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["Drug_ID","Drug_Name","Synonyms","Drug_Type","DrugBank_ID","DrugBank_Description","PubChem_ID","CasNo","Repositioning for NAFLD","SMILES","InChiKey","Molecular_Weight","DrugBank_Targets","DrugBank_MoA","DrugBank_Pharmacology","DrugBank_Indication","Targets","Therapeutic_Category","Clinical_Trial_Progress","Latest_Progress","Update"]
[1,"Acarbose",null,"Chemical drug","DB00284","Acarbose is a complex oligosaccharide that acts as an inhibitor of several enzymes responsible for the breakdown of complex carbohydrates in the intestines. It inhibits both pancreatic alpha-amylase and membrane-bound alpha-glucosidases - including intestinal glucoamylase, sucrase, maltase, and isomaltase - which are responsible for the metabolism of complex starches and oligo-, tri-, and disaccharides into absorbable simple sugars. By inhibiting the activity of these enzymes, acarbose limits the absorption of dietary carbohydrates and the subsequent postprandial increase in blood glucose and insulin levels. Acarbose is therefore used in conjunction with diet, exercise, and other pharmacotherapies for the management of blood sugar levels in patients with type 2 diabetes.\r\n\r\nAcarbose is one of only two approved alpha-glucosidase inhibitors (the other being ), receiving its first FDA approval in 1995 under the brand name Precose (since discontinued). This class of antidiabetic therapy is not widely used due to their relatively modest impact on A1c, their requirement for thrice-daily dosing, and the potential for significant gastrointestinal adverse effects.","41774","56180-94-0",true,"O([C@@H]1[C@@H](CO)O[C@@H]([C@@H]([C@H]1O)O)O[C@@H]([C@@H]([C@H](C=O)O)O)[C@@H](CO)O)[C@@H]1[C@H](O)[C@@H](O)[C@@H]([C@H](O1)C)N[C@H]1C=C(CO)[C@H]([C@@H]([C@H]1O)O)O","CEMXHAPUFJOOSV-XGWNLRGSSA-N",645.608,"Maltase-glucoamylase, intestinal inhibitor; Sucrase-isomaltase, intestinal inhibitor; Pancreatic alpha-amylase inhibitor; Lysosomal alpha-glucosidase inhibitor","Alpha-glucosidase enzymes are located in the brush-border of the intestinal mucosa and serve to metabolize oligo-, tri-, and disaccharides (e.g. sucrose) into smaller monosaccharides (e.g. glucose, fructose) which are more readily absorbed. These work in conjunction with pancreatic alpha-amylase, an enzyme found in the intestinal lumen that hydrolyzes complex starches to oligosaccharides.\r\n\r\nAcarbose is a complex oligosaccharide that competitively and reversibly inhibits both pancreatic alpha-amylase and membrane-bound alpha-glucosidases - of the alpha-glucosidases, inhibitory potency appears to follow a rank order of glucoamylase > sucrase > maltase > isomaltase. By preventing the metabolism and subsequent absorption of dietary carbohydrates, acarbose reduces postprandial blood glucose and insulin levels.","Acarbose is a complex oligosaccharide that competitively inhibits the ability of brush-border alpha-glucosidase enzymes to break down ingested carbohydrates into absorbable monosaccharides, reducing carbohydrate absorption and subsequent postprandial insulin levels. Acarbose requires the co-administration of carbohydrates in order to exert its therapeutic effect, and as such should be taken with the first bite of a meal three times daily.\r\n\r\nGiven its mechanism of action, acarbose in isolation poses little risk of contributing to hypoglycemia - this risk is more pronounced, however, when acarbose is used in conjunction with other antidiabetic therapies (e.g. sulfonylureas, insulin). Patients maintained on acarbose in addition to other antidiabetic agents should be aware of the symptoms and risks of hypoglycemia and how to treat hypoglycemic episodes. There have been rare post-marketing reports of the development of pneumatosis cystoides intestinalis following treatment with alpha-glucosidase inhibitors - patients experiencing significant diarrhea/constipation, mucus discharge, and/or rectal bleeding should be investigated and, if pneumatosis cystoides intestinalis is suspected, should discontinue therapy.","Acarbose is indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus.","MGAM inhibitor;AMY2A inhibitor; AMY2B inhibitor; GAA inhibitor","Improve insulin resistance","Phase 2 terminated (NCT00677521: Poor recruitment and no student currently interested in working on this project.)","Under clinical trials","2022-03-21"]
[2,"Acetaminophen","4-(Acetylamino)phenol; 4-acetamidophenol; 4'-hydroxyacetanilide; Acenol; Acetaminophen; APAP; N-acetyl-p-aminophenol; p-acetamidophenol; p-acetaminophenol; p-Acetylaminophenol; p-hydroxy-acetanilid; p-hydroxyacetanilide; p-hydroxyphenolacetamide","Chemical drug","DB00316","Acetaminophen (paracetamol), also commonly known as _Tylenol_, is the most commonly taken analgesic worldwide and is recommended as first-line therapy in pain conditions by the World Health Organization (WHO). It is also used for its antipyretic effects, helping to reduce fever. This drug was initially approved by the U.S. FDA in 1951 and is available in a variety of forms including syrup form, regular tablets, effervescent tablets, injection, suppository, and other forms.\r\n\r\nAcetaminophen is often found combined with other drugs in more than 600 over the counter (OTC) allergy medications, cold medications, sleep medications, pain relievers, and other products. Confusion about dosing of this drug may be caused by the availability of different formulas, strengths, and dosage instructions for children of different ages. Due to the possibility of fatal overdose and liver failure associated with the incorrect use of acetaminophen, it is important to follow current and available national and manufacturer dosing guidelines while this drug is taken or prescribed.","1983","103-90-2",true,"N(C(=O)C)c1ccc(cc1)O","RZVAJINKPMORJF-UHFFFAOYSA-N",151.165,"Prostaglandin E synthase 3 inhibitor; Prostaglandin G/H synthase 2 inhibitor; Prostaglandin G/H synthase 1 inhibitor; Transient receptor potential cation channel subfamily V member 1 activator","According to its FDA labeling, acetaminophen's exact mechanism of action has not been fully established - despite this, it is often categorized alongside NSAIDs (nonsteroidal anti-inflammatory drugs) due to its ability to inhibit the cyclooxygenase (COX) pathways. It is thought to exert central actions which ultimately lead to the alleviation of pain symptoms.\r\n\r\nOne theory is that acetaminophen increases the pain threshold by inhibiting two isoforms of cyclooxygenase, COX-1 and COX-2, which are involved in prostaglandin (PG) synthesis. Prostaglandins are responsible for eliciting pain sensations. Acetaminophen does not inhibit cyclooxygenase in peripheral tissues and, therefore, has no peripheral anti-inflammatory effects. Though acetylsalicylic acid (aspirin) is an irreversible inhibitor of COX and directly blocks the active site of this enzyme, studies have shown that acetaminophen (paracetamol) blocks COX indirectly. Studies also suggest that acetaminophen selectively blocks a variant type of the COX enzyme that is unique from the known variants COX-1 and COX-2. This enzyme has been referred to as _COX-3_. The antipyretic actions of acetaminophen are likely attributed to direct action on heat-regulating centers in the brain, resulting in peripheral vasodilation, sweating, and loss of body heat. The exact mechanism of action of this drug is not fully understood at this time, but future research may contribute to deeper knowledge.","Animal and clinical studies have determined that acetaminophen has both antipyretic and analgesic effects. This drug has been shown to lack anti-inflammatory effects. As opposed to the _salicylate_ drug class, acetaminophen does not disrupt tubular secretion of uric acid and does not affect acid-base balance if taken at the recommended doses. Acetaminophen does not disrupt hemostasis and does not have inhibitory activities against platelet aggregation. Allergic reactions are rare occurrences following acetaminophen use.","In general, acetaminophen is used for the treatment of mild to moderate pain and reduction of fever. It is available over the counter in various forms, the most common being oral forms.\r\n\r\nAcetaminophen _injection_ is indicated for the management of mild to moderate pain, the management of moderate to severe pain with adjunctive opioid analgesics, and the reduction of fever.\r\n\r\nBecause of its low risk of causing allergic reactions, this drug can be administered in patients who are intolerant to salicylates and those with allergic tendencies, including bronchial asthmatics. Specific dosing guidelines should be followed when administering acetaminophen to children.","PTGES3 inhibitor; TRPV1 activator","Antipyretic drug; non-narcotic analgesic","Clinical trial withdrawn (NCT02194894: (No patients enrolled)","Under clinical trials","2022-03-21"]
[3,"Acipimox",null,"Chemical drug","DB09055","Acipimox is a niacin derivative used as a hypolipidemic agent. It is used in low doses and may have less marked adverse effects, although it is unclear whether the recommended dose is as effective as are standard doses of nicotinic acid. Acipimox inhibits the production of triglycerides by the liver and the secretion of VLDL, which leads indirectly to a modest reduction in LDL and increase in HDL. Long-term administration is associated with reduced mortality, but unwanted effects limit its clinical use. Adverse effects include flushing (associated with Prostaglandin D2), palpitations, and GI disturbances. Flushing can be reduced by taking aspirin 20-30 min before taking Acipimox. High doses can cause disorders of liver function, impair glucose tolerance and precipitate gout.","5310993","51037-30-0",true,"C(=O)(O)c1cn(=O)c(cn1)C","DJQOOSBJCLSSEY-UHFFFAOYSA-N",154.125,null,"Acipimox inhibits the production of triglycerides by the liver and the secretion of VLDL, which leads indirectly to a modest reduction in LDL and increase in HDL.",null,"Used in the treatment of hyperlipidemias (abnormally elevated levels of any or all lipids and/or lipoproteins in the blood).","ADA inhibitor; TAG modulator","Hypolipidemic drug","Clinical trial on-going (ChiCTR-IPR-17012342)","Under clinical trials","2022-03-21"]
[5,"Aldafermin","NGM282; (phe5>met,ser6>arg,ala8>ser,gly9>ser,his11>leu) fibroblast growth factor 19 (human fgf19) (5-194)-peptide, produced in escherichia coli; Aldafermin; Engineered variant of recombinant human fibroblast growth factor 19","Biological drug","DB16086","Aldafermin is under investigation in clinical trial NCT03912532 (Evaluation of Efficacy, Safety and Tolerability of Aldafermin in a Phase 2b, Randomized, Double-blind, Placebo-controlled, Multi-center Study in Subjects With Nonalcoholic Steatohepatitis and Stage 2/3 Fibrosis (ALPINE 2/3)).",null,"1616639-03-2",false,{"$nulls":7},"FGF19 analog","Anti-fibrosis","Phase 2 completed (In a phase 2 trial of patients with NASH, aldafermin reduced liver fat and produced a trend toward fibrosis improvement. ClinicalTrials.gov, Number: NCT02443116.)","Under clinical trials","2022-03-21"]
[6,"Allopurinol","1,5-Dihydro-4H-pyrazolo(3,4-d)pyrimidin-4-one; 1,5-Dihydro-4H-pyrazolo(3,4-d)pyrimidine-4-one; 1H-Pyrazolo(3,4-d)pyrimidin-4-ol; 4-HPP; 4-Hydroxy-1H-pyrazolo(3,4-d)pyrimidine; 4-Hydroxy-3,4-pyrazolopyrimidine; 4-Hydroxypyrazolo(3,4-d)pyrimidine; 4-Hydroxypyrazolopyrimidine; 4-Hydroxypyrazolyl(3,4-d)pyrimidine; 4'-Hydroxypyrazolol(3,4-d)pyrimidine; 4H-Pyrazolo(3,4-d)pyrimidin-4-one; Allopurinol","Chemical drug","DB00437","Gout is a disease that occurs by the deposition of monosodium urate crystals (MSU) in body tissues, especially around joints .  This disease has been well-documented in historical medical records and appears in the biographies of several prominent, historically recognized individuals .\r\n\r\nAllopurinol is a xanthine oxidase enzyme inhibitor that is considered to be one of the most effective drugs used to decrease urate levels and is frequently used in the treatment of chronic gout . It was initially approved by the FDA in 1966  and is now formulated by several manufacturers .","135401907","315-30-0",true,"O=c1c2c(nc[nH]1)[nH]nc2","OFCNXPDARWKPPY-UHFFFAOYSA-N",136.114,"Xanthine dehydrogenase/oxidase inhibitor","Allopurinol is a structural analog of the natural purine base, hypoxanthine.  After ingestion, allopurinol is metabolized to its active metabolite, oxypurinol (_alloxanthine_) in the liver , which acts as an inhibitor of xanthine oxidase enzyme . \r\n\r\nAllopurinol and its active metabolite inhibit xanthine oxidase, the enzyme that converts hypoxanthine to xanthine and xanthine to uric acid. Inhibition of this enzyme is responsible for the effects of allopurinol. This drug increases the reutilization of hypoxanthine and xanthine for nucleotide and nucleic acid synthesis by a process that involves the enzyme hypoxanthine-guanine phosphoribosyltransferase (HGPRTase).  This process results in an increased nucleotide concentration, which causes feedback inhibition of de novo purine synthesis. The end result is decreased urine and serum uric acid concentrations , which decreases the incidence of gout symptoms. \r\n\r\nAccompanying the reduction of serum uric acid by allopurinol is an increase in the serum and urine concentrations of hypoxanthine and xanthine (due to inhibition of xanthine oxidase).  In the absence of allopurinol, regular urinary excretion of oxypurines almost entirely occurs in the form of uric acid. After the ingestion of allopurinol, the contents of excreted urine are hypoxanthine, xanthine, and uric acid. Because each substance has its own individual solubility, the concentration of uric acid in plasma is decreased without exposing the renal tissues to a high load of uric acid, thereby decreasing the risk of crystalluria. By lowering the uric acid concentration in the plasma below its limits of solubility, allopurinol encourages the dissolution of gout tophi. Although the levels of hypoxanthine and xanthine are found to be increased after allopurinol ingestion, the risk of deposition in renal tissues is less than that of uric acid, as they become more soluble and are rapidly excreted by the kidney .","Allopurinol decreases the production of uric acid by stopping the biochemical reactions that precede its formation .  This process decreases urate and relieves the symptoms of gout, which may include painful tophi, joint pain, inflammation, redness, decreased range of motion, and swelling .","Allopurinol is indicated in :\r\n\r\n1) the management of patients with signs and symptoms of primary or secondary gout (acute attacks, tophi, joint destruction, uric acid lithiasis, and/or nephropathy).\r\n\r\n2) the management of patients with leukemia, lymphoma and malignancies who are receiving cancer therapy which causes elevations of serum and urinary uric acid levels. Treatment with allopurinol should be discontinued when the potential for overproduction of uric acid is no longer present.\r\n\r\n3) the management of patients with recurrent calcium oxalate calculi whose daily uric acid excretion exceeds 800 mg/day in male patients and 750 mg/day in female patients. Therapy in such patients should be carefully assessed initially and reassessed periodically to determine in each case that treatment is beneficial and that the benefits outweigh the risks.","XO inhibitor",null,"Phase 3 on-going (IRCT20180404039187N2)","Under clinical trials","2022-03-21"]
[7,"Alpha-lipoic acid","(+)-alpha-Lipoic acid; (R)-(+)-Lipoate; (R)-(+)-lipoic acid; (R)-1,2-Dithiolane-3-pentanoic acid; (R)-1,2-dithiolane-3-valeric acid; (R)-6,8-thioctic acid; (R)-lipoic acid; Alpha lipoic acid; alpha-Lipoic acid; D-thioctic acid; Lipoic acid; R-(+)-thioctic acid; R-alpha-lipoic acid; Thioctic acid; Thioctic acid D-form; α-lipoic acid","Chemical drug","DB00166","A vitamin-like antioxidant.","6122","1200-22-2",true,"C(CCCC(=O)O)[C@@H]1CCSS1","AGBQKNBQESQNJD-SSDOTTSWSA-N",206.332,"Lipoyltransferase 1, mitochondrial; Lipoyl synthase, mitochondrial; Sodium-dependent multivitamin transporter","Lipoic Acid is generally involved in oxidative decarboxylations of keto acids and is presented as a growth factor for some organisms. Lipoic acid exists as two enantiomers, the R-enantiomer and the S-enantiomer. Normally only the R-enantiomer of an amino acid is biologically active, but for lipoic acid the S-enantiomer assists in the reduction of the R-enantiomer when a racemic mixture is given. Some recent studies have suggested that the S-enantiomer in fact has an inhibiting effect on the R-enantiomer, reducing its biological activity substantially and actually adding to oxidative stress rather than reducing it. Furthermore, the S-enantiomer has been found to reduce the expression of GLUT-4s in cells, responsible for glucose uptake, and hence reduce insulin sensitivity.","Lipoic acid (or &alpha;-lipoic acid) is able to pass the blood-brain barrier and is putatively used for detoxification of mercury attached to the brain cells. It can mobilise bound mercury into the blood stream as it is a mercaptan (sulfur compound which readily binds to the mercury). In the blood stream, another chelator such as dimercaptosuccinic acid (DMSA) or methylsulfonylmethane (MSM) is used to transfer mercury safely into the urine for excretion. Neither DMSA nor MSM can cross the blood-brain barrier, which is why both lipoic acid and DMSA are used. It is hypothesized that this treatment-along with carnitine, dimethylglycine (DMG), Vitamin B6, folic acid, and magnesium&mdash;could be used to treat autism and amalgam poisoning. In this hypothesis, the reason why autism is difficult to treat is that mercury is attached to the brain cells and most medicines and vitamin supplements do not penetrate the blood-brain barrier. However, &alpha;-lipoic acid and perhaps vitamin B12 could making it possible for other chelators to remove mercury safely out of the body and could perhaps one day be used as a treatment for autism. Because lipoic acid is related to cellular uptake of glucose and it is both soluble in water and fat, it is being used for treatment in diabetes. It may be helpful for people with Alzheimer's disease or Parkinson's disease.","For nutritional supplementation, also for treating dietary shortage or imbalance.","LIPT1","Antioxidant drug","Phase 4 on-going (NCT04475276)","Under clinical trials","2022-03-21"]
[8,"Alpha-tocopherol","(+)-α-tocopherol; (2R,4'R,8'R)-α-tocopherol; (R,R,R)-α-tocopherol; 5,7,8-trimethyltocol; alpha-tocopherol; d-α-tocopherol","Chemical drug","DB00163","In 1922, vitamin E was demonstrated to be an essential nutrient. Vitamin E is a term used to describe 8 different fat soluble tocopherols and tocotrienols, alpha-tocopherol being the most biologically active. Vitamin E acts as an antioxidant, protecting cell membranes from oxidative damage. The antioxidant effects are currently being researched for use in the treatment of diseases causing bone loss, cardiovascular diseases, diabetes mellitus and associated comorbidities, eye diseases, inflammatory diseases (including skin conditions), lipid disorders, neurological diseases, and radiation damage. Though this research is so far inconclusive, vitamin E remains a popular supplement and is generally considered safe by the FDA.","14985","59-02-9",true,"Cc1c2c(CC[C@](O2)(CCC[C@@H](CCC[C@@H](CCCC(C)C)C)C)C)c(c(c1C)O)C","GVJHHUAWPYXKBD-IEOSBIPESA-N",430.717,"Nuclear receptor subfamily 1 group I member 2; Protein kinase C beta type; Arachidonate 5-lipoxygenase; Protein kinase C alpha type; Diacylglycerol kinase alpha; Serine/threonine-protein phosphatase 2A catalytic subunit beta isoform; Serine/threonine-prot","The mechanism of action for most of vitamin E's effects are still unknown. Vitamin E is an antioxidant, preventing free radical reactions with cell membranes. Though in some cases vitamin E has been shown to have pro-oxidant activity.\r\n\r\nOne mechanism of vitamin E's antioxidant effect is in the termination of lipid peroxidation. Vitamin E reacts with unstable lipid radicals, producing stable lipids and a relatively stable vitamin E radical. The vitamin E radical is then reduced back to stable vitamin E by reaction with ascorbate or glutathione.","Vitamin E is a collective term used to describe 8 separate fat soluble antioxidants, most commonly alpha-tocopherol. Vitamin E acts to protect cells against the effects of free radicals, which are potentially damaging by-products of the body's metabolism. Vitamin E deficiency is seen in persons with abetalipoproteinemia, premature, very low birth weight infants (birth weights less than 1500 grams, or 3&frac12; pounds), cystic fibrosis, and cholestasis and severe liver disease. Preliminary research suggests vitamin E may help prevent or delay coronary heart disease and protect against the damaging effects of free radicals, which may contribute to the development of chronic diseases such as cancer. It also protects other fat-soluble vitamins (A and B group vitamins) from destruction by oxygen. Low levels of vitamin E have been linked to increased incidence of breast and colon cancer.","Vitamin E supplementation is indicated for treatment of vitamin E deficiency which can occur in cystic fibrosis, cholestasis and severe liver disease, abetalipoproteinemia or simply poor diet.","NR1I2; ALOX5; DGKA",null,"Phase 2 on-going (SLCTR/2019/038)","Under clinical trials","2022-03-21"]
[9,"ALS-L1023",null,"Chemical drug",{"$nulls":3},"141-78-6, 8014-71-9",false,"O(C(=O)C)CC","XEKOWRVHYACXOJ-UHFFFAOYSA-N",88.106,{"$nulls":4},"PPARA / Angiogenesis","Anti-inflammatory","Phase 2 on-going (NCT04342793)","Under clinical trials","2022-03-21"]
[10,"Amoxicillin","(2S,5R,6R)-6-{[(2R)-2-amino-2-(4-hydroxyphenyl)acetyl]amino}-3,3-dimethyl-7-oxo-4-thia-1-azabicyclo[3.2.0]heptane-2-carboxylic acid; 6-(p-hydroxy-α-aminophenylacetamido)penicillanic acid; Amox; Amoxicillin; Amoxicillin (anhydrous); Amoxicillin anhydrous; Amoxycillin; AX; p-Hydroxyampicillin; α-amino-p-hydroxybenzylpenicillin","Chemical drug","DB01060","Amoxicillin, or BRL-2333, is a penicillin G derivative first described in the literature in 1972. Amoxicillin has similar activity to  and , but leads to higher serum concentrations than ampicillin.\r\n\r\nAmoxicillin was granted FDA approval on 18 January 1974.","33613","26787-78-0",true,"C(=O)(O)[C@@H]1N2[C@H](SC1(C)C)[C@@H](C2=O)NC(=O)[C@H](N)c1ccc(cc1)O","LSQZJLSUYDQPKJ-NJBDSQKTSA-N",365.411,"Penicillin binding protein inhibitor","Amoxicillin competitively inhibits penicillin-binding protein 1 and other high molecular weight penicillin binding proteins.  Penicillin bind proteins are responsible for glycosyltransferase and transpeptidase reactions that lead to cross-linking of D-alanine and D-aspartic acid in bacterial cell walls. Without the action of penicillin binding proteins, bacteria upregulate autolytic enzymes and are unable to build and repair the cell wall, leading to bacteriocidal action.","Amoxicillin competitively inhibit penicillin binding proteins, leading to upregulation of autolytic enzymes and inhibition of cell wall synthesis. Amoxicillin has a long duration of action as it is usually given twice daily. Amoxicillin has a wide therapeutic range as mild overdoses are not associated with significant toxicity. Patients should be counselled regarding the risk of anaphylaxis, _Clostridium difficile_ infections, and bacterial resistance.","Amoxicillin alone is indicated to treat susceptible bacterial infections of the ear, nose, throat, genitourinary tract, skin, skin structure, and lower respiratory tract. Amoxicillin is given with calvulanic acid to treat acute bacterial sinusitis, community acquired pneumonia, lower respiratory tract infections, acute bacterial otitis media, skin and skin structure infections, and urinary tract infections. Amoxicillin is given with omeprazole in the treatment of _H. pylori_.",null,null,"Phase 2 completed  (NCT01876108)","Under clinical trials","2022-03-21"]
[11,"Anthocyanin",null,"Chemical drug",null,null,"145858","11029-12-2",false,"[o+]1c(c2ccccc2)ccc2c1cccc2","NWKFECICNXDNOQ-UHFFFAOYSA-N",207.252,{"$nulls":5},"Anti-inflammatory","Early phase 1 completed (NCT01940263:  Compared to controls, the anthocyanin group exhibited significant decreases (P < 0.05, all comparisons) in plasma alanine aminotransferase (-19.1% vs 3.1%), cytokeratin-18 M30 fragment (-8.8% vs 5.6%) and myeloperoxidase (-75.0% vs -44.8%). Significant decreases from baseline in fasting blood glucose and homeostasis model assessment for insulin resistance were observed in the anthocyanin group; however, these differences were not significant relative to placebo controls.)","Failed in clinical trials","2022-03-21"]
[12,"Apararenone","MT-3995","Chemical drug","DB15024","Apararenone is under investigation in clinical trial NCT02531568 (Drug Interaction Study of Warfarin and MT-3995).","24744336  ","945966-46-1",false,"O=C1N(c2c(OC1(C)C)cc(cc2)NS(=O)(=O)C)c1ccc(cc1)F","AZNHWXAFPBYFGH-UHFFFAOYSA-N",364.398,{"$nulls":4},"Aldosterone receptor","Improve insulin resistance","Phase 2 completed (NCT02923154)","Under clinical trials","2022-03-21"]
[13,"Aramchol",null,"Chemical drug","DB11860","Aramchol has been used in trials studying the treatment of HIV, Gallstones, Fatty Liver, Metabolic Syndrome, and Nonalcoholic Steatohepatitis, among others.","18738120","246529-22-6",false,"O[C@H]1[C@@H]2[C@@H]([C@@]3([C@H](C1)C[C@H](CC3)NC(=O)CCCCCCCCCCCCCCCCCCC)C)C[C@@H]([C@]1([C@H]2CC[C@@H]1[C@@H](CCC(=O)O)C)C)O","SHKXZIQNFMOPBS-OOMQYRRCSA-N",702.118,{"$nulls":4},"SCD-1","Enhance lipid metabolism","Phase 3 on-going (NCT04104321)","Under clinical trials","2022-03-21"]
[14,"ARI-3037MO",null,"Biological drug",{"$nulls":3},"2166482-73-9",false,{"$nulls":7},"GPR109A receptor agonist; GPR109B receptor agonist; Nicotinic acid analog",null,"Phase 2 on-going (NCT02574325)","Under clinical trials","2022-03-21"]
[15,"ARO-HSD",null,"Biological drug",{"$nulls":4},false,{"$nulls":7},"HSD17B13 inhibitor","Hepatoprotectants","Phase 1 completed (NCT04202354)","Under clinical trials","2022-03-21"]
[16,"Artichoke","Artichoke Leaf Extract; Cynara Scolymus L.","Biological extract","DB10638","Artichoke allergenic extract is used in allergenic testing.",null,"84012-14-6",true,{"$nulls":9},"Phase 2 on-going (IRCT20130126012278N3)","Under clinical trials","2022-03-21"]
[17,"ASP9831",null,"Miscellany",{"$nulls":4},false,{"$nulls":7},"PDE4 inhibitor",null,"Phase 2 completed (NCT00668070)","Under clinical trials","2022-03-21"]
[18,"Aspirin","2-Acetoxybenzenecarboxylic acid; 2-Acetoxybenzoic acid; Acetylsalicylate; ASA; Aspirin; o-acetoxybenzoic acid; O-acetylsalicylic acid; o-carboxyphenyl acetate; Salicylic acid acetate","Chemical drug","DB00945","Also known as _Aspirin_, acetylsalicylic acid (ASA) is a commonly used drug for the treatment of pain and fever due to various causes. Acetylsalicylic acid has both anti-inflammatory and antipyretic effects.  This drug also inhibits platelet aggregation and is used in the prevention of blood clots stroke, and myocardial infarction (MI) .  \r\n\r\nInterestingly, the results of various studies have demonstrated that long-term use of acetylsalicylic acid may decrease the risk of various cancers, including colorectal, esophageal, breast, lung, prostate, liver and skin cancer . Aspirin is classified as a _non-selective cyclooxygenase (COX) inhibitor_  and is available in many doses and forms, including chewable tablets, suppositories, extended release formulations, and others . \r\n\r\nAcetylsalicylic acid is a very common cause of accidental poisoning in young children. It should be kept out of reach from young children, toddlers, and infants .","2244","50-78-2",true,"C(=O)(O)c1c(OC(=O)C)cccc1","BSYNRYMUTXBXSQ-UHFFFAOYSA-N",180.159,"Prostaglandin G/H synthase 1 inhibitor; Prostaglandin G/H synthase 2 inhibitor; Aldo-keto reductase family 1 member C1 inhibitor; 5'-AMP-activated protein kinase activator; Endothelin-1 receptor inhibitor; Cellular tumor antigen p53 inducer; 78 kDa glucos","Acetylsalicylic acid (ASA) blocks prostaglandin synthesis. It is non-selective for COX-1 and COX-2 enzymes . Inhibition of COX-1 results in the inhibition of platelet aggregation for about 7-10 days (average platelet lifespan). The acetyl group of acetylsalicylic acid binds with a serine residue of the cyclooxygenase-1 (COX-1) enzyme, leading to irreversible inhibition. This prevents the production of pain-causing prostaglandins. This process also stops the conversion of arachidonic acid to thromboxane A2 (TXA2), which is a potent inducer of platelet aggregation .  Platelet aggregation can result in clots and harmful venous and arterial thromboembolism, leading to conditions such as pulmonary embolism and stroke. \r\n\r\nIt is important to note that there is 60% homology between the protein structures of COX-1 and COX-2. ASA binds to serine 516 residue on the active site of COX-2 in the same fashion as its binding to the serine 530 residue located on the active site of COX-1. The active site of COX-2 is, however, slightly larger than the active site of COX-1, so that arachidonic acid (which later becomes prostaglandins) manages to bypass the aspirin molecule inactivating COX-2 .  ASA, therefore, exerts more action on the COX-1 receptor rather than on the COX-2 receptor . A higher dose of acetylsalicylic acid is required for COX-2 inhibition .","**Effects on pain and fever**\r\n\r\nAcetylsalicylic acid disrupts the production of prostaglandins throughout the body by targeting cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) . Prostaglandins are potent, irritating substances that have been shown to cause headaches and pain upon injection into humans.  Prostaglandins increase the sensitivity of pain receptors and substances such as histamine and bradykinin. Through the disruption of the production and prevention of release of prostaglandins in inflammation, this drug may stop their action at pain receptors, preventing symptoms of pain. Acetylsalicylic acid is considered an antipyretic agent because of its ability to interfere with the production of brain prostaglandin E1. Prostaglandin E1 is known to be an extremely powerful fever-inducing agent . \r\n\r\n**Effects on platelet aggregation**\r\n\r\nThe inhibition of platelet aggregation by ASA occurs because of its interference with thromboxane A2 in platelets, caused by COX-1 inhibition. Thromboxane A2 is an important lipid responsible for platelet aggregation, which can lead to clot formation and future risk of heart attack or stroke  . \r\n\r\n**A note on cancer prevention**\r\n\r\nASA has been studied in recent years to determine its effect on the prevention of various malignancies . In general, acetylsalicylic acid is involved in the interference of various cancer signaling pathways, sometimes inducing or upregulating tumor suppressor genes . Results of various studies suggest that there are beneficial effects of long-term ASA use in the prevention of several types of cancer, including stomach, colorectal, pancreatic, and liver cancers .   Research is ongoing.","**Pain, fever, and inflammation**\r\n\r\nAcetylsalicylic acid (ASA), in the regular tablet form (immediate-release), is indicated to relieve pain, fever, and inflammation associated with many conditions, including the flu, the common cold, neck and back pain, dysmenorrhea, headache, tooth pain, sprains, fractures, myositis, neuralgia, synovitis, arthritis, bursitis, burns, and various injuries. It is also used for symptomatic pain relief after surgical and dental procedures . \r\n\r\nThe _extra strength_ formulation of acetylsalicylic acid is also indicated for the management migraine pain with photophobia (sensitivity to light) and phonophobia (sensitivity to sound).\r\n\r\n**Other indications**\r\n\r\nASA is also indicated for various other purposes, due to its ability to inhibit platelet aggregation. These include: \r\n\r\nReducing the risk of cardiovascular death in suspected cases of myocardial infarction (MI) . \r\n\r\nReducing the risk of a first non-fatal myocardial infarction in patients, and for reducing the risk of morbidity and mortality in cases of unstable angina and in those who have had a prior myocardial infarction .\r\n\r\nFor reducing the risk of transient ischemic attacks (TIA) and to prevent atherothrombotic cerebral infarction (in conjunction with other treatments) .\r\n\r\nFor the prevention of thromboembolism after hip replacement surgery . \r\n\r\nFor decreasing platelet to platelet adhesion following carotid endarterectomy, aiding in the prevention of transient ischemic attacks (TIA) .\r\n\r\nUsed for patients undergoing hemodialysis with a silicone rubber arteriovenous cannula inserted to prevent thrombosis at the insertion site . \r\n\r\n**Important note regarding use of the extended-release formulation **\r\n\r\nIn the setting of acute myocardial infarction, or before percutaneous interventions, the extended-release form of acetylsalicylic acid should not be used. Use immediate-release formulations in scenarios requiring rapid onset of action . The extended-release form is taken to decrease the incidence of mortality and myocardial infarction (MI) for individuals diagnosed with chronic coronary artery disease (CAD), including patients with previous myocardial infarction (MI) or unstable angina or with chronic stable angina. Additionally, the extended-release form is used to decrease the risk of death and recurrent episodes of stroke in patients with a history of stroke or TIA .\r\n\r\n\r","AKR1C1 inhibitor; PCNA downregulator","Enhance lipid metabolism","Phase 1&2 on-going (NCT04031729)","Under clinical trials","2022-03-21"]
[19,"Astaxanthin",null,"Chemical drug","DB06543","Astaxanthin is a keto-carotenoid in the terpenes class of chemical compounds. It is classified as a xanthophyll but it is a carotenoid with no vitamin A activity. It is found in the majority of aquatic organisms with red pigment. Astaxanthin has shown to mediate anti-oxidant and anti-inflammatory actions. It may be found in fish feed or some animal food as a color additive.","5281224","472-61-7",false,"C(=C\\C(=C\\C=C\\C(=C\\C=C\\C=C(\\C=C\\C=C(\\C=C\\C1=C(C)C(=O)[C@H](CC1(C)C)O)/C)/C)\\C)\\C)/C1=C(C)C(=O)[C@H](CC1(C)C)O","MQZIGYBFDRPAKN-UWFIBFSHSA-N",596.852,"NF-kappa-B inhibitor alpha",null,null,"Investigated for use/treatment in eye disorders/infections, cancer/tumors (unspecified), and asthma.",null,null,"Clinical trial on-going (JPRN-UMIN000008524)","Under clinical trials","2022-03-21"]
[20,"Atorvastatin","Atorvastatin","Chemical drug","DB01076","Atorvastatin (Lipitor®), is a lipid-lowering drug included in the statin class of medications. By inhibiting the endogenous production of cholesterol in the liver, statins lower abnormal cholesterol and lipid levels, and ultimately reduce the risk of cardiovascular disease. More specifically, statin medications competitively inhibit the enzyme hydroxymethylglutaryl-coenzyme A (HMG-CoA) Reductase, which catalyzes the conversion of HMG-CoA to mevalonic acid. This conversion is a critical metabolic reaction involved in the production of several compounds involved in lipid metabolism and transport, including cholesterol, low-density lipoprotein (LDL) (sometimes referred to as \"bad cholesterol\"), and very-low-density lipoprotein (VLDL). Prescribing statins is considered standard practice for patients following any cardiovascular event, and for people who are at moderate to high risk of developing cardiovascular disease. The evidence supporting statin use, coupled with minimal side effects and long term benefits, has resulted in wide use of this medication in North America.\r\n\r\nAtorvastatin and other statins including , , , , and  are considered first-line treatment options for dyslipidemia. The increasing use of this class of drugs is largely attributed to the rise in cardiovascular diseases (CVD) (such as heart attack, atherosclerosis, angina, peripheral artery disease, and stroke) in many countries. An elevated cholesterol level (elevated low-density lipoprotein (LDL) levels in particular) is a significant risk factor for the development of CVD. Several landmark studies demonstrate that the use of statins is associated with both a reduction in LDL levels and CVD risk. Statins were shown to reduce the incidences of all-cause mortality, including fatal and non-fatal CVD, as well as the need for surgical revascularization or angioplasty following a heart attack. Some evidence has shown that even for low-risk individuals (with <10% risk of a major vascular event occurring within five years) statin use leads to a 20%-22% relative reduction in the number of major cardiovascular events (heart attack, stroke, coronary revascularization, and coronary death) for every 1 mmol/L reduction in LDL without any significant side effects or risks.\r\n\r\nAtorvastatin was first synthesized in 1985 by Dr. Bruce Roth and approved by the FDA in 1996. It is a pentasubstituted pyrrole  formed by two contrasting moieties with an achiral heterocyclic core unit and a 3,5-dihydroxypentanoyl side chain identical to its parent compound. Unlike other members of the statin group, atorvastatin is an active compound and therefore does not require activation.","60823","134523-00-5",true,"C(=O)(Nc1ccccc1)c1c(c(n(c1C(C)C)CC[C@H](C[C@H](CC(=O)O)O)O)c1ccc(cc1)F)c1ccccc1","XUKUURHRXDUEBC-KAYWLYCHSA-N",558.65,"3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor; Dipeptidyl peptidase 4 inhibitor; Aryl hydrocarbon receptor agonist; Histone deacetylase 2 inhibitor; Nuclear receptor subfamily 1 group I member 3 ligand","Atorvastatin is a statin medication and a competitive inhibitor of the enzyme HMG-CoA (3-hydroxy-3-methylglutaryl coenzyme A) reductase, which catalyzes the conversion of HMG-CoA to mevalonate, an early rate-limiting step in cholesterol biosynthesis. Atorvastatin acts primarily in the liver, where decreased hepatic cholesterol concentrations stimulate the upregulation of hepatic low-density lipoprotein (LDL) receptors, which increases hepatic uptake of LDL. Atorvastatin also reduces Very-Low-Density Lipoprotein-Cholesterol (VLDL-C), serum triglycerides (TG) and Intermediate Density Lipoproteins (IDL), as well as the number of apolipoprotein B (apo B) containing particles, but increases High-Density Lipoprotein Cholesterol (HDL-C). \r\n\r\n_In vitro_ and _in vivo_ animal studies also demonstrate that atorvastatin exerts vasculoprotective effects independent of its lipid-lowering properties, also known as the pleiotropic effects of statins. These effects include improvement in endothelial function, enhanced stability of atherosclerotic plaques, reduced oxidative stress and inflammation, and inhibition of the thrombogenic response. Statins were also found to bind allosterically to β2 integrin function-associated antigen-1 (LFA-1), which plays an essential role in leukocyte trafficking and T cell activation.","Atorvastatin is an oral antilipemic agent that reversibly inhibits HMG-CoA reductase. It lowers total cholesterol, low-density lipoprotein-cholesterol (LDL-C), apolipoprotein B (apo B), non-high density lipoprotein-cholesterol (non-HDL-C), and triglyceride (TG) plasma concentrations while increasing HDL-C concentrations. High LDL-C, low HDL-C and high TG concentrations in the plasma are associated with increased risk of atherosclerosis and cardiovascular disease. The total cholesterol to HDL-C ratio is a strong predictor of coronary artery disease, and high ratios are associated with a higher risk of disease. Increased levels of HDL-C are associated with lower cardiovascular risk. By decreasing LDL-C and TG and increasing HDL-C, atorvastatin reduces the risk of cardiovascular morbidity and mortality. \r\n\r\nElevated cholesterol levels (and high low-density lipoprotein (LDL) levels in particular) are an important risk factor for the development of CVD. Clinical studies have shown that atorvastatin reduces LDL-C and total cholesterol by 36-53%. In patients with dysbetalipoproteinemia, atorvastatin reduced the levels of intermediate-density lipoprotein cholesterol. It has also been suggested that atorvastatin can limit the extent of angiogenesis, which can be useful in the treatment of chronic subdural hematoma.\r\n\r\n**Myopathy/Rhabdomyolysis**\r\n\r\nAtorvastatin, like other HMG-CoA reductase inhibitors, is associated with a risk of drug-induced myopathy characterized by muscle pain, tenderness, or weakness in conjunction with elevated levels of creatine kinase (CK). Myopathy often manifests as rhabdomyolysis with or without acute renal failure secondary to myoglobinuria. The risk of statin-induced myopathy is dose-related, and the symptoms of myopathy are typically resolved upon drug discontinuation. Results from observational studies suggest that 10-15% of people taking statins may experience muscle aches at some point during treatment.\r\n\r\n**Liver Dysfunction**\r\n\r\nStatins, like some other lipid-lowering therapies, have been associated with biochemical abnormalities of liver function. Persistent elevations (> 3 times the upper limit of normal  occurring on two or more occasions) in serum transaminases occurred in 0.7% of patients who received atorvastatin in clinical trials. This effect appears to be dose-related.\r\n\r\n**Endocrine Effects**\r\n\r\nStatins are associated with a risk of increased serum HbA1c and glucose levels. An _in vitro_ study demonstrated a dose-dependent cytotoxic effect on human pancreatic islet β cells following treatment with atorvastatin. Moreover, insulin secretion rates decreased relative to control.\r\n\r\nHMG-CoA reductase inhibitors interfere with cholesterol synthesis and may theoretically interfere with the production of adrenal and/or gonadal steroids. Clinical studies with atorvastatin and other HMG-CoA reductase inhibitors have suggested that these agents do not affect plasma cortisol concentrations, basal plasma testosterone concentration, or adrenal reserve. However, the effect of statins on male fertility has not been fully investigated. The effects of statins on the pituitary-gonadal axis in premenopausal women are unknown.\r\n\r\n**Cardiovascular**\r\n\r\nSignificant decreases in circulating ubiquinone levels in patients treated with atorvastatin and other statins have been observed. The clinical significance of a potential long-term statin-induced deficiency of ubiquinone has not been established. It has been reported that a decrease in myocardial ubiquinone levels could lead to impaired cardiac function in patients with borderline congestive heart failure.\r\n\r\n**Lipoprotein A**\r\n\r\nIn some patients, the beneficial effect of lowered total cholesterol and LDL-C levels may be partly blunted by the concomitant increase in Lp(a) lipoprotein concentrations. Present knowledge suggests the importance of high Lp(a) levels as an emerging risk factor for coronary heart disease. Further studies have demonstrated statins affect Lp(a) levels differently in patients with dyslipidemia depending on their apo(a) phenotype; statins increase Lp(a) levels exclusively in patients with the low molecular weight apo(a) phenotype.","Atorvastatin is indicated for the treatment of several types of dyslipidemias, including primary hyperlipidemia and mixed dyslipidemia in adults, hypertriglyceridemia, primary dysbetalipoproteinemia, homozygous familial hypercholesterolemia, and heterozygous familial hypercholesterolemia in adolescent patients with failed dietary modifications.\r\n\r\nDyslipidemia describes an elevation of plasma cholesterol, triglycerides or both as well as to the presence of low levels of high-density lipoprotein. This condition represents an increased risk for the development of atherosclerosis. \r\n\r\nAtorvastatin is indicated, in combination with dietary modifications, to prevent cardiovascular events in patients with cardiac risk factors and/or abnormal lipid profiles.\r\n\r\nAtorvastatin can be used as a preventive agent for myocardial infarction, stroke, revascularization, and angina, in patients without coronary heart disease but with multiple risk factors and in patients with type 2 diabetes without coronary heart disease but multiple risk factors.\r\n\r\nAtorvastatin may be used as a preventive agent for non-fatal myocardial infarction, fatal and non-fatal stroke, revascularization procedures, hospitalization for congestive heart failure and angina in patients with coronary heart disease.\r\n\r\nPrescribing of statin medications is considered standard practice following any cardiovascular events and for people with a moderate to high risk of development of CVD. Statin-indicated conditions include diabetes mellitus, clinical atherosclerosis (including myocardial infarction, acute coronary syndromes, stable angina, documented coronary artery disease, stroke, trans ischemic attack (TIA), documented carotid disease, peripheral artery disease, and claudication), abdominal aortic aneurysm, chronic kidney disease, and severely elevated LDL-C levels.","DPP4 inhibitor; AHR agonist; HDAC2 inhibitor; NR1I3 ligand","Enhance lipid metabolism","Clinical trial on-going (TCTR20180425001)","Under clinical trials","2022-03-21"]
[21,"AXA1125","LIVRQNac","Combinatory",{"$nulls":4},false,{"$nulls":9},"Phase 2 on-going (NCT04880187); Clinical trial completed (NCT04073368: Both compositions showed multitargeted activity on relevant NAFLD pathways. AXA1125 demonstrated the greatest activity over 16 weeks, warranting continued clinical investigation in nonalcoholic steatohepatitis subjects.)","Under clinical trials","2022-03-21"]
[22,"AXA1957",null,"Miscellany",{"$nulls":4},false,{"$nulls":8},"Hepatoprotectants","Clinical trial completed (NCT04073368: Both compositions showed multitargeted activity on relevant NAFLD pathways. AXA1125 demonstrated the greatest activity over 16 weeks, warranting continued clinical investigation in nonalcoholic steatohepatitis subjects.)","Under clinical trials","2022-03-21"]
[23,"AZD4017",null,"Chemical drug","DB14875","AZD-4017 is under investigation in clinical trial NCT01173471 (A Phase IIa Study to Assess the Tolerability, Safety, and Efficacy of AZD4017 for Raised Intra-ocular Pressure).","24946280","1024033-43-9",false,"S(CCC)c1nc(ccc1C(=O)NC1CCCCC1)N1C[C@H](CC(=O)O)CCC1","NCDZABJPWMBMIQ-INIZCTEOSA-N",419.591,{"$nulls":4},"11B-HSD1 inhibitor",null,"Phase 2 terminated  (NCT02605616: Astra Zeneca notified Dr. Rita Basu that they will not manufacture new drug due to business reasons and study was stopped.)","Under clinical trials","2022-03-21"]
[24,"AZD4076",null,"Biological drug",{"$nulls":3},"1967845-94-8",false,{"$nulls":7},"miR-103 antagonist;miR-107 antagonist",null,"Phase 1 completed (NCT02826525)","Under clinical trials","2022-03-21"]
[25,"Azithromycin","Azithromycin","Chemical drug","DB00207","Azithromycin is a broad-spectrum macrolide antibiotic with a long half-life and a high degree of tissue penetration . It was initially approved by the FDA in 1991 .\r\n\r\nIt is primarily used for the treatment of respiratory, enteric and genitourinary infections and may be used instead of other macrolides for some sexually transmitted and enteric infections. It is structurally related to erythromycin .\r\n\r\nAzithromycin  is a part of the _azalide_ subclass of macrolides, and contains a 15-membered ring, with a methyl-substituted nitrogen instead of a carbonyl group at the 9a position on the aglycone ring, which allows for the prevention of its metabolism. This differentiates azithromycin from other types of macrolides .\r\n\r\nIn March 2020, a small study was funded by the French government to investigate the treatment of COVID-19 with a combination of azithromycin and the anti-malaria drug . The results were positive, all patients taking the combination were virologically cured within 6 days of treatment, however, larger studies are required.","447043","83905-01-5",true,"O([C@@H]1[C@@H](C)[C@H](O[C@H]2C[C@](OC)(C)[C@H]([C@@H](O2)C)O)[C@@H](C)C(=O)O[C@H](CC)[C@@]([C@@H]([C@H](N(C[C@@H](C[C@@]1(C)O)C)C)C)O)(C)O)[C@H]1[C@H](O)[C@@H](N(C)C)C[C@H](O1)C","MQTOSJVFKKJCRP-BICOPXKESA-N",748.996,"23S ribosomal RNA inhibitor; Protein-arginine deiminase type-4 inhibitor","In order to replicate, bacteria require a specific process of protein synthesis, enabled by ribosomal proteins . Azithromycin binds to the 23S rRNA of the bacterial 50S ribosomal subunit. It stops bacterial protein synthesis by inhibiting the transpeptidation/translocation step of protein synthesis and by inhibiting the assembly of the 50S ribosomal subunit , . This results in the control of various bacterial infections , .   The strong affinity of macrolides, including azithromycin, for bacterial ribosomes, is consistent with their broad‐spectrum antibacterial activities .\r\n\r\n\r\nAzithromycin is highly stable at a low pH, giving it a longer serum half-life and increasing its concentrations in tissues compared to erythromycin . \r\n\r","Macrolides stop bacterial growth by inhibiting protein synthesis and translation, treating bacterial infections .\r\nAzithromycin has additional immunomodulatory effects and has been used in chronic respiratory inflammatory diseases for this purpose .\r\n\r","Azithromycin should be used only to treat or prevent infections that are proven or strongly suspected to be caused by susceptible bacteria in order to prevent the development antimicrobial resistance and maintain the efficacy of azithromycin .\r\n\r\nAzithromycin is indicated for the treatment of patients with mild to moderate infections caused by susceptible strains of the microorganisms listed in the specific conditions below. Recommended dosages, duration of therapy and considerations for various patient populations may vary among these infections. Refer to the FDA label and \"Indications\" section of this drug entry for detailed information . \r\n\r\n**Adults**:\r\n\r\nAcute bacterial exacerbations of chronic obstructive pulmonary disease due to _Haemophilus influenzae_, _Moraxella catarrhalis_ or _Streptococcus pneumoniae_\r\n\r\nAcute bacterial sinusitis due to _Haemophilus influenzae_, _Moraxella catarrhalis_ or _Streptococcus pneumoniae_\r\n\r\nCommunity-acquired pneumonia due to _Chlamydophila pneumoniae_, _Haemophilus influenzae_, _Mycoplasma pneumoniae_ or _Streptococcus pneumoniae_ in patients appropriate for oral therapy\r\n\r\nPharyngitis/tonsillitis caused by _Streptococcus pyogenes_ as an alternative to first-line therapy in individuals who cannot use first-line therapy.\r\nUncomplicated skin and skin structure infections due to _Staphylococcus aureus_, _Streptococcus pyogenes_, or _Streptococcus agalactiae_. Abscesses usually require surgical drainage.\r\n\r\nUrethritis and cervicitis due to _Chlamydia trachomatis_ or _Neisseria gonorrhoeae_.\r\n\r\nGenital ulcer disease in men due to _Haemophilus ducreyi_ (chancroid). Due to the small number of women included in clinical trials, the efficacy of azithromycin in the treatment of chancroid in women has not been established.\r\n\r\n**Pediatric Patients**\r\n\r\nAcute otitis media caused by _Haemophilus influenzae_, _Moraxella catarrhalis_ or _Streptococcus pneumoniae_\r\n\r\nCommunity-acquired pneumonia due to _Chlamydophila pneumoniae_, _Haemophilus influenzae_, _Mycoplasma pneumoniae_ or _Streptococcus pneumoniae_ in patients appropriate for oral therapy.\r\n\r\nPharyngitis/tonsillitis caused by _Streptococcus pyogenes_ as an alternative to first-line therapy in individuals who cannot use first-line therapy.",null,null,"Phase 2 completed  (NCT01876108)","Under clinical trials","2022-03-21"]
[26,"Bacillus coagulans",null,"Biological extract",{"$nulls":3},"68038-65-3",true,{"$nulls":9},"Clinical trial on-going (IRCT20100524004010N23)","Under clinical trials","2022-03-21"]
[27,"Bayberry Juice","Chinese Bayberry Juice; Myrica rubra (Lour.) S. et Zucc.","Biological extract",{"$nulls":3},"8038-77-5",false,{"$nulls":9},"Clinical trial completed (NCT01707914: The consumption of bayberry juice for a period of 4 wk can protect against NAFLD in young adults by improving the plasma antioxidant status and inhibiting the inflammatory and apoptotic responses that are involved in this disease.)","Under clinical trials","2022-03-21"]
[28,"Belapectin","GR-MD-02; Belapectin","Chemical drug","DB15125","Belapectin is under investigation in clinical trial NCT02575404 (GR-MD-02 Plus Pembrolizumab in Melanoma, Non-small Cell Lung Cancer, and Squamous Cell Head and Neck Cancer Patients).",null,"1980787-47-0",false,{"$nulls":7},"Gelactin-3 inhibitor; LGALS3 inhibitor","Anti-fibrosis","Phase 2 completed (In a phase 2b study of 162 patients with NASH, cirrhosis, and portal hypertension, 1 year of biweekly infusion of belapectin was safe but not associated with significant reduction in HVPG or fibrosis compared with placebo. However, in a subgroup analysis of patients without esophageal varices, 2 mg/kg belapectin did reduce HVPG and development of varices. ClinicalTrials.gov number: NCT02462967.)","Failed in clinical trials","2022-03-21"]
[29,"Berberine",null,"Chemical drug","DB04115","An alkaloid from Hydrastis canadensis L., Berberidaceae. It is also found in many other plants. It is relatively toxic parenterally, but has been used orally for various parasitic and fungal infections and as antidiarrheal.","2353","2086-83-1",true,"O(C)c1c2c[n+]3c(cc2ccc1OC)c1c(CC3)cc2c(c1)OCO2","YBHILYKTIRIUTE-UHFFFAOYSA-N",336.367,"HTH-type transcriptional regulator QacR; Baculoviral IAP repeat-containing protein 5",{"$nulls":3},"AMPK activator","Improve insulin resistance","Clinical trial completed (NCT04049396)","Under clinical trials","2022-03-21"]
[30,"Bergamot","Bergamot; Bergamot Fruit Extract; Bergamot Oil, Cold-pressed; Bergamot Oil, Coldpressed; Bergamot Orange Oil; Bergamot,imitation; Citri Bergamia Aetheroleum; Citrus Aurantium Bergamia (Bergamot) Fruit Extract; Citrus Aurantium Bergamia (Bergamot) Fruit Oil; Citrus Aurantium Bergamia (Bergamot) Fruit Water; Citrus Aurantium Bergamia (Bergamot) Peel Oil; Citrus Aurantium Subsp. Bergamia Fruit Rind Oil; Citrus Aurantium Subsp. Bergamia Oil; Citrus Bergamia (Bergamot) Peel Oil; Citrus Bergamia Extract; Citrus Bergamia Fruit Rind Oil; Citrus Bergamia Oil; Citrus Bergamia Risso & Poiteau.; Citrus X Aurantium Subsp. Bergamia Fruit Rind Oil; Oil Bergamot; Oil of Bergamot","Biological drug","DB14335","Bergamot oil is a plant/plant extract used in some OTC (over-the-counter) products. It is not an approved drug.","8294","115-95-7",false,"C(CCC=C(C)C)(OC(=O)C)(C=C)C","UWKAYLJWKGQEPM-UHFFFAOYSA-N",196.29,{"$nulls":5},"Enhance lipid metabolism","Clinical trial on-going (ISRCTN33165861)","Under clinical trials","2022-03-21"]
[31,"Besifovir","Besifovir","Chemical drug","DB15671",null,"5270766","441785-25-7",false,"C(C1(OCP(=O)(O)O)CC1)n1c2c(nc1)cnc(n2)N","KDNSSKPZBDNJDF-UHFFFAOYSA-N",299.227,{"$nulls":4},"DNA-directed DNA polymerase; Hepatitis B virus replication",null,"Phase 4 on-going (NCT03604016)","Under clinical trials","2022-03-21"]
[32,"Betaine","2-(Trimethylammonio)Acetate; 2-N,N,N-trimethylammonio acetate; 2-trimethylammonioacetate; Abromine; Acidol; Betaine; Betaine, anhydrous; Glycine betaine; Glycinebetaine; N,N,N-trimethylammonioacetate; N,N,N-Trimethylglycine; TMG; Trimethylaminoacetate; Trimethylammonioacetate; Trimethylglycine; Trimethylglycocoll","Chemical drug","DB06756","Betaine is a methyl group donor that functions in the normal metabolic cycle of methionine and reduces homocystinuria in patients with inborn errors of methionine metabolism. In the United States, betaine is distributed under the brand name Cystadane® by Rare Disease Therapeutics. Many reports have shown that betaine's therapeutic effectiveness is limited, and does not lower tHcy levels or prevent clinical symptoms .","247","107-43-7",true,"[O-]C(=O)C[N+](C)(C)C","KWIUHFFTVRNATP-UHFFFAOYSA-N",117.148,"Apoptosis regulator Bcl-2","Betaine acts as a methyl group donor in the remethylation of homocysteine to methionine in patients with homocystinuria.",null,"Betaine is indicated for the treatment of homocystinuria to decrease elevated homocysteine blood levels. Included within the category of homocystinuria are deficiencies or defects in: 1. cystathionine beta-synthase (CBS), 2. 5,10-methylenetetrahydrofolate reductase (MTHFR), 3. cobalamin cofactor metabolism (cbl).","DNMTs stimulant","Improve insulin resistance","Phase 2 completed (NCT00586911)","Under clinical trials","2022-03-21"]
[33,"Bezafibrate","2-(p-(2-(p-Chlorobenzamido)ethyl)phenoxy)-2-methylpropionic acid; Bezafibrate","Chemical drug","DB01393","Antilipemic agent that lowers cholesterol and triglycerides. It decreases low density lipoproteins and increases high density lipoproteins.","39042","41859-67-0",true,"CC(C(O)=O)(OC1=CC=C(CCNC(C2=CC=C(Cl)C=C2)=O)C=C1)C","IIBYAHWJQTYFKB-UHFFFAOYSA-N",361.825,"Peroxisome proliferator-activated receptor alpha agonist; Peroxisome proliferator-activated receptor delta agonist; Peroxisome proliferator-activated receptor gamma agonist; Nuclear receptor subfamily 1 group I member 2 partial agonist; Retinoic acid rece","It is generally accepted that bezafibrate is likely an agonist of PPAR-alpha. However, certain other investigations have also suggested that the substance might also elicit some effects on PPAR-gamma and PPAR-delta too.","Bezafibrate is an antilipemic agent that lowers cholesterol and triglycerides. It decreases low density lipoproteins and increases high density lipoproteins. Bezafibrate lowers elevated blood lipids (triglycerides and cholesterol). Elevated VLDL and LDL are reduced by treatment with bezafibrate, whilst HDL-levels are increased. The activity of triglyceride lipases (lipoprotein lipase and hepatic lipoproteinlipase) involved in the catabolism of triglyceride-rich lipoproteins is increased by bezafibrate. In the course of the intensified degradation of triglyceride-rich lipoproteins (chylomicrons, VLDL) precursors for the formation of HDL are formed which explains an increase in HDL. Furthermore, cholesterol biosynthesis is reduced by bezafibrate, which is accompanied by a stimulation of the LDL-receptor-mediated lipoprotein catabolism. Elevated fibrinogen appears to be an important risk-factor, alongside the lipids, smoking and hypertension, in the development of atheroma. Fibrinogen plays an important role in viscosity, and therefore blood flow, and also appears to play an important role in thrombus development and lysability. Bezafibrate exerts an effect on thrombogenic factors. A significant decrease in elevated plasma fibrinogen levels can be achieved. This may lead, amongst other things, to a reduction in both blood and plasma viscosity. Inhibition of platelet aggregation has also been observed. A reduction in blood glucose concentration due to an increase in glucose tolerance has been reported in diabetic patients. In the same patients, the concentration of fasting and postprandial free fatty acids was reduced by bezafibrate.","For the treatment of primary hyperlipidaemia types IIa, IIb, III, IV and V (Fredrickson classification) corresponding to groups I, II and III of the European Atherosclerosis Society guidelines - when diet alone or improvements in lifestyle such as increased exercise or weight reduction do not lead to an adequate response. Also for the treatment of secondary hyperlipidaemias, e.g. severe hypertriglyceridemias, when sufficient improvement does not occur after correction of the underlying disorder (e.g. diabetes mellitus).","PPARA agonist; PPARD agonist; PPARG agonist; NR1I2 partial agonist","Improve insulin resistance; Anti-inflammatory","Phase 0 on-going (ChiCTR2000036225)","Under clinical trials","2022-03-21"]
[34,"BFKB8488A",null,"Biological drug",{"$nulls":4},false,{"$nulls":7},"KLB inhibitor; Type 1 FGFR antagonist",null,"Phase 2 on-going (NCT04171765)","Under clinical trials","2022-03-21"]
[35,"Bhunimba kshara",null,"Herbal medicine",{"$nulls":4},false,{"$nulls":9},"Phase 2&3 on-going (CTRI/2019/03/018039)","Under clinical trials","2022-03-21"]
[36,"BI 1467335","BI467335; BI-467335","Chemical drug",null,null,"71812246","1478364-68-9",false,"Cl.C(=O)(NC(C)(C)C)c1ccc(cc1)OC/C(=C/F)/CN","AEMZEDNMNLIDSL-YGCVIUNWSA-N",316.804,{"$nulls":4},"AOC3 activator",null,"Phase 2 completed (NCT03166735)","Failed in clinical trials","2022-03-21"]
[37,"Bifidobacterium longum","Bifidobacterium infantis; Bifidobacterium infantis whole; Bifidobacterium lactentis whole; Bifidobacterium liberorum whole; Bifidobacterium longum bv. infantis whole; Bifidobacterium longum infantis whole; Bifidobacterium longum subsp. infantis; Bifidobacterium longum subsp. infantis whole","Biological drug","DB14222",null,"9047",null,false,{"$nulls":9},"Phase 2 on-going (IRCT201301223140N6)","Under clinical trials","2022-03-21"]
[38,"Biguanide",null,"Chemical drug","DB13100","Biguanide has been investigated for the treatment of Diabetes Mellitus.","5939","56-03-1",true,"N(C(=N)N)C(=N)N","XNCOSPRUTUOJCJ-UHFFFAOYSA-N",101.113,{"$nulls":6},"Clinical trial on-going (CTRI/2019/03/018039)","Under clinical trials","2022-03-21"]
[39,"Bio-25",null,"Biological drug",{"$nulls":3},"63148-53-8",false,{"$nulls":9},"Clinical trial on-going (NCT01922830)","Under clinical trials","2022-03-21"]
[40,"BIO89-100",null,"Biological drug",{"$nulls":4},false,{"$nulls":7},"FGF21 analog","Improve insulin resistance; Enhance lipid metabolism","Phase 2 on-going (NCT04929483)","Under clinical trials","2022-03-21"]
[41,"BioE-1115",null,"Biological drug",null,null,"50922674",null,false,{"$nulls":9},"Phase 1 on-going (ACTRN12619000417189)","Under clinical trials","2022-03-21"]
[42,"BioFemale",null,"Biological drug",{"$nulls":4},false,{"$nulls":9},"Phase 1 terminated  (NCT00808990: Time table was unfulfilled due to incompetent research coordinator. Inaccurate results and No conclusions can be withdrawn)","Under clinical trials","2022-03-21"]
[43,"Bismuth subcitrate","Bismuth subcitrate potassium anhydrous","Chemical drug","DB09275","A bismuth compound used for peptic ulcer and gastro-oesophageal reflux disease (GORD).","10101269","57644-54-9",true,"[K].C(CC(=O)O)(CC(=O)O)(C(=O)O)O.[Bi]","ZBCVUEHBBZTSOB-UHFFFAOYSA-N",null,"ATP-dependent Clp protease ATP-binding subunit ClpX antagonist","Colloidal bismuth subcitrate is very effective in the treatment of gastroduodenal disorders and appears to act via several mechanisms. It has little acid-neutralizing effect and does not affect acid secretion. It is uncertain whether it affects pepsin secretion, but it does inhibit peptic activity. It causes an increase in mucus glycoprotein secretion and may also bind to the gastric mucus layer to act as a diffusion barrier to HCl. It accelerates ulcer healing and causes an accumulation of epidermal growth factor around the ulcer. In addition, it has a cytoprotective effect and increases mucosal secretion of prostaglandins and bicarbonate. It has bactericidal effects against Helicobacter pylori (which is associated with gastritis and peptic ulcers). It also prevents adhesion of H. pylori to epithelial cells and can inhibit enzymes secreted by H. pylori, such as proteases, lipases, glycosidases, and phospholipases.","Bismuth subcitrate  is very effective in the treatment of gastroduodenal disorders and appears to act via several mechanisms. It has little acid-neutralizing effect and does not affect acid secretion.","For the treatment of peptic ulcer and gastro-oesophageal reflux disease (GORD).\r\nTreatment of inflammatory and erosive-ulcerous diseases of gastric and duodenal mucosa:  gastritis, ulcer disease of the stomach and duodenum, functional non-ulcerous dyspepsia, erosive duodenitis, post-operative inflammatory and erosive changes – anastomositis, peptic ulcer of anastomosis",null,null,"Phase 2 completed  (NCT01876108)","Under clinical trials","2022-03-21"]
[44,"Black cumin","Nigella sativa; Roman coriander; black caraway; black seed; fennel flower; kalonji","Herbal medicine",{"$nulls":4},false,{"$nulls":9},"Phase 2 on-going (IRCT2017012232109N1)","Under clinical trials","2022-03-21"]
[45,"BLD-0409",null,"Miscellany",{"$nulls":4},false,{"$nulls":7},"ENPP2 inhibitor; ATX inhibitor","Anti-fibrosis","Phase 1 completed  (NCT04146805)","Under clinical trials","2022-03-21"]
[46,"Pegbelfermin","BMS-986036; PEG-FGF21; FALCON 2; FALCON 1","Biological drug","DB15365","Pegbelfermin is under investigation in clinical trial NCT03486899 (A Study of Experimental Medication BMS-986036 in Adults With Nonalcoholic Steatohepatitis (NASH) and Stage 3 Liver Fibrosis).",null,"1966977-70-7",false,{"$nulls":7},"FGF21 analog","Improve insulin resistance; Enhance lipid metabolism; Anti-fibrosis","Phase 2 completed (NCT02413372: Treatment with subcutaneously administered pegbelfermin for 16 weeks was generally well tolerated and significantly reduced hepatic fat fraction in patients with non-alcoholic steatohepatitis. Further study of pegbelfermin is warranted in patients with non-alcoholic steatohepatitis. Additional studies that use liver biopsies would allow for the assessment of pegbelfermin's effects on liver histology. Moreover, further studies should allow assessments of the safety and effectiveness of pegbelfermin in a larger number of patients.)","Under clinical trials","2022-03-21"]
[47,"BMS-986251",null,"Chemical drug",null,null,"132123624",null,false,"S(=O)(=O)([C@]12[C@H](N(CC1)C(=O)[C@H]1[C@H](C[C@@H](CC1)C(=O)O)C)CCc1c2ccc(c1)C(F)(C(F)(F)F)C(F)(F)F)c1ccc(F)cc1","JQORWGARJVSRBA-QOTTZFGFSA-N",667.615,{"$nulls":4},"RORGt inverse agonist",null,"Phase 1&2 terminated  (NCT03329885: Adverse change in the risk/benefit)","Failed in clinical trials","2022-03-21"]
[48,"BMS-986263",null,"Biological drug",{"$nulls":4},false,{"$nulls":7},"HSP inhibitor",null,"Phase 2 on-going (NCT04267393)","Under clinical trials","2022-03-21"]
[49,"Bovine Colostrum","Bovine colostrum powder","Supplement",{"$nulls":4},false,{"$nulls":9},"Phase 1&2 completed  (NCT01016418: These results suggest that BC can decrease levels of blood glucose and ketones, as well as reduce cholesterol and TGs, all of which may cause complications in Type 2 diabetic patients.)","Under clinical trials","2022-03-21"]
[50,"Branched-chain amino acids","BCAA","Biological drug",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (JPRN-UMIN000012351)","Under clinical trials","2022-03-21"]
[51,"Brewed chicory leaf","Cichorium intybus L.","Herbal medicine",{"$nulls":4},false,{"$nulls":9},"Phase 3 on-going (IRCT20190819044565N2)","Under clinical trials","2022-03-21"]
[52,"BRM4","rice bran arabinoxylan compound (RBAC)","Supplement",{"$nulls":4},false,{"$nulls":9},"Clinical trial completed (NCT02568787)","Under clinical trials","2022-03-21"]
[54,"Calcitriol","(1S,3R,5Z,7E)-9,10-secocholesta-5,7,10-triene-1,3,25-triol; (1α,3β,5Z,7E)-9,10-secocholesta-5,7,10(19)-triene-1,3,25-triol; (5Z,7E)-(1S,3R)-9,10-secocholesta-5,7,10(19)-triene-1,3,25-triol; 1-alpha-25-Dihydroxyvitamin D3; 1,25-DHCC; 1,25-dihydroxycholecalciferol; 1α,25-dihydroxycholecalciferol; 1α,25-dihydroxyvitamin D3; 1α,25(OH)2D3","Supplement","DB00136","Calcitriol is an active metabolite of vitamin D with 3 hydroxyl (OH) groups and is commonly referred to as 1,25-dihydroxycholecalciferol, or 1alpha,25-dihydroxyvitamin D<sub>3</sub>, 1,25-dihydroxyvitamin D<sub>3</sub>. It is produced in the body after series of conversion steps of 7-dehydrocholesterol from exposure to UV light. 7-dehydrocholesterol is converted to  (vitamin D3) in the skin, which is then converted to  in the liver and kidneys.  undergoes hydroxylation to form calcitriol via 1α-hydroxylase (CYP27B1) activity . Calcitriol is considered to be the most potent metabolite of vitamin D in humans . Renal production of calcitriol is stimulated in response to PTH, low calcium and low phosphate . Calcitriol plays a role in plasma calcium regulation in concert with parathyroid hormone (PTH) by enhancing absorption of dietary calcium and phosphate from the gastrointestinal tract, promoting renal tubular reabsorption of calcium in the kidneys, and stimulating the release of calcium stores from the skeletal system. In addition to promoting fatty acid synthesis and inhibiting lipolysis, calcitriol has been demonstrated to increase energy efficiency by suppressing UCP2 expression, which is modulated by signaling pathways of classical nuclear receptors (nVDR), where calcitriol acts as a natural ligand . There is also evidence that calcitriol modulates the action of cytokines and may regulate immune and inflammatory response, cell turnover, cell differentiation . \r\n\r\nAdministered orally and intravenously, calcitriol is commonly used as a medication in the treatment of secondary hyperparathyroidism and resultant metabolic bone disease, hypocalcemia in patients undergoing chronic renal dialysis, and osteoporosis. It is also available in topical form for the treatment of mild to moderate plaque psoriasis in adults. Calcitriol is marketed under various trade names including Rocaltrol (Roche), Calcijex (Abbott) and Decostriol (Mibe, Jesalis).","5280453","32222-06-3",true,"C[C@]12[C@H](/C(=C/C=C/3\\C(=C)[C@@H](O)C[C@@H](C3)O)/CCC2)CC[C@@H]1[C@@H](CCCC(C)(C)O)C","GMRQFYUYWCNGIN-NKMMMXOESA-N",416.646,"Vitamin D3 receptor antagonist; Homeobox protein Hox-A10","The mechanism of action of calcitriol in the treatment of psoriasis is accounted for by their antiproliferative activity for keratinocytes and their stimulation of epidermal cell differentiation. The anticarcinogenic activity of the active form of Calcitriol appears to be correlated with cellular vitamin D receptor (VDR) levels. Vitamin D receptors belong to the superfamily of steroid-hormone zinc-finger receptors. VDRs selectively bind 1,25-(OH)<sub>2</sub>-D3 and retinoic acid X receptor (RXR) to form a heterodimeric complex that interacts with specific DNA sequences known as vitamin D-responsive elements. VDRs are ligand-activated transcription factors. The receptors activate or repress the transcription of target genes upon binding their respective ligands. It is thought that the anticarcinogenic effect of Calcitriol is mediated via VDRs in cancer cells. The immunomodulatory activity of calcitriol is thought to be mediated by vitamin D receptors (VDRs) which are expressed constitutively in monocytes but induced upon activation of T and B lymphocytes. 1,25-(OH)<sub>2</sub>-D3 has also been found to enhance the activity of some vitamin D-receptor positive immune cells and to enhance the sensitivity of certain target cells to various cytokines secreted by immune cells.\r\n\r\nA study suggests that calcitriol plays an immunoregulatry role by suppressing the aryl hydrocarbon receptor (AhR) expression in human Th9, a pro-inflammatory CD4 T cell subset . This suppression subsequently leads to repressed expression of BATF, a transcription factor essential for Th9 . Calcitriol has also been found to induce monocyte differentiation and to inhibit lymphocyte proliferation and production of cytokines, including interleukin IL-1 and IL-2, as well as to suppress immunoglobulin secretion by B lymphocytes.","Calcitriol is a biologically active calcitrophic hormone with anti-osteoporotic, immunomodulatory, anticarcinogenic, antipsoriatic, antioxidant, and mood-modulatory activities. Its main sites of action are the intestine, bone, kidney and parathyroid hormone . Calcitriol is a ligand for the vitamin D nuclear receptor, which is expressed in, but not limited to, gastrointestinal (GI) tissues, bones, and kidneys . As an active form of vitamin D<sub>3</sub>, calcitriol elevates the plasma levels of calcium by stimulating intestinal calcium uptake, increasing reabsorption of calcium by the kidneys, and possibly increasing the release of calcium from skeletal stores. The duration of pharmacologic activity of a single dose of exogenous calcitriol is expected to be about 3 to 5 days . \r\n\r\nIn addition to its important role in calcium metabolism, other pharmacological effects of calcitriol have been studied in various conditions including cancer models. Various studies demonstrated expression of vitamin D receptors in cancer cell lines, including mouse myeloid leukemia cells . Calcitriol has been found to induce differentiation and/or inhibit cell proliferation _in vitro_ and _in vivo_ in many cell types, such as malignant cell lines carcinomas of the breast, prostate, colon, skin, and brain, myeloid leukemia cells, and others . In early human prostate cancer trials, administration of 1.5 µg/d calcitriol in male participants resulted in a reduction in the rate of PSA rise in most participants, however it was coincided with dose-limiting hypercalcemia in most participants . Hypercalcemia and hypercalcuria were evident in numerous initial trials, and this may be due to these trials not testing the drug at concentrations that are active in preclinical systems . Findings from preclinical data show an additive or synergistic antineoplastic action of calcitriol when combined with agents including dexamethasone, retinoids, and radiation, as well as several cytotoxic chemotherapy drugs such as platinum compounds . \r\n\r\nVitamin D deficiency has long been suspected to increase the susceptibility to tuberculosis. The active form of calcitriol, 1,25-(OH)<sub>2</sub>-D3, has been found to enhance the ability of mononuclear phagocytes to suppress the intracellular growth of <i>Mycobacterium tuberculosis</i>. 1,25-(OH)<sub>2</sub>-D3 has demonstrated beneficial effects in animal models of such autoimmune diseases as rheumatoid arthritis. Vitamin D appears to demonstrate both immune-enhancing and immunosuppressive effects.","Used to treat vitamin D deficiency or insufficiency, refractory rickets (vitamin D resistant rickets), familial hypophosphatemia and hypoparathyroidism, and in the management of hypocalcemia and renal osteodystrophy in patients with chronic renal failure undergoing dialysis. Also used in conjunction with calcium in the management and prevention of primary or corticosteroid-induced osteoporosis.",null,null,"Phase 3 on-going (IRCT2017053034222N1)","Under clinical trials","2022-03-21"]
[55,"Calcium","Calcium, elemental; Elemental calcium","Chemical drug","DB01373","Calcium plays a vital role in the anatomy, physiology and biochemistry of organisms and of the cell, particularly in signal transduction pathways. The skeleton acts as a major mineral storage site for the element and releases Ca2+ ions into the bloodstream under controlled conditions. Circulating calcium is either in the free, ionized form or bound to blood proteins such as serum albumin. Although calcium flow to and from the bone is neutral, about 5 mmol is turned over a day. Bone serves as an important storage point for calcium, as it contains 99% of the total body calcium. Low calcium intake may also be a risk factor in the development of osteoporosis. The best-absorbed form of calcium from a pill is a calcium salt like carbonate or phosphate. Calcium gluconate and calcium lactate are absorbed well by pregnant women. Seniors absorb calcium lactate, gluconate and citrate better unless they take their calcium supplement with a full breakfast.","5460341","7440-70-2",false,"[Ca]","OYPRJOBELJOOCE-UHFFFAOYSA-N",42.094,"Voltage-dependent L-type calcium channel subunit alpha-1C ligand; Calcium-transporting ATPase type 2C member 1 agonist; Troponin C, skeletal muscle agonist; Troponin C, slow skeletal and cardiac muscles agonist; Spectrin beta chain, non-erythrocytic 1 ago","Calcium plays a vital role in the anatomy, physiology and biochemistry of organisms and of the cell, particularly in signal transduction pathways. More than 500 human proteins are known to bind or transport calcium.   The skeleton acts as a major mineral storage site for the element and releases Ca2+ ions into the bloodstream under controlled conditions. Circulating calcium is either in the free, ionized form or bound to blood proteins such as serum albumin. Parathyroid hormone (secreted from the parathyroid gland) regulates the resorption of Ca2+ from bone. Calcitonin stimulates incorporation of calcium in bone, although this process is largely independent of calcitonin. Although calcium flow to and from the bone is neutral, about 5 mmol is turned over a day. Bone serves as an important storage point for calcium, as it contains 99% of the total body calcium.  Low calcium intake may also be a risk factor in the development of osteoporosis.  The best-absorbed form of calcium from a pill is a calcium salt like carbonate or phosphate. Calcium gluconate and calcium lactate are absorbed well by pregnant women. Seniors absorb calcium lactate, gluconate and citrate better unless they take their calcium supplement with a full breakfast. The currently recommended calcium intake is 1,500 milligrams per day for women not taking estrogen and 800 milligrams per day for women on estrogen. There is close to 300 milligrams of calcium in one cup of fluid milk. Calcium carbonate is currently the best and least expensive form of calcium supplement available.","Calcium (Ca2+) plays a pivotal role in the physiology and biochemistry of organisms and the cell. It plays an important role in signal transduction pathways, where it acts as a second messenger, in neurotransmitter release from neurons, contraction of all muscle cell types, and fertilization. Many enzymes require calcium ions as a cofactor, those of the blood-clotting cascade being notable examples. Extracellular calcium is also important for maintaining the potential difference across excitable cell membranes, as well as proper bone formation.","Calcium plays a vital role in the anatomy, physiology and biochemistry of organisms and of the cell, particularly in signal transduction pathways. It is vital in cell signaling, muscular contractions, bone health, and signalling cascades.","CAST; COMP; CP; BMP4; MGP",null,"Phase 3 on-going (IRCT201408312709N29)","Under clinical trials","2022-03-21"]
[56,"Camelina oil","Camelina Crantz","Biological extract",{"$nulls":3},"1024002-90-1",false,{"$nulls":9},"Phase 3 on-going (IRCT20150205020965N5)","Under clinical trials","2022-03-21"]
[57,"Camu camu","Myrciaria dubia","Herbal medicine",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (NCT04130321)","Under clinical trials","2022-03-21"]
[58,"Canagliflozin","Canagliflozin; Canagliflozin anhydrous; Canaglifrozin","Chemical drug","DB08907","Canagliflozin, also known as _Invokana_, is a sodium-glucose cotransporter 2 (SGLT2) inhibitor used in the management of type 2 diabetes mellitus along with lifestyle changes including diet and exercise .\r\n\r\nIt was initially approved by the FDA in 2013 for the management of diabetes and later approved in 2018 for a second indication of reducing the risk of cardiovascular events in patients diagnosed with type 2 diabetes mellitus , . \r\n\r\nCanagliflozin is the first oral antidiabetic drug approved for the prevention of cardiovascular events in patients with type 2 diabetes . Cardiovascular disease is the most common cause of death in these patients .","24812758","842133-18-0",true,"O[C@H]1[C@@H](O[C@@H]([C@H]([C@@H]1O)O)CO)c1cc(Cc2sc(cc2)c2ccc(cc2)F)c(cc1)C","XTNGUQKDFGDXSJ-ZXGKGEBGSA-N",444.524,"Sodium/glucose cotransporter 2 inhibitor","The sodium-glucose co-transporter2 (SGLT2), is found in the proximal tubules of the kidney, and reabsorbs filtered glucose from the renal tubular lumen. Canagliflozin inhibits the SGLT2 co-transporter. This inhibition leads to lower reabsorption of filtered glucose into the body and decreases the renal threshold for glucose (RTG), leading to increased glucose excretion in the urine .","This drug increases urinary glucose excretion and decreases the renal threshold for glucose (RTG) in a dose-dependent manner . The renal threshold is defined as the lowest level of blood glucose associated with the appearance of detectable glucose in the urine .  The end result of canagliflozin administration is increased urinary excretion of glucose and less renal absorption of glucose, decreasing glucose concentration in the blood and improving glycemic control. \r\n\r\n**A note on type 2 diabetes and cardiovascular disease**\r\n\r\nThe risk of cardiovascular events in diabetes type 2 is increased due to the damaging effects of diabetes on blood vessels and nerves in the cardiovascular system.  In particular, there is a tendency for hyperglycemia to create pro-atherogenic (plaque forming) lesions in blood vessels, leading to various fatal and non-fatal events including stroke and myocardial infarction .  Long-term glycemic control has been proven to be effective in the prevention of cardiovascular events such as myocardial infarction and stroke in patients with type 2 diabetes .\r","This drug is used in conjunction with diet and exercise to increase glycemic control in adults diagnosed with type 2 diabetes mellitus .\r\n\r\nAnother indication for canagliflozin is the prevention of major cardiovascular events (myocardial infarction, stroke, or death due to a cardiovascular cause) in patients with type 2 diabetes, as well as hospitalization for heart failure in patients with type 2 diabetes.\r\n\r\nIn addition to the above, canagliflozin can be used to lower the risk of end-stage kidney disease and major increases in serum creatinine and cardiovascular death for patients with a combination of type 2 diabetes mellitus, diabetic nephropathy, and albuminuria.\r\n\r\nIt is important to note that this drug is **not** indicated for the treatment of type 1 diabetes mellitus or diabetic ketoacidosis .","SGLT2 inhibitor","Improve insulin resistance","Phase 1 completed (NCT02009488: Canagliflozin improves hepatic insulin sensitivity and insulin secretion and clearance in patients with T2DM. IHTG decreases in proportion to the magnitude of body weight loss, which tended to be greater and occur more often with canagliflozin.)","Under clinical trials","2022-03-21"]
[59,"Cappris pickle",null,"Supplement",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (IRCT2015122425686N1)","Under clinical trials","2022-03-21"]
[60,"Cardo Mariano",null,"Miscellany",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (RBR-8dp876)","Under clinical trials","2022-03-21"]
[61,"Cardoon extract","Cynara cardunculus","Biological extract",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (ISRCTN12833814)","Under clinical trials","2022-03-21"]
[62,"Carnitine complex","Godex; (-)-Carnitine; (-)-L-Carnitine; (R)-Carnitine; 3-Carboxy-2-hydroxy-N,N,N-trimethyl-1-propanaminium hydroxide, inner salt; Carnitine; L-Carnitine; Levocarnitine; Vitamin BT","Supplement","DB00583","Constituent of striated muscle and liver. It is used therapeutically to stimulate gastric and pancreatic secretions and in the treatment of hyperlipoproteinemias.","10917","541-15-1, 836627-73-7",true,null,null,161.201,"Solute carrier family 22 member 4; Solute carrier family 22 member 5; Carnitine O-acetyltransferase; Mitochondrial carnitine/acylcarnitine carrier protein CACL; Mitochondrial carnitine/acylcarnitine carrier protein; Peroxisomal carnitine O-octanoyltransfe","Levocarnitine can be synthesised within the body from the amino acids lysine or methionine. Vitamin C (ascorbic acid) is essential to the synthesis of carnitine. Levocarnitine is a carrier molecule in the transport of long chain fatty acids across the inner mitochondrial membrane. It also exports acyl groups from subcellular organelles and from cells to urine before they accumulate to toxic concentrations. Only the L isomer of carnitine (sometimes called vitamin BT) affects lipid metabolism. Levocarnitine is handled by several proteins in different pathways including carnitine transporters, carnitine translocases, carnitine acetyltransferases and carnitine palmitoyltransferases.","Levocarnitine is a carrier molecule in the transport of long chain fatty acids across the inner mitochondrial membrane. It also exports acyl groups from subcellular organelles and from cells to urine before they accumulate to toxic concentrations. Lack of carnitine can lead to liver, heart, and muscle problems. Carnitine deficiency is defined biochemically as abnormally low plasma concentrations of free carnitine, less than 20 &micro;mol/L at one week post term and may be associated with low tissue and/or urine concentrations. Further, this condition may be associated with a plasma concentration ratio of acylcarnitine/levocarnitine greater than 0.4 or abnormally elevated concentrations of acylcarnitine in the urine. Only the L isomer of carnitine (sometimes called vitamin BT) affects lipid metabolism. The \"vitamin BT\" form actually contains D,L-carnitine, which competitively inhibits levocarnitine and can cause deficiency. Levocarnitine can be used therapeutically to stimulate gastric and pancreatic secretions and in the treatment of hyperlipoproteinemias.","For treatment of primary systemic carnitine deficiency, a genetic impairment of normal biosynthesis or utilization of levocarnitine from dietary sources, or for the treatment of secondary carnitine deficiency resulting from an inborn error of metabolism such as glutaric aciduria II, methyl malonic aciduria, propionic acidemia, and medium chain fatty acylCoA dehydrogenase deficiency. Used therapeutically to stimulate gastric and pancreatic secretions and in the treatment of hyperlipoproteinemias. Parenteral levocarnitine is indicated for the prevention and treatment of carnitine deficiency in patients with end-stage renal disease.","SLC22A4; SLC22A5; CRAT; MPO",null,"Phase 4 on-going (KCT0000505)","Under clinical trials","2022-03-21"]
[63,"Catechin-contained green tea","Catechin beverage","Herbal medicine",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (JPRN-UMIN000018361)","Under clinical trials","2022-03-21"]
[64,"CB4211",null,"Biological drug",{"$nulls":4},false,{"$nulls":7},"MOTS-c analog",null,"Phase 1 completed  (NCT03998514)","Under clinical trials","2022-03-21"]
[65,"CC-90001",null,"Chemical drug",{"$nulls":3},"1403859-14-2",false,"N(c1c(C(=O)N)cnc(n1)NC(C)(C)C)[C@H]1C[C@@H](O)[C@@H](CC1)C","QBBRJRLJWXRSHQ-CKYFFXLPSA-N",321.425,{"$nulls":4},"serine kinase inhibitor",null,"Phase 2 terminated  (NCT04048876: Business objectives have changed)","Under clinical trials","2022-03-21"]
[66,"Celery seed","Apium graveolens L.","Biological extract",{"$nulls":3},"8015-90-5",false,{"$nulls":9},"Phase 2 on-going (IRCT20191124045488N1)","Under clinical trials","2022-03-21"]
[67,"Celsentri",null,"Chemical drug","DB04835","Maraviroc (brand-named Selzentry, or Celsentri outside the U.S.) is a chemokine receptor antagonist drug developed by the drug company Pfizer that is designed to act against HIV by interfering with the interaction between HIV and CCR5. It was originally labelled as UK-427857 during development but was assigned the Maraviroc name as it entered trials. It was approved for use by the FDA in August, 2007.","3002977","376348-65-1",true,"C(C[C@H](NC(=O)C1CCC(CC1)(F)F)c1ccccc1)N1[C@@H]2C[C@@H](C[C@H]1CC2)n1c(C(C)C)nnc1C","GSNHKUDZZFZSJB-QYOOZWMWSA-N",513.677,"C-C chemokine receptor type 5 antagonist","Maraviroc is an entry inhibitor and works by blocking HIV from entering human cells. Specifically maraviroc is a selective, slowly reversible, small molecule antagonist of the interaction between human CCR5 and HIV-1 gp120. Maraviroc selectively binds to the human chemokine receptor CCR5 present on the membrane of CD4 cells (T-cells), preventing the interaction of HIV-1 gp120 and CCR5 necessary for CCR5-tropic HIV-1 to enter cells.","Maraviroc is a chemokine receptor antagonist drug developed by the drug company Pfizer that is designed to act against HIV by interfering with the interaction between HIV and CCR5.","For treatment-experienced adult patients infected with only CCR5-tropic HIV-1 detectable, who have evidence of viral replication and HIV-1 strains resistant to multiple antiretroviral agents.",null,null,"Clinical trial on-going (EUCTR2017-003172-32-DE)","Under clinical trials","2022-03-21"]
[68,"Cenicriviroc","Cenicriviroc","Chemical drug","DB11758","Cenicriviroc has been used in trials studying the treatment of HIV-infection/AIDS, AIDS Dementia Complex, Nonalcoholic Steatohepatitis, Human Immunodeficiency Virus, and HIV-1-Associated Cognitive Motor Complex.","11285792","497223-25-3",false,"C(C(C)C)N1c2c(cc(cc2)c2ccc(cc2)OCCOCCCC)C=C(CCC1)C(=O)Nc1ccc(cc1)S(=O)Cc1n(CCC)cnc1","PNDKCRDVVKJPKG-UHFFFAOYSA-N",696.958,{"$nulls":4},"CCR2 inhibitor; CCR5 inhibitor","Anti-fibrosis","Phase 3 terminated (NCT03028740: This study was terminated early due to lack of efficacy based on the results of the planned interim analysis of Part 1 data.)","Failed in clinical trials","2022-03-21"]
[69,"CF102",null,"Chemical drug","DB12885","CF-102 has been used in trials studying the treatment of Chronic Hepatitis C and Hepatocellular Carcinoma.","3035850","163042-96-4",false,"O[C@H]1[C@H](n2c3c(nc2)c(NCc2cc(I)ccc2)nc(n3)Cl)O[C@@H]([C@H]1O)C(=O)NC","IPSYPUKKXMNCNQ-PFHKOEEOSA-N",544.737,{"$nulls":4},"ADORA3 receptor antagonist activity","Anticancer agent","Phase 2 completed  (NCT02927314: A3AR is a valid target; namodenoson 25 mg b.d. was safe and demonstrated efficacy signals.)","Under clinical trials","2022-03-21"]
[70,"CH-001",null,"Miscellany",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (Clinical trial on-going ())","Under clinical trials","2022-03-21"]
[71,"Chicory","Cichorium intybus L.","Biological extract",{"$nulls":3},"68650-43-1",false,{"$nulls":9},"Phase 3 on-going (IRCT20190819044565N2)","Under clinical trials","2022-03-21"]
[72,"Chitosan","Poliglusam low molecular weight (20-200 mpa.s)","Chemical drug","DB14155",null,"71853","9012-76-4",false,"O([C@H]1[C@H](O)[C@@H](N)[C@H](O[C@H]2[C@H](O)[C@@H](NC(=O)OC)[C@@H](O[C@@H]2CO)O[C@H]2[C@H](O)[C@@H](N)[C@@H](O[C@@H]2CO)O[C@H]2[C@H](O)[C@@H](N)[C@@H](O[C@@H]2CO)O)O[C@@H]1CO)[C@@H]1O[C@@H]([C@@H](O[C@@H]2O[C@@H]([C@@H](O[C@@H]3O[C@@H]([C@@H](O[C@@H]4O[C@@H]([C@@H](O[C@@H]5O[C@@H]([C@@H](O)[C@H](O)[C@H]5N)CO)[C@H](O)[C@H]4N)CO)[C@H](O)[C@H]3N)CO)[C@H](O)[C@H]2N)CO)[C@H](O)[C@H]1N)CO","FLASNYPZGWUPSU-SICDJOISSA-N",1526.464,{"$nulls":6},"Clinical trial on-going (IRCT20180412039284N2)","Under clinical trials","2022-03-21"]
[73,"Chlorella Volgaris",null,"Biological extract",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (IRCT2014101619554N1)","Under clinical trials","2022-03-21"]
[74,"Cholestyramine","Cholestyramine resin; Colestyramine","Chemical drug","DB01432","Cholestyramine or colestyramine is a bile acid sequestrant. Bile acid sequestrants are polymeric compounds which serve as ion exchange resins. Cholestyramine resin is quite hydrophilic, but insoluble in water.","70695641","11041-12-6",true,"[N+](c1ccc(CCC(c2ccc(cc2)CC)C)cc1)(C)(C)C","HGMSJMJPXGGEBP-UHFFFAOYSA-N",296.478,"Bile acids binder","Cholestyramine forms a resin that acts as a bile acid sequestrant to limit the reabsorption of bile acids in the gastrointestinal tract. Cholestyramine resin is a strong anion exchange resin, allowing it to exchange its chloride anions with anionic bile acids present in the gastrointestinal tract and form a strong resin matrix. Cholestyramine consists of a functional group, which is a quaternary ammonium group attached to an inert styrene-divinylbenzene copolymer, in the anion exchange resin.","Cholesterol is probably the sole precursor of bile acids. During normal digestion, bile acids are secreted into the intestines. A major portion of the bile acids is absorbed from the intestinal tract and returned to the liver via the enterohepatic circulation. Only very small amounts of bile acids are found in normal serum. Cholestyramine resin adsorbs and combines with the bile acids in the intestine to form an insoluble complex which is excreted in the feces. This results in a partial removal of bile acids from the enterohepatic circulation by preventing their absorption.","Indicated as adjunctive therapy to diet for the reduction of elevated serum cholesterol in patients with primary hypercholesterolemia (elevated low density lipoprotein  cholesterol) who do not respond adequately to diet. Also for the relief of pruritus associated with partial biliary obstruction.",null,"Hypolipidemic drug","Phase 2 completed  (NCT04235205: Elobixibat resolved constipation in the short-term, and was well tolerated with both short-term and long-term treatment. The evidence supports the use of this novel approach to increase intracolonic concentrations of endogenous bile acid for the treatment of chronic constipation.)","Under clinical trials","2022-03-21"]
[75,"Choline","Bilineurine; Choline ion; N-trimethylethanolamine; N,N,N-trimethylethanol-ammonium; trimethylethanolamine; Vitamin J","Supplement","DB00122","A basic constituent of lecithin that is found in many plants and animal organs. It is important as a precursor of acetylcholine, as a methyl donor in various metabolic processes, and in lipid metabolism.","305","62-49-7",true,"C([N+](C)(C)C)CO","OEYIOHPDSNJKLS-UHFFFAOYSA-N",104.173,"Choline-phosphate cytidylyltransferase B product of; Acetylcholinesterase product of; Choline-phosphate cytidylyltransferase A product of; Phospholipase D2 product of; Cholinesterase product of; Phospholipase D1 product of; Phosphoethanolamine/phosphochol","Choline is a major part of the polar head group of phosphatidylcholine. Phosphatidylcholine's role in the maintenance of cell membrane integrity is vital to all of the basic biological processes: information flow, intracellular communication and bioenergetics. Inadequate choline intake would negatively affect all these processes. Choline is also a major part of another membrane phospholipid, sphingomyelin, also important for the maintenance of cell structure and function. It is noteworthy and not surprising that choline deficiency in cell culture causes apoptosis or programmed cell death. This appears to be due to abnormalities in cell membrane phosphatidylcholine content and an increase in ceramide, a precursor, as well as a metabolite, of sphingomyelin. Ceramide accumulation, which is caused by choline deficiency, appears to activate Caspase, a type of enzyme that mediates apoptosis. Betaine or trimethylglycine is derived from choline via an oxidation reaction. Betaine is one of the factors that maintains low levels of homocysteine by resynthesizing L-methionine from homocysteine. Elevated homocysteine levels are a significant risk factor for atherosclerosis, as well as other cardiovascular and neurological disorders. Acetylcholine is one of the major neurotransmitters and requires choline for its synthesis. Adequate acetylcholine levels in the brain are believed to be protective against certain types of dementia, including Alzheimer's disease.","This compound is needed for good nerve conduction throughout the CNS (central nervous system) as it is a precursor to acetylcholine (ACh). Choline is also needed for gallbladder regulation, liver function and lecithin (a key lipid) formation. Choline also aids in fat and cholesterol metabolism and prevents excessive fat build up in the liver. Choline has been used to mitigate the effects of Parkinsonism and tardive dyskinesia. Choline deficiencies may result in excessive build-up of fat in the liver, high blood pressure, gastric ulcers, kidney and liver dysfunction and stunted growth.","For nutritional supplementation, also for treating dietary shortage or imbalance","PLD2 product of; PLD1 product of",null,"Phase 2 on-going (JPRN-UMIN000006192)","Under clinical trials","2022-03-21"]
[76,"Chromium picolinate","Chromium(III) picolinate","Chemical drug","DB11255","Chromium picolinate has a chemical formula CrPic3 and reddish-pink color. It is a coordination complex consisting of chromium(III) and picolinic acid. Chromium picolinate is used as a nutritional supplement for optimal insulin function in patients with Type 2 diabetes or promotion of weight loss. Chromium ions are shown to regulate insulin by promoting glucose utilization and increasing the sensitivity of the insulin receptor .","151932","14639-25-9",true,"[Cr+3].[O-]C(=O)c1ncccc1.[O-]C(=O)c1ncccc1.[O-]C(=O)c1ncccc1","CBDQOLKNTOMMTL-UHFFFAOYSA-K",418.305,{"$nulls":6},"Clinical trial on-going (IRCT20100123003140N15)","Under clinical trials","2022-03-21"]
[77,"Cichorium Intybus L.",null,"Herbal medicine",{"$nulls":3},"68650-43-1",false,{"$nulls":9},"Phase 2 on-going (IRCT2016061228411N1)","Under clinical trials","2022-03-21"]
[78,"Cilofexor","GS-9674","Chemical drug","DB15168","Cilofexor is under investigation in clinical trial NCT02943447 (Safety, Tolerability, and Efficacy of Cilofexor in Adults With Primary Biliary Cholangitis Without Cirrhosis).","71228883","1418274-28-8",false,"C(Oc1cc(Cl)c(cc1)C1(O)CN(C1)c1cc(C(=O)O)ccn1)c1c(noc1C1CC1)c1c(Cl)cccc1Cl","KZSKGLFYQAYZCO-UHFFFAOYSA-N",586.859,{"$nulls":4},"FXR agonist","Enhance lipid metabolism","Phase 2 completed (Cilofexor for 24 weeks was well-tolerated and provided significant reductions in hepatic steatosis, liver biochemistry, and serum bile acids in patients with NASH. ClinicalTrials.gov No. NCT02854605.)","Under clinical trials","2022-03-21"]
[79,"Cinnamon",null,"Biological drug","DB10520","Cinnamon allergenic extract is used in allergenic testing.",null,null,false,{"$nulls":9},"Phase 2 on-going (IRCT201207114010N9)","Under clinical trials","2022-03-21"]
[80,"Citrulline","(S)-2-Amino-5-ureidopentanoic acid; 2-Amino-5-ureidovaleric acid; alpha-amino-delta-Ureidovaleric acid; Cit; Citrulline; delta-Ureidonorvaline; L-2-Amino-5-ureidovaleric acid; L-Citrulline; N(5)-(Aminocarbonyl)-L-ornithine; N(delta)-Carbamylornithine; N5-(Aminocarbonyl)ornithine; N5-Carbamoyl-L-ornithine; N5-carbamoylornithine; α-amino-δ-ureidovaleric acid; δ-ureidonorvaline","Chemical drug","DB00155","Citrulline is an amino acid. It is made from ornithine and carbamoyl phosphate in one of the central reactions in the urea cycle. It is also produced from arginine as a by-product of the reaction catalyzed by NOS family. Its name is derived from citrullus, the Latin word for watermelon, from which it was first isolated.","9750","372-75-8",true,"C(CCNC(=O)N)[C@@H](C(=O)O)N","RHGKLRLOHDJJDR-BYPYZUCNSA-N",175.188,"Argininosuccinate synthase; N(G),N(G)-dimethylarginine dimethylaminohydrolase 2; Argininosuccinate synthetase, isoform CRA_a; N(G),N(G)-dimethylarginine dimethylaminohydrolase 1; Ornithine carbamoyltransferase, mitochondrial; Nitric oxide synthase, brain;","L-citrulline is converted to L-arginine by argininosuccinate synthase. L-arginine is in turn responsible for citrulline's therapeutic affects. Many of L-arginine's activities, including its possible anti-atherogenic actions, may be accounted for by its role as the precursor to nitric oxide or NO. NO is produced by all tissues of the body and plays very important roles in the cardiovascular system, immune system and nervous system. NO is formed from L-arginine via the enzyme nitric oxide synthase or synthetase (NOS), and the effects of NO are mainly mediated by 3',5' -cyclic guanylate or cyclic GMP. NO activates the enzyme guanylate cyclase, which catalyzes the synthesis of cyclic GMP from guanosine triphosphate or GTP. Cyclic GMP is converted to guanylic acid via the enzyme cyclic GMP phosphodiesterase. <br/><br/>NOS is a heme-containing enzyme with some sequences similar to cytochrome P-450 reductase. Several isoforms of NOS exist, two of which are constitutive and one of which is inducible by immunological stimuli. The constitutive NOS found in the vascular endothelium is designated eNOS and that present in the brain, spinal cord and peripheral nervous system is designated nNOS. The form of NOS induced by immunological or inflammatory stimuli is known as iNOS. iNOS may be expressed constitutively in select tissues such as lung epithelium. <br/><br/>All the nitric oxide synthases use NADPH (reduced nicotinamide adenine dinucleotide phosphate) and oxygen (O<sub>2</sub>) as cosubstrates, as well as the cofactors FAD (flavin adenine dinucleotide), FMN (flavin mononucleotide), tetrahydrobiopterin and heme. Interestingly, ascorbic acid appears to enhance NOS activity by increasing intracellular tetrahydrobiopterin. eNOS and nNOS synthesize NO in response to an increased concentration of calcium ions or in some cases in response to calcium-independent stimuli, such as shear stress. <i>In vitro</i> studies of NOS indicate that the Km of the enzyme for L-arginine is in the micromolar range. The concentration of L-arginine in endothelial cells, as well as in other cells, and in plasma is in the millimolar range. What this means is that, under physiological conditions, NOS is saturated with its L-arginine substrate. In other words, L-arginine would not be expected to be rate-limiting for the enzyme, and it would not appear that supraphysiological levels of L-arginine which could occur with oral supplementation of the amino acid would make any difference with regard to NO production. The reaction would appear to have reached its maximum level. However, <i>in vivo</i> studies have demonstrated that, under certain conditions, e.g. hypercholesterolemia, L-arginine could enhance endothelial-dependent vasodilation and NO production.","A non-essential amino acid and a precursor of arginine. Citrulline supplements have been claimed to promote energy levels, stimulate the immune system and help detoxify ammonia (a cell toxin). L-citrulline is made from L-ornithine and carbamoyl phosphate in one of the central reactions in the urea cycle. It is also produced from L-arginine as a by-product of the reaction catalyzed by the enzyme NO synthase. L-citrulline, while being an amino acid, is not involved in protein synthesis and is not one of the amino acids coded for by DNA. Although citrulline cannot be incorporated in proteins during protein synthesis, several proteins are known to contain citrulline as an amino acid. These citrulline residues are generated by a family of enzymes called peptidylarginine deiminases (PADs), which convert the amino acid arginine into citrulline. Proteins that contain citrulline residues include myelin basic protein (MBP), fillagrin and several histone proteins.","Used for nutritional supplementation, also for treating dietary shortage or imbalance.",null,null,"Clinical trial on-going (IRCT201703194010N18)","Under clinical trials","2022-03-21"]
[81,"Citrus unshiu",null,"Herbal medicine",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (JPRN-UMIN000014736)","Under clinical trials","2022-03-21"]
[82,"CK-18",null,"Miscellany",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (ChiCTR1900021534)","Under clinical trials","2022-03-21"]
[83,"CLA","Conjugated linoleic acid; 6-O-methyl erythromycin; 6-O-methylerythromycin; 6-O-methylerythromycin A; CLA; Clarithromycin","Chemical drug","DB01211","Clarithromycin, a semisynthetic macrolide antibiotic derived from erythromycin, inhibits bacterial protein synthesis by binding to the bacterial 50S ribosomal subunit. Binding inhibits peptidyl transferase activity and interferes with amino acid translocation during the translation and protein assembly process. Clarithromycin may be bacteriostatic or bactericidal depending on the organism and drug concentration.","5282796","1839-11-8",true,"C(CC=CC=CCCCCCC)CCCCCC(=O)O","JBYXPOFIGCOSSB-UHFFFAOYSA-N",280.452,"50S ribosomal protein L10 inhibitor; Potassium voltage-gated channel subfamily H member 2; Solute carrier organic anion transporter family member 1B1; Solute carrier organic anion transporter family member 1B3","Clarithromycin is first metabolized to 14-OH clarithromycin, which is active and works synergistically with its parent compound. Like other macrolides, it then penetrates bacteria cell wall and reversibly binds to domain V of the 23S ribosomal RNA of the 50S subunit of the bacterial ribosome, blocking translocation of aminoacyl transfer-RNA and polypeptide synthesis. Clarithromycin also inhibits the hepatic microsomal CYP3A4 isoenzyme and P-glycoprotein, an energy-dependent drug efflux pump.","Clarithromycin is a macrolide antibiotic whose spectrum of activity includes many gram-positive (<i>Staphylococcus aureus, S. pneumoniae, and S. pyogenes</i>) and gram-negative aerobic bacteria (<i>Haemophilus influenzae, H. parainfluenzae, and Moraxella catarrhalis</i>), many anaerobic bacteria, some mycobacteria, and some other organisms including <i>Mycoplasma, Ureaplasma, Chlamydia, Toxoplasma</i>, and <i>Borrelia</i>. Other aerobic bacteria that clarithromycin has activity against include <i>C. pneumoniae and M. pneumoniae</i>. Clarithromycin has an in-vitro activity that is similar or greater than that of erythromycin against erythromycin-susceptible organisms. Clarithromycin is usually bacteriostatic, but may be bactericidal depending on the organism and the drug concentration.","An alternative medication for the treatment of acute otitis media caused by <i>H. influenzae, M. catarrhalis, or S. pneumoniae</i> in patients with a history of type I penicillin hypersensitivity. Also for the treatment of pharyngitis and tonsillitis caused by susceptible <i>Streptococcus pyogenes</i>, as well as respiratory tract infections including acute maxillary sinusitis, acute bacterial exacerbations of chronic bronchitis, mild to moderate community-acquired pneuomia, Legionnaires' disease, and pertussis. Other indications include treatment of uncomplicated skin or skin structure infections, helicobacter pylori infection, duodenal ulcer disease, bartonella infections, early Lyme disease, and encephalitis caused by <i>Toxoplasma gondii</i> (in HIV infected patients in conjunction with pyrimethamine). Clarithromycin may also decrease the incidence of cryptosporidiosis, prevent the occurence of α-hemolytic (viridans group) streptococcal endocarditis, as well as serve as a primary prevention for <i>Mycobacterium avium</i> complex (MAC) bacteremia or disseminated infections (in adults, adolescents, and children with advanced HIV infection).","KCNH2; SLCO1B1; SLCO1B3",null,"Clinical trial on-going (IRCT2014020516491N1)","Under clinical trials","2022-03-21"]
[84,"Coenzyme Q10","Coenzyme Q-10; Coenzyme Q10; Ubidecarenone","Chemical drug","DB09270","Ubidecarenone, also called coenzyme Q10, is a 1,4-benzoquinone. From his name (Q10), the Q refers to the constitutive quinone group, and 10 is related to the number of isoprenyl subunits in its tail. It is a powerful antioxidant, a lipid-soluble and essential cofactor in mitochondrial oxidative phosphorylation. The ubidecarenone is the coenzyme destined for mitochondrial enzyme complexes involved in oxidative phosphorylation in the production of ATP. It is fundamental for cells that have a high metabolic demand. Ubidecarenone is sold as a dietary supplement and is not FDA approved as a drug thus, it is not meant to treat, cure or prevent any disease. FDA does not approve this dietary supplements before sold nor regulate the manufacturing process.","5281915","303-98-0",true,"C(/C=C(/CC/C=C(/CC/C=C(/CC/C=C(/CC/C=C(/CC/C=C(/CC/C=C(/CC/C=C(/CC/C=C(/CCC=C(C)C)\\C)\\C)\\C)\\C)\\C)\\C)\\C)\\C)\\C)C1=C(C)C(=O)C(=C(C1=O)OC)OC","ACTIUHUUMQJHFO-UPTCCGCDSA-N",863.365,"NADH dehydrogenase [ubiquinone] flavoprotein 3, mitochondrial cofactor; Succinate dehydrogenase [ubiquinone] flavoprotein subunit, mitochondrial cofactor","Ubidecarenone is an essential cofactor in the mitochondrial electron transport chain. Its functions are the acceptance of electrons from the complex I and II and this activity is vital for the production of ATP. It acts as a mobile redox agent shuttling electrons and protons in the electron transport chain. Ubidecarenone also presents antioxidant activity in mitochondria and cellular membranes, protecting against peroxidation of lipid membranes as well as inhibiting oxidation of LDL-cholesterol.","Ubidecarenon has roles in many prysiological process including sulfide oxidation, regulation of mitochondrial permeability transition pore and translocation of protons and calcium ions accross biological membranes. Studies have shown its benefitial effect in treating cancer, statin myopathy, congestive heart failure and hypertension.","The diet supplements containing ubidecarenone are indicated, as stated in the product label, to assist individuals with cardiovascular complaints including congestive heart failure and systolic hypertension. In the product, ubidecarenone is used to increase the cardiac input as well as for the prevention of several other diseases like Parkinson, fibromyalgia, migraine, periodontal disease and diabetes, based on preclinical studies. It is important to highlight that these products are not FDA approved and it is recommended to use under discretion.",null,null,"Phase 2 on-going (RBR-26cq7n)","Under clinical trials","2022-03-21"]
[85,"Colesevelam","Colesevelam","Chemical drug","DB00930","Colesevelam is a bile acid sequestrant. Colesevelam is used with exercise and diet changes (restriction of cholesterol and fat intake) to reduce the amount of cholesterol and certain fatty substances in the blood. It works by binding bile acids in the intestine. Bile acids are made when cholesterol is broken down in the body. Removing these bile acids helps to lower blood cholesterol.","56843207","182815-43-6",true,"C(CCCCNCC=C)C[N+](C)(C)C.C(CCCNCC=C)CCCCCC.C(=C)CN.C(Cl)C1CO1.[Cl-]","NXOLVMFMAFCDSR-UHFFFAOYSA-M",581.802,"Bile acids binder","Colesevelam binds bile acids in the intestine and prevents their reabsorption. Colesevelam is not absorbed itself. The depletion of bile acid causes the upregulation of cholesterol 7-alpha-hydroxylase and conversion of cholesterol to bile acid. this increases the production and activity of hydroxymethyl-glutaryl-coenzyme A (HMG-CoA) reductase in the liver as well as an increase in the number of low density lipoprotein (LDL) receptors. This process clears LDL cholesterol from the blood.\r\n\r\nSerum triglyceride levels may increase or remain unchanged. The end result is increased clearance of LDL-cholesterol from the blood with decreased serum LDL-cholesterol.","Colesevelam is a high capacity bile-acid binding molecule. Colesevelam binds to bile acids in the intestine which reduces the amount of bile acids that are returned to the liver via enterohepatic circulation. Clinical studies have demonstrated that elevated levels of total cholesterol (total-C), LDL-C, and apolipoprotein B (Apo B, a protein associated with LDL-C) are associated with an increased risk of atherosclerosis in humans. Similarly, decreased levels of high-density lipoprotein cholesterol (HDL-C) are associated with the development of atherosclerosis. Epidemiological investigations have established that cardiovascular morbidity and mortality vary directly with the levels of total-C and LDL-C, and inversely with the level of HDL-C. The combination of colesevelam and an HMG-CoA reductase inhibitor is effective in further lowering serum total-C and LDL-C levels beyond that achieved by either agent alone.","For use, alone or in combination with an HMG-CoA reductase inhibitor, as adjunctive therapy to diet and exercise for the reduction of elevated LDL cholesterol in patients with primary hypercholesterolemia (Fredrickson Type IIa).",null,"Anticholesteremic drug","Phase 2 completed  (NCT01066364)","Under clinical trials","2022-03-21"]
[86,"Miricorilant","CORT118335","Chemical drug","DB16234","Miricorilant is under investigation in clinical trial NCT03818256 (Study Evaluating the Safety, Efficacy, and Pharmacokinetics of Miricorilant (CORT118335) in Obese Adult Patients With Schizophrenia and Recent Weight Gain While Taking Antipsychotic Medications (GRATITUDE)).","66550324","1400902-13-7",false,"C(c1c([nH]c(=O)[nH]c1=O)[C@H]1CC[C@@H](CC1)c1ccccc1)c1cc(C(F)(F)F)ccc1","GVVUZBSCYAVFTI-IYARVYRRSA-N",428.454,{"$nulls":4},"GCR antagonist; MCR antagonist","Hepatoprotectants","Phase 1 on-going (NCT05117489); Phase 2 terminated  (NCT03823703: Suspended by sponsor, pending investigation of abnormal laboratory values in patients with NASH)","Under clinical trials","2022-03-21"]
[87,"Costus speciosus","Thebu","Biological extract",{"$nulls":3},"89997-95-5",false,{"$nulls":9},"Phase 2 on-going (SLCTR/2015/019)","Under clinical trials","2022-03-21"]
[88,"CP-945598","Otenabant; Otenabant","Chemical drug","DB11745","Otenabant has been investigated for the treatment of Obesity.","10052040","686344-29-6",false,"O=C(N)C1(NCC)CCN(C=2N=CN=C3C2N=C(C=4C=CC=CC4Cl)N3C5=CC=C(Cl)C=C5)CC1","UNAZAADNBYXMIV-UHFFFAOYSA-N",510.429,"Cannabinoid receptor 1","Pre-clinical and clinical trial data suggest that CB-1 antagonists may have favorable effects on glucose metabolism in patients with type 2 diabetes and may also be an effective therapy for the treatment of obesity.",null,null,"CNR1; CB-1 antagonist",null,"Phase 1 completed  (NCT00706537)","Under clinical trials","2022-03-21"]
[89,"Cranberry",null,"Biological drug","DB10631","Cranberry allergenic extract is used in allergenic testing.","13506","915-67-3",true,"[Na].N(=N\\c1c2c(c(cc1)S(=O)(=O)O)cccc2)/c1c2c(cc(c1O)S(=O)(=O)O)cc(cc2)S(=O)(=O)O","KSQCYWPBMKMMHA-QUABFQRHSA-N",562.535,{"$nulls":6},"Phase 3 on-going (IRCT20150124020765N2)","Under clinical trials","2022-03-21"]
[90,"Crocin",null,"Chemical drug","DB11874","Crocin has been investigated for the treatment of Hyperglycemia, Metabolic Syndrome, Hypertriglyceridemia, and Hypercholesterolemia.","5281233  ","42553-65-1",false,"C(O[C@@H]1O[C@H](CO)[C@H]([C@@H]([C@H]1O)O)O)[C@H]1O[C@@H](OC(=O)/C(=C/C=C/C(=C/C=C/C=C(/C=C/C=C(/C(=O)O[C@@H]2O[C@H](CO[C@@H]3O[C@H](CO)[C@H]([C@@H]([C@H]3O)O)O)[C@H]([C@@H]([C@H]2O)O)O)\\C)\\C)/C)/C)[C@@H]([C@H]([C@@H]1O)O)O","SEBIKDIMAPSUBY-RTJKDTQDSA-N",976.972,{"$nulls":6},"Phase 3 on-going (IRCT20180513039634N1)","Under clinical trials","2022-03-21"]
[91,"CRV431",null,"Chemical drug",null,null,"134812041","1383420-08-3",false,"[C@H]([C@@H](CCCCCCNC(=O)C)C)(O)[C@@H]1N(C)C(=O)[C@H](C(C)C)N(C)C(=O)[C@H](CC(C)C)N(C)C(=O)[C@H](CC(C)C)N(C)C(=O)[C@@H](C)NC(=O)[C@H](C)NC(=O)[C@@H](N(C(=O)[C@@H](NC(=O)[C@@H](N(C(=O)[C@H](N(C(=O)[C@@H](NC1=O)CC)C)C)C)CC(C)C)C(C)C)C)CC(C)C","KBARHGHBFILILC-NGIJKBHDSA-N",1303.784,{"$nulls":4},"CyP inhibitor",null,"Phase 2 completed  (NCT04480710)","Under clinical trials","2022-03-21"]
[92,"Curcumin","Turmeric","Chemical drug","DB11672","Curcumin, also known as diferuloylmethane, is an active component in the golden spice turmeric (Curcuma longa) and in . It is a highly pleiotropic molecule that exhibits antibacterial, anti-inflammatory, hypoglycemic, antioxidant, wound-healing, and antimicrobial activities . Due to these properties, curcumin has been investigated for the treatment and supportive care of clinical conditions including proteinuria, breast cancer, multiple myeloma, depression, and Non Small Cell Lung Cancer (NSCLC). Despite proven efficacy against numerous experimental models, poor bioavailability due to poor absorption, rapid metabolism, and rapid systemic elimination have been shown to limit the therapeutic efficacy of curcumin . Curcumin is under investigation for the treatment and supportive care of various clinical conditions including mucositis, rectal cancer, prostate cancer, chronic schizophrenia, and Mild Cognitive Impairment (MCI) .","969516","458-37-7",true,"C(=C\\C(=O)CC(=O)/C=C/c1cc(OC)c(cc1)O)/c1cc(OC)c(cc1)O","VFLDPWHFBUODDF-FCXRPNKRSA-N",368.385,"Peroxisome proliferator-activated receptor gamma; Vitamin D3 receptor; Multidrug resistance-associated protein 5 inhibitor; Carbonyl reductase [NADPH] 1; Glutathione S-transferase P","Curcumin acts as a scavenger of oxygen species, such as hydroxyl radical, superoxide anion, and singlet oxygen and inhibit lipid peroxidation as well as peroxide-induced DNA damage . Curcumin mediates potent anti-inflammatory agent and anti-carcinogenic actions via modulating various signalling molecules. It suppresses a number of key elements in cellular signal transduction pathways pertinent to growth, differentiation, and malignant transformation; it was demonstrated _in vitro_ that curcumin inhibits protein kinases, c-Jun/AP-1 activation, prostaglandin biosynthesis, and the activity and expression of the enzyme cyclooxygenase (COX)-2 .","Intravenous application of 25 mg/kg bw curcumin to rats resulted in an increase in bile flow by 80 and 120% . In the rat model of inflammation, curcumin was shown to inhibit edema formation. In nude mouse that had been injected subcutaneously with prostate cancer cells, administration of curcumin caused a marked decrease in the extent of cell proliferation, a significant increase of apoptosis and micro-vessel density . Curcumin may exert choleretic effects by increasing biliary excretion of bile salts, cholesterol, and bilirubin, as well as increasing bile solubility . Curcumin inhibited arachidonic acid-induced platelet aggregation _in vitro_ .","No approved therapeutic indications.","PPARG; COX inhibitor","Anticancer agent; NSAID","Phase 2 on-going (NCT04315350)","Under clinical trials","2022-03-21"]
[93,"Cynara","Cynara scolymus L.","Biological extract",{"$nulls":3},"11051-97-1",false,{"$nulls":9},"Clinical trial completed (ISRCTN33165861)","Under clinical trials","2022-03-21"]
[94,"Cysteamine","2-amino-1-ethanethiol; 2-amino-ethanethiol; 2-aminoethanethiol; beta-aminoethanethiol; beta-Mercaptoethylamine; Cysteamine; MEA; Mercaptamine; Thioethanolamine; β-aminoethylthiol; β-MEA","Chemical drug","DB00847","Cystinosis is a rare disease caused by mutations in the CTNS gene that encodes for cystinosin, a protein responsible for transporting cystine out of the cell lysosome. A defect in cystinosin function is followed by cystine accumulation throughout the body, especially the eyes and kidneys.\r\n\r\nSeveral preparations of cysteamine exist for the treatment of cystinosis manifestations, some in capsule form, and others in ophthalmic solution form. In particular, cystine deposits on the eye can cause significant discomfort throughout the day and require frequent treatment with eye drops, typically every waking hour.\r\n\r\nOn August 25th 2020, the first ophthalmic solution for cystinosis requiring only 4 daily treatments was granted FDA approval.  Cysteamine eye drops are a practical and effective option for those affected by ocular cystinosis. Marketed by Recordati Rare Diseases Inc., CYSTADROPS® reduce the burden of multiple frequent medications normally administered to those with cystinosis.","6058","60-23-1",true,"C(CS)N","UFULAYFCSOUIOV-UHFFFAOYSA-N",77.152,"Cystine cleavage; Neuropeptide Y receptor type 2 other/unknown","Individuals born without the ability to metabolize cystine suffer from cystinosis, a rare genetic disorder characterized by the widespread accumulation of cystine crystals throughout the body and eye tissues. The cystine crystals may cause considerable damage, particularly in the renal tissues and corneal tissues. In some cases, renal failure can occur during childhood if the condition is left untreated. Other organs that may be affected by cystinosis include the CNS, thyroid, pancreas, muscle tissues, and gonads. \r\n\r\nCysteamine converts cystine to cysteine and cysteine-cysteamine mixed disulfides, reducing the buildup of corneal cystine crystals. This drug participates in a thiol-disulfide interchange reaction with lysosomes, leading to cysteine exit from the lysosome in patients diagnosed with cystinosis.","Cystine accumulation is the cause of organ damage in cystinosis. Cysteamine prevents the accumulation of cystine crystals in the body and is specifically prescribed to prevent kidney and eye damage. Cysteamine converts cystine into a form that may easily exit cells, preventing harmful accumulation.\r\n\r","The bitartrate salt of cysteamine is used for the oral treatment of nephropathic cystinosis and cystinuria in children 6 years old and above, and adults. The hydrochloride salt, used in eye drop preparations, is indicated for the treatment of corneal cystine crystal accumulation in patients with cystinosis.\r","GSS stimulant","Renal drug","Phase 1&2 completed  (NCT00799578: Enteric-coated cysteamine reduces ALT and AST levels in children with NAFLD without reduction in body mass index. Further studies will evaluate optimal cysteamine therapeutic dose and effect on liver histology in NAFLD.)","Under clinical trials","2022-03-21"]
[95,"Cysteamine bitartrate","2-amino-1-ethanethiol; 2-amino-ethanethiol; 2-aminoethanethiol; beta-aminoethanethiol; beta-Mercaptoethylamine; Cysteamine; MEA; Mercaptamine; Thioethanolamine; β-aminoethylthiol; β-MEA","Chemical drug","DB00847","Cystinosis is a rare disease caused by mutations in the CTNS gene that encodes for cystinosin, a protein responsible for transporting cystine out of the cell lysosome. A defect in cystinosin function is followed by cystine accumulation throughout the body, especially the eyes and kidneys.\r\n\r\nSeveral preparations of cysteamine exist for the treatment of cystinosis manifestations, some in capsule form, and others in ophthalmic solution form. In particular, cystine deposits on the eye can cause significant discomfort throughout the day and require frequent treatment with eye drops, typically every waking hour.\r\n\r\nOn August 25th 2020, the first ophthalmic solution for cystinosis requiring only 4 daily treatments was granted FDA approval.  Cysteamine eye drops are a practical and effective option for those affected by ocular cystinosis. Marketed by Recordati Rare Diseases Inc., CYSTADROPS® reduce the burden of multiple frequent medications normally administered to those with cystinosis.","23111531","27761-19-9",true,"C(CS)N.[C@@H]([C@H](C(=O)O)O)(C(=O)O)O","NSKJTUFFDRENDM-ZVGUSBNCSA-N",227.238,"Cystine cleavage; Neuropeptide Y receptor type 2 other/unknown","Individuals born without the ability to metabolize cystine suffer from cystinosis, a rare genetic disorder characterized by the widespread accumulation of cystine crystals throughout the body and eye tissues. The cystine crystals may cause considerable damage, particularly in the renal tissues and corneal tissues. In some cases, renal failure can occur during childhood if the condition is left untreated. Other organs that may be affected by cystinosis include the CNS, thyroid, pancreas, muscle tissues, and gonads. \r\n\r\nCysteamine converts cystine to cysteine and cysteine-cysteamine mixed disulfides, reducing the buildup of corneal cystine crystals. This drug participates in a thiol-disulfide interchange reaction with lysosomes, leading to cysteine exit from the lysosome in patients diagnosed with cystinosis.","Cystine accumulation is the cause of organ damage in cystinosis. Cysteamine prevents the accumulation of cystine crystals in the body and is specifically prescribed to prevent kidney and eye damage. Cysteamine converts cystine into a form that may easily exit cells, preventing harmful accumulation.\r\n\r","The bitartrate salt of cysteamine is used for the oral treatment of nephropathic cystinosis and cystinuria in children 6 years old and above, and adults. The hydrochloride salt, used in eye drop preparations, is indicated for the treatment of corneal cystine crystal accumulation in patients with cystinosis.\r",null,null,"Phase 2&3 completed  (NCT01529268: In a randomized trial, we found that 1 year of CBDR did not reduce overall histologic markers of NAFLD compared with placebo in children. Children receiving CBDR, however, had significant reductions in serum aminotransferase levels and lobular inflammation.)","Under clinical trials","2022-03-21"]
[96,"Dabigatran Etexilate","Dabigatran etexilate","Chemical drug","DB06695","Dabigatran etexilate is an oral prodrug that is hydrolyzed to the competitive and reversible direct thrombin inhibitor . Dabigatran etexilate may be used to decrease the risk of venous thromboembolic events in patients in whom anticoagulation therapy is indicated. In contrast to warfarin, because its anticoagulant effects are predictable, lab monitoring is not necessary. Dabigatran etexilate was approved by the FDA in 2010.","135565674","211915-06-9",true,"Cn1c2c(nc1CNc1ccc(cc1)C(=N)NC(=O)OCCCCCC)cc(cc2)C(=O)N(CCC(=O)OCC)c1ccccn1","KSGXQBZTULBEEQ-UHFFFAOYSA-N",227.238,"Prothrombin inhibitor","Hemostasis is a complex process that balances coagulation to prevent excessive thrombus formation or excessive bleeding. Central to the coagulation process is the serine protease thrombin (FIIa), which is synthesized as inactive prothrombin (FII) and subsequently activated by FXa/FVa, leading to a positive feedback loop and the production of large quantities of thrombin; once enough thrombin is formed, it cleaves soluble fibrinogen to form insoluble fibrin fibres that, together with aggregated platelets, form a clot. Although beneficial in wound healing, aberrant thrombus formation can lead to serious health consequences.\r\n\r\nDabigatran is a univalent reversible direct thrombin inhibitor (DTI) that competitively inhibits thrombin with a K<sub>i</sub> of 4.5 ± 0.2 nmol/L. Furthermore, the reversible nature of the inhibition is believed to allow for some normal physiological thrombin function, which may help alleviate some adverse effects associated with anticoagulation therapy. In addition, dabigatran has several glucuronidated metabolites, all of which have been shown to possess _in vitro_ activity similar to the parent compound.\r\n\r\nIn addition to a direct effect on thrombin activity, dabigatran has also been shown to inhibit platelet aggregation, another step in the coagulation pathway. However, the mechanism remains unclear as dabigatran inhibits platelet aggregation stimulated by thrombin and von Willebrand factor (vWF), but not by other pathways such as ADP- or thromboxane A2-induced aggregation.","Dabigatran etexilate is a double prodrug that is hydrolyzed to the active  by intestinal and hepatic carboxylesterases. Dabigatran is a reversible competitive thrombin inhibitor that directly inhibits the conversion by thrombin of fibrinogen to fibrin, impairing the clotting process and acting as an anticoagulant. Dabigatran use prolongs coagulation markers such as the activated partial thromboplastin time (aPTT), ecarin clotting time (ECT), thrombin time (TT), and dilute thrombin time (dTT), but not the international normalized ratio (INR), which cannot be used in this context as it can in  monitoring.\r\n\r\nAs with all anticoagulant therapies, dabigatran carries a risk of bleeding, which may increase with concomitant use of antiplatelet agents, fibrinolytic therapy, heparins, or chronic NSAID use, and should be monitored for. Premature discontinuation of dabigatran, in the absence of an alternative anticoagulant, also carries an increased risk of thromboembolic events. Due to the risk of an epidural or spinal hematoma, dabigatran should generally not be used in the context of neuraxial anesthesia or spinal puncture; if such use is unavoidable, careful monitoring should be employed. Dabigatran should not be used in patients with prosthetic heart valves due to an increased occurrence of major bleeding and thromboembolic events. Dabigatran is a substrate of the P-gp transporter and should generally not be administered together with P-gp inhibitors or inducers, especially in patients with impaired renal function. Lastly, dabigatran or any other direct-acting oral anticoagulant should not be administered in patients with triple-positive antiphospholipid syndrome (APS) due to an increased risk of recurrent thrombotic events. In case of the need for emergency reversal,  is available for use in adult patients; the safety and efficacy of  has not been established in pediatric patients yet, for whom reversal may be achieved through hemodialysis, prothrombin complex concentrates, or recombinant FVIIa. However, none of these have been sufficiently evaluated in clinical trials.","Dabigatran etexilate is available in both oral pellet and capsule form. Dabigatran etexilate pellets are indicated for the treatment of venous thromboembolic events (VTE) in pediatric patients between three months and 12 years of age who have been treated with a parenteral anticoagulant for at least 5 days. They are also indicated in the same age group to reduce the risk of recurrence of VTE in patients who have been previously treated.\r\n\r\nIn capsule form, dabigatran etexilate is indicated in adults to reduce the risk of stroke and systemic embolism associated with non-valvular atrial fibrillation and for the treatment of deep venous thrombosis (DVT) and pulmonary embolism (PE) in patients who have been treated with a parenteral anticoagulant for 5-10 days. It is also indicated in adults to reduce the risk of recurrence of DVT and PE in patients who have been previously treated and for the prophylaxis of DVT and PE in patients who have undergone hip replacement surgery. Lastly, it is indicated in pediatric patients between eight and 18 years of age for the treatment of venous thromboembolic events (VTE) in patients who have been treated with a parenteral anticoagulant for at least 5 days and to reduce the risk of recurrence of VTE in patients who have been previously treated.","thrombin inhibitor",null,"Phase 1 completed  (NCT03143166: The DE tablet demonstrated BE to the capsule; however, at high gastric pH, BA of the tablet was reduced by approximately 70%, which may lead to reduced efficacy. Data indicate the importance of examining not only BE under standard conditions, but relative BA at elevated gastric pH. Such investigations may avoid the reduced BA at elevated pH that is quite common in the target population (the elderly and/or patients treated with gastric-acid modifying co-medications), and therefore reduce treatment failure with DE.)","Under clinical trials","2022-03-21"]
[97,"Daesiho-tang",null,"Herbal medicine",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (KCT0003554)","Under clinical trials","2022-03-21"]
[98,"Dan Shao Gan Kang",null,"Traditional medicine",{"$nulls":4},false,{"$nulls":9},"Phase 2 completed  (CTR20140038)","Under clinical trials","2022-03-21"]
[99,"Dandelion","dandelion pollen extract","Biological drug","DB10755","Taraxacum officinale pollen is the pollen of the Taraxacum officinale plant. Taraxacum officinale pollen is mainly used in allergenic testing.",null,"68990-74-9",true,{"$nulls":9},"Clinical trial on-going (IRCT20161205031252N10)","Under clinical trials","2022-03-21"]
[100,"Danggui Shaoyao Powder",null,"Traditional medicine",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (ChiCTR2000038111)","Under clinical trials","2022-03-21"]
[101,"Dapagliflozin","(2S,3R,4R,5S,6R)-2-(4-Chloro-3-(4-ethoxybenzyl)phenyl)-6- (hydroxymethyl)tetrahydro-2H-pyran-3,4,5-triol; Dapagliflozin","Chemical drug","DB06292","Dapagliflozin is a sodium-glucose cotransporter 2 inhibitor indicated for managing diabetes mellitus type 2. When combined with diet and exercise in adults, dapagliflozin helps to improve glycemic control by inhibiting glucose resorption in the proximal tubule of the nephron and causing glycosuria. Dapagliflozin was approved by the FDA on Jan 08, 2014.","9887712","461432-26-8",true,"O[C@H]1[C@@H](O[C@@H]([C@H]([C@@H]1O)O)CO)c1cc(Cc2ccc(cc2)OCC)c(cc1)Cl","JVHXJTBJCFBINQ-ADAARDCZSA-N",408.878,"Sodium/glucose cotransporter 2 antagonist&inhibitor","Dapagliflozin inhibits the sodium-glucose contransporter 2(SGLT2) which is primarily located in the proximal tubule of the nephron. SGLT2 facilitates 90% of glucose resorption in the kidneys and so its inhibition allows for glucose to be excreted in the urine. This excretion allows for better glycemic control and potentially weight loss in patients with type 2 diabetes mellitus.","Dapagliflozin inhibits the sodium-glucose contransporter 2(SGLT2) which is primarily located in the proximal tubule of the nephron. SGLT2 facilitates 90% of glucose resorption in the kidneys and so its inhibition allows for glucose to be excreted in the urine. This excretion allows for better glycemic control and potentially weight loss in patients with type 2 diabetes mellitus.","Dapagliflozin is indicated to improve glycemic control in adult patients with type 2 diabetes mellitus along with diet and exercise.","SLC5A2 antagonist; SLC5A2 inhibitor","Antidiabetic drug","Phase 2 completed (NCT02426541: In this study, 8 weeks of treatment with dapagliflozin reduced liver PDFF and the volume of visceral adipose tissue in obese patients with type 2 diabetes. Although glycemic control was improved, no effect on tissue-level insulin sensitivity was observed.)","Under clinical trials","2022-03-21"]
[102,"Dawa al-Blaghm",null,"Miscellany",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (IRCT2017073135415N1)","Under clinical trials","2022-03-21"]
[103,"Deferasirox","Deferasirox","Chemical drug","DB01609","Deferasirox is an iron chelator and the first oral medication FDA approved for chronic iron overload in patients receiving long term blood transfusions.","214348","201530-41-8",true,"Oc1c(c2n(nc(n2)c2c(O)cccc2)c2ccc(cc2)C(=O)O)cccc1","BOFQWVMAQOTZIW-UHFFFAOYSA-N",373.368,"Iron chelator","Two molecules of deferasirox are capable of binding to 1 atom of iron. Deferasirox works in treating iron toxicity by binding trivalent (ferric) iron (for which it has a strong affinity), forming a stable complex which is eliminated via the kidneys.","Deferasirox is an orally active chelator that is selective for iron (as Fe3+). It is a tridentate ligand that binds iron with high affinity in a 2:1 ratio. Although deferasirox has very low affinity for zinc and copper there are variable decreases in the serum concentration of these trace metals after the administration of deferasirox. The clinical significance of these decreases is uncertain.","For the treatment of chronic iron overload due to blood transfusions (transfusional hemosiderosis) in patients 2 years of age and older.",null,"Chelating agent","Phase 1&2 completed  (NCT01278056)","Under clinical trials","2022-03-21"]
[104,"Delta-tocotrienol",null,"Chemical drug",null,null,"5282350","25612-59-3",false,"Cc1c2c(CC[C@](O2)(CC/C=C(/CC/C=C(/CCC=C(C)C)\\C)\\C)C)cc(c1)O","ODADKLYLWWCHNB-LDYBVBFYSA-N",396.615,{"$nulls":6},"Phase 2 on-going (SLCTR/2019/038)","Under clinical trials","2022-03-21"]
[105,"DHA","(4Z,7Z,10Z,13Z,16Z,19Z)-Docosahexaenoic acid; 22:6-4, 7,10,13,16,19; 22:6(n-3); 4,7,10,13,16,19-docosahexaenoic acid; all-cis-4,7,10,13,16,19-docosahexaenoic acid; all-cis-DHA; cervonic acid; DHA; Doconexent; docosa-4,7,10,13,16,19-hexaenoic acid; Docosahexaenoic acid","Chemical drug","DB03756","A mixture of fish oil and primrose oil, doconexent is used as a high-docosahexaenoic acid (DHA) supplement. DHA is a 22 carbon chain with 6 cis double bonds with anti-inflammatory effects. It can be biosythesized from alpha-linolenic acid or commercially manufactured from microalgae. It is an omega-3 fatty acid and primary structural component of the human brain, cerebral cortex, skin, and retina thus plays an important role in their development and function. The amino-phospholipid DHA is found at a high concentration across several brain subcellular fractions, including nerve terminals, microsomes, synaptic vesicles, and synaptosomal plasma membranes .","15608515","6217-54-5",true,"C(=C\\C/C=C\\CCC(=O)O)\\C/C=C\\C/C=C\\C/C=C\\C/C=C\\CC","MBMBGCFOFBJSGT-KUBAVDMBSA-N",328.496,"Peroxisome proliferator-activated receptor alpha ligand; Peroxisome proliferator-activated receptor gamma ligand; Retinoic acid receptor RXR-alpha activator; Retinoic acid receptor RXR-beta activator; Retinoic acid receptor RXR-gamma activator; Sterol reg","DHA and its conversion to other lipid signalling moleccules compete with the arachidonic acid cascade from endogenous phospholipids and shift the inflammatory state to being more anti-inflammatory. DHA inhibits endotoxin-stimulated production of IL-6 and IL-8 in human endothelial cells. Derivatives of DHA are anti-inflammatory lipid mediators. Lipid mediators resolvin D1 and protectin D1 all inhibit transendothelial migration of neutrophils, so preventing neutrophilic infiltration at sites of inflammation, resolvin D1 inhibits IL-1β production, and protectin D1 inhibits TNF and IL-1β production . Monoxydroxy derivative of DHA converted by LOX inhibit thromboxane-induced platelet aggregation. DHA supplementation has also shown to reduce the levels of serum C-reactive protein (CRP) and other circulating markers of inflammation such as neutrophils in hypertriglyceridemic men . \r\nDHA acts as a ligand at peroxisome proliferator-activated receptor (PPAR) gamma and alpha that regulate lipid signalling molecule-mediated transduction pathways and modulate inflammation. \r\nAs a natural ligand, DHA induces a protective effect in retinal tissues by activating retinoid x receptors and subsequent ERK/MAPK signaling pathway in photoreceptors to promote their survival and differentiation, stimulating the expression of antiapoptotic proteins such as Bcl-2 and preserving mitochondrial membrane potential .","DHA in the central nervous system is found in the phospholipid bilayers where it modulates the physical environment and increase the free volume within the membrane bilayer. It influences the G-protein coupled receptor activity and affects transmembrane transport and cell interaction with the exterior world. It is also reported to promote apoptosis, neuronal differentiation and ion channel activity. Like other polyunsaturated fatty acids, DHA acts as a ligand at PPARs that plays an anti-inflammatory effect and regulate inflammatory gene expression and NFκB activation. DHA also gives rise to resolvins and related compounds (e.g., protectins) through pathways involving cyclooxygenase and lipoxygenase enzymes to resolve the inflammatory responses.","Used as a high-docosahexaenoic acid (DHA) oral supplement.","PPARA ligand; PPARG ligand","Anti-inflammatory","Phase 1&2 completed  (NCT00885313: DHA supplementation improves liver steatosis and insulin sensitivity in children with NAFLD.)","Under clinical trials","2022-03-21"]
[106,"DHA-EE",null,"Chemical drug",null,null,"9831416  ","81926-94-5",true,"C(=C\\C/C=C\\C/C=C\\C/C=C\\C/C=C\\C/C=C\\CC)\\CCC(OCC)=O","ITNKVODZACVXDS-YNUSHXQLSA-N",356.55,{"$nulls":6},"Phase 2 on-going (NCT04198805)","Under clinical trials","2022-03-21"]
[107,"Diacerein","Diacerein","Chemical drug","DB11994","Diacerein is a prodrug which is metabolized to rhein. It is currently approved in France for the treatment of osteoarthritis although the use of diacerein is restricted due to the side effects including severe diarrhea . Diacerein is under investigation for the treatment of Insulin Resistance, Diabetes Mellitus (Type 2), and Diabetes-Related Complications.","26248","13739-02-1",true,"O(C(=O)C)c1c2c(C(=O)c3c(C2=O)c(OC(=O)C)ccc3)cc(c1)C(=O)O","TYNLGDBUJLVSMA-UHFFFAOYSA-N",368.297,"Oxysterols receptor LXR-alpha inhibitor; Oxysterols receptor LXR-beta inhibitor; Arylamine N-acetyltransferase inhibitor; Arachidonate 5-lipoxygenase inhibitor; Cytochrome P450 1A2 inhibitor; Cytochrome P450 3A Subfamily inhibitor; Cytochrome P450 2E1 inh","Diacerein's active metabolite rhein  reduces cartilage destruction by decreasing expression of matrix metalloproteinase (MMP)-1 and -3 as well as upregulating tissue inhibitor of matrix metalloproteinases which serve to reduce the activity of several MMPs . The anti-inflammatory action of rhein reduces the level of interleukin-1beta activity which plays a large role in reduction of extracellular matrix production, MMP activity, and continued inflammation . Rhein reduces abnormal osteoblast synthetic activity through an unknown mechanism .","Decreases inflammation and cartilage destruction and also corrects altered osteoblast acitivity   .","For the treatment of osteoarthritis affecting the hip or knee .","ALOX5 inhibitor","Antiarthritic drug; antiinflammatory agent","Phase 3 completed  (NCT02242149: Diacerein reduced mean HbA1c levels, with peak of effect at the 24th week of treatment. The drug was well tolerated and may be indicated as adjunct treatment in patients with type 2 diabetes, particularly in those with osteoarthritis.)","Under clinical trials","2022-03-21"]
[108,"Diamel","1-(p-chlorobenzenesulfonyl)-3-propylurea; 1-(p-chlorophenylsulfonyl)-3-propylurea; 1-propyl-3-(p-chlorobenzenesulfonyl)urea; 4-chloro-N-((propylamino)carbonyl)benzenesulfonamide; 4-chloro-N-[(propylamino)carbonyl]benzenesulfonamide; N-(4-chlorophenylsulfonyl)-N'-propylurea; N-(p-chlorobenzenesulfonyl)-N'-propylurea; n-propyl-N'-(p-chlorobenzenesulfonyl)urea; n-propyl-N'-p-chlorophenylsulfonylcarbamide","Chemical drug","DB00672","Chlorpropamide is an oral antihyperglycemic agent used for the treatment of non-insulin-dependent diabetes mellitus (NIDDM). It belongs to the sulfonylurea class of insulin secretagogues, which act by stimulating β cells of the pancreas to release insulin. Sulfonylureas increase both basal insulin secretion and meal-stimulated insulin release. Medications in this class differ in their dose, rate of absorption, duration of action, route of elimination and binding site on their target pancreatic β cell receptor. Sulfonylureas also increase peripheral glucose utilization, decrease hepatic gluconeogenesis and may increase the number and sensitivity of insulin receptors. Sulfonylureas are associated with weight gain, though less so than insulin. Due to their mechanism of action, sulfonylureas may cause hypoglycemia and require consistent food intake to decrease this risk. The risk of hypoglycemia is increased in elderly, debilitated and malnourished individuals. Chlorpropamide is not recommended for the treatment of NIDDM as it increases blood pressure and the risk of retinopathy (UKPDS-33). Up to 80% of the single oral dose of chlorpropramide is metabolized, likely in the liver; 80-90% of the dose is excreted in urine as unchanged drug and metabolites. Renal and hepatic dysfunction may increase the risk of hypoglycemia.","2727","94-20-2",false,"S(=O)(=O)(NC(=O)NCCC)c1ccc(cc1)Cl","RKWGIWYCVPQPMF-UHFFFAOYSA-N",276.745,"ATP-binding cassette sub-family C member 8 inhibitor","Sulfonylureas such as chlorpropamide bind to ATP-sensitive potassium channels on the pancreatic cell surface, reducing potassium conductance and causing depolarization of the membrane. Depolarization stimulates calcium ion influx through voltage-sensitive calcium channels, raising intracellular concentrations of calcium ions, which induces the secretion, or exocytosis, of insulin.","Chlorpropamide, a second-generation sulfonylurea antidiabetic agent, is used with diet to lower blood glucose levels in patients with diabetes mellitus type II. Chlorpropamide is twice as potent as the related second-generation agent glipizide.","For treatment of NIDDM in conjunction with diet and exercise.",null,null,"Phase 3 completed  (NCT00820651: This report presents the first randomized controlled trial with Diamel. Although the study was not double-blind, Diamel seems to be useful in improving metabolic control and beta cell\r\nfunction at least during the 6 months of follow-up. )","Under clinical trials","2022-03-21"]
[109,"Diammonium glycyrrhizate",null,"Chemical drug",{"$nulls":3},"80658-20-4",false,"N.C[C@@]12[C@@H]([C@]3(C)[C@@H](CC2)C(C)(C)[C@H](CC3)O[C@@H]2[C@H](O[C@@H]3O[C@H](C(=O)O)[C@H]([C@@H]([C@H]3O)O)O)[C@@H](O)[C@@H]([C@H](O2)C(=O)O)O)C(=O)C=C2[C@@]1(C)CC[C@@]1([C@@H]2C[C@](CC1)(C(=O)O)C)C","ILRKKHJEINIICQ-LEEOIRFPSA-N",839.973,{"$nulls":6},"Clinical trial on-going (ChiCTR1800018629)","Under clinical trials","2022-03-21"]
[110,"Diane-35",null,"Chemical drug",null,null,"107694","60528-19-0",false,"C[C@@]12[C@@H]3[C@@H](C3)C(=O)C=C2C(=C[C@@H]2[C@@H]1CC[C@]1([C@H]2CC[C@]1(OC(=O)C)C(=O)C)C)Cl.C[C@]12[C@H]([C@H]3[C@H](CC2)c2c(CC3)cc(cc2)O)CC[C@]1(C#C)O","RWYFURDDADFSHT-BGWUALDMSA-N",713.355,{"$nulls":6},"Phase 0 on-going (ChiCTR1900024310)","Under clinical trials","2022-03-21"]
[111,"Digestive enzymes","Digestive enzyme","Supplement",{"$nulls":4},false,{"$nulls":9},"Phase 2 on-going (JPRN-UMIN000017266)","Under clinical trials","2022-03-21"]
[112,"Digoxin","12β-hydroxydigitoxin; Digoxin","Chemical drug","DB00390","Digoxin is one of the oldest cardiovascular medications used today. It is a common agent used to manage atrial fibrillation and the symptoms of heart failure. Digoxin is classified as a cardiac glycoside and was initially approved by the FDA in 1954.\r\n\r\nThis drug originates from the foxglove plant, also known as the _Digitalis_ plant, studied by William Withering, an English physician and botanist in the 1780s. Prior to this, a Welsh family, historically referred to as the _Physicians of Myddvai_, formulated drugs from this plant. They were one of the first to prescribe cardiac glycosides, according to ancient literature dating as early as the 1250s.","2724385","20830-75-5",true,"O[C@]12[C@@](C)([C@H](CC2)C2=CC(=O)OC2)[C@H](O)C[C@H]2[C@H]1CC[C@H]1[C@]2(C)CC[C@@H](C1)O[C@H]1C[C@H](O)[C@@H]([C@H](O1)C)O[C@H]1C[C@H](O)[C@@H]([C@H](O1)C)O[C@H]1C[C@H](O)[C@@H]([C@H](O1)C)O","LTMHDMANZUZIPE-PUGKRICDSA-N",780.949,"Sodium/potassium-transporting ATPase subunit alpha-1 inhibitor","Digoxin exerts hemodynamic, electrophysiologic, and neurohormonal effects on the cardiovascular system. It reversibly inhibits the Na-K ATPase enzyme, leading to various beneficial effects.  The Na-K ATPase enzyme functions to maintain the intracellular environment by regulating the entry and exit of sodium, potassium, and calcium (indirectly). Na-K ATPase is also known as the _sodium pump_. The inhibition of the sodium pump by digoxin increases intracellular sodium and increases the calcium level in the myocardial cells, causing an increased contractile force of the heart. This improves the left ventricular ejection fraction (EF), an important measure of cardiac function.\r\n\r\nDigoxin also stimulates the parasympathetic nervous system via the vagus nerve leading to sinoatrial (SA) and atrioventricular (AV) node effects, decreasing the heart rate. Part of the pathophysiology of heart failure includes neurohormonal activation, leading to an increase in norepinephrine. Digoxin helps to decrease norepinephrine levels through activation of the parasympathetic nervous system.","Digoxin is a positive inotropic and negative chronotropic drug, meaning that it increases the force of the heartbeat and decreases the heart rate. The decrease in heart rate is particularly useful in cases of atrial fibrillation, a condition characterized by a fast and irregular heartbeat. The relief of heart failure symptoms during digoxin therapy has been demonstrated in clinical studies by increased exercise capacity and reduced hospitalization due to heart failure and reduced heart failure-related emergency medical visits. Digoxin has a narrow therapeutic window.\r\n\r\n**A note on cardiovascular risk**\r\n\r\nDigoxin poses a risk of rapid ventricular response that can cause ventricular fibrillation in patients with an accessory atrioventricular (AV) pathway. Cardiac arrest as a result of ventricular fibrillation is fatal. An increased risk of fatal severe or complete heart block is present in individuals with pre-existing sinus node disease and AV block who take digoxin.\r\n\r","Digoxin is indicated in the following conditions: 1) For the treatment of mild to moderate heart failure in adult patients. 2) To increase myocardial contraction in children diagnosed with heart failure. 3) To maintain control ventricular rate in adult patients diagnosed with chronic atrial fibrillation.\r\n\r\nIn adults with heart failure, when it is clinically possible, digoxin should be administered in conjunction with a diuretic and an angiotensin-converting enzyme (ACE) inhibitor for optimum effects.\r\n\r","ATP1A1 inhibitor; ATP1A2 inhibitor; ATP1A3 inhibitor; ATP1A4 inhibitor","Antiarrhythmic","Phase 2 on-going (NCT04216693: These data identify PKM2 as a mediator and therapeutic target for regulating liver sterile inflammation, and demonstrate a novel role for digoxin that can effectively protect the liver from ASH and NASH.)","Under clinical trials","2022-03-21"]
[113,"Dihydromyricetin","(+)-ampelopsin; (+)-dihydromyricetin; Ampelopsin; Ampeloptin; Telocapil","Chemical drug","DB15645","Dihydromyricetin is under investigation in clinical trial NCT03606694 (Effect of Dihydromirycetin on Glycemic Control, Insulin Sensitivity and Insulin Secretion in Type 2 Diabetes Mellitus).","161557","27200-12-0",false,"O=C1c2c(O[C@@H]([C@H]1O)c1cc(O)c(c(c1)O)O)cc(cc2O)O","KJXSIXMJHKAJOD-LSDHHAIUSA-N",320.253,{"$nulls":6},"Clinical trial on-going (ChiCTR-TRC-12002377)","Under clinical trials","2022-03-21"]
[114,"Doxycycline","5-hydroxy-α-6-deoxytetracycline; 6-alpha-deoxy-5-oxytetracycline; 6alpha-deoxy-5-oxytetracycline; 6α-deoxy-5-oxytetracycline; Anhydrous doxycycline; Doxycycline; Doxycycline (anhydrous); Doxycycline anhydrous","Chemical drug","DB00254","Doxycycline is a broad-spectrum antibiotic synthetically derived from oxytetracycline .  This drug is a second-generation tetracycline, exhibiting lesser toxicity than first-generation tetracyclines . Doxycycline may be used to treat a wide range of bacterial infections, depending on the results of antibiotic susceptibility testing.","54671203","564-25-0",false,"O[C@@]12[C@H]([C@H](N(C)C)C(=C(C2=O)C(=O)N)O)[C@@H](O)[C@H]2C(=C1O)C(=O)c1c([C@@H]2C)cccc1O","JBIWCJUYHHGXTC-AKNGSSGZSA-N",444.44,"16S ribosomal RNA binder","In bacterial replication, an interaction that is important for translation initiation of proteins occurs at the 3′ end of the 16S rRNA, found on the ribosome on the 30S subunit , ,  .  The 30S subunit is the smaller subunit of the ribosome of prokaryotes, including bacteria. \r\n\r\n Tetracyclines such as doxycycline are thought to inhibit translation by binding to the 16S rRNA portion of the ribosome , preventing binding of tRNA to the RNA-30S bacterial ribosomal subunit,  which is necessary for the delivery of amino acids for protein synthesis.  As a result of the above actions, the initiation of protein synthesis by polyribosome formation is blocked. This stops the replication of bacteria and produces a bacteriostatic effect  .","The tetracyclines, including doxycycline, are mainly bacteriostatic and are thought to exert antimicrobial effects by the inhibition of protein synthesis.   Bacteriostatic antibiotics suppress the growth of bacteria, or keep them in the stationary phase of growth . The tetracyclines, including doxycycline, have a similar antimicrobial spectrum of activity against a variety of gram-positive and gram-negative microorganisms, treating numerous infectious diseases. Cross-resistance of these microorganisms to tetracyclines is a common occurrence .   Doxycycline shows favorable intra-cellular penetration, with bacteriostatic activity on a wide range of bacteria . Doxycycline has antiparasitic effects , , . In addition to the above effects, this drug has demonstrated anti-inflammatory actions, which may help to manage inflammatory conditions such as rosacea .","Doxycycline is indicated for the treatment of various infections by gram-positive and gram-negative bacteria, aerobes and anaerobes, as well other types of bacteria. A complete list of organisms is available in the FDA label and in the \"indications\" section of this drug entry .\r\n\r\nThe following are some of the major infections that may be treated with doxycycline :\r\n\r\nRocky mountain spotted fever, typhus fever and the typhus group, Q fever, rickettsialpox, and tick fevers caused by Rickettsiae\r\n\r\nRespiratory tract infections caused by Mycoplasma pneumoniae\r\n\r\nLymphogranuloma venereum caused by Chlamydia trachomatis\r\n\r\nPsittacosis (ornithosis) caused by Chlamydia psittaci\r\n\r\nTrachoma caused by Chlamydia trachomatis, although the infectious agent is not always eliminated as judged by immunofluorescence\r\n\r\nInclusion conjunctivitis caused by Chlamydia trachomatis\r\n\r\nUncomplicated urethral, endocervical or rectal infections in adults caused by Chlamydia trachomatis\r\n\r\nNongonococcal urethritis caused by Ureaplasma urealyticum\r\n\r\nRelapsing fever due to Borrelia recurrentis\r\n\r\n**A note regarding anti-microbial resistance**\r\n\r\nIt is important to note that doxycycline is not the drug of choice in the treatment of any type of staphylococcal infection.\r\nUp to 44 percent of strains of Streptococcus pyogenes and 74 percent of Streptococcus faecalis have been found to be resistant to tetracyclines. Therefore, tetracyclines such as doxycycline should not be used to treat streptococcal infections unless the microorganism has been demonstrated to be susceptible .",null,null,"Clinical trial on-going (EUCTR2006-001774-24-GB)","Under clinical trials","2022-03-21"]
[115,"DS102",null,"Miscellany",{"$nulls":4},false,{"$nulls":9},"Phase 2 completed  (NCT02941549: These data suggest epeleuton may have potential for cardiovascular risk reduction and nonalcoholic fatty liver disease by simultaneously targeting hypertriglyceridemia, hyperglycemia, and systemic inflammation. Further trials are planned.)","Under clinical trials","2022-03-21"]
[116,"Dulaglutide","LY2189265","Biological drug","DB09045","Dulaglutide, marketed by Eli Lilly as Trulicity, is a once-weekly subcutaneous glucagon-like peptide-1 (GLP-1) receptor agonist designed using recombinant DNA technology; it has been approved as an adjunct therapy to diet and exercise in the management of  2 diabetes (T2DM). Dulaglutide was initially approved by the FDA in 2014, and in February 2020 was approved for use in patients with T2DM and multiple cardiovascular risk factors for the prevention of cardiovascular events. It is the first T2DM drug approved to reduce major adverse cardiovascular events (MACE) risk in primary and secondary prevention populations.",null,"923950-08-7",true,{"$nulls":3},"Glucagon-like peptide 1 receptor agonist","Dulaglutide activates the GLP-1 receptor found in pancreatic beta cells, increasing intracellular cyclic AMP (cAMP) in beta cells, leading to insulin release and subsequent reduction of blood glucose concentrations. Additionally, dulaglutide decreases glucagon secretion and slows gastric emptying.","Dulaglutide reduces fasting glucose concentrations and reduces postprandial glucose (PPG) concentrations in patients with type 2 diabetes mellitus through the agonism of the GLP-1 receptor. This drug primarily acts as an incretin mimetic hormone or analog of human glucagon-like peptide-1, which normally acts on the GLP-1 receptor.","Dulaglutide is as an adjunct therapy to diet and exercise for glycemic control in adults with type 2 diabetes mellitus. Additionally, it is indicated to reduce the risk of major adverse cardiovascular events (MACE) in adult type 2 diabetes mellitus patients with cardiovascular disease or multiple cardiovascular risk factors.","GLP1R agonist","Improve insulin resistance","Clinical trial completed (NCT03590626: When included in the standard treatment for type 2 diabetes, dulaglutide significantly reduces LFC and improves GGT levels in participants with NAFLD. There were non-significant reductions in PFC, liver stiffness, serum AST and serum ALT levels. Dulaglutide could be considered for the early treatment of NAFLD in patients with type 2 diabetes.)","Under clinical trials","2022-03-21"]
[117,"EDP-305",null,"Chemical drug",{"$nulls":3},"1933507-63-1",false,"O[C@H]1[C@@H]2[C@@H]([C@@]3([C@H]([C@H]1CC)C[C@@H](CC3)O)C)CC[C@]1([C@H]2CC[C@@H]1[C@@H](CCNC(=O)NS(=O)(=O)c1ccc(cc1)C(C)(C)C)C)C","SJKLCUGQVVYDCX-HRNVLBFRSA-N",630.936,{"$nulls":4},"FXR agonist","Enhance lipid metabolism","Phase 2 completed (NCT03421431: Non-alcoholic fatty liver disease is a chronic hepatic disease that can progress to non-alcoholic steatohepatitis (NASH), which is associated with an increased risk of cirrhosis and liver cancer. Results from this phase II study support continued development of EDP-305, an oral farnesoid X receptor agonist, for the treatment of patients with NASH.)","Under clinical trials","2022-03-21"]
[118,"Efamax",null,"Miscellany",{"$nulls":3},"13292-46-1, 62534-43-4",false,{"$nulls":8},"Antimycobacterial drug","Phase 2 completed  (NCT00819338)","Under clinical trials","2022-03-21"]
[119,"Elafibranor","Elafibranor","Chemical drug","DB05187","Elafibranor (code name GFT505) is a multimodal and pluripotent medication for treatment of atherogenic dyslipidemia for an overweight patient with or without diabetes. It is an oral treatment that acts on the 3 sub-types of PPAR (PPARa, PPARg, PPARd) with a preferential action on PPARa. As of February 2016, elafibranor has completed 8 clinical trials and a phase III is in progress.","9864881","923978-27-2",false,"CC1=C(OC(C)(C(O)=O)C)C(C)=CC(/C([H])=C([H])/C(C2=CC=C(SC)C=C2)=O)=C1","AFLFKFHDSCQHOL-IZZDOVSWSA-N",384.497,"Peroxisome proliferator-activated receptor alpha; Peroxisome proliferator-activated receptor delta; Peroxisome proliferator-activated receptor gamma","GFT505 is an oral treatment that acts on the 3 sub-types of PPAR (PPARa, PPARg, PPARd) with a preferential action on PPARa. It has a sophisticated mechanism of action. It is able to differentially recruit cofactors to the nuclear receptor, which subsequently lead to differential regulation of genes and biological effect. Therefore, the ability to identify and profile the activity of selective nuclear receptor modulator (SNuRMs) is a powerful approach to select innovative drug candidates with improved efficacy and diminished side effects. These pluripotent and multimodal molecules have significant positive effects on obesity, insulin-resistance and diabetes, atherosclerosis, inflammation, and the lipid triad (increasing of HDL cholesterol, lowering of triglycerides and LDL cholesterol).\r",null,"Investigated for use/treatment in atherosclerosis and diabetes mellitus type 2.","PPARA; PPARD; PPARG","Anti-inflammatory","Phase 3 terminated (NCT02704403: Study did not meet the predefined primary surrogate efficacy endpoint, no safety issues identified.)","Failed in clinical trials","2022-03-21"]
[120,"Elobixibat","Elobixibat","Chemical drug","DB12486","Elobixibat has been used in trials studying the treatment and basic science of Dyslipidemia, Constipation, Chronic Constipation, Functional Constipation, and Chronic Idiopathic Constipation.","9939892","439087-18-0",false,"O=S1(=O)c2c(N(CC(C1)(CCCC)CCCC)c1ccccc1)cc(c(c2)OCC(=O)N[C@@H](C(=O)NCC(=O)O)c1ccccc1)SC","XFLQIRAKKLNXRQ-UUWRZZSWSA-N",695.904,{"$nulls":4},"SLC10A1 inhibitor","Gastrointestinal drug","Phase 2 completed  (NCT04235205: Elobixibat resolved constipation in the short-term, and was well tolerated with both short-term and long-term treatment. The evidence supports the use of this novel approach to increase intracolonic concentrations of endogenous bile acid for the treatment of chronic constipation.)","Under clinical trials","2022-03-21"]
[121,"Embryonic Bovine Liver Extract Tablets",null,"Biological extract",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (ChiCTR-TRC-09000404)","Under clinical trials","2022-03-21"]
[122,"Empagliflozin","(1S)-1,5-anhydro-1-(4-chloro-3-{4-[(3S)-tetrahydrofuran-3-yloxy]benzyl}phenyl)-D-glucitol; 1-chloro-4-(glucopyranos-1-yl)-2-(4-(tetrahydrofuran-3-yloxy)benzyl)benzene; Empagliflozin","Chemical drug","DB09038","Empagliflozin is an inhibitor of sodium-glucose co-transporter-2 (SGLT2), the transporters primarily responsible for the reabsorption of glucose in the kidney. It is used clinically as an adjunct to diet and exercise, often in combination with other drug therapies, for the management of type 2 diabetes mellitus.\r\n\r\nThe first known inhibitor of SGLTs, phlorizin, was isolated from the bark of apple trees in 1835 and researched extensively into the 20th century, but was ultimately deemed inappropriate for clinical use given its lack of specificity and significant gastrointestinal side effects. Attempts at overcoming these limitations first saw the development of O-glucoside analogs of phlorizin (e.g. ), but these molecules proved relatively pharmacokinetically unstable. The development of C-glucoside phlorizin analogs remedied the issues observed in the previous generation, and led to the FDA approval of  in 2013 and both  and empagliflozin in 2014. As the most recently approved of the \"flozin\" drugs, empagliflozin carries the highest selectivity for SGLT2 over SGLT1 (approximately 2700-fold).","11949646","864070-44-0",true,"O[C@H]1[C@H](c2cc(Cc3ccc(cc3)O[C@H]3CCOC3)c(cc2)Cl)O[C@@H]([C@H]([C@@H]1O)O)CO","OBWASQILIWPZMG-QZMOQZSNSA-N",450.915,"Sodium/glucose cotransporter 2 inhibitor","The vast majority of glucose filtered through the glomerulus is reabsorbed within the proximal tubule, primarily via SGLT2 (sodium-glucose linked co-transporter-2) which is responsible for ~90% of the total glucose reabsorption within the kidneys. Na<sup>+</sup>/K<sup>+</sup>-ATPase on the basolateral membrane of proximal tubular cells utilize ATP to actively pump Na+ ions into the interstitium surrounding the tubule, establishing a Na<sup>+</sup> gradient within the tubular cell. SGLT2 on the apical membrane of these cells then utilize this gradient to facilitate secondary active co-transport of both Na+ and glucose out of the filtrate, thereby reabsorbing glucose back into the blood – inhibiting this co-transport, then, allows for a marked increase in glucosuria and decrease in blood glucose levels. Empagliflozin is a potent inhibitor of renal SGLT2 transporters located in the proximal tubules of the kidneys and works to lower blood glucose levels via an increase in glucosuria.\r\n\r\nEmpagliflozin also appears to exert cardiovascular benefits - specifically in the prevention of heart failure - independent of its blood glucose-lowering effects, though the exact mechanism of this benefit is not precisely understood. Several theories have been posited, including the potential inhibition of Na<sup>+</sup>/H<sup>+</sup> exchanger (NHE) 1 in the myocardium and NHE3 in the proximal tubule, reduction of pre-load via diuretic/natriuretic effects and reduction of blood pressure, prevention of cardiac fibrosis via suppression of pro-fibrotic markers, and reduction of pro-inflammatory adipokines.","Empagliflozin lowers blood glucose levels by preventing glucose reabsorption in the kidneys, thereby increasing the amount of glucose excreted in the urine. It has a relatively long duration of action requiring only once-daily dosing. Patients should be monitored closely for signs and symptoms of ketoacidosis regardless of blood glucose level as empagliflozin may precipitate diabetic ketoacidosis in the absence of hyperglycemia. As its mechanism of action is contingent on the renal excretion of glucose, empagliflozin may be held in cases of acute kidney injury and/or discontinued in patients who develop chronic renal disease. \r\n\r\nThe overexcretion of glucose creates a sugar-rich urogenital environment which increases the risk of urogenital infections - including urosepsis, pyelonephritis, mycotic infections, and even Fournier's gangrene - in both male and female patients - monitor closely for signs and symptoms of developing infection.","Empagliflozin is indicated as an adjunct to diet and exercise to improve glycemic control in adult patients with type 2 diabetes. It is also indicated to reduce the risk of cardiovascular death in adult patients with both type 2 diabetes mellitus and established cardiovascular disease.\r\n\r\nEmpagliflozin is also available as a combination product with either metformin and linagliptin as an adjunct to diet and exercise in the management of type 2 diabetes mellitus in adults.\r\n\r\nAn extended-release combination product containing empagliflozin, metformin, and linagliptin was approved by the FDA in January 2020 for the improvement of glycemic control in adults with type 2 diabetes mellitus when used adjunctively with diet and exercise.\r\n\r\nEmpagliflozin is also approved to reduce the risk of cardiovascular mortality and hospitalization in adults with heart failure with reduced ejection fraction regardless of whether or not the patient has concomitant diabetes.\r\n\r\nEmpagliflozin is not approved for use in patients with type 1 diabetes.","SLC5A2 inhibitor; SGLT-2 inhibitor","Improve insulin resistance","Clinical trial completed (NCT02686476: When included in the standard treatment for type 2 diabetes, empagliflozin reduces liver fat and improves ALT levels in patients with type 2 diabetes and NAFLD.)","Under clinical trials","2022-03-21"]
[123,"Emricasan","IDN-6556","Chemical drug","DB05408","Emricasan is the first caspase inhibitor tested in human which has received orphan drug status by FDA. It is developed by Pfizer and made in such a way that it protects liver cells from excessive apoptosis.","12000240","254750-02-2",false,"N(C(=O)C(=O)N[C@H](C(=O)N[C@H](C(=O)COc1c(F)c(F)cc(c1F)F)CC(=O)O)C)c1c(C(C)(C)C)cccc1","SCVHJVCATBPIHN-SJCJKPOMSA-N",569.508,"Caspase-1; Caspase-3; Caspase-7","IDN-6556 significantly improves markers of liver damage in patients infected with the Hepatitis C virus (HCV), an infection that affects up to 170m patients worldwide. IDN-6556 represents a new class of drugs that protect the liver from inflammation and cellular damage induced by viral infections and other causes. Various studies have also shown that it  significantly lowers aminotransferase activity in HCV patients and appeared to be well tolerated.",null,"Investigated for use/treatment in hepatitis (viral, C), liver disease, and transplantation (organ or tissue).","caspase inhibitor","Anti-inflammatory","Phase 2 completed (Emricasan treatment did not improve liver histology in patients with NASH fibrosis despite target engagement and may have worsened fibrosis and ballooning. Caspase inhibition lowered serum alanine aminotransferase in the short-term but may have directed cells to alternative mechanisms of cell death, resulting in more liver fibrosis and hepatocyte ballooning. Clinical trial number: Clinical Trials.gov #NCT02686762.)","Failed in clinical trials","2022-03-21"]
[124,"EPA-E",null,"Chemical drug",null,null,"9831415","73310-10-8",false,"C(CCCCCCCCCCCCCCC)CCCC(=O)OCC","YBKSMWBLSBAFBQ-UHFFFAOYSA-N",340.592,{"$nulls":4},"DGAT1 inhibitor; PLA2 inhibitor","Antiinflammatory agent; Neuroprotective drug","Phase 2 completed (In a phase 2 trial, EPA-E had no significant effect on the histologic features of NASH. EPA-E reduced subjects' levels of triglyceride compared with placebo, without any increase in serious adverse events. Clinicaltrials.gov Number: 01154985.)","Failed in clinical trials","2022-03-21"]
[125,"Epanova","n-3 fatty acids; Omega 3 fatty acids; Omega-3; Omega-3 acid; Omega-3 acid triglycerides; Omega-3 fatty acid; Omega-3 phospholipids; Omega-3 polyunsaturated fatty acids; Omega-3 polyunsaturates; Omega-3-acid triglycerides; Phospholipids; ω-3 fatty acids","Chemical drug","DB11133","Omega-3 fatty acids are polyunsaturated fatty acids (PUFAs) with a double bond at the third carbon atom from the end of the carbon chain. The three types of omega-3 fatty acids involved in human physiology are α-linolenic acid (ALA) (found in plant oils), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA) (both commonly found in fish oil that originally come from microalgae that is further consumed by phytoplankton, a source of diet for fish). Omega-3 fatty acids play a critical role in metabolism and cellular function and they are available as daily supplements. On September 8, 2004, the U.S. Food and Drug Administration gave \"qualified health claim\" status to EPA and DHA omega-3 fatty acids. Therapeutic products containing omega-3 fatty acid and its derivatives for treatment of hypertriglyceridemia include Lovaza, Omtryg, Epanova, and Vascepa.","56842239","329042-31-1",true,"OC(=O)CCCCCCC/C=C\\C/C=C\\C/C=C\\CC.OC(=O)CCC/C=C\\C/C=C\\C/C=C\\C/C=C\\C/C=C\\CC.OC(=O)CC/C=C\\C/C=C\\C/C=C\\C/C=C\\C/C=C\\C/C=C\\CC","QPEOIOLHJXXJFN-GNGJDXFDSA-N",909.39,"Peroxisome proliferator-activated receptor gamma ligand; Peroxisome proliferator-activated receptor alpha activator; Sterol regulatory element-binding protein 1 inhibitor","Omega-3 fatty acids mediate anti-inflammatory effects and increased levels of EPA or DHA has shown to decrease the levels of PGE2 and 4 series-LT. \r\nEicosapentaenoic acids compete with constitutive levels of arachidonic acid in cell membranes for the same desaturation enzymes and produce 3-series prostaglandins and thromboxanes, and 5-series leukotrienes which have low pro-inflammatory potential. The alteration in leukotriene biosynthesis due to higher concentration of omega-3 fatty acids compared to arachidonic acid underlies the anti-inflammatory effects. \r\nEPA and DHA also give rise to resolvins and related lipid signalling molecules such as protectins via cyclooxygenase and lipoxygenase pathways, which have anti-inflammatory effects. They inhibit transendothelial migration of neutrophils and inhibit TNF and IL-1β production. Omega-3 fatty acids also decrease adhesion molecule expression on leukocytes and on endothelial cells and decrease intercellular adhesive interactions.\r\nOmega-3 (or n-3) polyunsaturated fatty acids (PUFAs) and their metabolites are natural ligands for peroxisome proliferator-activated receptor (PPAR) gamma that regulates inflammatory gene expression and NFκB activation. PPAR alpha activation is also associated with induction of COX-2 expression. \r\nThe role of EPA and DHA in reducing triglyceride levels include inhibition of acyl-CoA:1,2-diacylglycerol acyltransferase, increased mitochondrial and peroxisomal-beta-oxidation in the liver, decreased lipogenesis in the liver, and increased plasma lipoprotein lipase activity. They also may reduce triglyceride synthesis because they are poor substrates for the enzymes responsible for TG synthesis, and EPA and DHA inhibit esterification of other fatty acids.","Omega-3 fatty acids are triglycerides that get broken down into smaller fatty acid units. They act to reduce plasma triglyceride levels however increase the cholesterol levels and are thought to possess potent antiarrythmic effects. Polyunsaturated fatty acids including eicosapentaenoic and docosahexaenoic acid mediate important cellular function such as inhibition of platelet function, prolongation of bleeding time, anti-inflammatory effects and reduction of plasma fibrinogen. Polyunsaturated fatty acids are components of the phospholipids that form the structures of the cell membranes and also serve as energy source. They form eicosanoids which are important signalling molecules with wide-ranging functions in the body's cardiovascular, pulmonary, immune and endocrine systems. DHA tends to exist in high concentrations in the retina, brain (via uptake by Mfsd2a as a transporter), and sperm.","Provided as daily supplements. Aa preparation of omega-3-acid ethyl esters is licensed in UK for prevention of recurrent events after myocardial infarction in addition to treatment of hypertriglyceridaemia.","PPARG ligand; PPARA activator","Enhance lipid metabolism","Clinical trial completed (NCT04281121)","Under clinical trials","2022-03-21"]
[126,"Ergocalciferol","(3β,5Z,7E,22E)-9,10-secoergosta-5,7,10(19),22-tetraen-3-ol; (5Z,7E,22E)-(3S)-9,10-seco-5,7,10(19),22-ergostatetraen-3-ol; (5Z,7E,22E)-(3S)-9,10-secoergosta-5,7,10(19),22-tetraen-3-ol; Activated ergosterol; Ercalciol; Oleovitamin D2; Viosterol; Vitamin D2","Supplement","DB00153","Ergocalciferol is an inactivated vitamin D analog. It is synthesized by some plants in the presence of UVB light. The production of ergocalciferol was prompted by the identification of dietary deficiency, more specifically vitamin D, as the main causative factor for the development of rickets. Ergocalciferol was isolated for the first time from yeast in 1931 and its structure was elucidated in 1932.\r\n\r\nErgocalciferol is considered the first vitamin D analog and is differentiated from  by the presence of a double bond between C22 and C23 and the presence of a methyl group at C24. These modifications reduce the affinity of ergocalciferol for the vitamin D binding protein resulting in faster clearance, limits its activation, and alters its catabolism.\r\n\r\nThe first approved product containing ergocalciferol under the FDA records was developed by US Pharm Holdings and was FDA approved in 1941.","5280793","50-14-6",true,"C[C@]12[C@H](/C(=C/C=C/3\\C(=C)CC[C@@H](C3)O)/CCC2)CC[C@@H]1[C@@H](/C=C/[C@@H](C(C)C)C)C","MECHNRXZTMCUDQ-RKHKHRCZSA-N",396.659,"Vitamin D3 receptor agonist; Voltage-dependent calcium channel inducer","For its activity, ergocalciferol is required to be transformed to its major active circulating hydroxylated metabolite and transported to the target organs in order to bind to its target, the vitamin D receptor.\r\n\r\nThe activation of the vitamin D receptor is part of the vitamin D endocrine system and it is described by the production of a change in the transcription rates of the vitamin D receptor target genes. The target genes in the DNA affected by the presence of ergocalciferol are called vitamin D response elements which are dependent on co-modulators.\r\n\r\nThe vitamin D receptor is a transcription factor and member of the steroid hormone nuclear receptor family. It presents a DNA binding domain (VDRE) that, when activated, recruits coregulatory complexes to regulate the genomic activity.\r\n\r\nAdditionally, ergocalciferol presents nongenomic effects such as the stimulation of intestinal calcium transport via transcaltachia.","After the activation of the vitamin D receptor, some of the biological changes produced by ergocalciferol include mobilization and accretion of calcium and phosphorus in the bone, absorption of calcium and phosphorus in the intestine, and reabsorption of calcium and phosphorus in the kidney. \r\n\r\nSome other effects known to be produced due to the presence of vitamin D are osteoblast formation, fetus development, induction of pancreatic function, induction of neural function, improvement of immune function, cellular growth and cellular differentiation.\r\n\r\nWhen compared to its vitamin D counterpart , ergocalciferol has been shown to present a reduced induction of calcidiol and hence, it is less potent.\r\n\r\nErgocalciferol supplementation in patients with end-stage renal disease has been shown to generate a significant benefit in lab parameters of bone and mineral metabolism as well as improvement in glycemic control, serum albumin levels and reduced levels of inflammatory markers.","Ergocalciferol is indicated for the treatment of hypoparathyroidism, refractory rickets, and familial hypophosphatemia.\r\n\r\nHypoparathyroidism is the result of inadequate parathyroid hormone production that occurs due to the presence of damage or removal of the parathyroid glands. This condition produces decreased calcium and increased phosphorus levels.\r\n\r\nRickets is a condition produced due to a deficiency in vitamin D, calcium or phosphorus. However, this condition can also be related to renal diseases. It is characterized to present weak or soft bones.\r\n\r\nFamilial hypophosphatemia is characterized by the impaired transport of phosphate and an altered vitamin D metabolism in the kidneys. The presence of this condition can derive in the presence of osteomalacia, bone softening and rickets.","VDR agonist; VDR modulator","Calcium regulator; Vitamin source drug","Phase 3 completed  (NCT02132442)","Under clinical trials","2022-03-21"]
[127,"Eubacterium hallii",null,"Supplement",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (NTR4913)","Under clinical trials","2022-03-21"]
[128,"Evogliptin","Evoglitin","Chemical drug","DB12625","Evogliptin has been used in trials studying the treatment and screening of Osteoporosis, Renal Impairment, Type 2 Diabetes Mellitus, Diabetes Mellitis Type 2, and Diabetes Mellitus, Type 2.","25022354","1222102-29-5",false,"C(=O)(C[C@@H](Cc1c(F)cc(c(c1)F)F)N)N1[C@H](COC(C)(C)C)C(=O)NCC1","LCDDAGSJHKEABN-MLGOLLRUSA-N",401.429,{"$nulls":4},"DPP4 inhibitor",null,"Phase 4 completed  (NCT03910361)","Under clinical trials","2022-03-21"]
[129,"Exenatide","Exenatide; Exenatide synthetic; Exendin 4; Exendin-4; Synthetic exendin-4","Biological drug","DB01276","Exenatide is a glucagon-like peptide-1 (GLP-1) analog. It functions to activate the GLP-1 receptor and increases insulin secretion, decrease glucagon secretion, and slow gastric emptying to improve glycemic control. Exenatide was given FDA approval on April 28, 2005.","45588096","141758-74-9",true,"S(CC[C@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)CNC(=O)[C@@H](NC(=O)CNC(=O)[C@@H](N)Cc1nc[nH]c1)CCC(=O)O)[C@H](O)C)Cc1ccccc1)[C@H](O)C)CO)CC(=O)O)CC(C)C)CO)CCCCN)CCC(=O)N)C(=O)N[C@H](C(=O)N[C@H](C(=O)N[C@H](C(=O)N[C@H](C(=O)N[C@@H](C(C)C)C(=O)N[C@@H](CCCNC(=N)N)C(=O)N[C@@H](CC(C)C)C(=O)N[C@H](C(=O)N[C@@H]([C@H](CC)C)C(=O)N[C@H](C(=O)N[C@H](C(=O)N[C@H](C(=O)N[C@H](C(=O)N[C@H](C(=O)NCC(=O)NCC(=O)N1[C@H](C(=O)N[C@H](C(=O)N[C@H](C(=O)NCC(=O)N[C@H](C(=O)N2[C@H](C(=O)N3[C@@H](CCC3)C(=O)N3[C@@H](CCC3)C(=O)N[C@@H](CO)C(=O)N)CCC2)C)CO)CO)CCC1)CC(=O)N)CCCCN)CC(C)C)Cc1c2c([nH]c1)cccc2)CCC(=O)O)Cc1ccccc1)C)CCC(=O)O)CCC(=O)O)CCC(=O)O)C","HTQBXNHDCUEHJF-XWLPCZSASA-N",4186.637,"Glucagon-like peptide 1 receptor agonist","Exenatide is a human glucacon-like peptide-1(GLP-1) receptor agonist. By activating this receptor, insulin secretion is increased and glucagon secretion is decreased in a glucose dependant manner. Exenatide also slows gastric emptying and decreases food intake. These effects work synergistically to improve glycemic control by reducing the likelihood of hyper and hypoglycemia.","When patients take exenatide the body's natural response to glucose is modulated. More insulin and less glucagon are released in response to glucose, though in cases of hypoglycemia a normal amount of glucagon is released. Exenatide also slows gastric emptying, leading to a slower and prolonged release of glucose into the systemic circulation. Together these effects prevent hyper and hypoglycemia.","Exenatide is indicated for improving glycemic control in adults with type 2 diabetes mellitus along with diet and exercise.","GLP1R activator; GLP1R agonist","Improve insulin resistance","Phase 4 completed  (NCT02303730: All three agents showed efficacy regarding glycaemic control and metabolic benefits; however, exenatide showed the greatest efficacy. β-cell function improved in all treatment groups; hence, early initiation of β-cell-protective therapy may halt the decline in β-cell function in type 2 diabetes.)","Under clinical trials","2022-03-21"]
[130,"EYP001a",null,"Chemical drug",{"$nulls":4},false,{"$nulls":7},"FXR agonist;FXR modulator","Enhance lipid metabolism","Phase 2 completed  (NCT03812029)","Under clinical trials","2022-03-21"]
[131,"Ezetimibe","Ezetimibe","Chemical drug","DB00973","Ezetimibe is a lipid-lowering compound that inhibits intestinal cholesterol and phytosterol absorption. The discovery and research of this drug began in the early 1990s, after the intravenous administration of radiolabelled ezetimibe in rats revealed that it was being localized within enterocytes of the intestinal villi - this prompted studies investigating the effect of ezetimibe on intestinal cholesterol absorption. Ezetimibe is used as an adjunctive therapy to a healthy diet to lower cholesterol levels in primary hyperlipidemia, mixed hyperlipidemia, homozygous familial hypercholesterolemia (HoFH), and homozygous sitosterolemia (phytosterolemia).\r\n\r\nUnlike other classes of cholesterol-reducing compounds including statins and bile acid sequestrants, ezetimibe has a distinct mechanism of action involving the sterol transporter Niemann-Pick C1-Like 1 (NPC1L1), and is unique in that it does not affect the absorption of fat-soluble nutrients such as fat-soluble vitamins, triglycerides, or bile acids. In genetically NPC1L1-deficient mice, a 70% reduction in intestinal cholesterol absorption was seen, and these mice were insensitive to ezetimibe treatment - it was determined based on these findings that NPC1L1 plays an essential role in promoting intestinal cholesterol uptake via an ezetimibe-sensitive pathway. By interfering with the intestinal uptake of cholesterol and phytosterols, ezetimibe reduces the delivery of intestinal cholesterol to the liver.","150311","163222-33-1",true,"C(C[C@H](O)c1ccc(cc1)F)[C@@H]1[C@H](N(C1=O)c1ccc(cc1)F)c1ccc(cc1)O","OLNTVTPDXPETLC-XPWALMASSA-N",409.432,"Niemann-Pick C1-like protein 1 inhibitor; Sterol O-acyltransferase 1 inhibitor; Aminopeptidase N other","Ezetimibe mediates its blood cholesterol-lowering effect via selectively inhibiting the absorption of cholesterol and phytosterol by the small intestine without altering the absorption of fat-soluble vitamins and nutrients. The primary target of ezetimibe is the cholesterol transport protein Niemann-Pick C1-Like 1 (NPC1L1) protein. NPC1L1 is expressed on enterocytes/gut lumen (apical) as well as the hepatobiliary (canalicular) interface and plays a role in facilitating internalization of free cholesterol into the enterocyte in conjunction with the adaptor protein 2 (AP2) complex and clathrin. Once cholesterol in the gut lumen or bile is incorporated into the cell membrane of enterocytes, it binds to the sterol-sensing domain of NPC1L1 and forms a NPC1L1/cholesterol complex. The complex is then internalized or endocytosed by joining to AP2 clathrin, forming a vesicle complex that is translocated for storage in the endocytic recycling compartment.\r\n\r\nEzetimibe does not require exocrine pancreatic function for its pharmacological activity; rather, it localizes and appears to act at the brush border of the small intestine. Ezetimibe selectively blocks the NPC1L1 protein in the jejunal brush border, reducing the uptake of intestinal lumen micelles into the enterocyte. Overall, ezetimibe causes a decrease in the delivery of intestinal cholesterol to the liver and reduction of hepatic cholesterol stores and an increase in clearance of cholesterol from the blood. While the full mechanism of action of ezetimibe in reducing the entry of cholesterol into both enterocytes and hepatocytes is not fully understood, one study proposed that ezetimibe prevents the NPC1L1/sterol complex from interacting with AP2 in clathrin coated vesicles and induces a conformational change in NPC1L1, rendering it incapable of binding to sterols. Another study suggested that ezetimibe disrupts the function of other protein complexes involved in regulating cholesterol uptake, including the CAV1–annexin 2 heterocomplex.","Ezetimibe was shown to reduce the levels of total cholesterol (total-C), low-density lipoprotein cholesterol (LDL-C), apoprotein B (Apo B), non-high-density lipoprotein cholesterol (non-HDL-C), and triglycerides (TG), and increase high-density lipoprotein cholesterol (HDL-C) in patients with hyperlipidemia. This therapeutic effect was more profound when ezetimibe was co-administered with a statin or fenofibrate compared to either treatment alone. In clinical trials involving patients with homozygous and heterozygous familial hypercholesterolemia and in those with sitosterolemia, a recommended therapeutic dose of ezetimibe was effective in reducing the LDL levels by 15-20% while increasing HDL-C by 2.5-5%.\r\n\r\nThe effects of increased exposure to ezetimibe secondary to moderate-severe hepatic impairment have not been assessed - patients meeting these criteria should avoid the use of ezetimibe. Post-marketing reports indicate the potential for myopathy and rhabdomyolysis in patients taking ezetimibe, and this risk appears to be exacerbated in patients concurrently receiving, or having recently received, statin therapy.","Ezetimibe is indicated to reduce elevated total-C, LDL-C, Apo B, and non-HDL-C in patients with primary hyperlipidemia, alone or in combination with an HMG-CoA reductase inhibitor (statin). It is also indicated to reduce elevated total-C, LDL-C, Apo B, and non-HDL-C in patients with mixed hyperlipidemia in combination with fenofibrate, and to reduce elevated total-C and LDL-C in patients with homozygous familial hypercholesterolemia (HoFH), in combination with atorvastatin or simvastatin. Ezetimibe may also be used to reduce elevated sitosterol and campesterol in patients with homozygous sitosterolemia (phytosterolemia).","SOAT1 inhibitor;","Enhance lipid metabolism","Phase 2 completed  (NCT01766713: Ezetimibe improved FRS whereas placebo did not. FRS and CAC scores improved in a greater proportion of patients with ezetimibe; this trend did not reach significance. These findings indicate the utility and feasibility of monitoring cardiovascular risk in a NASH trial. The utility of CAC scores may be higher in trials of longer duration (⩾52 weeks) and with older patients (age ⩾45).)","Under clinical trials","2022-03-21"]
[132,"Femarelle","DT56a","Biological extract",{"$nulls":3},"670226-96-7",false,{"$nulls":8},"Immunomodulator","Phase 4 withdrawn (NCT01269320: Sponsors decision)","Under clinical trials","2022-03-21"]
[133,"Fenofibrate","2-(4-(4-Chlorobenzoyl)phenoxy)-2-methylpropanoic acid 1-methylethyl ester; Fenofibrate; Finofibrate; FNF; Isopropyl (4'-(p-chlorobenzoyl)-2-phenoxy-2-methyl)propionate; Isopropyl 2-(4-(4-chlorobenzoyl)phenoxy)-2-methylpropionate; Procetofen","Chemical drug","DB01039","Fenofibrate is a fibric acid derivative like  and . Fenofibrate is used to treat primary hypercholesterolemia, mixed dyslipidemia, severe hypertriglyceridemia.\r\n\r\nFenofibrate was granted FDA approval on 31 December 1993.","3339","49562-28-9",true,"CC(OC(C(C)(OC1=CC=C(C(C2=CC=C(Cl)C=C2)=O)C=C1)C)=O)C","YMTINGFKWWXKFG-UHFFFAOYSA-N",360.837,"Peroxisome proliferator-activated receptor alpha agonist; Matrix metalloproteinase-25 inhibitor; Nuclear receptor subfamily 1 group I member 2 partial agonist","Fenofibrate activates peroxisome proliferator activated receptor alpha (PPARα), increasing lipolysis, activating lipoprotein lipase, and reducing apoprotein C-III. PPARα is a nuclear receptor and its activation alters lipid, glucose, and amino acid homeostasis. Activation of PPARα activates transcription of gene transcription and translation that generates peroxisomes filled with hydrogen peroxide, reactive oxygen species, and hydroxyl radicals that also participate in lipolysis. This mechanism of increased lipid metabolism is also associated with increased oxidative stress on the liver. In rare cases this stress can lead to cirrhosis and chronic active hepatitis.","Fenofibrate is a fibrate that activates peroxisome proliferator activated receptor alpha (PPARα) to alter lipid metabolism and treat primary hypercholesterolemia, mixed dyslipidemia, and severe hypertriglyceridemia. Fenofibrate requires once daily dosing and has a half life of 19-27 hours so its duration of action is long. Fenofibrate capsules are given at a dose of 50-150mg daily so the therapeutic index is wide. Patients should be counselled about the risk of rhabdomyolysis, myopathy, and cholelithiasis when taking fibrates.","Fenofibrate is indicated as adjunctive therapy to diet to reduce elevated LDL-C, Total-C, Triglycerides, and Apo B, and to increase HDL-C adults with primary hypercholesterolemia or mixed dyslipidemia. Fenofibrate is also indicated to treat adults with severe hypertriglyceridemia.","PPARA agonist; NR1I2 partial agonist","Anti-inflammatory","Phase 2 completed  (NCT02354976: OM-3CA and fenofibrate reduced serum triglycerides but did not reduce liver fat. Fenofibrate increased total liver volume and total liver fat volume vs OM-3CA, indicating a complex effect of fenofibrate on human hepatic lipid metabolism.)","Under clinical trials","2022-03-21"]
[134,"Fenretinide","4-HPR; 4-hydroxy(phenyl)retinamide; 4-hydroxyphenyl retinamide; Fenretinide; N-(4-hydroxyphenyl)all-trans retinamide","Chemical drug","DB05076","A synthetic retinoid that is used orally as a chemopreventive against prostate cancer and in women at risk of developing contralateral breast cancer. It is also effective as an antineoplastic agent.","5288209","65646-68-6",false,"C(=C\\C(=C\\C=C\\C(=C\\C(=O)Nc1ccc(cc1)O)\\C)\\C)/C1=C(C)CCCC1(C)C","AKJHMTWEGVYYSE-FXILSDISSA-N",391.555,null,"Fenretinide inhibits the growth of several human cancer cell lines, acting through both retinoid-receptor-dependent and retinoid-receptor-independent mechanisms.1In vivo, fenretinide selectively accumulates in breast tissue and is particularly active in inhibiting rat mammary carcinogenesis.1 An important feature of fenretinide is its ability to inhibit cell growth through the induction of apoptosis rather than through differentiation, an effect that is strikingly different from that of vitamin A.1 In contrast to tamoxifen, which inhibits only estrogen receptor (ER)-positive tumors, fenretinide induces apoptosis in both ER-positive and ER-negative breast cancer cell lines.2 All of these properties render fenretinide an attractive candidate for breast cancer chemoprevention.",null,"Investigated for use/treatment in macular degeneration.","RARB agonist; RARG agonist","Anti-fibrosis","Phase 2 suspended (NCT00546455: This study was terminated due to expired drug with possibility of re-starting in the future.)","Under clinical trials","2022-03-21"]
[135,"Fenugreek","Trigonella Foenum-graecum Seed Extract","Biological extract",{"$nulls":3},"8016-13-5",false,"O1[C@@H]2[C@@H]([C@@]3([C@H]([C@H]4[C@@H]([C@@]5([C@@H](CC4)C[C@@H](O[C@@H]4O[C@@H]([C@@H](O)[C@H](O)[C@H]4O)CO[C@@H]4OC[C@@H](O)[C@H](O)[C@H]4O)[C@H](O)C5)C)CC3)C2)C)[C@@H]([C@@]1(O)CC[C@H](CO[C@@H]1O[C@@H]([C@@H](O)[C@H](O)[C@H]1O)CO)C)C","TVNGRDSDHVARNR-SYQAKRSCSA-N",907.057,{"$nulls":6},"Phase 2&3 completed (NCT02303314)","Under clinical trials","2022-03-21"]
[136,"Firsocostat","GS-0976; GS-ACC; ND-630; NDI-010976; Firsocostat","Chemical drug","DB16166","Firsocostat is under investigation in clinical trial NCT02781584 (Safety, Tolerability, and Efficacy of Selonsertib, Firsocostat, and Cilofexor in Adults With Nonalcoholic Steatohepatitis (NASH)).","71528744","1434635-54-7",false,"C([C@H](OC1CCOCC1)c1c(OC)cccc1)n1c2c(c(=O)n(c1=O)C(C(=O)O)(C)C)c(c(s2)c1ncco1)C","ZZWWXIBKLBMSCS-FQEVSTJZSA-N",569.636,{"$nulls":4},"ACC inhibitor","Enhance lipid metabolism","Phase 2 completed (In a randomized placebo-controlled trial of patients with NASH, we found 12-week administration of GS-0976 20 mg decreased hepatic steatosis, selected markers of fibrosis, and liver biochemistry. ClinicalTrials.gov ID NCT02856555.)","Under clinical trials","2022-03-21"]
[137,"Fish oil","Fish oil containing omega-3 acids; Fish oils; Omega-3 fish oil","Biological drug","DB13961","Fish oil is a component of SMOFLIPID, which was FDA approved in July 2016. It is indicated in adults as a source of calories and essential fatty acids for parenteral nutrition when oral or enteral nutrition is not possible, insufficient, or contraindicated.\r\n\r\nMore commonly, fish oil refers to the omega-3-fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) . In general, dietary or pharmaceutical intake of these acids is primarily the only way to increase their levels in the human body where they are overall an essential element to dietary health as they have demonstrated abilities in minimizing or preventing hypertriglyceridemia when taken as an adjunct to a healthy diet .\r\n\r\nSuch fish oils are available in both non-prescription and prescription-only varieties at different concentrations. For many individuals, taking non-prescription fish oils as part of their multivitamin regimen is an effective way to supplement their diets with the healthy fatty acids. However, prescription-only fish oil products are sometimes prescribed for individuals who demonstrate severe (>= 500 mg/dL) hypertriglyceridemia .\r\n\r\nFurthermore, a variety of studies regarding additional potential actions of fish oil omega-3-fatty acids EPA and DHA are ongoing. Such experimental actions include inflammation modulation, cardioprotective effects, the attenuation of oxidative stress, and more. Regardless, the specific mechanisms of action for these effects have yet to be formally elucidated.",null,"8016-13-5",true,{"$nulls":3},"Diacylglycerol O-acyltransferase 2 agonist; Prostaglandin G/H synthase 2 inhibitor; Free fatty acid receptor 4 agonist&inhibits downstream inflammation cascades; Voltage gated L-type calcium channel inhibitor; Sodium channel protein inhibitor; Free radica","The specific mechanism of action by which the fish oil EPA and DHA acids are capable of reducing serum triglyceride levels is not yet fully understood . Nevertheless, it is proposed that such omega-3-fatty acids may not be the preferred substrates of the enzyme diacylglycerol O-acyltransferase that participates in the generation of triglycerides; that  they might interact with nuclear transcription factors that manage lipogenesis; or that their presence and increase in levels can cause cellular metabolism to subsequently shift toward a decrease in triglyceride synthesis and an increase in fatty acid oxidation . Moreover, the EPA and DHA acids are also believed to be able to promote apolipoprotein B degradation in the liver through the stimulation of an autophagic process . It may also be possible that these fish oil acids can accelerate the clearance of very-low-density lipoprotein (VLDL) particles and chylomicron . The combination of all these actions results in fewer VLDL particles being assembled and secreted, which is of considerable importance as VLDL particles are the major endogenous source of triglycerides .\r\n\r\nMoreover, new paradigms of how inflammation is contained and dissipated involve various newly discovered chemical mediators, resolvins, and protectins . Such agents are believed to be directly involved in blocking neutrophil migration, infiltration, recruitment, as well as blocking T-cell migration and promoting T-cell apoptosis . Additionally, such protectins can also reduce tumor necrosis factor and interferon secretion . Of particular importance, however, is the fact that protectins and resolvins are exclusively derived from omega-3-fatty acids and that EPA is the substrate of the resolvins family and DHA can be converted to both resolvins and protectins . It is believed that these effects of such fish oil acids underlie the actions that fish oil have demonstrated on eliciting stability for vulnerable inflammatory plaques .\r\n\r\nFinally, fish oil acids have demonstrated certain direct electrophysiological effects on the myocardium . In animal studies, it was shown that the ventricular fibrillation threshold could be increased in both animals fed or infused with omega-3-fatty acids . Further studies subsequently revealed that such fatty acids could reduce both sodium currents and L-type calcium currents on a cellular and ion channel level . It is consequently hypothesized that during ischemia, a reduction in the sodium ion current protects hyperexcitable tissue, and a reduction in the calcium ion current could reduce arrhythmogenic depolarizing currents - and that perhaps the use of EPA and DHA fish oil acids could facilitate such activity . For the time being, however, omega-3-fatty acids in pharmaceutical supplement form have not been shown to elicit such protection against heart conditions .","In general, the only practical method of obtaining and increasing the levels of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) fish oil omega-3-fatty acids in the body is to consume them directly from foods and/or dietary supplements . Having EPA and DHA is important because they facilitate numerous important functions in the human body. As an example, such supplementation of fish oil EPA and DHA demonstrates a legitimate ability to decrease triglyceride levels as their presence in the body can act as poor substrates for the enzymes that are ordinarily responsible for triglyceride synthesis and also inhibit the esterification of other fatty acids, among other mechanisms .\r\n\r\nMoreover, such fish oil acids can become important components of the phospholipids that form the structures of cell membranes . Specifically, DHA is particularly high in the retina, brain, and sperm . Additionally, these acids also provide energy for the body and are used to form eicosanoids - signaling molecules that have similar chemical structures to the fish oil fatty acids from which they are derived . Furthermore, such eicosanoids possess wide-ranging functions in the cardiovascular, pulmonary, immune, and endocrine systems .","Under FDA approval, fish oil pharmaceuticals are typically products consisting of a combination of the omega-3-fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) and are indicated primarily as an adjunct to diet to reduce triglyceride levels in adult patients with severe (>=500 mg/dL) hypertriglyceridemia .\r\n\r\nUnder EMA approval, such fish oil pharmaceuticals comprised of virtually the same fish and fish oil derived omega-3-fatty acids EPA and DHA are indicated specifically for (a) adjuvant treatment in secondary prevention after myocardial infarction, in addition to other standard therapy (ie. statins, antiplatelet medicinal products, beta blockers, ACE inhibitors), and (b) as a supplement to diet when dietary measures alone are insufficient to produce an adequate response, particularly with type IV hypertriglyceridemia in monotherapy or type IIb/III in combination with statins, when control of triglycerides is insufficient . In addition, prescribing information for EMA approved fish oil pharmaceuticals are also indicated as an adjunct to diet to reduce very high (>=500 mg/dL) triglyceride levels in adult patients, much like similar FDA approved indications .",null,null,"Phase 2&3 completed  (NCT00681408: N-3 PUFAs at 3000 mg/day for one year did not lead to an improvement in the primary outcome of histological activity in NASH patients (⩾ 2 point NAS reduction). N-3 led to reduced liver fat by multiple measures. Other metabolic effects were not seen, although no detrimental effects were apparent. Whether longer duration, higher dose, or different composition of n-3 therapy would lead to additional benefits is uncertain.)","Under clinical trials","2022-03-21"]
[138,"Flaxseed","flaxseed allergenic extract; Flaxseed extract","Biological drug","DB10708","Flax seed allergenic extract is used in allergenic testing.","164475","8001-26-1, 94350-04-6",true,"O1[C@@H]([C@@H](O)[C@H](O)[C@@H](O)[C@@H]1O)CO.OC[C@@H]([C@@H](Cc1cc(OC)c(O)cc1)CO)Cc1cc(OC)c(O)cc1","MJYQFWSXKFLTAY-OVEQLNGDSA-N",542.578,{"$nulls":5},"Anti-inflammatory; Antioxidant; Antineoplastic drug","Clinical trial on-going (NCT03734510)","Under clinical trials","2022-03-21"]
[139,"Fluconazole","Diflucan; Difluconazole; Fluconazole; Triflucan","Chemical drug","DB00196","Fluconazole, commonly known as _Diflucan_, is an antifungal drug used for the treatment of both systemic and superficial fungal infections in a variety of tissues.  It was initially approved by the FDA in 1990. This drug is an _azole_ antifungal, in the same drug family as  and . Fluconazole has many advantages over the other antifungal drugs including the option of oral administration. The side effect profile of this drug is minimal. It has been demonstrated as an efficacious treatment for vaginal yeast infections in one single dose.","3365","86386-73-4",true,"C(Cn1cncn1)(Cn1cncn1)(O)c1c(F)cc(cc1)F","RFHAOTPXVQNOHP-UHFFFAOYSA-N",306.276,"Cytochrome P450 51 inhibitor","Fluconazole is a very selective inhibitor of fungal cytochrome P450 dependent enzyme _lanosterol 14-α-demethylase_. This enzyme normally works to convert _lanosterol_ to _ergosterol_, which is necessary for fungal cell wall synthesis.  The free nitrogen atom located on the azole ring of fluconazole binds with a single iron atom located in the heme group of lanosterol 14-α-demethylase. This prevents oxygen activation and, as a result, inhibits the demethylation of lanosterol, halting the process of ergosterol biosynthesis.  Methylated sterols are then found to accumulate in the fungal cellular membrane, leading to an arrest of fungal growth. These accumulated sterols negatively affect the structure and function of the fungal cell plasma membrane.\r\n\r\nFluconazole resistance may arise from an alteration in the amount or function of the target enzyme (lanosterol 14-α-demethylase), altered access to this enzyme, or a combination of the above. Other mechanisms may also be implicated, and studies are ongoing.","Fluconazole has been demonstrated to show fungistatic activity against the majority of strains of the following microorganisms, curing fungal infections:\r\n\r\n_Candida albicans, Candida glabrata (Many strains are intermediately susceptible), Candida parapsilosis, Candida tropicalis, Cryptococcus neoformans_\r\n\r\nThis is achieved through steroidal inhibition in fungal cells, interfering with cell wall synthesis and growth as well as cell adhesion, thereby treating fungal infections and their symptoms.\r\n\r\nThe fungistatic activity of fluconazole has also been shown in normal and immunocompromised animal models with both systemic and intracranial fungal infections caused by _Cryptococcus neoformans_ and for systemic infections caused by Candida albicans.  It is important to note that resistant organisms have been found against various strains of organisms treated with fluconazole. This further substantiates the need to perform susceptibility testing when fluconazole is considered as an antifungal therapy. \r\n\r\n\r\n**A note on steroidal effects of fluconazole**\r\n\r\nThere has been some concern that fluconazole may interfere with and inactivate human steroids/hormones due to the inhibition of hepatic cytochrome enzymes.  Fluconazole has demonstrated to be more selective for _fungal_ cytochrome P-450 enzymes than for a variety of mammalian cytochrome P-450 enzymes. Fluconazole 50 mg administered daily for up to 28 days in individuals of reproductive age has been show to have no effect on testosterone plasma concentrations of males and plasma concentrations of steroids in females. A 200-400 mg dose of fluconazole showed no clinically relevant effect on steroid levels or on ACTH-stimulated steroid response in healthy males, in one clinical study mentioned on the European Medicines Agency label. Other studies have shown no significant effects of fluconazole on steroid levels, further confirming these data.","Fluconazole can be administered in the treatment of the following fungal infections:\r\n\r\n 1) Vaginal yeast infections caused by Candida\r\n 2) Systemic Candida infections\r\n 3) Both esophageal and oropharyngeal candidiasis \r\n 4) Cryptococcal meningitis\r\n 5) UTI (urinary tract infection) by Candida\r\n 6) Peritonitis (inflammation of the peritoneum) caused by Candida\r\n\r\n**A note on fungal infection prophylaxis**\r\n\r\nPatients receiving bone marrow transplantation who are treated with cytotoxic chemotherapy and/or radiation therapy may be predisposed to candida infections, and may receive fluconazole as prophylactic therapy.\r\n\r\n**A note on laboratory testing**\r\n\r\nObtaining specimens for fungal culture and other important laboratory studies such as serology or pathology is advised before starting fluconazole therapy in order to isolate the organisms to be eliminated through treatment. It is permissible to start therapy before the results are available, however, adjusting the therapy once laboratory results confirm the causative organism may be necessary.\r","CYP51A1 inhibitor","Antifungal","Phase 1 completed (NCT03610945)","Under clinical trials","2022-03-21"]
[140,"Folic acid","Vitamin B9; Folacin; Folate; Folic acid; N-[(4-{[(2-amino-4-oxo-1,4-dihydropteridin-6-yl)methyl]amino}phenyl)carbonyl]-L-glutamic acid; N-pteroyl-L-glutamic acid; PGA; PteGlu; Pteroyl-L-glutamate; Pteroyl-L-glutamic acid; Pteroyl-L-monoglutamic acid; Pteroylglutamic acid; Vitamin B9; Vitamin Bc; Vitamin M","Supplement","DB00158","Folic acid, also known as folate or Vitamin B9, is a member of the B vitamin family and an essential cofactor for enzymes involved in DNA and RNA synthesis. More specifically, folic acid is required by the body for the synthesis of purines, pyrimidines, and methionine before incorporation into DNA or protein. Folic acid is particularly important during phases of rapid cell division, such as infancy, pregnancy, and erythropoiesis, and plays a protective factor in the development of cancer. As humans are unable to synthesize folic acid endogenously, diet and supplementation is necessary to prevent deficiencies. For example, folic acid is present in green vegetables, beans, avocado, and some fruits.\r\n\r\nIn order to function within the body, folic acid must first be reduced by the enzyme dihydrofolate reductase (DHFR) into the cofactors dihydrofolate (DHF) and tetrahydrofolate (THF). This important pathway, which is required for de novo synthesis of nucleic acids and amino acids, is disrupted by anti-metabolite therapies such as  as they function as DHFR inhibitors to prevent DNA synthesis in rapidly dividing cells, and therefore prevent the formation of DHF and THF. When used in high doses such as for cancer therapy, or in low doses such as for Rheumatoid Arthritis or psoriasis,  impedes the body's ability to create folic acid. This results in a deficiency of coenzymes and a resultant buildup of toxic substances that are responsible for numerous adverse side effects. As a result, supplementation with 1-5mg of folic acid is recommended to prevent deficiency and a number of side effects associated with MTX therapy including mouth ulcers and gastrointestinal irritation.  (also known as folinic acid) supplementation is typically used for high-dose MTX regimens for the treatment of cancer. Levoleucovorin and leucovorin are analogs of tetrahydrofolate (THF) and are able to bypass DHFR reduction to act as a cellular replacement for the co-factor THF.\r\n\r\nThere are also several antiepileptic drugs (AEDs) that are associated with reduced serum and red blood cell folate, including  (CBZ),  (PHT), or barbiturates. Folic acid is therefore often provided as supplementation to individuals using these medications, particularly to women of child-bearing age. \r\n\r\nInadequate folate levels can result in a number of health concerns including cardiovascular disease, megaloblastic anemias, cognitive deficiencies, and neural tube defects (NTDs). Folic acid is typically supplemented during pregnancy to prevent the development of NTDs and in individuals with alcoholism to prevent the development of neurological disorders, for example.","135398658","59-30-3",true,"O=c1c2c([nH]cc(n2)CNc2ccc(cc2)C(=O)N[C@@H](CCC(=O)O)C(=O)O)nc(n1)N","OVBPIULPVIDEAO-LBPRGKRZSA-N",441.404,"Folate receptor gamma binder; Folate receptor beta binder; Folate receptor alpha","Folic acid, as it is biochemically inactive, is converted to tetrahydrofolic acid and methyltetrahydrofolate by dihydrofolate reductase (DHFR). These folic acid congeners are transported across cells by receptor-mediated endocytosis where they are needed to maintain normal erythropoiesis, synthesize purine and thymidylate nucleic acids, interconvert amino acids, methylate tRNA, and generate and use formate. Using vitamin B12 as a cofactor, folic acid can normalize high homocysteine levels by remethylation of homocysteine to methionine via methionine synthetase.","Folic acid is a water-soluble B-complex vitamin found in foods such as liver, kidney, yeast, and leafy, green vegetables. Also known as folate or Vitamin B9, folic acid is an essential cofactor for enzymes involved in DNA and RNA synthesis. More specifically, folic acid is required by the body for the synthesis of purines, pyrimidines, and methionine before incorporation into DNA or protein. Folic acid is the precursor of tetrahydrofolic acid, which is involved as a cofactor for transformylation reactions in the biosynthesis of purines and thymidylates of nucleic acids. Impairment of thymidylate synthesis in patients with folic acid deficiency is thought to account for the defective deoxyribonucleic acid (DNA) synthesis that leads to megaloblast formation and megaloblastic and macrocytic anemias. Folic acid is particularly important during phases of rapid cell division, such as infancy, pregnancy, and erythropoiesis, and plays a protective factor in the development of cancer. As humans are unable to synthesize folic acid endogenously, diet and supplementation is necessary to prevent deficiencies. In order to function properly within the body, folic acid must first be reduced by the enzyme dihydrofolate reductase (DHFR) into the cofactors dihydrofolate (DHF) and tetrahydrofolate (THF). This important pathway, which is required for de novo synthesis of nucleic acids and amino acids, is disrupted by anti-metabolite therapies such as  as they function as DHFR inhibitors to prevent DNA synthesis in rapidly dividing cells, and therefore prevent the formation of DHF and THF. \r\n\r\nIn general, folate serum levels below 5 ng/mL indicate folate deficiency, and levels below 2 ng/mL usually result in megaloblastic anemia.","Folic acid is indicated for the treatment of folic acid deficiency, megaloblastic anemia, and in anemias of nutritional origins, pregnancy, infancy, or childhood.","FOLR2 binder",null,"Phase 3 on-going (IRCT20150819023685N2)","Under clinical trials","2022-03-21"]
[141,"Foralumab","Foralumab","Biological drug","DB16170","Foralumab is under investigation in clinical trial NCT03291249 (Assessment of the Safety of Foralumab, an Oral Anti-cd3 Antibody, in Patients With NASH and T2DM).",null,"946415-64-1",false,{"$nulls":9},"Phase 2 withdrawn (NCT03291249: Due to MOH request.)","Under clinical trials","2022-03-21"]
[142,"Fructose",null,"Chemical drug","DB04173",null,"2723872","30237-26-4",true,"[C@H]([C@@H](C(=O)CO)O)([C@@H](CO)O)O","BJHIKXHVCXFQLS-UYFOZJQFSA-N",180.156,"Maltoporin",{"$nulls":4},"Intravenous nutrition drug","Clinical trial on-going (NCT03783195)","Under clinical trials","2022-03-21"]
[143,"FT-4101",null,"Miscellany",{"$nulls":4},false,{"$nulls":7},"FASN inhibitor","Enhance lipid metabolism","Phase 1&2 terminated  (NCT04004325: sponsor decision)","Under clinical trials","2022-03-21"]
[144,"FTZ",null,"Chemical drug",null,null,"16015442",null,false,"Clc1c(CNc2nc([nH]n2)c2occc2)c(F)ccc1","AHOHWELPUXLPOF-UHFFFAOYSA-N",292.701,{"$nulls":6},"Clinical trial on-going (ChiCTR1900025938)","Under clinical trials","2022-03-21"]
[145,"Fucoidan",null,"Chemical drug",null,null,"92023653","9072-19-9",false,"S(=O)(=O)(O[C@H]1[C@@H](O)[C@H](O)[C@H](O[C@H]1C)C)O","NLMDZXKCTWKRSQ-IBISWUOJSA-N",242.249,{"$nulls":6},"Clinical trial completed (NCT02875392: Altogether, these studies suggest the possibility for future development of fucoxanthin as a one-compound-multiple-target or pro-drug type pharmaceutical or nutraceutical treatment for neurodegenerative disorders.)","Under clinical trials","2022-03-21"]
[146,"FucoVital",null,"Supplement",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (NCT03625284)","Under clinical trials","2022-03-21"]
[147,"Garlic",null,"Biological drug","DB10532","Garlic allergenic extract is used in allergenic testing.","6850761",null,true,"S(=O)(CC(N)C(=O)O)CC=C.S(=O)(SCC=C)CC=C","NEVNZJWAVFPOQZ-UHFFFAOYSA-N",339.504,{"$nulls":6},"Clinical trial on-going (IRCT20170206032417N4)","Under clinical trials","2022-03-21"]
[148,"GB1211",null,"Chemical drug",null,null,"132201704",null,false,"C1=C(C=C(C(=C1F)F)F)C2=CN(N=N2)C3C(C(OC(C3O)SC4=CC(=CN=C4)Br)CO)O","FNCLKJPMEFPXOR-UHFFFAOYSA-N",533.3,{"$nulls":4},"Gelactin-3 inhibitor","Anti-fibrosis","Phase 1 completed  (NCT03809052)","Under clinical trials","2022-03-21"]
[149,"Gemcabene","Gemcabene","Chemical drug","DB05123","Gemcabene is a new drug that lowers low-density lipoprotein cholesterol (LDL-C), decreases triglycerides, and raises high-density lipoprotein cholesterol (HDL-C).","157692","183293-82-5",false,"CC(C(O)=O)(C)CCCCOCCCCC(C)(C)C(O)=O","SDMBRCRVFFHJKR-UHFFFAOYSA-N",302.411,{"$nulls":3},"Investigated for use/treatment in atherosclerosis, cardiovascular disorders, and hyperlipidemia.","ACC inhibitor; apo C-III inhibitor; CRP inhibitor; CCR2 receptor antagonist; CCR5 receptor antagonist; lipoprotein A inhibitor; PPAR agonist; sulfatase inhibitor","Enhance lipid metabolism; Anti-fibrosis","Phase 2 terminated  (NCT03436420: Terminated due to lack of efficacy and safety concerns.)","Failed in clinical trials","2022-03-21"]
[150,"Genistein","4',5,7-trihydroxyisoflavone; 5,7-dihydroxy-3-(4-hydroxyphenyl)-4H-1-benzopyran-4-one; 5,7,4'-trihydroxyisoflavone; Genistein; Genisteol; Genisterin","Chemical drug","DB01645","An isoflavonoid derived from soy products. It inhibits protein-tyrosine kinase and topoisomerase-II (DNA topoisomerases, type II) activity and is used as an antineoplastic and antitumor agent. Experimentally, it has been shown to induce G2 phase arrest in human and murine cell lines.\r\n\r\nAdditionally, genistein has antihelmintic activity. It has been determined to be the active ingredient in <I>Felmingia vestita</I>, which is a plant traditionally used against worms. It has shown to be effective in the treatment of common liver fluke, pork trematode and poultry cestode.\r\n\r\nFurther, genistein is a phytoestrogen which has selective estrogen receptor modulator properties. It has been investigated in clinical trials as an alternative to classical hormone therapy to help prevent cardiovascular disease in postmenopausal women .  \r\n\r\nNatural sources of genistein include tofu, fava beans, soybeans, kudzu, and lupin.","5280961","446-72-0",false,"O=c1c2c(occ1c1ccc(cc1)O)cc(cc2O)O","TZBJGXHYKVUXJN-UHFFFAOYSA-N",270.24,"Estrogen receptor beta; DNA topoisomerase 2-alpha; Protein-tyrosine kinase 2-beta; Nuclear receptor coactivator 1; Estrogen receptor alpha; Nuclear receptor coactivator 2; Steroid hormone receptor ERR2 agonist; Steroid hormone receptor ERR1 agonist; Nucle","Genistein may inhibit cancer cell growth by blocking enzymes required for cell growth. \r\n\r\nGenistein may decrease cardiovascular risk in postmenopausal women by interacting with the nuclear estrogen receptors to alter the transcription of cell specific genes. In randomized clinical trials, genistein was seen to increase the ratio of nitric oxide to endothelin and improved flow-mediated endothelium dependent vasodilation in healthy postmenopausal women . In addition, genistein may have beneficial effects on glucose metabolism by inhibiting islet tyrosine kinase activity as well as insulin release dependent on glucose and sulfonylurea .",null,"Currently Genistein is being studied in clinical trials as a treatment for prostate cancer.","NCOA1; NCOA2; NR1I2",null,"Phase 3 on-going (IRCT201506222480N6)","Under clinical trials","2022-03-21"]
[151,"Ginger","zingiber officinale","Herbal medicine","DB10344","Ginger allergenic extract is used in allergenic testing.","6850776","91770-91-1, 91770-92-2",true,"O=C(CC(CCCCC)C)CCc1cc(OC)c(O)cc1.O=C(CCc1cc(OC)c(O)cc1)/C=C/CCCCC","QCVRFSPGUWEKFC-ILHSMLOTSA-N",568.795,{"$nulls":5},"Antiallergic drug","Phase 2&3 completed  (NCT02535195)","Under clinical trials","2022-03-21"]
[152,"Ginseng","Aralia ginseng root; Asian ginseng root; Chinese ginseng root; Ginseng (panax ginseng); Ginseng extract; Ginseng, asian; Hong shen root; Insam root; Korean ginseng; Korean ginseng root; Ninjin root; Panax ginseng; Panax ginseng root; Panax ginseng root extract; Panax schinseng root; Panax verus root; Red ginseng; Ren seng root; Ren shen; Ren shen root; True ginseng root; Ginseng Powder","Herbal medicine","DB01404","Ginseng is promoted as an adaptogen (a product that increases the body's resistance to stress), one which can to a certain extent be supported with reference to its anticarcinogenic and antioxidant properties. Ginseng is also known to contain phytoestrogens.","420552","1830107-15-7",true,"OC1C(C2C(C3C(C4(C(=CC3)C3C(CC4)(CCC(C3)(C)C)C(=O)OC3OC(C(O)C(O)C3O)CO)CO)(CC2)C)(CC1O)C)(C)C(=O)OC1OC(C(O)C(O)C1O)CO","YDQIRODFTJGGMP-UHFFFAOYSA-N",842.973,"Interleukin-6 antagonist; Prostaglandin G/H synthase 2 inhibitor; Aryl hydrocarbon receptor agonist",{"$nulls":3},"AHR agonist",null,"Clinical trial completed (NCT03260543: Our results suggest that GBCK25 supplementation has beneficial effects on liver function.)","Under clinical trials","2022-03-21"]
[153,"Gliclazide","1-(3-azabicyclo(3.3.0)oct-3-yl)-3-(p-tolylsulfonyl)urea; 1-(hexahydrocyclopenta(c)pyrrol-2(1H)-yl)-3-(p-tolylsulfonyl)urea; Gliclazide","Chemical drug","DB01120","Gliclazide is an oral antihyperglycemic agent used for the treatment of non-insulin-dependent diabetes mellitus (NIDDM). It has been classified differently according to its drug properties in which based on its chemical structure, gliclazide is considered a first-generation sulfonylurea due to the structural presence of a sulfonamide group able to release a proton and the presence of one aromatic group. On the other hand, based on the pharmacological efficacy, gliclazide is considered a second-generation sulfonylurea which presents a higher potency and a shorter half-life. Gliclazide belongs to the sulfonylurea class of insulin secretagogues, which act by stimulating &beta; cells of the pancreas to release insulin. Sulfonylureas increase both basal insulin secretion and meal-stimulated insulin release. Medications in this class differ in their dose, rate of absorption, duration of action, route of elimination and binding site on their target pancreatic &beta; cell receptor. Sulfonylureas also increase peripheral glucose utilization, decrease hepatic gluconeogenesis and may increase the number and sensitivity of insulin receptors. Sulfonylureas are associated with weight gain, though less so than insulin. Due to their mechanism of action, sulfonylureas may cause hypoglycemia and require consistent food intake to decrease this risk. The risk of hypoglycemia is increased in elderly, debilitated and malnourished individuals. Gliclazide has been shown to decrease fasting plasma glucose, postprandial blood glucose and glycosolated hemoglobin (HbA1c) levels (reflective of the last 8-10 weeks of glucose control). Gliclazide is extensively metabolized by the liver; its metabolites are excreted in both urine (60-70%) and feces (10-20%).","3475","21187-98-4",true,"N(C(=O)NS(=O)(=O)c1ccc(cc1)C)N1CC2C(C1)CCC2","BOVGTQGAOIONJV-UHFFFAOYSA-N",323.418,"ATP-binding cassette sub-family C member 8 binder; Vascular endothelial growth factor A other/unknown","Gliclazide binds to the &beta; cell sulfonyl urea receptor (SUR1). This binding subsequently blocks the ATP sensitive potassium channels. The binding results in closure of the channels and leads to a resulting decrease in potassium efflux leads to depolarization of the &beta; cells. This opens voltage-dependent calcium channels in the &beta; cell resulting in calmodulin activation, which in turn leads to exocytosis of insulin containing secretorty granules.","Based on the pharmacological properties, gliclazide is a second generation sulphonylurea which acts as a hypoglycemic agent. It stimulates &beta; cells of the islet of Langerhans in the pancreas to release insulin. It also enhances peripheral insulin sensitivity. Overall, it potentiates insulin release and improves insulin dynamics.","For the treatment of NIDDM in conjunction with diet and exercise.","VEGFA other/unknown","Antidiabetic drug","Phase 4 completed (NCT03068065)","Under clinical trials","2022-03-21"]
[154,"Glimepiride","Glimepiride","Chemical drug","DB00222","First introduced in 1995, glimepiride is a member of the second-generation sulfonylurea (SU) drug class used for the management of type 2 diabetes mellitus (T2DM) to improve glycemic control. Type 2 diabetes is a metabolic disorder with increasing prevalences worldwide; it is characterized by insulin resistance in accordance with progressive β cell failure and long-term microvascular and macrovascular complications that lead to co-morbidities and mortalities. Sulfonylureas are one of the insulin secretagogues widely used for the management of type 2 diabetes to lower blood glucose levels. The main effect of SUs is thought to be effective when residual pancreatic β-cells are present, as they work by stimulating the release of insulin from the pancreatic beta cells and they are also thought to exert extra-pancreatic effects, such as increasing the insulin-mediated peripheral glucose uptake. \r\n\r\nGlimepiride works by stimulating the secretion of insulin granules from pancreatic islet beta cells by blocking ATP-sensitive potassium channels (K<SUB>ATP</SUB> channels) and causing depolarization of the beta cells. Compared to , another second SU drug, glimepiride has a longer duration of action. It is sometimes classified as a third-generation SU because it has larger substitutions than other second-generation SUs. Compared to other SUs, glimepiride was associated with a lower risk of developing hypoglycemia and weight gain in clinical trials  as well as fewer cardiovascular effects than other SUs due to minimal effects on ischemic preconditioning of cardiac myocytes. It is effective in reducing fasting plasma glucose, postprandial glucose, and glycosylated hemoglobin levels and is considered to be a useful, cost-effective treatment option for managing type 2 diabetes mellitus. Glimepiride was approved by the Food and Drug Administration (FDA) in the United States in 1995 for the treatment of T2DM. It is commonly marketed under the brand name Amaryl as oral tablets and is typically administered once daily.","3476","93479-97-1",true,"C(=O)(NCCc1ccc(cc1)S(=O)(=O)NC(=O)N[C@H]1CC[C@@H](CC1)C)N1C(=O)C(=C(C1)C)CC","WIGIZIANZCJQQY-RUCARUNLSA-N",490.626,"ATP-sensitive inward rectifier potassium channel 11 inhibitor; ATP-sensitive inward rectifier potassium channel 1 inhibitor; ATP-binding cassette sub-family C member 8 inducer","ATP-sensitive potassium channels on pancreatic beta cells that are gated by intracellular ATP and ADP. The hetero-octomeric complex of the channel is composed of four pore-forming Kir6.2 subunits and four regulatory sulfonylurea receptor (SUR) subunits. Alternative splicing allows the formation of channels composed of varying subunit isoforms expressed at different concentrations in different tissues. In pancreatic beta cells, ATP-sensitive potassium channels play a role as essential metabolic sensors and regulators that couple membrane excitability with glucose-stimulated insulin secretion (GSIS). When there is a decrease in the ATP:ADP ratio, the channels are activated and open, leading to K+ efflux from the cell, membrane hyperpolarization, and suppression of insulin secretion. In contrast, increased uptake of glucose into the cell leads to elevated intracellular ATP:ADP ratio, leading to the closure of channels and membrane depolarization. Depolarization leads to activation and opening of the voltage-dependent Ca2+ channels and consequently an influx of calcium ions into the cell. Elevated intracellular calcium levels causes the contraction of the filaments of actomyosin responsible for the exocytosis of insulin granules stored in vesicles. Glimepiride blocks the ATP-sensitive potassium channel by binding non-specifically to the B sites of both sulfonylurea receptor-1 (SUR1) and sulfonylurea receptor-2A (SUR2A) subunits as well as the A site of SUR1 subunit of the channel to promote insulin secretion from the beta cell.","Glimepiride stimulates the secretion of insulin granules from the pancreatic beta cells and improves the sensitivity of peripheral tissues to insulin to increase peripheral glucose uptake, thus reducing plasma blood glucose levels and glycated hemoglobin (HbA1C) levels. A multi-center, randomized, placebo-controlled clinical trial evaluated the efficacy of glimepiride (1–8 mg) as monotherapy titrated over 10 weeks compared with placebo in T2DM subjects who were not controlled by diet alone. In this study, there was a reduction in fasting plasma glucose (FPG) by 46 mg/dL, post-prandial glucose (PPG) by 72 mg/dL, and HbA1c by 1.4% more than the placebo. In another randomized study comprising of patients with T2DM receiving either placebo or one of the three doses (1, 4, or 8 mg) of glimepiride during a 14-week study period, all glimepiride regimens significantly reduced FPG, PPG, and HbA1c values (P < 0.001) compared to placebo by the end of the study period. The 4- and 8-mg doses of glimepiride were more effective than the 1-mg dose; however, the 4-mg dose provided a nearly maximal antihyperglycemic effect.","Glimepiride is indicated for the management of type 2 diabetes in adults as an adjunct to diet and exercise to improve glycemic control as monotherapy. \r\n\r\nIt may also be indicated for use in combination with metformin or insulin to lower blood glucose in patients with type 2 diabetes whose high blood sugar levels cannot be controlled by diet and exercise in conjunction with an oral hypoglycemic (a drug used to lower blood sugar levels) agent alone.","ABCC8 binder; KCNJ1 inhibitor; KCNJ11 inhibitor; KCNJ11 potassium channel inhibitor","Antidiabetic drug","Clinical trial on-going (JPRN-UMIN000016306)","Under clinical trials","2022-03-21"]
[155,"Glucagon","Glucagon; Glucagon (recombinant dna origin); Glucagon recombinant; Glucagon, human; Glucagon, porcine; Glucagone","Biological drug","DB00040","Glucagon is a 29 amino acid hormone used as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and to treat severe hypoglycemia. Glucagon raises blood sugar through activation of hepatic glucagon receptors, stimulating glycogenolysis and the release of glucose.\r\n\r\nGlucagon was granted FDA approval on 14 November 1960.","16132283","9007-92-5",false,"S(CC[C@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)CNC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](N)Cc1[nH]cnc1)CO)CCC(=O)N)[C@H](O)C)Cc1ccccc1)[C@H](O)C)CO)CC(=O)O)Cc1ccc(O)cc1)CO)CCCCN)Cc1ccc(O)cc1)CC(C)C)CC(=O)O)CO)CCCNC(=N)N)CCCNC(=N)N)C)CCC(=O)N)CC(=O)O)Cc1ccccc1)C(C)C)CCC(=O)N)Cc1c2c([nH]c1)cccc2)CC(C)C)C(=O)N[C@@H](CC(=O)N)C(=O)N[C@@H]([C@H](O)C)C(=O)O)C","MASNOZXLGMXCHN-ZLPAWPGGSA-N",3482.802,"Glucagon receptor agonist; Glucagon-like peptide 2 receptor agonist; Glucagon-like peptide 1 receptor agonist","Glucagon binds to the glucagon receptor activating G<sub>s</sub>α and G<sub>q</sub>. This activation activates adenylate cyclase, which increases intracellular cyclic AMP and activates protein kinase A. Activating G<sub>q</sub> activates phospholipase C, increases production of inositol 1,4,5-triphosphate, and releases intracellular calcium. Protein kinase A phosphorylates glycogen phosphorylase kinase, which phosphorylates glycogen phosphorylase, which phosphorylates glycogen, causing its breakdown.\r\n\r\nGlucagon also relaxes smooth muscle of the stomach, duodenum, small bowel, and colon.","Glucagon is indicated as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and severe hypoglycemia. Glucagon raises blood sugar through activation of hepatic glucagon receptors, stimulating glycogenolysis and the release of glucose. Glucagon has a short duration of action. Glucagon may cause hyperglycemia in diabetic patients.","Glucagon is indicated as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and to treat severe hypoglycemia.","GCGR agonist","Antidiabetic drug","Clinical trial on-going (NCT04859322)","Under clinical trials","2022-03-21"]
[156,"Glucomannan","GLUCOMANNAN","Chemical drug","DB14963","Konjac mannan is under investigation in clinical trial NCT01709955 (The Effects of Glucomannan on Weight Loss).","24892726","11078-31-2",false,"O([C@H]1[C@H](O)[C@H](O)[C@@H](O[C@@H]1CO)OC1[C@H](O)[C@H](O)[C@@H](O[C@@H]1CO)O)[C@@H]1O[C@@H]([C@@H](O[C@@H]2O[C@@H]([C@@H](O)[C@H](O)[C@@H]2O)CO)[C@H](O)[C@H]1O)CO","LUEWUZLMQUOBSB-FSKGGBMCSA-N",666.579,{"$nulls":5},"Anorexic","Phase 2 completed  (NCT01553500)","Under clinical trials","2022-03-21"]
[157,"Glucophage","1,1-Dimethylbiguanide; Dimethylbiguanid; Metformin; Metformine","Chemical drug","DB00331","Metformin is an antihyperglycemic agent of the _biguanide_ class, used for the management of type II diabetes) .  Currently, metformin is the first drug of choice for the management of type II diabetes and is prescribed to at least 120 million people worldwide . \r\n\r\nMetformin is considered an antihyperglycemic drug because it lowers blood glucose concentrations in type II diabetes without causing hypoglycemia. Metformin is commonly described as an _insulin sensitizer_ leading to a decrease in insulin resistance and a clinically significant reduction of plasma fasting insulin levels . Another well-known benefit of this drug is modest weight loss. Metformin is the drug of choice for obese type II diabetes patients .\r\n\r\nMetformin was first approved in Canada in 1972 , followed by 1995 in the USA . This drug is available in regular and extended-release forms .","14219","1115-70-4",true,"C(=N)(NC(=N)N)N(C)C.Cl","OETHQSJEHLVLGH-UHFFFAOYSA-N",165.628,"5'-AMP-activated protein kinase subunit beta-1 inducer&activator; Electron transfer flavoprotein-ubiquinone oxidoreductase, mitochondrial inhibitor; Glycerol-3-phosphate dehydrogenase [NAD(+)], cytoplasmic inhibitor","Metformin's mechanisms of action are unique from other classes of oral antihyperglycemic drugs. Metformin decreases blood glucose levels by decreasing hepatic glucose production (gluconeogenesis), decreasing the intestinal absorption of glucose, and increasing insulin sensitivity by increasing peripheral glucose uptake and utilization . It is well established that metformin inhibits mitochondrial complex I activity, and it has since been generally postulated that its potent antidiabetic effects occur through this mechanism .   The above processes lead to a decrease in blood glucose, managing type II diabetes and exerting positive effects on glycemic control.\r\n\r\nAfter ingestion, the organic cation transporter-1 (OCT1) is responsible for the uptake of metformin into hepatocytes (liver cells). As this drug is positively charged, it accumulates in cells and in the mitochondria because of the membrane potentials across the plasma membrane as well as the mitochondrial inner membrane. Metformin inhibits mitochondrial complex I, preventing the production of mitochondrial ATP leading to increased cytoplasmic ADP:ATP and AMP:ATP ratios . These changes activate AMP-activated protein kinase (AMPK), an enzyme that plays an important role in the regulation of glucose metabolism . Aside from this mechanism, AMPK can be activated by a lysosomal mechanism involving other activators.  Following this process, increases in AMP:ATP ratio also inhibit _fructose-1,6-bisphosphatase_ enzyme, resulting in the inhibition of gluconeogenesis, while also inhibiting _adenylate cyclase_ and decreasing the production of cyclic adenosine monophosphate (cAMP) , a derivative of ATP used for cell signaling . Activated AMPK phosphorylates two isoforms of acetyl-CoA carboxylase enzyme, thereby inhibiting fat synthesis and leading to fat oxidation, reducing hepatic lipid stores and increasing liver sensitivity to insulin .  \r\n\r\nIn the intestines, metformin increases anaerobic glucose metabolism in enterocytes (intestinal cells), leading to reduced net glucose uptake and increased delivery of lactate to the liver. Recent studies have also implicated the gut as a primary site of action of metformin and suggest that the liver may not be as important for metformin action in patients with type 2 diabetes. Some of the ways metformin may play a role on the intestines is by promoting the metabolism of glucose by increasing glucagon-like peptide I (GLP-1) as well as increasing gut utilization of glucose  . \r\n\r\nIn addition to the above pathway, the mechanism of action of metformin may be explained by other ways, and its exact mechanism of action has been under extensive study in recent years .","**General effects**\r\n\r\nInsulin is an important hormone that regulates blood glucose levels . Type II diabetes is characterized by a decrease in sensitivity to insulin, resulting in eventual elevations in blood glucose when the pancreas can no longer compensate. In patients diagnosed with type 2 diabetes, insulin no longer exerts adequate effects on tissues and cells (called insulin resistance)  and insulin deficiency may also be present .\r\n\r\nMetformin reduces liver (hepatic) production of glucose, decreases the intestinal absorption of glucose, and enhances insulin sensitivity by increasing both peripheral glucose uptake and utilization. In contrast with drugs of the _sulfonylurea_ class, which lead to hyperinsulinemia, the secretion of insulin is unchanged with metformin use .\r\n\r\n**Effect on fasting plasma glucose (FPG) and Glycosylated hemoglobin (HbA1c)**\r\n\r\nHbA1c is an important periodic measure of glycemic control that is used to monitor diabetic patients. Fasting plasma glucose is also a useful and important measure of glycemic control. In a 29-week clinical trial of subjects diagnosed with type II diabetes, metformin decreased the fasting plasma glucose levels by an average of 59 mg/dL from baseline, compared to an average increase of 6.3 mg/dL from baseline in subjects taking a placebo .  Glycosylated hemoglobin (HbA1c) was decreased by about 1.4% in subjects receiving metformin, and increased by 0.4% in subjects receiving placebo only .","**Metformin tablet**\r\n \r\nMetformin is indicated as an adjunct to diet and exercise to increase glycemic control in _adults and pediatric patients_ 10 years of age and older diagnosed with type 2 diabetes mellitus.\r\n\r\n**Metformin extended-release tablet (XR)**\r\n\r\nThe extended-release form is indicated as an adjunct to diet and exercise to improve glycemic control in only _adults_ with type 2 diabetes mellitus. Safety in children has not been determined to this date.\r\n\r\nAn extended-release combination product containing empagliflozin, linagliptin, and metformin was approved by the FDA in January 2020 for the improvement of glycemic control in adults with type 2 diabetes mellitus when used adjunctively with diet and exercise.",null,null,"Clinical trial on-going (EUCTR2011-001010-34-AT)","Under clinical trials","2022-03-21"]
[158,"Glutathione","5-L-Glutamyl-L-cysteinylglycine; gamma-L-Glutamyl-L-cysteinyl-glycine; Glutathion; Glutathione; Glutathione-SH; GSH; N-(N-gamma-L-Glutamyl-L-cysteinyl)glycine; Reduced glutathione","Chemical drug","DB00143","A tripeptide with many roles in cells. It conjugates to drugs to make them more soluble for excretion, is a cofactor for some enzymes, is involved in protein disulfide bond rearrangement and reduces peroxides.","124886","70-18-8",true,"[C@H](C(=O)NCC(=O)O)(NC(=O)CC[C@@H](C(=O)O)N)CS","RWSXRVCMGQZWBV-WDSKDSINSA-N",307.328,"Microsomal glutathione S-transferase 3; Hematopoietic prostaglandin D synthase; Glutathione S-transferase A1; Glutathione S-transferase A2; Microsomal glutathione S-transferase 1; S-formylglutathione hydrolase; Gamma-glutamyltranspeptidase 1; Glutathione","Glutathione (GSH) participates in leukotriene synthesis and is a cofactor for the enzyme glutathione peroxidase. It also plays a role in the hepatic biotransformation and detoxification process; it acts as a hydrophilic molecule that is added to other lipophilic toxins or wastes prior to entering biliary excretion. It participates in the detoxification of methylglyoxal, a toxic by-product of metabolism, mediated by glyoxalase enzymes.  Glyoxalase I catalyzes the conversion of methylglyoxal and reduced glutathione to S-D-Lactoyl-glutathione. Glyoxalase II catalyzes the conversion of S-D-Lactoyl Glutathione to Reduced Glutathione and D-lactate. Glyoxalase I catalyzes the conversion of methylglyoxal and reduced glutathione to S-D-Lactoyl-glutathione. Glyoxalase II catalyzes the conversion of S-D-Lactoyl Glutathione to Reduced Glutathione and D-lactate. GSH is a cofactor of conjugation and reduction reactions that are catalyzed by glutathione S-transferase enzymes expressed in the cytosol, microsomes, and mitochondria. However, it is capable of participating in non-enzymatic conjugation with some chemicals, as it is hypothesized to do to a significant extent with n-acetyl-p-benzoquinone imine (NAPQI), the reactive cytochrome P450 reactive metabolite formed by toxic overdose of acetaminophen. Glutathione in this capacity binds to NAPQI as a suicide substrate and in the process detoxifies it, taking the place of cellular protein sulfhydryl groups which would otherwise be toxically adducted. The preferred medical treatment to an overdose of this nature, whose efficacy has been consistently supported in literature, is the administration (usually in atomized form) of N-acetylcysteine, which is used by cells to replace spent GSSG and allow a usable GSH pool.",null,"For nutritional supplementation, also for treating dietary shortage or imbalance","MGST3; HPGDS; GSTM2; GSTM5; GPX7 cofactor; MGST2; GSS; GSTM1; GSTK1; GSTM3; GSTM4; GPX1 cofactor; GPX2 cofactor; GPX3 cofactor",null,"Phase 3 on-going (CTRI/2010/091/000087)","Under clinical trials","2022-03-21"]
[159,"Green Cardamom","Elettaria Cardamomum","Herbal medicine",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (IRCT2015121317254N4)","Under clinical trials","2022-03-21"]
[160,"Growth Hormone","Growth hormone; Growth hormone (human); hGH; Human growth hormone; Recombinant human growth hormone; rhGH; Somatotropin (human); Somatotropin human; Somatotropin human growth hormone; Somatropin; Somatropin (rDNA origin); Somatropin (recombinant DNA origin); Somatropin [rDNA origin]; Somatropin recombinant; Somatropin(recombinant DNA origin)","Biological drug","DB00052","Human growth hormone (HGH), also known as somatotropin, is a peptide hormone that is synthesized and secreted by the somatotropic cells of the anterior pituitary gland. Growth hormone plays an essential role in growth regulation during childhood as well as other basal metabolic functions, muscle and fat mass regulation, blood glucose level regulation, and lipid regulation in both children and adults. Synthesized in a strain of _Escherichia coli_, recombinant HGH is a polypeptide hormone that contains 191 amino acid residues with a molecular weight of 22 kDa. It has an identical primary protein structure to endogenous human growth hormone. Recombinant HGH has been commercially available since 1985 after its development by Genentech.  was the first available recombinant HGH and was largely replaced by somatropin, another form of recombinant HGH. \r\n\r\nGrowth hormone therapy is approved for various disorders of growth hormone deficiency, growth failure, or short stature including Turner syndrome, chronic renal insufficiency before transplantation, Prader-Willi syndrome, a history of fetal growth restriction, short stature homeobox (SHOX) haploinsufficiency, Noonan syndrome, idiopathic short stature, and adult- or childhood-onset growth hormone deficiency. Recombinant growth hormone is available as a subcutaneous injection for children and adults under a wide variety of brand names.","72","9002-72-6",true,"Oc1cc(ccc1O)C(=O)O","YQUVCSBJEUQKSH-UHFFFAOYSA-N",154.121,"Growth hormone receptor ligand; Prolactin receptor ligand","In conditions of growth failure, growth hormone deficiency, low body mass, and malnutrition, somatotropin treatment acts to mimic and restore the actions of endogenous growth hormone of stimulating linear bone growth, increasing bone mass, increasing muscle and reduced fat mass, and regulating blood glucose and lipid levels. Somatotropin mediates its effects both directly by somatotropin and indirectly by insulin-like growth factor-1 (IGF-1), which is upregulated by growth hormone. It binds to the human growth hormone receptor (GHR), which is a dimeric receptor expressed in target cells in the liver and cartilage. Upon binding of growth hormone, GHR dimerizes and interacts with Janus kinase 2 (JAK2), subsequently leading to tyrosine phosphorylation of JAK2 and the GH receptor. The signal transducer activator of transcription (STAT) pathway is initiated, where transcription factors such as STAT1, STAT3, and STAT5 are translocated into the nucleus to stimulate target gene transcription. \r\n\r\nAt the epiphysis or growth plate, growth hormone increases linear growth by promoting differentiation of prechondrocytes and expansion of osteoblasts. Growth hormone binding to its receptor in the liver and cartilage promotes the production of IGF-1, which acts on type 1 IGF receptors to also stimulate linear growth. In the liver, activated growth hormone receptor signalling leads to increased production of IGF binding protein-3 (IGFBP-3) and acid-labile subunit (ALS), which are proteins that bind to IGF-1 in a ternary complex to increase its half-life.","Somatotropin induces growth in nearly every tissue and organ in the body. It stimulates linear growth and cartilaginous growth of long bones. In children with short stature, growth hormone increases both the number and size of muscle cells. It also promotes the growth of internal organs, and it also increases red cell mass. By promoting nitrogen retention, growth hormone increases cellular protein synthesis. Growth hormone also retains potassium and phosphorus in the serum, which may be the result of cell growth. Growth hormone stimulates the synthesis of chondroitin sulfate and collagen and increases the urinary excretion of hydroxyproline. It has negligible effects on serum calcium levels. Although increased calcium excretion in the urine is observed, calcium absorption from the intestine is simultaneously enhanced. In end-stage renal disease, growth hormone was shown to improve several nutritional parameters, such as increases in serum insulin-like growth factor-I (IGF-I), serum albumin, and transferrin, as well as a reduction in blood urea nitrogen.\r\n\r\nThe metabolic effects of growth hormone are caused by the upregulation of insulin-like growth factor-1. Generally, growth hormone leads cells to enter an anabolic protein state with increased amino acid uptake, protein synthesis, and decreased catabolism of proteins. The diabetogenic effect of larger doses of growth hormone is well documented in the literature: somatotropin antagonizes insulin action _in vivo_, causing insulin resistance and glucose intolerance. It increases glucose production through gluconeogenesis and glycogenolysis from the liver and kidney  and suppresses glucose uptake in the adipose tissue. In mice, growth hormone increased mRNA expression of 2 major gluconeogenic genes, phosphoenolpyruvate carboxy-kinase and glucose-6-phosphatase. The risk for impaired glucose tolerance and reduced insulin sensitivity may be increased in susceptible patients, especially in those with risk factors for diabetes mellitus, such as obesity, Turner syndrome, or a family history of diabetes mellitus. The development of new-onset type 2 Diabetes Mellitus was observed in patients receiving somatotropin treatment. \r\n\r\nGrowth hormone stimulates lipolysis via activation of the hormone-sensitive lipase in the adipose tissue, thereby increasing circulating levels of free fatty acids and triglycerides in the plasma. It also leads to a reduction of fat stores and decreased serum levels of low-density lipoprotein (LDL) cholesterol. In contrast to the effects seen in the adipose tissue, growth hormone promotes cellular uptake of free fatty acids in skeletal muscle by increasing the activity of lipoprotein lipase. Growth hormone may cause hyperinsulinism following beta-cell compensation for insulin resistance; however, there is some evidence that growth hormone directly promotes beta-cell proliferation and glucose-stimulated insulin secretion.","Somatotropin is indicated for the treatment of pediatric patients who have growth failure due to an inadequate secretion of endogenous growth hormone, short stature associated with Turner syndrome, Prader-Willi syndrome (PWS), idiopathic short stature (ISS), short stature or growth failure in short stature homeobox-containing gene (SHOX) deficiency, and short stature born small for gestational age (SGA). It is indicated for the treatment of growth failure in children associated with chronic kidney disease up to the time of renal transplantation.\r\n\r\nIt is also indicated for adults with adult-onset growth hormone deficiency, either alone or associated with multiple hormone deficiencies (hypopituitarism), as a result of pituitary disease, hypothalamic disease, surgery, radiation therapy, or trauma. It is also used to treat childhood-onset growth hormone deficiency in adults due to congenital, genetic, acquired, or idiopathic causes.\r\n\r\nSomatotropin is indicated for the treatment of wasting or cachexia in patients with human immunodeficiency virus (HIV) who are receiving antiretroviral therapy to increase lean body mass and body weight and improve physical endurance.\r\n\r\nSomatotropin is indicated for the treatment of short bowel syndrome in adult patients receiving specialized nutritional support.","GHR ligand; PRLR ligand",null,"Clinical trial on-going (ChiCTR2100042787)","Under clinical trials","2022-03-21"]
[161,"HEC96719",null,"Chemical drug",{"$nulls":4},false,{"$nulls":9},"Phase 1 completed  (NCT04546984)","Under clinical trials","2022-03-21"]
[162,"Hedan Capsule",null,"Traditional medicine",{"$nulls":4},false,{"$nulls":9},"Phase 2 on-going (CTR20131131)","Under clinical trials","2022-03-21"]
[163,"Hepafast",null,"Miscellany",{"$nulls":4},false,{"$nulls":9},"Phase 1 completed  (NCT02491229)","Under clinical trials","2022-03-21"]
[164,"Hepaguard","Phyllanthus urinaria","Herbal medicine",{"$nulls":3},"1841183-27-4",false,{"$nulls":9},"Clinical trial completed (NCT01210989: Phyllanthus is not superior to placebo in improving NAFLD activity score in NASH patients.)","Failed in clinical trials","2022-03-21"]
[165,"Hepar-P",null,"Biological extract",{"$nulls":3},"84775-91-7",false,{"$nulls":9},"Phase 2 on-going (NCT01680003)","Under clinical trials","2022-03-21"]
[166,"HepaStem",null,"Biological drug",{"$nulls":3},"2166483-24-3",false,{"$nulls":8},"Cell therapy drug","Phase 1&2 completed  (NCT03963921)","Under clinical trials","2022-03-21"]
[167,"Hepatoheal tablet",null,"Traditional medicine",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (IRCT2014042612438N6)","Under clinical trials","2022-03-21"]
[168,"Hepaxa",null,"Supplement",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (NCT03801577)","Under clinical trials","2022-03-21"]
[169,"Hesperidin","(S)-(−)-hesperidin; Cirantin; Ciratin; Hesperetin 7-O-rutinoside; Hesperidin; Hesperidoside","Chemical drug","DB04703","Hesperidin is a flavan-on glycoside found in citrus fruits.","10621","520-26-3",true,"O=C1c2c(O[C@@H](C1)c1cc(O)c(cc1)OC)cc(cc2O)O[C@@H]1O[C@H](CO[C@H]2[C@H](O)[C@H](O)[C@H]([C@@H](O2)C)O)[C@H]([C@@H]([C@H]1O)O)O","QUQPHWDTPGMPEX-QJBIFVCTSA-N",610.565,"Aurora kinase B",{"$nulls":3},"AURKB","Antiosteoporotic drug","Clinical trial on-going (NCT03377153)","Under clinical trials","2022-03-21"]
[170,"HL Tablet",null,"Herbal medicine",{"$nulls":4},false,{"$nulls":9},"Phase 2 completed  (NCT02491905)","Under clinical trials","2022-03-21"]
[171,"HM15211",null,"Biological drug",{"$nulls":4},false,{"$nulls":7},"GLP-1 agonist; GIP agonist; Glucagon triple agonist","Improve insulin resistance","Phase 2 on-going (NCT04505436)","Under clinical trials","2022-03-21"]
[172,"Hoodia Gordonii",null,"Biological extract",{"$nulls":3},"938077-10-2",false,{"$nulls":9},"Phase 1 completed  (NCT00816465)","Under clinical trials","2022-03-21"]
[173,"HPN-01",null,"Chemical drug",null,null,"15979284  ",null,false,"Clc1ccc(c2cc(c3ccc(S(=O)(=O)N)cc3)c(N)c(c2)C(=O)N)cc1","XJLFMRGTLRIXDT-UHFFFAOYSA-N",401.875,{"$nulls":6},"Phase 1 on-going (NCT04481594)","Under clinical trials","2022-03-21"]
[174,"HTD1801",null,"Chemical drug",{"$nulls":4},false,{"$nulls":7},"lipid modulator","Anticholesteremic; Anti-inflammatories; Antihyperlipidaemics; Hepatoprotectants","Phase 2 completed  (NCT03656744: We conclude that berberine ursodeoxycholate has a broad spectrum of metabolic activity in patients with presumed NASH and diabetes. It is relatively well tolerated and merits further development as a treatment for NASH with diabetes.)","Under clinical trials","2022-03-21"]
[175,"Hydroalcoholic extract of Berberis fruits integerrima","Berberis integerrima Bunge","Biological extract",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (IRCT20190714044196N1)","Under clinical trials","2022-03-21"]
[176,"Hydrolyzed oyster extract",null,"Biological extract",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (NCT02992470)","Under clinical trials","2022-03-21"]
[177,"Hydroxy citric acid","2-hydroxy-1,2,3-propanetricarboxyic acid; 2-Hydroxytricarballylic acid; 3-carboxy-3-hydroxypentane-1,5-dioic acid; Anhydrous citric acid; Citric acid monoglyceride; Citric acid, anhydrous; Citric acid,anhydrous","Chemical drug","DB04272","A key intermediate in metabolism. It is an acid compound found in citrus fruits. The salts of citric acid (citrates) can be used as anticoagulants due to their calcium chelating ability.\r\n\r\nCitric acid was one of active ingredients in Phexxi, a non-hormonal contraceptive agent that was approved by the FDA on May 2020.","22230","5949-29-1",true,"O.C(CC(=O)O)(CC(=O)O)(C(=O)O)O","YASYEJJMZJALEJ-UHFFFAOYSA-N",210.138,"Fumarate hydratase class II inhibitor; 6-phosphogluconolactonase; L-amino-acid oxidase; Carboxy-terminal domain RNA polymerase II polypeptide A small phosphatase 1; Cytochrome c peroxidase; Hepatocyte growth factor-regulated tyrosine kinase substrate; Inv",{"$nulls":3},"PGLS; HGS; CS; RTCA; CS; APRT; LYZ",null,"Clinical trial on-going (IRCT201503273320N11)","Under clinical trials","2022-03-21"]
[178,"Hydroxytyrosol","HXT","Chemical drug","DB12771","Hydroxytyrosol has been used in trials studying the prevention of Breast Cancer.","82755","10597-60-1",false,"C(CO)c1cc(O)c(cc1)O","JUUBCHWRXWPFFH-UHFFFAOYSA-N",154.165,{"$nulls":5},"Antioxidant","Phase 3 completed (NCT02842567: The treatment with HXT and VitE reduced the NAFLD-related systemic inflammation in children, mainly by an increase of IL-10 circulating levels that occurred in response to DNA damage recovery, ultimately improving steatosis and hypertriglyceridemia.)","Under clinical trials","2022-03-21"]
[179,"Icosabutate","Icosabutate","Chemical drug","DB12990","Icosabutate is under investigation in clinical trial NCT02373176 ( Icosabutate -A Phase I Absorption, Metabolism and Excretion Study).","78210211","1253909-57-7",false,"C(OCCCC/C=C\\C/C=C\\C/C=C\\C/C=C\\C/C=C\\CC)(C(=O)O)CC","VOGXDRFFBBLZBT-AAQCHOMXSA-N",374.565,{"$nulls":6},"Phase 2 on-going (NCT04052516)","Under clinical trials","2022-03-21"]
[180,"IdB 1016","Siliphos","Biological drug",null,null,"6450536","134499-06-2",false,{"$nulls":9},"Phase 2 completed  (NCT00443079: Silybin-phosphatidylcholine complexed as a phytosome provides significant liver protection and enhanced bioavailability over conventional silymarin.)","Under clinical trials","2022-03-21"]
[181,"IMM-124E",null,"Biological drug",{"$nulls":3},"1774337-30-2",false,{"$nulls":7},"LPS","Gut microbiome modulator","Phase 2 completed  (NCT02316717: the peptide AWRK6 ameliorates MAFLD by improving lipid and glucose metabolism homeostasis, and it is mediated by the PI3K/AKT/AMPK/ACC signaling pathway. Thus, AWRK6 has a potential in preventing MAFLD.)","Under clinical trials","2022-03-21"]
[182,"Insulin","High molecular weight insulin human; Human insulin; human insulin (rDNA); Insulin (human); Insulin human; Insulin human [rDNA origin]; Insulin Human Regular; Insulin human regular (rDNA); Insulin human, rDNA origin; Insulin recombinant human; Insulin recombinant purified human; Insulin regular; Insulin, human; Neutral insulin; Regular Insulin, human; Soluble insulin","Biological drug","DB00030","Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions.\r\n\r\nInsulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as , , or  have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. \r\n\r\nMarketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered \"bolus insulin\" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting \"basal insulin\" such as , , and  to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia.\r\n\r\nHuman insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets . Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA \"black box\" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. \r\n\r\nHuman Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. \r\n\r\nHuman insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH.\r\n\r\nWithout an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy.","16131098","9004-10-8",true,"S1SC[C@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@H]2NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)CN)[C@H](CC)C)C(C)C)CCC(=O)O)CCC(=O)N)CSSC2)CSSC[C@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](N)Cc2ccccc2)C(C)C)CC(=O)N)CCC(=O)N)Cc2[nH]cnc2)CC(C)C)C(=O)NCC(=O)N[C@H](C(=O)N[C@H](C(=O)N[C@@H](CC(C)C)C(=O)N[C@@H](C(C)C)C(=O)N[C@@H](CCC(=O)O)C(=O)N[C@H](C(=O)N[C@@H](CC(C)C)C(=O)N[C@H](C(=O)N[C@@H](CC(C)C)C(=O)N[C@@H](C(C)C)C(=O)N[C@H](C(=O)NCC(=O)N[C@H](C(=O)N[C@H](C(=O)NCC(=O)N[C@H](C(=O)N[C@H](C(=O)N[C@H](C(=O)N[C@H](C(=O)N2[C@@H](CCC2)C(=O)N[C@@H](CCCCN)C(=O)N[C@@H](C)C(=O)O)[C@H](O)C)Cc2ccc(O)cc2)Cc2ccccc2)Cc2ccccc2)CCCNC(=N)N)CCC(=O)O)C1)Cc1ccc(O)cc1)C)Cc1[nH]cnc1)CO)[C@H](O)C)CO)[C@H](CC)C)CO)CC(C)C)Cc1ccc(O)cc1)CCC(=O)N)CC(C)C)CCC(=O)O)CC(=O)N)Cc1ccc(O)cc1)C(=O)N[C@@H](CC(=O)N)C(=O)O","NOESYZHRGYRDHS-ZYCCASTOSA-N",5777.645,"Insulin receptor agonist; Insulin-like growth factor 1 receptor activator; Carboxypeptidase E modulator&product of; Protein NOV homolog downregulator; Low-density lipoprotein receptor-related protein 2 substrate; Insulin-like growth factor-binding protein","The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver.\r\nInsulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism.","Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis).","Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus.","INSR agonist; CPE modulator&product of",null,"Phase 2 on-going (NCT04616014)","Under clinical trials","2022-03-21"]
[183,"Insulin Glargine","Insulin glargine; Insulin glargine (rDNA origin); Insulin glargine recombinant; insulin glargine-yfgn","Biological drug","DB00047","Insulin glargine is a long-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Insulin is typically prescribed for the management of diabetes mellitus to mimic the activity of endogenously produced human insulin, a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis.\r\n\r\nInsulin is an important treatment in the management of Type 1 Diabetes (T1D), which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin, such as insulin glargine, to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after several oral medications such as , , or  have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. \r\n\r\nAvailable as the brand name product Lantus, insulin glargine has a duration of action up to 24 hours allowing for once-daily dosing, typically at bedtime. Due to its duration of action, Lantus is considered \"basal insulin\" as it provides low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Basal insulin is often combined with short-acting \"bolus insulin\" such as , , and  to provide higher doses of insulin that are required following meals. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. \r\n\r\nInsulin glargine is also available as the biosimilar, or \"follow-on\" product, Basaglar in the US and as Abasaglar in the EU. As of 2015, insulin glargine was reformulated by Sanofi as the product Toujeo in an extra-concentrated form containing 300IU/mL (compared to 100IU/mL contained in Lantus). Use of the higher concentrated Toujeo as compared to Lantus results in slightly different pharmacokinetics, with a later onset (up to 6 hours) and duration of action (up to 30 hours). In 2021, another biosimilar, Semglee (insulin glargine-yfgn), became the first interchangeable (with Lantus) biosimilar insulin to receive FDA approval.\r\n\r\nInsulin glargine is produced by recombinant DNA technology using a non-pathogenic laboratory strain of Escherichia coli (K12) as the production organism. Insulin glargine differs from endogenous human insulin by the replacement of an asparagine residue at position A21 of the A-chain with glycine and addition of two arginines to the C-terminus (positions B31 and 32) of the B-chain. The resulting protein is soluble at pH 4 and forms microprecipitates at physiological pH 7.4 allowing for the slow release of small amounts of insulin glargine, giving the drug a long duration of action and no pronounced peak concentration.\r\n\r\nWithout an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy.","118984454","160337-95-1",true,"S1SC[C@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@H]2NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)CN)[C@H](CC)C)C(C)C)CCC(=O)O)CCC(=O)N)CSSC2)CSSC[C@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](N)Cc2ccccc2)C(C)C)CC(=O)N)CCC(=O)N)Cc2nc[nH]c2)CC(C)C)C(=O)NCC(=O)N[C@H](C(=O)N[C@H](C(=O)N[C@@H](CC(C)C)C(=O)N[C@@H](C(C)C)C(=O)N[C@@H](CCC(=O)O)C(=O)N[C@H](C(=O)N[C@@H](CC(C)C)C(=O)N[C@H](C(=O)N[C@@H](CC(C)C)C(=O)N[C@H](C(=O)N[C@H](C(=O)NCC(=O)N[C@H](C(=O)N[C@H](C(=O)NCC(=O)N[C@H](C(=O)N[C@H](C(=O)N[C@H](C(=O)N[C@H](C(=O)N2[C@@H](CCC2)C(=O)N[C@@H](CCCCN)C(=O)N[C@@H]([C@H](O)C)C(=O)N[C@@H](CCCNC(=N)N)C(=O)N[C@@H](CCCNC(=N)N)C(=O)O)[C@H](O)C)Cc2ccc(O)cc2)Cc2ccccc2)Cc2ccccc2)CCCNC(=N)N)CCC(=O)O)C1)C(C)C)Cc1ccc(O)cc1)C)Cc1nc[nH]c1)CO)[C@H](O)C)CO)[C@H](CC)C)CO)CC(C)C)Cc1ccc(O)cc1)CCC(=O)N)CC(C)C)CCC(=O)O)CC(=O)N)Cc1ccc(O)cc1)C(=O)NCC(=O)O","COCFEDIXXNGUNL-RFKWWTKHSA-N",6062.997,"Insulin receptor agonist; Insulin-like growth factor 1 receptor activator","Insulin glargine binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signalling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism. Insulin glargine is completely soluble at pH 4, the pH of administered solution, and has low solubility at physiological pH 7.4. Upon subcuteous injection, the solution is neutralized resulting in the formation of microprecipitates. Small amounts of insulin glargine are released from microprecipitates giving the drug a relatively constant concentration over time profile over 24 hours with no pronounced peak. This release mechanism allows the drug to mimic basal insulin levels within the body.","Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, the pancreas produces a continuous supply of low levels of basal insulin along with spikes of insulin following meals. Increased insulin secretion following meals is responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin glargine is a long-acting insulin analogue with a flat and predictable action profile. It is used to mimic the basal levels of insulin in diabetic individuals.","Insulin glargine is indicated to improve glycemic control in adults and pediatric patients with type 1 diabetes mellitus and in adults with type 2 diabetes mellitus.","INSR agonist","Antidiabetic drug","Phase 4 completed (NCT02303730)","Under clinical trials","2022-03-21"]
[184,"INT-767",null,"Chemical drug",null,null,"23712772","1000403-03-1",false,"O[C@H]1[C@@H]2[C@@H]([C@@]3([C@H]([C@H]1CC)C[C@@H](CC3)O)C)CC[C@]1([C@H]2CC[C@@H]1[C@@H](CCOS(=O)(=O)O)C)C.[Na]","DQIGKAIZUNNJGO-PMWRKVJASA-N",496.686,{"$nulls":4},"FXR agonist; TGR5 agonist","Enhance lipid metabolism",null,"Under investigation","2022-03-21"]
[185,"Inulin","Inulin","Chemical drug","DB00638","A starch found in the tubers and roots of many plants. Since it is hydrolyzable to fructose, it is classified as a fructosan. It has been used in physiologic investigation for determination of the rate of glomerular function.","24763","9005-80-5",true,"O([C@@]1(O[C@@H]([C@@H](O)[C@@H]1O)CO)CO[C@@]1(O[C@@H]([C@@H](O)[C@@H]1O)CO)CO[C@@]1(O[C@@H]([C@@H](O)[C@@H]1O)CO)CO[C@@]1(O[C@@H]([C@@H](O)[C@@H]1O)CO)CO[C@@]1(O[C@@H]([C@@H](O)[C@@H]1O)CO)CO[C@@]1(O[C@@H]([C@@H](O)[C@@H]1O)CO)CO[C@@]1(O[C@@H]([C@@H](O)[C@@H]1O)CO)CO[C@@]1(O[C@@H]([C@@H](O)[C@@H]1O)CO)CO[C@@]1(O[C@@H]([C@@H](O)[C@@H]1O)CO)CO[C@@]1(O[C@@H]([C@@H](O)[C@@H]1O)CO)CO[C@@]1(O[C@@H]([C@@H](O)[C@@H]1O)CO)CO[C@@]1(O[C@@H]([C@@H](O)[C@@H]1O)CO)CO[C@@]1(O[C@@H]([C@@H](O)[C@@H]1O)CO)CO[C@@]1(O[C@@H]([C@@H](O)[C@@H]1O)CO)CO[C@@]1(O[C@@H]([C@@H](O)[C@@H]1O)CO)CO[C@@]1(O[C@@H]([C@@H](O)[C@@H]1O)CO)CO[C@@]1(O[C@@H]([C@@H](O)[C@@H]1O)CO)CO[C@@]1(O[C@@H]([C@@H](O)[C@@H]1O)CO)CO[C@@]1(O[C@@H]([C@@H](O)[C@@H]1O)CO)CO)C[C@@]1(OC[C@@]2(OC[C@@]3(OC[C@@]4(OC[C@@]5(OC[C@@]6(OC[C@@]7(OC[C@@]8(OC[C@@]9(OC[C@@]%10(OC[C@@]%11(OC[C@@]%12(OC[C@@]%13(OC[C@]%14(O[C@@H]([C@@H](O)[C@@H]%14O)CO)OC[C@]%14(O[C@@H]([C@@H](O)[C@@H]%14O)CO)OC[C@]%14(O[C@@H]([C@@H](O)[C@@H]%14O)CO)OC[C@]%14(O[C@@H]([C@@H](O)[C@@H]%14O)CO)OC[C@]%14(O[C@@H]([C@@H](O)[C@@H]%14O)CO)O[C@H]%14O[C@@H]([C@@H](O)[C@H](O)[C@H]%14O)CO)O[C@@H]([C@@H](O)[C@@H]%13O)CO)O[C@@H]([C@@H](O)[C@@H]%12O)CO)O[C@@H]([C@@H](O)[C@@H]%11O)CO)O[C@@H]([C@@H](O)[C@@H]%10O)CO)O[C@@H]([C@@H](O)[C@@H]9O)CO)O[C@@H]([C@@H](O)[C@@H]8O)CO)O[C@@H]([C@@H](O)[C@@H]7O)CO)O[C@@H]([C@@H](O)[C@@H]6O)CO)O[C@@H]([C@@H](O)[C@@H]5O)CO)O[C@@H]([C@@H](O)[C@@H]4O)CO)O[C@@H]([C@@H](O)[C@@H]3O)CO)O[C@@H]([C@@H](O)[C@@H]2O)CO)O[C@@H]([C@@H](O)[C@@H]1O)CO","JYJIGFIDKWBXDU-MNNPPOADSA-N",6179.373,"Cycloinulo-oligosaccharide fructanotransferase binder","As a diagnostic agent, inulin is readily soluble and essentially indigestible. It readily passes through the blood and into the urine. It is neither secreted nor resorbed by the kidney making it an excellent indicator for renal clearance rates. The inulin clearance test has largely been succeeded by the creatinine clearance test as a measure of glomerular filtration rate. \r\n\r\nInulin is a hypoglycemic agent. Since it is not digestible by human enzymes ptyalin and amylase, inulin passes through much of the digestive system intact. It is only in the colon that bacteria metabolise inulin, with the release of significant quantities of carbon dioxide and/or methane. Because inulin is not broken down into simple sugars (monosaccharides) by normal digestion, it does not elevate blood sugar levels, hence, helping diabetics regulate blood sugar levels.","The inulin test is a procedure by which the filtering capacity of the glomeruli (the main filtering structures of the kidney) is determined by measuring the rate at which inulin, the test substance, is cleared from blood plasma. Inulin is one of the more suitable and accurate substance to measure because it is a small, inert polysaccharide molecule that readily passes through the glomeruli. The inulin clearance test is performed by injecting inulin, waiting for it to be distributed, and then measuring plasma and urine inulin concentrations by various assays. As nutraceutical agents inulins may have antitumor, antimicrobial, hypolipidemic and hypoglycemic actions. They may also help to improve mineral absorption and balance and may have antiosteoporotic activity.","Historically used in an important medical test of renal function, specifically a measure of glomerular filtration rate. Sometimes used to help relieve symptoms of diabetes mellitus - a condition characterised by hyperglycemia and/or hyperinsulinemia.","CFT binder",null,"Clinical trial on-going (NCT03914495)","Under clinical trials","2022-03-21"]
[186,"ION 224","ISIS-DGAT2Rx; ION-224; IONIS-DGAT2Rx; ISIS 484137","Miscellany",{"$nulls":4},false,{"$nulls":7},"DGAT2 inhibitor","Enhance lipid metabolism","Phase 2 on-going (NCT04932512: ION 224 is still in clinical trials for Non-alcoholic steatohepatitis in the US, Canada, the UK, Poland, and Hungary)","Under clinical trials","2022-03-21"]
[187,"Ipragliflozin","Ipragliflozin","Chemical drug","DB11698","Ipragliflozin is under investigation in Type 2 Diabetes and Diabetes Mellitus, Type 2.","10453870","761423-87-4",false,"O[C@H]1[C@@H](O[C@@H]([C@H]([C@@H]1O)O)CO)c1cc(Cc2cc3c(s2)cccc3)c(cc1)F","AHFWIQIYAXSLBA-RQXATKFSSA-N",404.459,{"$nulls":4},"SGLT2 inhibitor","Improve insulin resistance","Phase 3 completed  (JPRN-jRCTs071180069: A total of 55 patients were included in the current study. In the 51 patients (ipragliflozin=25, control=26) without discontinuation, decrease in HbA1c of ipragliflozin group at 72-week from baseline was not significantly different comparing with the control group. Body weight of ipragliflozin group decreased from baseline significantly more than control group. Patients with improvement of liver fibrosis was significantly more frequent n the ipragliflozin group than the control group.)","Under clinical trials","2022-03-21"]
[188,"ISIS 703802",null,"Biological drug",{"$nulls":3},"2097587-62-5",false,{"$nulls":8},"Anticholesteremic drug","Phase 2 completed  (NCT03371355)","Under clinical trials","2022-03-21"]
[189,"Itraconazole","Itraconazole; Oriconazole","Chemical drug","DB01167","One of the triazole antifungal agents that inhibits cytochrome P-450-dependent enzymes resulting in impairment of ergosterol synthesis.  It has been used against histoplasmosis, blastomycosis, cryptococcal meningitis & aspergillosis.","55283","84625-61-6",true,"Clc1c([C@@]2(O[C@H](CO2)COc2ccc(N3CCN(CC3)c3ccc(n4c(=O)n(nc4)C(CC)C)cc3)cc2)Cn2ncnc2)ccc(Cl)c1","VHVPQPYKVGDNFY-ZPGVKDDISA-N",705.647,"Lanosterol 14-alpha demethylase inhibitor; Lanosterol 14-alpha demethylase inhibitor","Itraconazole interacts with 14-&alpha; demethylase, a cytochrome P-450 enzyme necessary to convert lanosterol to ergosterol. As ergosterol is an essential component of the fungal cell membrane, inhibition of its synthesis results in increased cellular permeability causing leakage of cellular contents. Itraconazole may also inhibit endogenous respiration, interact with membrane phospholipids, inhibit the transformation of yeasts to mycelial forms, inhibit purine uptake, and impair triglyceride and/or phospholipid biosynthesis.","Itraconazole is an imidazole/triazole type antifungal agent. Itraconazole is a highly selective inhibitor of fungal cytochrome P-450 sterol C-14 &alpha;-demethylation via the inhibition of the enzyme cytochrome P450 14&alpha;-demethylase. This enzyme converts lanosterol to ergosterol, and is required in fungal cell wall synthesis. The subsequent loss of normal sterols correlates with the accumulation of 14 &alpha;-methyl sterols in fungi and may be partly responsible for the fungistatic activity of fluconazole. Mammalian cell demethylation is much less sensitive to fluconazole inhibition. Itraconazole exhibits <i>in vitro</i> activity against <i>Cryptococcus neoformans</i> and <i>Candida spp.</i> Fungistatic activity has also been demonstrated in normal and immunocompromised animal models for systemic and intracranial fungal infections due to <i>Cryptococcus neoformans</i> and for systemic infections due to <i>Candida albicans</i>.","For the treatment of the following fungal infections in immunocompromised and non-immunocompromised patients: pulmonary and extrapulmonary blastomycosis, histoplasmosis, aspergillosis, and onychomycosis.","P450 inhibitor",null,"Phase 1 completed  (NCT04845646)","Under clinical trials","2022-03-21"]
[190,"Japanese apricot extract","Misatol GL; Prunus mume","Biological extract",{"$nulls":3},"2007931-41-9",false,{"$nulls":9},"Clinical trial completed (JPRN-jRCTs031180203: \t\r\nThe efficacy and safety of Misatol GL twice a day for 8 weeks after drinking were evaluated in patients with NASH or NAFLD. The primary and secondary endpoints of efficacy did not show any improvement in liver function of Misatol GL. There was no problem with the safety of Misatol GL.)","Failed in clinical trials","2022-03-21"]
[191,"Jiuwei Qingzhi Gao",null,"Traditional medicine",{"$nulls":4},false,{"$nulls":9},"Phase 0 on-going (ChiCTR1900021508)","Under clinical trials","2022-03-21"]
[192,"JKB-121","Nalmefene","Chemical drug","DB06230","Nalmefene is a 6-methylene analogue of naltrexone and opioid system modulator but with no opioid activity . It mediates a partial agonist effect on kappa receptors . It is primarily used in the management of alcohol dependence in adult patients in conjunction with continuous psychosocial support focused on treatment adherence and reducing alcohol consumption  when it is exists as the hydrochloride dihydrate form under the trade name Selincro. Selincro is orally administered as tablets. Nalmefene works to reduce alcohol consumption in individuals by positive reward effect of alcohol which involves the opioid system, as well as the sedative and dysphoric properties of alcohol . \r\n\r\nIt is also indicated to prevent or reverse the effects of opioids, including respiratory depression, sedation, and hypotension by acting on the opioid receptor as an antagonist  under the trade name Revex for intramuscular, intravenous and subcutaneous injection, where nalmefene hydrochloride is an active ingredient.","5284594","55096-26-9",false,"O[C@@]12[C@@]34c5c(O[C@H]3C(=C)CC2)c(O)ccc5C[C@H]1N(CC4)CC1CC1","WJBLNOPPDWQMCH-MBPVOVBZSA-N",339.435,"Mu-type opioid receptor antagonist; Kappa-type opioid receptor partial agonist; Delta-type opioid receptor antagonist","Nalmefene is an opioid system modulator with a distinct μ, δ, and κ receptor profile. It acts as a selective opioid receptor ligand with antagonist activity at the μ and δ receptors and partial agonist activity at the κ receptor . Animal studies suggest that the kappa receptor signalling responses lead to antagonism of acute reward and positive reinforcement effects of drugs by decreasing dopamine in the nucleus accumbens . Thus it is suggested that nalmefene may be more effective treatment for alcohol dependence than , which is a pure mu and delta receptor antagonist . In vivo studies and rat studies have demonstrated that nalmefene reduces self-administration of alcohol, possibly by modulating cortico-mesolimbic functions . \r\n\r\nNalmefene, a 6-methylene analogue of naltrexone, is a competitive opioid antagonist which binds with high affinity to the mu opioid receptor. Nalmefene itself does not induce any opioid activity, but prevents or reverses the effects of opioids such as respiratory depression and sedation when injected. Some pharmacodynamic studies showed that nalmefene has a longer duration of action than naloxone at fully reversing doses  however the relative potency of these two antagonists are reported to be similar .","Nalmefene has not been shown to produce tolerance, physical dependence, or abuse potential . \r\n\r\nWhen adminsitered as an antidote for opioid overdose, nalmefene is not known to produce any respiratory depression, psychomimetic effects, or pupillary constriction . In the absence of opioid agonists, there was no observable pharmacological activity. Nalmefene injection can produce acute withdrawal symptoms in individuals who are opioid-dependent.","Indicated for the reduction of alcohol consumption in adult patients with alcohol dependence who have a high drinking risk level (DRL), without physical withdrawal symptoms and who do not require immediate detoxification .\r\n\r\nIndicated for the complete or partial reversal of opioid drug effects, including respiratory depression - induced by either natural or synthetic opioids - or in the management of known or suspected opioid overdose .","TLR4 antagonist","Anti-inflammatory","Phase 2 completed  (NCT02442687)","Under clinical trials","2022-03-21"]
[193,"JKB-122",null,"Miscellany",{"$nulls":4},false,{"$nulls":7},"TLR4 antagonist","Anti-inflammatory","Phase 2 on-going (NCT04255069)","Under clinical trials","2022-03-21"]
[194,"Katuki churna","Katukyadi churna","Herbal medicine",{"$nulls":4},false,{"$nulls":9},"Phase 2&3 on-going (CTRI/2019/03/018039)","Under clinical trials","2022-03-21"]
[195,"Kestose",null,"Chemical drug",null,null,"9914062","562-68-5",false,"O([C@]1(CO)O[C@@H]([C@H]([C@@H]1O)O)CO[C@]1(CO)O[C@@H]([C@H]([C@@H]1O)O)CO)[C@H]1O[C@H](CO)[C@H]([C@@H]([C@H]1O)O)O","ODEHMIGXGLNAKK-OESPXIITSA-N",504.438,{"$nulls":6},"Clinical trial on-going (JPRN-jRCTs041180162)","Under clinical trials","2022-03-21"]
[196,"Lactobacillus acidophilus","Acidophilus; Bacillus acidophilus whole; Bacterium acidophilum whole; Lacteol; Lactobacillus acidophilus; Lactobacillus acidophilus whole; Lactobacterium acidophilum whole; Thermobacterium intestinale whole","Biological drug","DB15823",null,null,"68333-16-4",true,{"$nulls":9},"Phase 2 on-going (IRCT201301223140N6)","Under clinical trials","2022-03-21"]
[197,"Lactobacillus spp","Lactobacillus reuteri V3401","Supplement",{"$nulls":4},false,{"$nulls":9},"Clinical trial completed (NCT02972567: This is the first time that L. reuteri V3401 will be evaluated in patients with IRS. Therefore, this study will provide valuable scientific information about the effects of this strain in metabolic syndrome patients.)","Under clinical trials","2022-03-21"]
[198,"Lactulose","4-O-beta-D-Galactopyranosyl-D-fructofuranose; 4-O-beta-D-Galactopyranosyl-D-fructose; Lactulose","Chemical drug","DB00581","Lactulose is a synthetic disaccharide derivative of lactose that is most commonly used as a laxative agent despite also being formally indicated to serve as an adjunct therapy in treating portal-systemic encephalopathy (PSE). Despite being first synthesized in 1929, investigations regarding its possible use as a laxative for the treatment of chronic constipation did not occur until the 1960s and its first clinical use for treating PSE was not until 1966. \r\n\r\nNevertheless, although lactulose received formal FDA approval in 1977 and has since become a readily available generic and brand-name non-prescription medication listed on the World Health Organization's List of Essential Medicines as one of the most effective and safe medicines employed in a health system, data regarding its optimal place in therapy is often ambiguous.\r\n\r\nEspecially considering the use of lactulose as a laxative is typically only considered after lifestyle and dietary modifications fail and the fact that lactulose therapy cannot be ethically withheld from patients diagnosed with PSE in a placebo study, the substance may just be one of many options available for treating constipation and its efficacy in managing PSE may never be formally confirmed or refuted via clinical investigation.","3037557  ","4618-18-2",true,"O([C@@H]([C@@H](C(=O)CO)O)[C@@H](CO)O)[C@@H]1O[C@H](CO)[C@@H]([C@@H]([C@H]1O)O)O","PFCRQPBOOFTZGQ-VZXVHDRGSA-N",342.297,"Evolved beta-galactosidase subunit alpha other","Lactulose is a synthetic disaccharide derivative of lactose that consists of one molecule of galactose and one molecule of fructose. Saccharolytic bacteria present in the large intestine subsequently break the substance down into organic acids like lactic acid and small amounts of formic and acetic acids. Such resultant volatile fatty acid metabolites, in combination with hydrogen and methane that is also generated consequently enhance intraluminal gas formation, peristaltic gut motility, and elicit an osmotic effect that facilitates an increase in the water content of stool as well as associated stool softening. All of these actions ultimately assist in facilitating and increasing the frequency of bowel movements in patients experiencing constipation, although it may take 24 to 48 hours after using the medication for this laxative effect to become evident.\r\n\r\nAt the same time, the formation of such acids via the metabolism of lactulose by colonic bacteria also acidifies the contents of the colon, thereby contributing to the treatment of portal-systemic encephalopathy (PSE). As one of the principal features of PSE involves the accumulation of nitrogenous waste products like ammonia in the systemic circulation, a state in which the colonic contents become more acidic than blood allows ammonia in the circulation to diffuse into the colon.. Furthermore, ammonia that diffuses into the acidic colon is ionized to ammonium ions that are incapable of being absorbed back into the blood. These effects, combined with the laxative action of lactulose facilitates the excretion of excess ammonia. And finally, it is also believed that an acidic colonic environment results in the elimination of urease-producing bacteria that contribute to the formation of ammonia while surviving colonic bacteria use up any trapped ammonia in the colon as a source of nitrogen for protein synthesis.","Lactulose formulations are most commonly administered via the oral route or the rectal route. Consequently, because the substance experiences minimal absorption by the gut it typically remains localized in the gastrointestinal tract environment and ultimately demonstrates almost all of its pharmacologic effects within the gut. In particular, as lactulose elicits its laxative effects in enhancing stool amounts and softening stool, such biochemical and physiologic activities can cause increased bowel sounds (borborygmi), a feeling of bloatedness, belching, frequent flatus, and diarrhea.","Lactulose is indicated for use as a laxative in the treatment of chronic constipation in adults and geriatric patients.\r\n\r\nAdditionally, lactulose is also employed as an adjunct to protein restriction and supportive therapy for the prevention and treatment of portal-systemic encephalopathy (PSE), including both the hepatic pre-coma and coma variations. In particular, lactulose solution has been effective at managing PSE resulting from surgical portacaval shunts or from chronic hepatic diseases like cirrhosis.\r\n\r\nMoreover, there have also been studies demonstrating the capacity for lactulose to minimize the formation of gallstones and even some investigations regarding the experimental use of the agent in developing novel anticancer agents owing to its ability to bind galactin carbohydrates involved in various tumor progressions .",null,null,"Clinical trial on-going (IRCT2014010715879N3)","Under clinical trials","2022-03-21"]
[199,"L-alanine","(2S)-2-aminopropanoic acid; (S)-2-aminopropanoic acid; (S)-alanine; Alanine; L-2-Aminopropionic acid; L-alanine; L-alpha-Alanine; L-α-alanine","Chemical drug","DB00160","Alanine is a non-essential amino acid that occurs in high levels in its free state in plasma. It is produced from pyruvate by transamination. It is involved in sugar and acid metabolism, increases immunity, and provides energy for muscle tissue, brain, and the central nervous system.","5950","56-41-7",true,"[C@@H](C(=O)O)(C)N","QNAYBMKLOCPYGJ-REOHCLBHSA-N",89.094,"Serine--pyruvate aminotransferase; 4-aminobutyrate aminotransferase, mitochondrial inhibitor; Kynureninase; Alanine--tRNA ligase, mitochondrial; 5-phosphohydroxy-L-lysine phospho-lyase; Alanine aminotransferase 2; Alanine aminotransferase 1; Cysteine desu","L-Alanine is a non-essential amino acid that occurs in high levels in its free state in plasma. It is produced from pyruvate by transamination. It is involved in sugar and acid metabolism, increases immunity, and provides energy for muscle tissue, brain, and the central nervous system. BCAAs are used as a source of energy for muscle cells. During prolonged exercise, BCAAs are released from skeletal muscles and their carbon backbones are used as fuel, while their nitrogen portion is used to form another amino acid, Alanine. Alanine is then converted to Glucose by the liver. This form of energy production is called the Alanine-Glucose cycle, and it plays a major role in maintaining the body's blood sugar balance.","Is an important source of energy for muscle tissue, the brain and central nervous system; strengthens the immune system by producing antibodies; helps in the metabolism of sugars and organic acids.","Used for protein synthesis.","KYNU",null,"Clinical trial completed (NCT00586885: No therapeutic effect of L-alanine in patients with nonalcoholic steatohepatitis.)","Failed in clinical trials","2022-03-21"]
[200,"Lanifibranor","IVA337","Chemical drug","DB14801","Lanifibranor is under investigation in clinical trial NCT03008070 (Phase 2b Study in NASH to Assess IVA337).","68677842","927961-18-0",false,"OC(=O)CCCC1=CC2=C(C=CC(Cl)=C2)N1S(=O)(=O)C1=CC2=C(C=C1)N=CS2","OQDQIFQRNZIEEJ-UHFFFAOYSA-N",434.926,{"$nulls":4},"PPARD agonist; PPARA agonist; PPARG agonist","Dermatological drug","Phase 2 completed (NCT03008070: In this phase 2b trial involving patients with active NASH, the percentage of patients who had a decrease of at least 2 points in the SAF-A score without worsening of fibrosis was significantly higher with the 1200-mg dose of lanifibranor than with placebo. These findings support further assessment of lanifibranor in phase 3 trials.) \r\nPhase 3 on-going (NCT04849728)","Advanced in clinical trials","2022-03-21"]
[201,"L-Carnitine","(-)-Carnitine; (-)-L-Carnitine; (R)-Carnitine; 3-Carboxy-2-hydroxy-N,N,N-trimethyl-1-propanaminium hydroxide, inner salt; Carnitine; L-Carnitine; Levocarnitine; Vitamin BT","Supplement","DB00583","Constituent of striated muscle and liver. It is used therapeutically to stimulate gastric and pancreatic secretions and in the treatment of hyperlipoproteinemias.","10917","541-15-1",true,"C([N+](C)(C)C)[C@@H](CC(=O)[O-])O","PHIQHXFUZVPYII-ZCFIWIBFSA-N",161.201,"Solute carrier family 22 member 4; Solute carrier family 22 member 5; Carnitine O-acetyltransferase; Mitochondrial carnitine/acylcarnitine carrier protein CACL; Mitochondrial carnitine/acylcarnitine carrier protein; Peroxisomal carnitine O-octanoyltransfe","Levocarnitine can be synthesised within the body from the amino acids lysine or methionine. Vitamin C (ascorbic acid) is essential to the synthesis of carnitine. Levocarnitine is a carrier molecule in the transport of long chain fatty acids across the inner mitochondrial membrane. It also exports acyl groups from subcellular organelles and from cells to urine before they accumulate to toxic concentrations. Only the L isomer of carnitine (sometimes called vitamin BT) affects lipid metabolism. Levocarnitine is handled by several proteins in different pathways including carnitine transporters, carnitine translocases, carnitine acetyltransferases and carnitine palmitoyltransferases.","Levocarnitine is a carrier molecule in the transport of long chain fatty acids across the inner mitochondrial membrane. It also exports acyl groups from subcellular organelles and from cells to urine before they accumulate to toxic concentrations. Lack of carnitine can lead to liver, heart, and muscle problems. Carnitine deficiency is defined biochemically as abnormally low plasma concentrations of free carnitine, less than 20 &micro;mol/L at one week post term and may be associated with low tissue and/or urine concentrations. Further, this condition may be associated with a plasma concentration ratio of acylcarnitine/levocarnitine greater than 0.4 or abnormally elevated concentrations of acylcarnitine in the urine. Only the L isomer of carnitine (sometimes called vitamin BT) affects lipid metabolism. The \"vitamin BT\" form actually contains D,L-carnitine, which competitively inhibits levocarnitine and can cause deficiency. Levocarnitine can be used therapeutically to stimulate gastric and pancreatic secretions and in the treatment of hyperlipoproteinemias.","For treatment of primary systemic carnitine deficiency, a genetic impairment of normal biosynthesis or utilization of levocarnitine from dietary sources, or for the treatment of secondary carnitine deficiency resulting from an inborn error of metabolism such as glutaric aciduria II, methyl malonic aciduria, propionic acidemia, and medium chain fatty acylCoA dehydrogenase deficiency. Used therapeutically to stimulate gastric and pancreatic secretions and in the treatment of hyperlipoproteinemias. Parenteral levocarnitine is indicated for the prevention and treatment of carnitine deficiency in patients with end-stage renal disease.","SLC22A4; SLC22A5; CRAT; MPO",null,"Phase 3 on-going (IRCT20170628034786N2)","Under clinical trials","2022-03-21"]
[202,"LCQ908","Pradigastat","Chemical drug","DB12866","Pradigastat has been used in trials studying the treatment of Non-alcoholic Fatty Liver Disease (NAFLD).","53387035","956136-95-1",false,"N(c1ccc(nc1)c1ccc(cc1)[C@@H]1CC[C@H](CC1)CC(=O)O)c1ccc(nc1)C(F)(F)F","GXALXAKNHIROPE-QAQDUYKDSA-N",455.48,{"$nulls":4},"DGAT1 inhibitor","Hypolipidemic drug","Phase 2 completed  (NCT01811472)","Under clinical trials","2022-03-21"]
[203,"Levothyroxine","3,3',5,5'-Tetraiodo-L-thyronine; 3,5,3',5'-Tetraiodo-L-thyronine; 4-(4-Hydroxy-3,5-diiodophenoxy)-3,5-diiodo-L-phenylalanine; L-T4; L-Thyroxine; Levothyroxin; LT4; O-(4-Hydroxy-3,5-diidophenyl)-3,5-diiodo-L-tyrosine; O-(4-Hydroxy-3,5-diiodophenyl)-3,5-diiodo-L-tyrosine; T4; Thyroxine","Chemical drug","DB00451","Levothyroxine is a synthetically produced form of thyroxine, a major endogenous hormone secreted by the thyroid gland. Also known as L-thyroxine or the brand name product Synthroid, levothyroxine is used primarily to treat hypothyroidism, a condition where the thyroid gland is no longer able to produce sufficient quantities of the thyroid hormones T<sub>4</sub> (tetraiodothyronine or thyroxine) and T<sub>3</sub> (triiodothyronine or ), resulting in diminished down-stream effects of these hormones. Without sufficient quantities of circulating thyroid hormones, symptoms of hypothyroidism begin to develop such as fatigue, increased heart rate, depression, dry skin and hair, muscle cramps, constipation, weight gain, memory impairment, and poor tolerance to cold temperatures.\r\n\r\nIn response to Thyroid Stimulating Hormone (TSH) release by the pituitary gland, a normally functioning thyroid gland will produce and secrete T<sub>4</sub>, which is then converted through deiodination (by type I or type II 5′-deiodinases) into its active metabolite T<sub>3</sub>. While T<sub>4</sub> is the major product secreted by the thyroid gland,  T<sub>3</sub> exerts the majority of the physiological effects of the thyroid hormones; T<sub>4</sub> and T<sub>3</sub> have a relative potency of ~1:4 (T4:T3). T<sub>4</sub> and T<sub>3</sub> act on nearly every cell of the body, but have a particularly strong effect on the cardiac system. As a result, many cardiac functions including heart rate, cardiac output, and systemic vascular resistance are closely linked to thyroid status.\r\n\r\nPrior to the development of levothyroxine,  or desiccated thyroid, used to be the mainstay of treatment for hypothyroidism. However, this is no longer recommended for the majority of patients due to several clinical concerns including limited controlled trials supporting its use. Desiccated thyroid products contain a ratio of T4 to T3 of 4.2:1, which is significantly lower than the 14:1 ratio of secretion by the human thyroid gland. This higher proportion of T3 in desiccated thyroid products can lead to supraphysiologic levels of T3 which may put patients at risk of thyrotoxicosis if thyroid extract therapy is not adjusted according to the serum TSH.","5819","51-48-9",true,"O(c1cc(I)c(c(c1)I)O)c1c(I)cc(cc1I)C[C@@H](C(=O)O)N","XUIIKFGFIJCVMT-LBPRGKRZSA-N",776.872,"Thyroid hormone receptor alpha agonist; Thyroid hormone receptor beta agonist; Integrin alpha-V; Integrin beta-3","Levothyroxine is a synthetically prepared levo-isomer of the thyroid hormone thyroxine (T<sub>4</sub>, a tetra-iodinated tyrosine derivative) that acts as a replacement in deficiency syndromes such as hypothyroidism. T<sub>4</sub> is the major hormone secreted from the thyroid gland and is chemically identical to the naturally secreted T<sub>4</sub>: it increases metabolic rate, decreases thyroid-stimulating hormone (TSH) production from the anterior lobe of the pituitary gland, and, in peripheral tissues, is converted to T<sub>3</sub>. Thyroxine is released from its precursor protein thyroglobulin through proteolysis and secreted into the blood where is it then peripherally deiodinated to form triiodothyronine (T<sub>3</sub>) which exerts a broad spectrum of stimulatory effects on cell metabolism. T<sub>4</sub> and T<sub>3</sub> have a relative potency of ~1:4. \r\n\r\nThyroid hormone increases the metabolic rate of cells of all tissues in the body. In the fetus and newborn, thyroid hormone is important for the growth and development of all tissues including bones and the brain. In adults, thyroid hormone helps to maintain brain function, food metabolism, and body temperature, among other effects. The symptoms of thyroid deficiency relieved by levothyroxine include slow speech, lack of energy, weight gain, hair loss, dry thick skin and unusual sensitivity to cold.\r\n\r\nThe thyroid hormones have been shown to exert both genomic and non-genomic effects. They exert their genomic effects by diffusing into the cell nucleus and binding to thyroid hormone receptors in DNA regions called thyroid hormone response elements (TREs) near genes. This complex of T<sub>4</sub>, T<sub>3</sub>, DNA, and other coregulatory proteins causes a conformational change and a resulting shift in transcriptional regulation of nearby genes, synthesis of messenger RNA, and cytoplasmic protein production. For example, in cardiac tissues T<sub>3</sub> has been shown to regulate the genes for α- and β-myosin heavy chains, production of the sarcoplasmic reticulum proteins calcium-activated ATPase (Ca2+-ATPase) and phospholamban, β-adrenergic receptors, guanine-nucleotide regulatory proteins, and adenylyl cyclase types V and VI as well as several plasma-membrane ion transporters, such as Na+/K+–ATPase, Na+/Ca2+ exchanger, and voltage-gated potassium channels, including Kv1.5, Kv4.2, and Kv4.3.  As a result, many cardiac functions including heart rate, cardiac output, and systemic vascular resistance are closely linked to thyroid status.\r\n\r\nThe non-genomic actions of the thyroid hormones have been shown to occur through binding to a plasma membrane receptor integrin aVb3 at the Arg-Gly-Asp recognition site. From the cell-surface, T<sub>4</sub> binding to integrin results in down-stream effects including activation of mitogen-activated protein kinase (MAPK; ERK1/2) and causes subsequent effects on cellular/nuclear events including angiogenesis and tumor cell proliferation.","Oral levothyroxine is a synthetic hormone that exerts the same physiologic effect as endogenous T<sub>4</sub>, thereby maintaining normal T<sub>4</sub> levels when a deficiency is present. \r\n\r\nLevothyroxine has a narrow therapeutic index and is titrated to maintain a euthyroid state with TSH (thyroid stimulating hormone) within a therapeutic range of 0.4–4.0 mIU/L. Over- or under-treatment with levothyroxine may have negative effects on growth and development, cardiovascular function, bone metabolism, reproductive function, cognitive function, emotional state, gastrointestinal function and glucose and lipid metabolism. The dose of levothyroxine should be titrated slowly and carefully and patients should be monitored for their response to titration to avoid these effects. TSH levels should be monitored at least yearly to avoid over-treating with levothyroxine which can result in hyperthyroidism (TSH <0.1mIU/L) and symptoms of increased heart rate, diarrhea, tremor, hypercalcemia, and weakness to name a few.\r\n\r\nAs many cardiac functions including heart rate, cardiac output, and systemic vascular resistance are closely linked to thyroid status, over-treatment with levothyroxine may result in increases in heart rate, cardiac wall thickness, and cardiac contractility and may precipitate angina or arrhythmias, particularly in patients with cardiovascular disease and in elderly patients. In populations with any cardiac concerns, levothyroxine should be initiated at lower doses than those recommended in younger individuals or in patients without cardiac disease. Patients receiving concomitant levothyroxine and sympathomimetic agents should be monitored for signs and symptoms of coronary insufficiency. If cardiac symptoms develop or worsen, reduce the levothyroxine dose or withhold for one week and restart at a lower dose.\r\n\r\nIncreased bone resorption and decreased bone mineral density may occur as a result of levothyroxine over-replacement, particularly in post-menopausal women. The increased bone resorption may be associated with increased serum levels and urinary excretion of calcium and phosphorous, elevations in bone alkaline phosphatase and suppressed serum parathyroid hormone levels. Administer the minimum dose of levothyroxine that achieves the desired clinical and biochemical response to mitigate this risk.\r\n\r\nAddition of levothyroxine therapy in patients with diabetes mellitus may worsen glycemic control and result in increased antidiabetic agent or insulin requirements. Carefully monitor glycemic control after starting, changing or discontinuing levothyroxine.","Levothyroxine is indicated as replacement therapy in primary (thyroidal), secondary (pituitary) and tertiary (hypothalamic) congenital or acquired hypothyroidism. It is also indicated as an adjunct to surgery and radioiodine therapy in the management of thyrotropin-dependent well-differentiated thyroid cancer.","THRA agonist; THRB agonist","Anti-fibrosis","Phase 2 terminated  (NCT03281083: Difficult recruitment and end of funding.)","Under clinical trials","2022-03-21"]
[204,"Licogliflozin","LIK-066; LIK066","Chemical drug","DB15048","Licogliflozin is under investigation in clinical trial NCT03320941 (A Dose-finding Study to Evaluate the Change in Weight After Treatment With LIK066 in Japanese Patients With Obesity).","52913524","1291094-73-9",false,"O[C@H]1[C@@H](O[C@@H]([C@H]([C@@H]1O)O)CO)c1cc(Cc2cc3c(cc2)OCCO3)c(cc1)CC","XFJAMQQAAMJFGB-ZQGJOIPISA-N",416.47,{"$nulls":4},"SGLT1 inhibitor; SGLT2 inhibitor","Improve insulin resistance","Phase 2 completed  (NCT03205150)","Under clinical trials","2022-03-21"]
[205,"Linagliptin","(R)-8-(3-aminopiperidin-1-yl)-7-but-2-ynyl-3-methyl-1-(4-methylquinazolin-2-ylmethyl)-3,7-dihydro-purine-2,6-dione; Linagliptin","Chemical drug","DB08882","Linagliptin is a DPP-4 inhibitor developed by Boehringer Ingelheim for the treatment of type II diabetes . Linagliptin differs from other DPP-4 inhibitors in that it has a non-linear pharmacokinetic profile, is not primarily eliminated by the renal system, and obeys concentration dependant protein binding. Linagliptin was approved by the FDA on May 2, 2011.","10096344","668270-12-0",true,"C(C#CC)n1c2c(nc1N1C[C@H](N)CCC1)n(C)c(=O)n(c2=O)Cc1nc2c(c(n1)C)cccc2","LTXREWYXXSTFRX-QGZVFWFLSA-N",472.553,"Dipeptidyl peptidase 4 inhibitor","Linagliptin is a competitive, reversible DPP-4 inhibitor. Inhibition of this enzyme slows the breakdown of GLP-1 and glucose-dependant insulinotropic polypeptide (GIP). GLP-1 and GIP stimulate the release of insulin from beta cells in the pancreas while inhibiting release of glucagon from pancreatic beta cells. These effects together reduce the breakdown of glycogen in the liver and increase insulin release in response to glucose.","A 5mg oral dose of linagliptin results in >80% inhibition of dipeptidyl peptidase 4 (DPP-4) for ≥24 hours. Inhibition of DPP-4 increases the concentration of glucagon-like peptide 1 (GLP-1), leading to decreased glycosylated hemoglobin and fasting plasma glucose.","Linagliptin is indicated for the treatment of type II diabetes in addition to diet and exercise. It should not be used to treat type I diabetes or in diabetic ketoacidosis. An extended-release combination product containing empagliflozin, linagliptin, and metformin was approved by the FDA in January 2020 for the improvement of glycemic control in adults with type 2 diabetes mellitus when used adjunctively with diet and exercise.","DPP4 inhibitor",null,"Clinical trial on-going (JPRN-UMIN000014864)","Under clinical trials","2022-03-21"]
[206,"Lingguizhugan decoction","Fulin, Guizhi, Baizhu, Gancao","Traditional medicine",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (ChiCTR1800014364)","Under clinical trials","2022-03-21"]
[207,"Liraglutide","Arg34Lys26-(N-ε-(γ-Glu(N-α-hexadecanoyl)))-GLP-1[7-37]; Liraglutide; Liraglutide (genetical recombination); Liraglutide (rDNA origin); Liraglutide recombinant; N²⁶-(hexadecanoyl-gamma-glutamyle)-[34-arginine]GLP-1-(7-37)-peptide; N²⁶-(N-Hexadecanoyl-L-gamma-glutamyl)-[34-L-arginine]glucagon-like peptide 1-(7-37)-peptide","Biological drug","DB06655","Victoza contains liraglutide, a synthetic analog of human glucagon-like peptide-1(GLP-1) and acts as a GLP-1 receptor agonist. Liraglutide is 97% homologous to native human GLP-1 by substituting arginine for lysine at position 34. Liraglutide is made by attaching a C-16 fatty acid (palmitic acid) with a glutamic acid spacer on the remaining lysine residue at position 26 of the peptide precursor. Liraglutide was granted FDA approval on Januray 25, 2010.","16134956","204656-20-2",true,"O=C(N[C@@H](C(C)C)C(=O)N[C@@H](CCCNC(=N)N)C(=O)NCC(=O)N[C@@H](CCCNC(=N)N)C(=O)NCC(=O)O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)CNC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)CNC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](N)Cc1[nH]cnc1)C)CCC(=O)O)[C@H](O)C)Cc1ccccc1)[C@H](O)C)CO)CC(=O)O)C(C)C)CO)CO)Cc1ccc(O)cc1)CC(C)C)CCC(=O)O)CCC(=O)N)C)C)CCCCNC(=O)CC[C@H](NC(=O)CCCCCCCCCCCCCCC)C(=O)O)CCC(=O)O)Cc1ccccc1)[C@H](CC)C)C)Cc1c2c([nH]c1)cccc2)CC(C)C","YSDQQAXHVYUZIW-QCIJIYAXSA-N",3751.262,"Glucagon-like peptide 1 receptor agonist","Liraglutide is an acylated synthetic glucagon-like peptide-1 analog. Liraglutide is an agonist of the glucagon-like peptide-1 receptor which is coupled to adenylate cyclase. The increase in cyclic AMP stimulates the glucose dependant release of insulin, inhibits the glucose dependant release of glucagon, and slows gastric emptying to increase control of blood sugar.","Liraglutide is a once-daily GLP-1 derivative for the treatment of type 2 diabetes. The prolonged action of liraglutide is achieved by attaching a fatty acid molecule at position 26 of the GLP-1 molecule, enabling it to bind reversibly to albumin within the subcutaneous tissue and bloodstream and be released slowly over time. Binding with albumin results in slower degradation and reduced elimination of liraglutide from the circulation by the kidneys compared to GLP-1. The effect of liraglutide is the increased secretion of insulin and decreased secretion of glucagon in response to glucose as well as slower gastric emptying. Liraglutide also does not adversely affect glucagon secretion in response to low blood sugar.","Liraglutide is indicated in combination with diet and exercise to improve glycemic control in patients 10 years and older with type 2 diabetes mellitus. It is also indicated to reduce the risk of major adverse cardiovascular events in patients with type 2 diabetes mellitus as well as cardiovascular disease.","GLP1R activator; GLP1R agonist; GCG receptor antagonist activity","Improve insulin resistance","Phase 2 completed (NCT01237119: Liraglutide was safe, well tolerated, and led to histological resolution of non-alcoholic steatohepatitis, warranting extensive, longer-term studies.)","Under clinical trials","2022-03-21"]
[208,"Lobeglitazone","Lobeglitazone","Chemical drug","DB09198","Lobeglitazone is an antidiabetic medication from the thiazolidinedione class of drugs. It primarily functions as an insulin sensitizer by binding and activating Peroxisome Proliferator-Activated Receptors (PPAR) gamma within fat cells. By activating PPAR-gamma and promoting the binding of insulin at fat cells, lobeglitazone thereby has been shown to reduce blood sugar levels, lower hemoglobain A1C (HbA1C) levels, and improve lipid and liver profiles . Unlike , which is a dual PPAR agonist at PPAR-alpha and PPAR-gamma, Lobeglitazone is a pure PPAR-alpha agonist. \r\n\r\nLobeglitazone was approved by the Ministry of Food and Drug Safety (South Korea) in 2013, and is being monitored by postmarketing surveillance until 2019. Lobeglitazone is not approved for use by either the Food and Drug Administration (USA), Health Canada, or by the European Medicines Agency for use in the management of diabetes.","9826451","607723-33-1",false,"COC1=CC=C(OC2=NC=NC(=C2)N(C)CCOC2=CC=C(CC3SC(=O)NC3=O)C=C2)C=C1","CHHXEZSCHQVSRE-UHFFFAOYSA-N",480.546,"Peroxisome proliferator-activated receptor gamma activator","Lobeglitazone acts as an insulin sensitizer by binding and activating Peroxisome Proliferator-Activated Receptors (PPAR) gamma within fat cells. By promoting the binding of insulin at fat cells, lobeglitazone has been shown to reduce blood sugar levels, lower hemoglobain A1C (HbA1C) levels, and improve lipid and liver profiles . Unlike , which is a dual PPAR agonist at PPAR-alpha and PPAR-gamma, Lobeglitazone is a pure PPAR-alpha agonist.",null,"Lobeglitazone was approved by the Ministry of Food and Drug Safety (South Korea) in 2013, and is being monitored by postmarketing surveillance until 2019. Lobeglitazone is not approved for use by either the Food and Drug Administration (USA), Health Canada, or by the European Medicines Agency for use in the management of diabetes.","PPARG activator","Improve insulin resistance","Phase 4 completed  (NCT02285205: Lobeglitazone treatment reduced intrahepatic fat content, as assessed by transient liver elastography, and improved glycemic, liver, and lipid profiles in T2D patients with NAFLD. Further randomized controlled trials using liver histology as an end point are necessary to evaluate the efficacy of lobeglitazone for NAFLD treatment.)","Under clinical trials","2022-03-21"]
[209,"Losartan","(2-butyl-4-chloro-1-{[2'-(1H-tetrazol-5-yl)biphenyl-4-yl]methyl}-1H-imidazol-5-yl)methanol; 2-n-butyl-4-chloro-5-hydroxymethyl-1-[(2'-(1H-tetrazol-5-yl)biphenyl-4-yl)methyl]imidazole; Losartan","Chemical drug","DB00678","Losartan is an angiotensin II receptor blocker (ARB) used to treat hypertension. Angiotensin-converting enzyme (ACE) inhibitors are used for a similar indication but are associated with a cough. When patients with ACE inhibitor associated coughs are switched to ARBs like losartan, they have an incidence of cough similar to placebo or . Losartan is available as losartan potassium oral tablets as well as a combination tablet of losartan potassium and hydrochlorothiazide. Patients taking losartan should have their renal function and potassium levels monitored. Losartan was granted FDA approval on 14 April 1995.","3961","114798-26-4",true,"C(n1c(CCCC)nc(c1CO)Cl)c1ccc(cc1)c1c(cccc1)c1[nH]nnn1","PSIFNNKUMBGKDQ-UHFFFAOYSA-N",422.92,"Type-1 angiotensin II receptor antagonist","Losartan reversibly and competitively prevents angiotensin II binding to the AT<sub>1</sub> receptor in tissues like vascular smooth muscle and the adrenal gland. Losartan and its active metabolite bind the AT<sub>1</sub> receptor with 1000 times more affinity than they bind to the AT<sub>2</sub> receptor. The active metabolite of losartan is 10-40 times more potent by weight than unmetabolized losartan as an inhibitor of AT<sub>1</sub> and is a non-competitive inhibitor. Losartan's prevention of angiotensin II binding causes vascular smooth muscle relaxation, lowering blood pressure.\r\n\r\nAngiotensin II would otherwise bind to the AT<sub>1</sub> receptor and induce vasoconstriction, raising blood pressure.","Losartan is an angiotensin II receptor blocker used to treat hypertension, diabetic nephropathy, and to reduce the risk of stroke. Losartan has a long duration of action as it is given once daily. Patients taking losartan should be regularly monitored for hypotension, renal function, and potassium levels.","Losartan is indicated to treat hypertension in patients older than 6 years, reduce the risk of stroke in patients with hypertension and left ventricular hypertrophy (though this benefit may not extend to patients with African heritage), and to treat diabetic nephropathy with elevated serum creatinine and proteinuria in patients with type 2 diabetes and hypertension. Losartan with hydrochlorothiazide is indicated to treat hypertension and to reduce the risk of stroke in patients with hypertension and left ventricular hypertrophy (though this benefit may not extend to patients with African heritage).","AGTR1 antagonist&binder","Anti-fibrosis","Phase 3 on-going (IRCT20180412039283N1)","Under clinical trials","2022-03-21"]
[210,"Lovaza","Omega-3 fatty acid ethyl esters; Omega-3-acid ethyl esters","Chemical drug","DB09539","Omega-3-acid ethyl esters are prescription drugs that contain eicosapentaenoic acid-ethyl ester (EPA) and docosahexaenoic acid-ethyl ester (DHA) that are used in combination with changes in diet to lower triglyceride levels in adults with severe (≥ 500 mg/dL) hypertriglyceridemia. Omega-3-acid ethyl esters are currently marketed in the US, EU, and many other regions under the brand name Lovaza.","9831414","861006-80-6",true,"C(=C\\C/C=C\\C/C=C\\C/C=C\\C/C=C\\C/C=C\\CC)\\CCC(=O)OCC.C(=C\\C/C=C\\C/C=C\\C/C=C\\C/C=C\\CC)\\CCCC(=O)OCC","DTMGIJFHGGCSLO-FIAQIACWSA-N",687.062,"Sterol regulatory element-binding protein 1 inhibitor","Omega-3-acid ethyl esters reduce triglyceride production by the liver but this mechanism is not well understood. Omega-3-acid ethyl esters inhibit acyl-CoA:1,2-diacylglycerol acyltransferase, reducing triglyceride synthesis and increasing paroxysmal beta-oxidation, which increases fatty aside metabolism. Omega-3-acid ethyl esters also inhibit the release of fatty acids by competing for enzymes involved in the synthesis of triglycerides, increase triglyceride clearance by increasing the activity of lipoprotein lipase, and decrease production of VLDL-C.","Omega-3-acid ethyl esters reduce triglyceride production, increase fatty acid metabolism, inhibit the release of fatty acids, increase triglyceride clearance, and decrease production of very low density lipoprotein cholesterol(VLDL-C).","Omega-3-Acid Ethyl Esters capsules, USP are indicated as an adjunct to diet to reduce triglyceride (TG) levels in adult patients with severe (≥500 mg/dL) hypertriglyceridemia (HTG).","SREBF1 inhibitor","Hypolipidemic drug","Clinical trial on-going (NCT00941642)","Under clinical trials","2022-03-21"]
[211,"LPCN 1144",null,"Biological drug",{"$nulls":4},false,{"$nulls":7},"AR activator","Metabolic disorder drug","Phase 2 on-going (NCT04685993)","Under clinical trials","2022-03-21"]
[212,"Lubiprostone","Lubiprostone","Chemical drug","DB01046","Lubiprostone is a medication used in the management of idiopathic chronic constipation. A prostaglandin E1 derivative, lubiprostone is a bicyclic fatty acid that activates ClC-2 chloride channels located on the apical side of the gastrointestinal epithelial cells. Activation of these channels promotes the secretion of a chloride-rich fluid that soften the stool, increase gastrointestinal motility, and induce spontaneous bowel movements (SBM).","157920","333963-40-9, 136790-76-6",true,"C(CCCC)(F)(F)[C@]1(O)O[C@H]2[C@H](CC1)[C@H](C(=O)C2)CCCCCCC(=O)O","WGFOBBZOWHGYQH-MXHNKVEKSA-N",390.467,"Chloride channel protein 2 inducer","Lubiprostone acts by specifically activating ClC-2 chloride channels, which is a normal constituent of the apical membrane of the human intestine, in a protein kinase A action independent fashion. Activation of ClC-2 chloride channels causes an efflux of chloride ions into the lumen, which in turn leads to an efflux of sodium ions through a paracellular pathway to maintain isoelectric neutrality. As a result, water follows sodium into the lumen in order to maintain isotonic equilibrium, thereby increasing intestinal fluid secretion. By increasing intestinal fluid secretion, lubiprostone increases motility in the intestine, thereby increasing the passage of stool and alleviating symptoms associated with chronic idiopathic constipation. Activation of ClC-2 chloride channels may also stimulate the recovery of muscosal barrier function by restoring tight junction protein complexes in the intestine. Patch clamp cell studies in human cell lines have indicated that the majority of the beneficial biological activity of lubiprostone and its metabolites is observed only on the apical (luminal) portion of the gastrointestinal epithelium.","Chronic idiopathic constipation is generally defined by infrequent or difficult passage of stool. The signs and symptoms associated with chronic idiopathic constipation (i.e., abdominal pain or discomfort, bloating, straining, and hard or lumpy stools) may be the result of abnormal colonic motility that can delay the transit of intestinal contents and impede the evacuation of rectal contents. One approach to the treatment of chronic idiopathic constipation is the secretion of fluid into the abdominal lumen through the activation of chloride channels in the apical membrane of the gastrointestinal epithelium. Lubiprostone is a locally acting chloride channel activator that increases intestinal chloride and fluid secretion without altering sodium and potassium concentrations in the serum.","For the treatment of chronic idiopathic constipation in the adult population. Also used for the treatment of irritable bowel syndrome with constipation in women who are 18 years of age or older.",null,null,"Clinical trial on-going (JPRN-UMIN000026635)","Under clinical trials","2022-03-21"]
[213,"Luseogliflozin","Luseogliflozin","Chemical drug","DB12214","Luseogliflozin has been used in trials studying the treatment of Diabetes Melltius, Type 2.","11988953","898537-18-3",false,"O(C)c1c(cc(c(c1)C)Cc1ccc(cc1)OCC)[C@@H]1S[C@H](CO)[C@H]([C@@H]([C@H]1O)O)O","WHSOLWOTCHFFBK-ZQGJOIPISA-N",434.554,{"$nulls":6},"Phase 0 on-going (JPRN-jRCTs031190238)","Under clinical trials","2022-03-21"]
[214,"LYS006",null,"Chemical drug",null,null,"118166566",null,false,"C1=CC(=CC=C1C2=NN(N=N2)CC(CC(=O)O)N)OC3=C(C=C(C=N3)Cl)F","ZEGMEJVULDALSH-UHFFFAOYSA-N",392.77,{"$nulls":6},"Phase 2 terminated  (NCT04147195: Sponsor Decision)","Under clinical trials","2022-03-21"]
[215,"Maple Syrup",null,"Supplement",{"$nulls":3},"8029-81-0",false,{"$nulls":9},"Clinical trial completed (NCT04117802)","Under clinical trials","2022-03-21"]
[216,"Maraviroc",null,"Chemical drug","DB04835","Maraviroc (brand-named Selzentry, or Celsentri outside the U.S.) is a chemokine receptor antagonist drug developed by the drug company Pfizer that is designed to act against HIV by interfering with the interaction between HIV and CCR5. It was originally labelled as UK-427857 during development but was assigned the Maraviroc name as it entered trials. It was approved for use by the FDA in August, 2007.","3002977","376348-65-1",true,"C(C[C@H](NC(=O)C1CCC(CC1)(F)F)c1ccccc1)N1[C@@H]2C[C@@H](C[C@H]1CC2)n1c(C(C)C)nnc1C","GSNHKUDZZFZSJB-QYOOZWMWSA-N",513.677,"C-C chemokine receptor type 5 antagonist","Maraviroc is an entry inhibitor and works by blocking HIV from entering human cells. Specifically maraviroc is a selective, slowly reversible, small molecule antagonist of the interaction between human CCR5 and HIV-1 gp120. Maraviroc selectively binds to the human chemokine receptor CCR5 present on the membrane of CD4 cells (T-cells), preventing the interaction of HIV-1 gp120 and CCR5 necessary for CCR5-tropic HIV-1 to enter cells.","Maraviroc is a chemokine receptor antagonist drug developed by the drug company Pfizer that is designed to act against HIV by interfering with the interaction between HIV and CCR5.","For treatment-experienced adult patients infected with only CCR5-tropic HIV-1 detectable, who have evidence of viral replication and HIV-1 strains resistant to multiple antiretroviral agents.","CCR5 antagonist; CCR5 binder","Anti-fibrosis","Phase 2&3 completed  (NCT03129113)","Under clinical trials","2022-03-21"]
[217,"Mastiha","Pistacia lentiscus","Biological extract",{"$nulls":3},"61789-92-2",false,{"$nulls":9},"Clinical trial completed (NCT03135873: Mastiha supplementation improved the TAS levels among NAFLD patients with severe obesity. We identified several novel genome-wide significant nutrigenetic interactions, influencing the antioxidant and inflammatory status in NAFLD.)","Under clinical trials","2022-03-21"]
[218,"Matricaria chamomilla L.",null,"Biological extract",{"$nulls":3},"8002-66-2",false,{"$nulls":9},"Clinical trial on-going (IRCT20180903040941N1)","Under clinical trials","2022-03-21"]
[219,"Maxicor",null,"Chemical drug",{"$nulls":3},"1446486-27-6",false,"C(=C\\C/C=C\\C/C=C\\C/C=C\\CC)\\C/C=C\\CCCC(=O)O.C(=C\\C/C=C\\CCC(=O)O)\\C/C=C\\C/C=C\\C/C=C\\C/C=C\\CC.C(=C\\CCCCC(=O)O)\\C/C=C\\C/C=C\\C/C=C\\CC","RLRFGEJRYONIMT-ZMQSKEMKSA-N",907.374,{"$nulls":6},"Clinical trial completed (NCT02647294)","Under clinical trials","2022-03-21"]
[220,"MB12066",null,"Chemical drug","DB11948","Lapachone has been used in trials studying the treatment of Cancer, Carcinoma, Advanced Solid Tumors, Head and Neck Neoplasms, and Carcinoma, Squamous Cell.","3885","4707-32-8",false,{"$nulls":3},"Retinol-binding protein 3",{"$nulls":5},"Phase 2 terminated  (NCT02029586: Lack of recruitment)","Under clinical trials","2022-03-21"]
[221,"MEDI0382","Cotadutide","Chemical drug","DB15194","Cotadutide is under investigation in clinical trial NCT03444584 (Study of MEDI0382 in Combination With Dapagliflozin and Metformin in Overweight/Obese Subject With Type 2 Diabetes).","134694273","1686108-82-6",false,"O=C(N[C@@H](CC(C)C)C(=O)N[C@@H](CCC(=O)O)C(=O)N[C@@H](C)C(=O)NCC(=O)NCC(=O)O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)CNC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](N)Cc1nc[nH]c1)CO)CCC(=O)N)[C@H](O)C)Cc1ccccc1)[C@H](O)C)CO)CC(=O)O)CCCCNC(=O)CC[C@H](NC(=O)CCCCCCCCCCCCCCC)C(=O)O)CO)CCC(=O)O)Cc1ccc(O)cc1)CC(C)C)CC(=O)O)CO)CCC(=O)O)CCCNC(=N)N)C)CCCNC(=N)N)CC(=O)O)Cc1ccccc1)C(C)C)C)Cc1c2c([nH]c1)cccc2","YEKUUBPJRPXMBM-PTCFZACGSA-N",3728.092,{"$nulls":4},"GLP1R inhibitor; GCGR inhibitor","Improve insulin resistance","Phase 2 completed (NCT04019561)","Under clinical trials","2022-03-21"]
[222,"Melatonin","5-methoxy-N-acetyltryptamine; Melatonin; N-[2-(5-methoxyindol-3-yl)ethyl]acetamide; N-Acetyl-5-methoxytryptamine","Chemical drug","DB01065","Melatonin is a biogenic amine that is found in animals, plants and microbes. Aaron B. Lerner of Yale University is credited for naming the hormone and for defining its chemical structure in 1958.  In mammals, melatonin is produced by the pineal gland. The pineal gland is small endocrine gland, about the size of a rice grain and shaped like a pine cone (hence the name), that is located in the center of the brain (rostro-dorsal to the superior colliculus) but outside the blood-brain barrier. The secretion of melatonin increases in darkness and decreases during exposure to light, thereby regulating the circadian rhythms of several biological functions, including the sleep-wake cycle. In particular, melatonin regulates the sleep-wake cycle by chemically causing drowsiness and lowering the body temperature.  Melatonin is also implicated in the regulation of mood, learning and memory, immune activity, dreaming, fertility and reproduction. Melatonin is also an effective antioxidant.  Most of the actions of melatonin are mediated through the binding and activation of melatonin receptors. Individuals with autism spectrum disorders (ASD) may have lower than normal levels of melatonin. A 2008 study found that unaffected parents of individuals with ASD also have lower melatonin levels, and that the deficits were associated with low activity of the ASMT gene, which encodes the last enzyme of melatonin synthesis. Reduced melatonin production has also been proposed as a likely factor in the significantly higher cancer rates in night workers.","896","73-31-4",true,"C(CNC(=O)C)c1c2c([nH]c1)ccc(c2)OC","DRLFMBDRBRZALE-UHFFFAOYSA-N",232.283,"Melatonin receptor type 1A agonist; Melatonin receptor type 1B agonist; Estrogen receptor alpha antagonist; Nuclear receptor ROR-beta agonist; Calmodulin; Myeloperoxidase inhibitor; Eosinophil peroxidase inhibitor; Calreticulin; Acetylserotonin O-methyltr","Melatonin is a derivative of tryptophan. It binds to melatonin receptor type 1A, which then acts on adenylate cylcase and the inhibition of a cAMP signal transduction pathway. Melatonin not only inhibits adenylate cyclase, but it also activates phosphilpase C. This potentiates the release of arachidonate. By binding to melatonin receptors 1 and 2, the downstream signallling cascades have various effects in the body. The melatonin receptors are G protein-coupled receptors and are expressed in various tissues of the body. There are two subtypes of the receptor in humans, melatonin receptor 1 (MT1) and melatonin receptor 2 (MT2). Melatonin and melatonin receptor agonists, on market or in clinical trials, all bind to and activate both receptor types.The binding of the agonists to the receptors has been investigated for over two decades or since 1986. It is somewhat known, but still not fully understood. When melatonin receptor agonists bind to and activate their receptors it causes numerous physiological processes.\r\nMT1 receptors are expressed in many regions of the central nervous system (CNS): suprachiasmatic nucleus of the hypothalamus (SNC), hippocampus, substantia nigra, cerebellum, central dopaminergic pathways, ventral tegmental area and nucleus accumbens. MT1 is also expressed in the retina, ovary, testis, mammary gland, coronary circulation and aorta, gallbladder, liver, kidney, skin and the immune system. MT2 receptors are expressed mainly in the CNS, also in the lung, cardiac, coronary and aortic tissue, myometrium and granulosa cells, immune cells, duodenum and adipocytes.\r\nThe binding of melatonin to melatonin receptors activates a few signaling pathways. MT1 receptor activation inhibits the adenylyl cyclase and its inhibition causes a rippling effect of non activation; starting with decreasing formation of cyclic adenosine monophosphate (cAMP), and then progressing to less protein kinase A (PKA) activity, which in turn hinders the phosphorilation of cAMP responsive element-binding protein (CREB binding protein) into P-CREB. MT1 receptors also activate phospholipase C (PLC), affect ion channels and regulate ion flux inside the cell. The binding of melatonin to MT2 receptors inhibits adenylyl cyclase which decreases the formation of cAMP. As well it hinders guanylyl cyclase and therefore the forming of cyclic guanosine monophosphate (cGMP). Binding to MT2 receptors probably affects PLC which increases protein kinase C (PKC) activity. Activation of the receptor can lead to ion flux inside the cell.","Melatonin is a hormone normally produced in the pineal gland and released into the blood. The essential amino acid L-tryptophan is a precursor in the synthesis of melatonin. It helps regulate sleep-wake cycles or the circadian rhythm. Production of melatonin is stimulated by darkness and inhibited by light. High levels of melatonin induce sleep and so consumption of the drug can be used to combat insomnia and jet lag.\r\nMT1 and MT2 receptors may be a target for the treatment of circadian and non circadian sleep disorders because of their differences in pharmacology and function within the SCN. SCN is responsible for maintaining the 24 hour cycle which regulates many different body functions ranging from sleep to immune functions\r","Used orally for jet lag, insomnia, shift-work disorder, circadian rhythm disorders in the blind (evidence for efficacy), and benzodiazepine and nicotine withdrawal. Evidence indicates that melatonin is likely effective for treating circadian rhythm sleep disorders in blind children and adults. It has received FDA orphan drug status as an oral medication for this use. A number of studies have shown that melatonin may be effective for treating sleep-wake cycle disturbances in children and adolescents with mental retardation, autism, and other central nervous system disorders. It appears to decrease the time to fall asleep in children with developmental disabilities, such as cerebral palsy, autism, and mental retardation. It may also improve secondary insomnia associated with various sleep-wake cycle disturbances. Other possible uses for which there is some evidence for include: benzodiazepine withdrawal, cluster headache, delayed sleep phase syndrome (DSPS), primary insomnia, jet lag, nicotine withdrawal, preoperative anxiety and sedation, prostate cancer, solid tumors (when combined with IL-2 therapy in certain cancers), sunburn prevention (topical use), tardive dyskinesia, thrombocytopenia associated with cancer, chemotherapy and other disorders.","MPO inhibitor; EPX inhibitor; CALR; ASMT",null,"Phase 3 on-going (IRCT20200531047614N2)","Under clinical trials","2022-03-21"]
[223,"Metabolic Cofactor Supplementation","combined metabolic activators; CMA","Supplement",{"$nulls":4},true,{"$nulls":9},"Phase 2 on-going (NCT04330326: CMA can be used to develop a pharmacological treatment strategy in NAFLD patients.)","Under clinical trials","2022-03-21"]
[224,"Metadoxine","Pyridoxine mixture with Pyrrolidonecarboxylic Acid; Pyridoxine pyroglutamate","Chemical drug","DB16554",null,"115198","74536-44-0",false,"C(=O)(O)[C@H]1NC(=O)CC1.C(O)c1c(CO)cnc(c1O)C","RYKKQQUKJJGFMN-HVDRVSQOSA-N",298.295,{"$nulls":5},"Antialcoholic drug","Phase 3 suspended (NCT02541045: lack of resources to finance the project)","Under clinical trials","2022-03-21"]
[225,"Metformin","1,1-Dimethylbiguanide; Dimethylbiguanid; Metformin; Metformine","Chemical drug","DB00331","Metformin is an antihyperglycemic agent of the _biguanide_ class, used for the management of type II diabetes) .  Currently, metformin is the first drug of choice for the management of type II diabetes and is prescribed to at least 120 million people worldwide . \r\n\r\nMetformin is considered an antihyperglycemic drug because it lowers blood glucose concentrations in type II diabetes without causing hypoglycemia. Metformin is commonly described as an _insulin sensitizer_ leading to a decrease in insulin resistance and a clinically significant reduction of plasma fasting insulin levels . Another well-known benefit of this drug is modest weight loss. Metformin is the drug of choice for obese type II diabetes patients .\r\n\r\nMetformin was first approved in Canada in 1972 , followed by 1995 in the USA . This drug is available in regular and extended-release forms .","4091","657-24-9",true,"C(=N)(NC(=N)N)N(C)C","XZWYZXLIPXDOLR-UHFFFAOYSA-N",129.167,"5'-AMP-activated protein kinase subunit beta-1 inducer&activator; Electron transfer flavoprotein-ubiquinone oxidoreductase, mitochondrial inhibitor; Glycerol-3-phosphate dehydrogenase [NAD(+)], cytoplasmic inhibitor","Metformin's mechanisms of action are unique from other classes of oral antihyperglycemic drugs. Metformin decreases blood glucose levels by decreasing hepatic glucose production (gluconeogenesis), decreasing the intestinal absorption of glucose, and increasing insulin sensitivity by increasing peripheral glucose uptake and utilization . It is well established that metformin inhibits mitochondrial complex I activity, and it has since been generally postulated that its potent antidiabetic effects occur through this mechanism .   The above processes lead to a decrease in blood glucose, managing type II diabetes and exerting positive effects on glycemic control.\r\n\r\nAfter ingestion, the organic cation transporter-1 (OCT1) is responsible for the uptake of metformin into hepatocytes (liver cells). As this drug is positively charged, it accumulates in cells and in the mitochondria because of the membrane potentials across the plasma membrane as well as the mitochondrial inner membrane. Metformin inhibits mitochondrial complex I, preventing the production of mitochondrial ATP leading to increased cytoplasmic ADP:ATP and AMP:ATP ratios . These changes activate AMP-activated protein kinase (AMPK), an enzyme that plays an important role in the regulation of glucose metabolism . Aside from this mechanism, AMPK can be activated by a lysosomal mechanism involving other activators.  Following this process, increases in AMP:ATP ratio also inhibit _fructose-1,6-bisphosphatase_ enzyme, resulting in the inhibition of gluconeogenesis, while also inhibiting _adenylate cyclase_ and decreasing the production of cyclic adenosine monophosphate (cAMP) , a derivative of ATP used for cell signaling . Activated AMPK phosphorylates two isoforms of acetyl-CoA carboxylase enzyme, thereby inhibiting fat synthesis and leading to fat oxidation, reducing hepatic lipid stores and increasing liver sensitivity to insulin .  \r\n\r\nIn the intestines, metformin increases anaerobic glucose metabolism in enterocytes (intestinal cells), leading to reduced net glucose uptake and increased delivery of lactate to the liver. Recent studies have also implicated the gut as a primary site of action of metformin and suggest that the liver may not be as important for metformin action in patients with type 2 diabetes. Some of the ways metformin may play a role on the intestines is by promoting the metabolism of glucose by increasing glucagon-like peptide I (GLP-1) as well as increasing gut utilization of glucose  . \r\n\r\nIn addition to the above pathway, the mechanism of action of metformin may be explained by other ways, and its exact mechanism of action has been under extensive study in recent years .","**General effects**\r\n\r\nInsulin is an important hormone that regulates blood glucose levels . Type II diabetes is characterized by a decrease in sensitivity to insulin, resulting in eventual elevations in blood glucose when the pancreas can no longer compensate. In patients diagnosed with type 2 diabetes, insulin no longer exerts adequate effects on tissues and cells (called insulin resistance)  and insulin deficiency may also be present .\r\n\r\nMetformin reduces liver (hepatic) production of glucose, decreases the intestinal absorption of glucose, and enhances insulin sensitivity by increasing both peripheral glucose uptake and utilization. In contrast with drugs of the _sulfonylurea_ class, which lead to hyperinsulinemia, the secretion of insulin is unchanged with metformin use .\r\n\r\n**Effect on fasting plasma glucose (FPG) and Glycosylated hemoglobin (HbA1c)**\r\n\r\nHbA1c is an important periodic measure of glycemic control that is used to monitor diabetic patients. Fasting plasma glucose is also a useful and important measure of glycemic control. In a 29-week clinical trial of subjects diagnosed with type II diabetes, metformin decreased the fasting plasma glucose levels by an average of 59 mg/dL from baseline, compared to an average increase of 6.3 mg/dL from baseline in subjects taking a placebo .  Glycosylated hemoglobin (HbA1c) was decreased by about 1.4% in subjects receiving metformin, and increased by 0.4% in subjects receiving placebo only .","**Metformin tablet**\r\n \r\nMetformin is indicated as an adjunct to diet and exercise to increase glycemic control in _adults and pediatric patients_ 10 years of age and older diagnosed with type 2 diabetes mellitus.\r\n\r\n**Metformin extended-release tablet (XR)**\r\n\r\nThe extended-release form is indicated as an adjunct to diet and exercise to improve glycemic control in only _adults_ with type 2 diabetes mellitus. Safety in children has not been determined to this date.\r\n\r\nAn extended-release combination product containing empagliflozin, linagliptin, and metformin was approved by the FDA in January 2020 for the improvement of glycemic control in adults with type 2 diabetes mellitus when used adjunctively with diet and exercise.","PRKAB1 inducer activator; ETEDH inhibitor; GPD1 inhibitor","Improve insulin resistance","Phase 1&2 completed (NCT01084486: Metformin treatment was associated with a significant decrease in OPG levels in patients with NAFLD. The effect on OPG was associated with exposure to metformin per se.); Phase 3 on-going (IRCT20210922052550N1)","Under clinical trials","2022-03-21"]
[226,"Metreleptin","N-Methionylleptin; r-metHuLeptin","Biological drug","DB09046","Metreleptin, a recombinant analog of the human hormone leptin, is an orphan drug used to treat complications of leptin deficiency in people with congenital or acquired lipodystrophy. Affecting less than 500 people worldwide, lipodystrophy is characterized by a lack of adipose tissue, fat deposition in the muscles and liver, and metabolic complications such as hypertriglyceridemia, insulin resistance, diabetes mellitus, and fatty liver disease. These metabolic abnormalities are often aggravated by excessive food intake, which is further aggravated by leptin deficiency, a protein secreted by adipose tissue. Administration of Metreleptin results in improvement of metabolic symptoms including improvements in insulin resistance, reduced HbA1c and fasting glucose, reduced triglycerides, and reductions in food intake. Metreleptin is produced in E. coli and differs from native human leptin by the addition of a methionine residue at its amino terminus. It is administered as a once daily subcutaneous injection. On Feb. 24, 2014, Metreleptin was approved by the FDA for the treatment of complications of leptin deficiency, in addition to diet, in patients with congenital generalized or acquired generalized lipodystrophy. Metreleptin is marketed under the brand Myalept® by Aegerion Pharmaceuticals, Inc.",null,"186018-45-1",true,{"$nulls":3},"Leptin receptor agonist","Metreleptin functions by binding to and activating the human leptin receptor (ObR), which belongs to the Class I cytokine family of receptors that signals through the JAK/STAT transduction pathway.","In patients with leptin deficiency, clinical trials demonstrated that exogenous leptin administration results in weight loss, reduction in mean HbA1c and fasting glucose levels, reduced blood insulin, and reduced triglyceride levels leading to improved insulin sensitivity and reductions in food intake.","Metreleptin is indicated as an adjunct to diet as replacement therapy to treat the complications of leptin deficiency in patients with congenital or acquired generalized lipodystrophy.","LEPR agonist","CNS drug","Phase 2 completed  (NCT02654977)","Under clinical trials","2022-03-21"]
[227,"Milled chia seeds","Salvia hispanica L.","Herbal medicine",{"$nulls":4},true,{"$nulls":9},"Clinical trial completed (NCT03942822: The results of the present study show that 25 g/day of milled chia ameliorates NAFLD. Chia is an accessible vegetal source of omega-3 fatty acids, antioxidants, and fiber, which could have the potential to prevent metabolic abnormalities in NAFLD patients. Considering that there is no pharmacological treatment approved for NAFLD, the findings of the present study suggest that a chia-supplemented diet could be an innovative alternative to control this disease.)","Under clinical trials","2022-03-21"]
[228,"Misatol GL","MK615; heat-concentrated extract from Japanese green apricot; Prunus mume","Biological extract",{"$nulls":3},"2007931-41-9",true,{"$nulls":9},"Clinical trial completed (JPRN-jRCTs031180203: \t\r\nThe efficacy and safety of Misatol GL twice a day for 8 weeks after drinking were evaluated in patients with NASH or NAFLD. The primary and secondary endpoints of efficacy did not show any improvement in liver function of Misatol GL. There was no problem with the safety of Misatol GL.)","Failed in clinical trials","2022-03-21"]
[229,"MitoQ","Mitoquinone cation; Mitoquinone ion","Chemical drug","DB05063","Mitoquinone is based on a novel technology, targeted lipophilic cations, that transport and concentrate antioxidants into the mitochondria -- organelles inside cells that provide energy for life processes -- where they accumulate up to a thousand fold. In 2004, a genomic study of hereditary early-onset Parkinson's disease demonstrated a direct molecular link between mitochondrial dysfunction and the pathogenesis of Parkinson's disease. Mitochondrial dysfunction also has been shown to represent an early critical event in the pathogenesis of the sporadic form of Parkinson's disease. Clinical studies by the Parkinson's Study Group show that very high doses of an antioxidant called Coenzyme Q (which Mitoquinone effectively targets into mitochondria) appear to slow the progression of Parkinson's disease symptoms.","11388331","444890-41-9",true,"[P+](CCCCCCCCCCC1=C(C)C(=O)C(=C(C1=O)OC)OC)(c1ccccc1)(c1ccccc1)c1ccccc1","OIIMUKXVVLRCAF-UHFFFAOYSA-N",583.729,null,"Mitoquinone is targeted to mitochondria by covalent attachment to a lipophilic triphenylphosphonium cation. Because of the large mitochondria membrane potential, the cations accumulate within cellular mitochondria up to 1,000 fold, compared to non-targeted antioxidants such as Coenzyme Q or its analogues, enabling the antioxidant moiety to block lipid peroxidation and protect mitochondria from oxidative damage. By selectively blocking mitochondrial oxidative damage, it prevents cell death.","Mitoquinone may help to prevent the nerve cell damage that leads to Parkinson's disease. It aims to slow or halt Parkinson's disease at its cause by tackling cell damage caused when mitochondria cease to function normally. It is anticipated that MitoQ will slow or arrest the progression of Parkinson's disease symptoms.\r\nHepatits C virus can directly alter mitochondrial function, leading to increased reactive oxygen species (free-radical) production that can lead to scarring of the liver and cirrhosis. Mitoquinone could be used to halt or decrease liver inflammation and fibrosis progression, even in the absence of sustained virologic response.\r\nMitoquinone directly affects the mitochondria in two steps: a targeting component directs the drug to the mitochondria; and an antioxidant component helps to prevent cell damage.","Investigated for use/treatment in hepatitis (viral, C) and parkinson's disease.",null,"Antiparkinsonian drug","Phase 2 terminated (NCT01167088: This study has been terminated due to poor participant recruitment)","Under clinical trials","2022-03-21"]
[230,"MK-4074",null,"Chemical drug",null,null,"24964679","1039758-22-9",true,"O=C1CC2(Oc3c1cc(cc3)c1cc(C(=O)O)cnc1)CCN(CC2)C(=O)c1cc2n(cc(c2c(c1)OC)C)C1CC1","WDBNGXLHMZSUEI-UHFFFAOYSA-N",565.626,{"$nulls":4},"ACC inhibitor",null,"Phase 1 completed  (NCT01431521)","Under clinical trials","2022-03-21"]
[231,"MN-001","Tipelukast","Chemical drug","DB12435","Tipelukast is under investigation for the treatment of IPF and Idiopathic pulmonary fibrosis.","9893228","125961-82-2",true,"C(CC)c1c(OCCCC(=O)O)c(C(=O)C)ccc1OCCCSc1c(CCC)c(O)c(cc1)C(=O)C","KPWYNAGOBXLMSE-UHFFFAOYSA-N",530.683,{"$nulls":6},"Phase 2 completed  (NCT02681055)","Under clinical trials","2022-03-21"]
[232,"Moxonidine","(2R,4R)-1-[(2S)-5-[(aminoiminomethyl)amino]-1-oxo-2-[[(1,2,3,4-tetrahydro-3-methyl-8- quinolinyl)sulfonyl]amino]pentyl]-4-methyl-2-piperidinecarboxylic acid; Moxonidine","Chemical drug","DB09242","Moxonidine is a new-generation centrally acting antihypertensive drug approved for the treatment of mild to moderate essential hypertension. It is suggested to be effective in cases where other agents such as thiazides, beta-blockers, ACE inhibitors, and calcium channel blockers are not appropriate or irresponsive. As well, moxonidine has been shown to present blood pressure-independent beneficial effects on insulin resistance syndrome.","4810","75438-57-2",true,"N(c1c(OC)nc(nc1Cl)C)C1=NCCN1","WPNJAUFVNXKLIM-UHFFFAOYSA-N",241.682,"Alpha-2A adrenergic receptor agonist; Nischarin agonist","Stimulation of central alpha 2-adrenergic receptors is associated with sympathoadrenal suppression and subsequent reduction of blood pressure. As this class was further explored it was discovered that sympathoadrenal activity can also be suppressed by a second pathway with a newly discovered drug target specific to imidazolines . Specifically, moxonidine binds the imidazoline receptor subtype 1 (I1) and to a lesser extent αlpha-2-adrenoreceptors in the RSV causing a reduction of sympathetic activity, reducing systemic vascular resistance and thus arterial blood pressure. \r\n\r\nMoreover, since alpha-2-adrenergic receptors are considered the primary molecular target that facilitates the most common side effects of sedation and dry mouth that are elicited by most centrally acting antihypertensives, moxonidine differs from these other centrally acting antihypertensives by demonstrating only low affinity for central alpha-2-adrenoceptors compared to the aforementioned I1-imidazoline receptors .","Antihypertensive agent whose site of action is the Central Nervous System (CNS), specifically involving interactions with I1- imidazoline and alpha-2-adrenergic rececptors within the rostral ventrolateral medulla (RSV).","For the treatment of mild to moderate essential or primary hypertension . Effective as most first-line antihypertensives when used as monotherapy .","NISCH agonist",null,"Phase 4 on-going (ACTRN12617000948392)","Under clinical trials","2022-03-21"]
[233,"MSDC-0602K",null,"Chemical drug",null,null,"87355566","1314533-27-1",false,"C(C1SC(=O)NC1=O)c1ccc(cc1)OCC(=O)c1cc(OC)ccc1.[K]","WUPYCVYXBXCSQK-UHFFFAOYSA-N",411.52,{"$nulls":4},"MPC modulator","Antidiabetic drug","Phase 2 completed (MSDC-0602K did not demonstrate statistically significant effects on primary and secondary liver histology endpoints. However, effects on non-invasive measures of liver cell injury and glucose metabolism support further exploration of MSDC-0602K's safety and potential efficacy in patients with type 2 diabetes and liver injury. [ClinicalTrials.gov Identifier: NCT02784444].)","Failed in clinical trials","2022-03-21"]
[234,"Muliv strong syrup",null,"Supplement",{"$nulls":4},false,{"$nulls":9},"Phase 2 on-going (CTRI/2019/12/022578)","Under clinical trials","2022-03-21"]
[235,"N-acetyl cysteine",null,"Chemical drug",null,null,"12035","7218-04-4",true,"C(NC(=O)C)(C(=O)O)CS","PWKSKIMOESPYIA-UHFFFAOYSA-N",163.198,{"$nulls":4},"SLC7A11 activator; GSS stimulator","Antiviral","Phase 2 on-going (NCT02117700)","Under clinical trials","2022-03-21"]
[236,"Nanocurcumin",null,"Biological extract",{"$nulls":4},false,{"$nulls":8},"Anticancer agent; NSAID","Clinical trial on-going (IRCT2016071915536N3)","Under clinical trials","2022-03-21"]
[237,"Nesinaact","Alogliptin/pioglitazone","Chemical drug",{"$nulls":4},false,{"$nulls":7},"CD26 antigen inhibitor; PPARG agonist","Improve insulin resistance","Phase 4 on-going (NCT03950505)","Under clinical trials","2022-03-21"]
[238,"NGM395",null,"Miscellany",{"$nulls":4},false,{"$nulls":7},"GDNF receptor agonist","Hormones, hepatoprotectants","Phase 1 completed  (NCT04187339)","Under clinical trials","2022-03-21"]
[239,"Niacin","3-carboxypyridine; 3-Pyridinecarboxylic acid; 3-Pyridylcarboxylic acid; anti-pellagra vitamin; m-pyridinecarboxylic acid; Niacin; Nicotinic acid; pyridine-β-carboxylic acid; β-pyridinecarboxylic acid","Supplement","DB00627","Niacin is a B vitamin used to treat vitamin deficiencies as well as hyperlipidemia, dyslipidemia, hypertriglyceridemia, and to reduce the risk of myocardial infarctions.","938","59-67-6",true,"C(=O)(O)c1cccnc1","PVNIIMVLHYAWGP-UHFFFAOYSA-N",123.111,"Hydroxycarboxylic acid receptor 3 agonist; Hydroxycarboxylic acid receptor 2 agonist; Nicotinate-nucleotide pyrophosphorylase [carboxylating] binder; Nicotinamide N-methyltransferase binder","Niacin performs a number of functions in the body and so has many mechanisms, not all of which have been fully described. Niacin can decrease lipids and apolipoprotein B (apo B)-containing lipoproteins by modulating triglyceride synthesis in the liver, which degrades apo B, or by modulating lipolysis in adipose tissue.\r\n\r\nNiacin inhibits hepatocyte diacylglycerol acyltransferase-2. This action prevents the final step of triglyceride synthesis in hepatocytes, limiting available triglycerides for very low density lipoproteins (VLDL). This activity also leads to intracellular degradation of apo B and decreased production of low density lipoproteins, the catabolic product of VLDL.\r\n\r\nNiacin also inhibits a high density lipoprotein (HDL) catabolism receptor, which increases the levels and half life of HDL.","Niacin is a B vitamin used to treat vitamin deficiencies as well as hyperlipidemia, dyslipidemia, hypertriglyceridemia, and to reduce the risk of myocardial infarctions. Niacin acts to decrease levels of very low density lipoproteins and low density lipoproteins, while increasing levels of high density lipoproteins. Niacin has a wide therapeutic window with usual oral doses between 500mg and 2000mg. Patients with diabetes, renal failure, uncontrolled hypothyroidism, and elderly patients taking niacin with simvastatin or lovastatin are at increased risk of myopathy and rhabdomyolysis.","Niacin is indicated to prevent vitamin deficiencies in pediatric and adult patients receiving parenteral nutrition as part of multivitamin intravenous injections. Niacin oral tablets are indicated as a monotherapy or in combination with simvastatin or lovastatin to treat primary hyperlipidemia and mixed dyslipidemia. It can also be used to reduce the risk of nonfatal myocardial infarctions in patients with a history of myocardial infarction and hyperlipidemia. Niacin is also indicated with bile acid binding resins to treat atherosclerosis in patients with coronary artery disease and hyperlipidemia or to treat primary hyperlipidemia. Finally niacin is indicated to treat severe hypertriglyceridemia.","NNMT binder","Hypolipidemic drug","Phase 2 completed  (NCT03850886: Nicotinamide at a dose of 1000 mg daily was tolerable, improved metabolic abnormalities and QOL of diabetic NAFLD patients with no effect on liver fibrosis or steatosis.)","Under clinical trials","2022-03-21"]
[240,"Nicotinamide","3-pyridinecarboxamide; Niacinamide; Nicotinamide; Nicotinic acid amide; Nicotinic amide; β-pyridinecarboxamide","Chemical drug","DB02701","An important compound functioning as a component of the coenzyme NAD. Its primary significance is in the prevention and/or cure of blacktongue and pellagra. Most animals cannot manufacture this compound in amounts sufficient to prevent nutritional deficiency and it therefore must be supplemented through dietary intake.","936","98-92-0",false,"C(=O)(N)c1cccnc1","DFPAKSUCGFBDDF-UHFFFAOYSA-N",122.127,"Exotoxin A product of; L-lactate dehydrogenase A chain; Poly [ADP-ribose] polymerase 1 binder; NAD-dependent protein deacylase sirtuin-5, mitochondrial; ADP-ribosyl cyclase 2 product of",{"$nulls":3},"PARP inhibitor","Metabolic disorder drug","Phase 2 completed  (NCT03850886: Nicotinamide at a dose of 1000 mg daily was tolerable, improved metabolic abnormalities and QOL of diabetic NAFLD patients with no effect on liver fibrosis or steatosis.)","Under clinical trials","2022-03-21"]
[241,"Nidufexor","LMB763","Chemical drug","DB16255","Nidufexor is under investigation in clinical trial NCT03804879 (Safety, Tolerability and Efficacy of LMB763 in Patients With Diabetic Nephropathy).","118063735","1773489-72-7",false,"Cn1c2c(c(n1)C(=O)N(Cc1ccc(cc1)C(=O)O)Cc1ccccc1)COc1c2cc(cc1)Cl","JYTIXGYXBIBOMN-UHFFFAOYSA-N",487.943,{"$nulls":4},"FXR modulator","Enhance lipid metabolism","Phase 2 terminated  (NCT02913105)","Under clinical trials","2022-03-21"]
[242,"Nigella Sativa",null,"Biological extract",{"$nulls":3},"90064-32-7",false,{"$nulls":8},"Gastrointestinal drug","Phase 2 on-going (IRCT2017012232109N1)","Under clinical trials","2022-03-21"]
[243,"Nitazoxanide","Nitazoxanide","Chemical drug","DB00507","Nitazoxanide belongs to the class of drugs known as _thiazolides_.  Nitazoxanide (NTZ) is a broad-spectrum anti-infective drug that markedly modulates the survival, growth, and proliferation of a range of extracellular and intracellular protozoa, helminths, anaerobic and microaerophilic bacteria, in addition to viruses. This drug is effective in the treatment of gastrointestinal infections including Cryptosporidium parvum or Giardia lamblia in healthy subjects. It is generally well tolerated. Nitazoxanide is a first-line, standard treatment for illness caused by C. parvum or G. lamblia infection in healthy (not immunosuppressed) adults and children and may also be considered in the treatment of illnesses caused by other protozoa or helminths .  Recently, this drug has been studied as a broad-spectrum antiviral agent due to its ability to inhibit the replication of several RNA and DNA viruses .","41684","55981-09-4",true,"C(=O)(Nc1sc(cn1)N(=O)=O)c1c(OC(=O)C)cccc1","YQNQNVDNTFHQSW-UHFFFAOYSA-N",307.287,"Pyruvate-flavodoxin oxidoreductase antagonist&inhibitor","The most widely accepted mechanism of NTZ is believed to be the disruption of the energy metabolism in anaerobic microbes by inhibition of the pyruvate: ferredoxin/flavodoxin oxidoreductase (PFOR) cycle . In parasitic-protozoa, Nitazoxanide also induces lesions in the cell membranes and depolarizes the mitochondrial membrane while inhibiting quinone oxidoreductase NQO1, nitroreductase-1 and protein disulphide isomerase enzymes. In addition, this drug also inhibits the glutathione-S-transferase (a major detoxifying enzyme) and modulates the Avr-14 gene, encoding for the alpha-type subunit of glutamate-gated chloride ion channel present in nematodes. Aside from its well understood non-competitive inhibition of the PFOR in anaerobic bacteria, NTZ also demonstrates various other antibacterial mechanisms. It inhibits pyruvate dehydrogenase in E Coli, disrupts the membrane potential and pH homeostasis in the Mycobacterium tuberculosis, suppresses the chaperone/usher (CU) pathway of the gram-negative bacteria,  and stimulates host macrophage autophagy in tuberculosis patients . NTZ also suppresses viral replication by inhibiting the maturation of the viral hemagglutinin and the viral transcription factor immediate early 2 (IE2) as well as by activating the eukaryotic translation initiation factor 2α (an antiviral intracellular protein). Lastly, NTZ exhibits an inhibitory effect on tumor cell progression by altering drug detoxification (glutathione-S-transferase P1), unfolded protein response, autophagy, anti-cytokines activity, and c-Myc inhibition .","The general effect of this medication is the prevention of microbe activity through disruption of important energy pathways for survival and proliferation .  Nitazoxanide exhibits antiprotozoal activity by interfering with the pyruvate ferredoxin/flavodoxin oxidoreductase dependent electron transfer reaction, an essential reaction need for anaerobic energy metabolism of various microorganisms.  Sporozoites of Cryptosporidium parvum and trophozoites of Giardia lamblia are therefore inhibited, relieving symptoms of diahrrea . Interference with the PFOR enzyme-dependent electron transfer reaction may only be one of the many pathways by which nitazoxanide exhibits antiprotozoal activity .","For the treatment of diarrhea in adults and children caused by the protozoa <i>Giardia lamblia</i>,  and for the treatment of diarrhea in children caused by the protozoan,  <i>Cryptosporidium parvum</i> .\r\n\r\nNitazoxanide has not been shown to be superior to placebo medication for the management of diarrhea caused by Cryptosporidium parvum in patients with HIV/immunodeficiency .","POR inhibitor","Antiprotozoal drug","Phase 2 completed  (NCT03656068)","Under clinical trials","2022-03-21"]
[244,"Nivocasan","GS-9450","Chemical drug","DB12720","Nivocasan has been used in trials studying the treatment of HCV Infection and Nonalcoholic Steatohepatitis.","11633038","908253-63-4",false,"C(=O)(N[C@@H]1[C@](CF)(O)OC(=O)C1)[C@]1(C(C)C)CC(=NO1)c1c2c(ccn1)cccc2","VYFGDLGHHBUDTQ-ZLGUVYLKSA-N",415.421,{"$nulls":5},"Protective drug","Phase 2 completed  (NCT00740610)","Under clinical trials","2022-03-21"]
[245,"Norursodeoxycholic acid","24-norursodeoxycholic acid; Nor-ursodeoxycholic acid; Norucholic acid; NorUrsodeoxycholic Acid","Chemical drug","DB16260","norUrsodeoxycholic acid is under investigation in clinical trial NCT03872921 (Norursodeoxycholic Acid vs Placebo in PSC).","192254","99697-24-2",false,"C[C@]12[C@H]([C@H]3[C@H](CC2)[C@]2(C)[C@H](C[C@@H]3O)C[C@@H](CC2)O)CC[C@@H]1[C@@H](CC(=O)O)C","QYYDXDSPYPOWRO-JHMCBHKWSA-N",378.553,{"$nulls":6},"Phase 2 on-going (EudraCT number 2013-004605-38: Norursodeoxycholic acid at 1500 mg resulted in a significant reduction of serum ALT within 12 weeks of treatment when compared with placebo. Norursodeoxycholic acid was safe and well tolerated encouraging further studies.)","Under clinical trials","2022-03-21"]
[246,"NRL972","Cholyl-lysylfluorescein","Chemical drug",null,null,"70697664",null,false,"S=C(NCCCC[C@H](NC(=O)CC[C@H]([C@@H]1[C@@]2([C@H]([C@H]3[C@@H]([C@@]4([C@H](C[C@H]3O)C[C@H](O)CC4)C)C[C@@H]2O)CC1)C)C)C(=O)O)Nc1cc2c(C3(OC2=O)c2c(Oc4c3ccc(O)c4)cc(O)cc2)cc1","KHNJPPGHIWPDLG-DXNXUNFASA-N",926.142,{"$nulls":5},"Diagnostic contrast drug","Phase 2 completed  (NCT00794716)","Under clinical trials","2022-03-21"]
[247,"Nutraceutical mixture",null,"Supplement",{"$nulls":4},false,{"$nulls":9},"Clinical trial completed (NCT02369536)","Under clinical trials","2022-03-21"]
[248,"Obeticholic Acid","(3α,5β,6α,7α)-6-ethyl-3,7-dihydroxycholan-24-oic acid; 6-ECDCA; 6-Ethyl-CDCA; 6-ethylchenodeoxycholic acid; 6alpha-Ethyl-chenodeoxycholic acid; 6α-ethylchenodeoxycholic acid; Obeticholic acid; OCA; INT-747","Chemical drug","DB05990","Primary biliary cirrhosis, or PBC, is a progressive and chronic condition that leads to hepatic injury often resulting in end-stage liver failure that requires liver transplantation.\r\n\r\nObeticholic acid is a farnesoid-X receptor (FXR) agonist used to treat this condition, possibly allowing for increased survival.  In 2016, it was granted approval to treat primary biliary cholangitis in combination with , which was previously the mainstay treatment for this condition. In May 2021, the FDA updated its prescribing information to contraindicate the use of obeticholic acid in patients with PBC and advanced cirrhosis (e.g. those with portal hypertension or hepatic decompensation) due to a risk of liver failure, in some cases requiring liver transplantation. \r\n\r\nObeticholic acid is currently being considered for FDA approval to treat fibrosis caused by non-alcoholic liver steatohepatitis (NASH). The NDA from Intercept Pharmaceuticals was approved in November 2019 and obeticholic acid is expected to be granted full approval for this indication in 2020.","447715","459789-99-2",true,"C[C@@]12[C@@H]3[C@H]([C@H]4[C@@](CC3)(C)[C@H](CC4)[C@@H](CCC(=O)O)C)[C@@H]([C@@H]([C@@H]1C[C@@H](CC2)O)CC)O","ZXERDUOLZKYMJM-ZWECCWDJSA-N",420.634,"Bile acid receptor agonist","Primary biliary cirrhosis is an autoimmune process by which the bile ducts and liver are damaged progressively, leading to fibrosis and cirrhosis. Bile acids increase the risk of damage and fibrosis to the damaged bile ducts.  \r\n\r\nObeticholic acid is a potent agonist of the farnesoid X receptor, which serves to regulate the hepatic metabolism of bile and cholesterol. This drug acts by binding to the farnesoid X receptor (FXR), found in the nucleus of liver and intestinal cells, which in turn increases liver bile flow, suppressing its production and decreasing hepatocyte exposure to excess levels of bile with cholestasis. Cholestasis is a process that normally causes inflammation and cirrhosis of the liver.","The activation of the FXR by obeticholic acid acts to reduce the synthesis of bile acids, inflammation, and the resulting hepatic fibrosis. This may increase the survival of patients with PBC, but to date, an association between obeticholic acid and survival in PBC has not been established.\r\n\r\n\r","Obeticholic acid is indicated for the treatment of primary biliary cholangitis in combination with ursodeoxycholic acid (UDCA) in adults with an inadequate response to UDCA. It is also used as a monotherapy in adults with PBC that are unable to tolerate UDCA.\r\n\r\nObeticholic acid is currently being considered for FDA approval to treat fibrosis caused by non-alcoholic liver steatohepatitis (NASH), and is likely to be approved for this indication in 2020.","NR1H4 activator; NR1H4 agonist; FXR agonist","Enhance lipid metabolism","Phase 3 active (NCT02548351: Based on the REGENERATE Month 18 interim analysis, rapid and sustained improvements in various NITs were observed with OCA treatment. Dynamic changes in selected NITs separated histologic responders from non-responders. These results suggest that NITs may be useful in assessing histologic response to OCA therapy.)","Approval rejected","2022-03-21"]
[249,"Ocimum Basilicum",null,"Herbal medicine",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (IRCT2014101811763N17)","Under clinical trials","2022-03-21"]
[250,"Odevixibat","A4250; BRAVO-1","Chemical drug","DB16261","Odevixibat, or A4250, is an ileal sodium/bile acid cotransporter inhibitor indicated for the treatment of pruritus in patients older than 3 months, with progressive familiar intrahepatic cholestasis (PFIC). Odevixibat is the first approved non-surgical treatment option for PFIC. Previous therapies for PFIC included a bile acid sequestrant such as .\r\n\r\nOdevixibat was granted FDA approval on 20 July 2021.","10153627  ","501692-44-0",false,"O=S1(=O)c2c(N(CC(N1)(CCCC)CCCC)c1ccccc1)cc(c(c2)OCC(=O)N[C@@H](C(=O)N[C@H](C(=O)O)CC)c1ccc(cc1)O)SC","XULSCZPZVQIMFM-IPZQJPLYSA-N",740.945,"Ileal sodium/bile acid cotransporter inhibitor","Progressive familiar intrahepatic cholestasis (PFIC) is a group of autosomal recessive disorders leading to cholestasis, fibrosis, and eventually a need for liver transplantation. Patients with PFIC require liver transplants or develop hepatocellular carcinomas in their first few years of life. Many of these patients experience severe pruritus. The exact mechanism of pruritus is PFIC is not known, but lower concentrations of bile acids have been shown to reduce pruritus. Patients with certain forms of PFIC type 2, associated with a non-functional or absent bile salt export pump, are not expected to benefit from odevixibat treatment.\r\n\r\nThe ileal sodium/bile acid cotransporter is a transport glycoprotein responsible for reabsorption of 95% of bile acids in the distal ileum. Odevixibat is a reversible inhibitor of the ileal sodium/bile acid contransporter. Patients taking odevixibat for a week experienced a 56% reduction in bile acid area under the curve with a 3 mg once daily dose. A 1.5 mg daily dose lead to a 43% reduction in bile acid area under the curve.\r\n\r\nThe decreased reabsorption of bile acids, leads to reduced stimulation of FXR, which reduces expression of FGF19, reducing binding of FGF19 to FGF4R, decreasing inhibition of bile acid synthesis. Further synthesis of bile acids that will not be reabsorbed in the intestine contributes to lowering low density lipoprotein levels.","Odevixibat, or A4250, is an ileal sodium/bile acid cotransporter inhibitor indicated for the treatment of pruritus in patients older than 3 months, with progressive familiar intrahepatic cholestasis (PFIC). It has a moderate duration of action as it is given once daily. Odevixibat has a wide therapeutic index as patients were given single doses up to 10 mg while the maximum therapeutic dose is 6 mg daily. Patients should be counselled regarding the risks of elevated liver function tests, diarrhea, and fat soluble vitamin defiencies.","Odevixibat is indicated for the treatment of pruritus in patients older than 3 months, with progressive familiar intrahepatic cholestasis (PFIC).\r\n\r\nIt may not be effective in PFIC type 2 with ABCB11 variants. These patients lack a functional bile salt export pump.","SLC10A2 inhibitor; ASBT inhibitor",null,"Phase 2 withdrawn (NCT03451279)","Under clinical trials","2022-03-21"]
[251,"OKT3","Anti-CD3; Muromonab-CD3","Biological drug","DB00075","Murine monoclonal antibody specific to CD3 T-cell lymphocyte antigens. More specifically it is a purified murine (mouse) monoclonal antibody, directed against the CD3 (T3) receptor on the surface of human T-cells (T-lymphocytes) cultured using the murine ascites method. Muromonab is 93% monomeric immune globulin G type 2a (IgG2a).",null,"140608-64-6",true,{"$nulls":3},"T-cell surface glycoprotein CD3 delta chain; T-cell surface glycoprotein CD3 epsilon chain binder; T-cell surface glycoprotein CD3 gamma chain; T-cell surface glycoprotein CD3 zeta chain; Low affinity immunoglobulin gamma Fc region receptor III-B","Muromonab binds to the T-cell surface glycoprotein CD3 epsilon chain. It appears to kill CD-3 positive cells by inducing Fc mediated apoptosis, antibody mediated cytotoxicity and complement-dependent cytotoxicity.","Used in organ transplant prophylaxis, Muromonab or OKT-3 binds specifically to the CD-3 complex, which is involved in antigen recognition and cell stimulation, on the surface of T lymphocytes. Immediately after administration CD-3-positive T lymphocytes are abruptly removed from circulation. It has been effective in reversing corticosteroid-resistant acute rejection in renal, liver, and cardiac transplant recipients.","For treatment of organ transplant recipients, prevention of organ rejection","CD3E antagonist","Immunosuppressant","Phase 2 completed  (NCT01205087)","Under clinical trials","2022-03-21"]
[252,"Oleanolic Acid",null,"Chemical drug",null,null,"10494","508-02-1",false,"C[C@]12[C@@]3(C)C(=CC[C@@H]1[C@]1(C)[C@@H](CC2)C(C)(C)[C@H](CC1)O)[C@H]1[C@](CC3)(C(=O)O)CCC(C1)(C)C","MIJYXULNPSFWEK-GTOFXWBISA-N",456.711,{"$nulls":6},"Phase 4 on-going (ChiCTR1900021568)","Under clinical trials","2022-03-21"]
[253,"Oleoylethanolamide","N-(2-Hydroxyethyl)oleamide; N-OEA; N-oleoyl ethanolamine; N-oleoylethanolamine; OEA; Oleamide MEA; Oleoyl Ethanolamide; Oleoyl monoethanolamide; Oleoylethanolamide; Oleylethanolamide","Chemical drug","DB16495",null,"5283454","111-58-0",false,"C(CCCCC/C=C\\CCCCCCCC)CC(=O)NCCO","BOWVQLFMWHZBEF-KTKRTIGZSA-N",325.537,null,"Oleoylethanolamide (OEA) is a major N-acylethanolamine and an endogenous ethanolamide fatty acid. Although it is an endocannabinoids-like compound, it does not bind to cannabinoid receptors. Instead, this lipid sensor is an agonist at peroxisome proliferator-activated receptor-α (PPAR-α) agonist while also being an inhibitor of ceramidase and thereby the sphingolipid signaling pathway.",{"$nulls":4},"Phase 3 on-going (IRCT20110530006652N2)","Under clinical trials","2022-03-21"]
[254,"Oligofructose",null,"Supplement",{"$nulls":4},false,{"$nulls":9},"Clinical trial completed (NCT03184376: Independent of other lifestyle changes, prebiotic supplementation reduced histologically-confirmed steatosis in patients with NASH. Larger follow-up studies are warranted.)","Under clinical trials","2022-03-21"]
[255,"Olive oil","Olive oil","Biological drug","DB09567","Oil extracted from olives . Consists primarily of the glycerides of the fatty acids linoleic, oleic and palmitic. Used as a source of fatty acids in total parenteral nutrition and as an additive in some cosmetic products .","24753271","8001-25-0",true,"O(C(=O)CCCCCCCCCCCCCCCCC)CC.O(C(=O)CCCCCCCCCCCCCCC)CC.O(C(=O)CCCCCCC/C=C\\CCCCCCCC)CC.O(C(=O)CCCCCCC/C=C\\C/C=C\\CCCCC)CC.O(C(=O)CCCCCCC/C=C\\C/C=C\\C/C=C\\CC)CC","NWUIOBPENFDKLG-IBAIYALWSA-N",1522.54,null,"Fatty acids act as a substrate in energy production through beta-oxidation as well as important components of cell membrane structures and prescursors for bioactive molecules like prostaglandins .","Provides a source of calories and fatty acids .","For use in adults as a source of calories and fatty acids in total parenteral nutrition . Sometimes used as an additive in cosmetic products.",null,null,"Clinical trial on-going (IRCT2016011825957N2)","Under clinical trials","2022-03-21"]
[256,"Oltipraz",null,"Chemical drug","DB12539","Oltipraz has been used in trials studying the treatment and prevention of Lung Cancer, Liver Fibrosis, Liver Cirrhosis, and Non-alcoholic Fatty Liver Disease.","47318","64224-21-1",false,"Cc1c(ssc1=S)c1cnccn1","CKNAQFVBEHDJQV-UHFFFAOYSA-N",226.351,{"$nulls":5},"Anticancer agent; antiviral","Phase 3 on-going (NCT04142749)","Under clinical trials","2022-03-21"]
[257,"OMACOR","Omega-3 fatty acid ethyl esters; Omega-3-acid ethyl esters","Chemical drug","DB09539","Omega-3-acid ethyl esters are prescription drugs that contain eicosapentaenoic acid-ethyl ester (EPA) and docosahexaenoic acid-ethyl ester (DHA) that are used in combination with changes in diet to lower triglyceride levels in adults with severe (≥ 500 mg/dL) hypertriglyceridemia. Omega-3-acid ethyl esters are currently marketed in the US, EU, and many other regions under the brand name Lovaza.","9831414","861006-80-6",true,"C(=C\\C/C=C\\C/C=C\\C/C=C\\C/C=C\\CC)\\CCCC(=O)OCC.C(=C\\C/C=C\\C/C=C\\C/C=C\\C/C=C\\C/C=C\\CC)\\CCC(=O)OCC","DTMGIJFHGGCSLO-FIAQIACWSA-N",687.062,"Sterol regulatory element-binding protein 1 inhibitor","Omega-3-acid ethyl esters reduce triglyceride production by the liver but this mechanism is not well understood. Omega-3-acid ethyl esters inhibit acyl-CoA:1,2-diacylglycerol acyltransferase, reducing triglyceride synthesis and increasing paroxysmal beta-oxidation, which increases fatty aside metabolism. Omega-3-acid ethyl esters also inhibit the release of fatty acids by competing for enzymes involved in the synthesis of triglycerides, increase triglyceride clearance by increasing the activity of lipoprotein lipase, and decrease production of VLDL-C.","Omega-3-acid ethyl esters reduce triglyceride production, increase fatty acid metabolism, inhibit the release of fatty acids, increase triglyceride clearance, and decrease production of very low density lipoprotein cholesterol(VLDL-C).","Omega-3-Acid Ethyl Esters capsules, USP are indicated as an adjunct to diet to reduce triglyceride (TG) levels in adult patients with severe (≥500 mg/dL) hypertriglyceridemia (HTG).",null,"Hypolipidemic drug","Phase 3 completed  (NCT01277237)","Under clinical trials","2022-03-21"]
[258,"Omega 3 PUFA","n-3 fatty acids; Omega 3 fatty acids; Omega-3; Omega-3 acid; Omega-3 acid triglycerides; Omega-3 fatty acid; Omega-3 phospholipids; Omega-3 polyunsaturated fatty acids; Omega-3 polyunsaturates; Omega-3-acid triglycerides; Phospholipids; ω-3 fatty acids","Chemical drug","DB11133","Omega-3 fatty acids are polyunsaturated fatty acids (PUFAs) with a double bond at the third carbon atom from the end of the carbon chain. The three types of omega-3 fatty acids involved in human physiology are α-linolenic acid (ALA) (found in plant oils), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA) (both commonly found in fish oil that originally come from microalgae that is further consumed by phytoplankton, a source of diet for fish). Omega-3 fatty acids play a critical role in metabolism and cellular function and they are available as daily supplements. On September 8, 2004, the U.S. Food and Drug Administration gave \"qualified health claim\" status to EPA and DHA omega-3 fatty acids. Therapeutic products containing omega-3 fatty acid and its derivatives for treatment of hypertriglyceridemia include Lovaza, Omtryg, Epanova, and Vascepa.","6842239","329042-31-1",true,"OC(=O)CCCCCCC/C=C\\C/C=C\\C/C=C\\CC.OC(=O)CCC/C=C\\C/C=C\\C/C=C\\C/C=C\\C/C=C\\CC.OC(=O)CC/C=C\\C/C=C\\C/C=C\\C/C=C\\C/C=C\\C/C=C\\CC","QPEOIOLHJXXJFN-GNGJDXFDSA-N",909.39,"Peroxisome proliferator-activated receptor gamma ligand; Peroxisome proliferator-activated receptor alpha activator; Sterol regulatory element-binding protein 1 inhibitor","Omega-3 fatty acids mediate anti-inflammatory effects and increased levels of EPA or DHA has shown to decrease the levels of PGE2 and 4 series-LT. \r\nEicosapentaenoic acids compete with constitutive levels of arachidonic acid in cell membranes for the same desaturation enzymes and produce 3-series prostaglandins and thromboxanes, and 5-series leukotrienes which have low pro-inflammatory potential. The alteration in leukotriene biosynthesis due to higher concentration of omega-3 fatty acids compared to arachidonic acid underlies the anti-inflammatory effects. \r\nEPA and DHA also give rise to resolvins and related lipid signalling molecules such as protectins via cyclooxygenase and lipoxygenase pathways, which have anti-inflammatory effects. They inhibit transendothelial migration of neutrophils and inhibit TNF and IL-1β production. Omega-3 fatty acids also decrease adhesion molecule expression on leukocytes and on endothelial cells and decrease intercellular adhesive interactions.\r\nOmega-3 (or n-3) polyunsaturated fatty acids (PUFAs) and their metabolites are natural ligands for peroxisome proliferator-activated receptor (PPAR) gamma that regulates inflammatory gene expression and NFκB activation. PPAR alpha activation is also associated with induction of COX-2 expression. \r\nThe role of EPA and DHA in reducing triglyceride levels include inhibition of acyl-CoA:1,2-diacylglycerol acyltransferase, increased mitochondrial and peroxisomal-beta-oxidation in the liver, decreased lipogenesis in the liver, and increased plasma lipoprotein lipase activity. They also may reduce triglyceride synthesis because they are poor substrates for the enzymes responsible for TG synthesis, and EPA and DHA inhibit esterification of other fatty acids.","Omega-3 fatty acids are triglycerides that get broken down into smaller fatty acid units. They act to reduce plasma triglyceride levels however increase the cholesterol levels and are thought to possess potent antiarrythmic effects. Polyunsaturated fatty acids including eicosapentaenoic and docosahexaenoic acid mediate important cellular function such as inhibition of platelet function, prolongation of bleeding time, anti-inflammatory effects and reduction of plasma fibrinogen. Polyunsaturated fatty acids are components of the phospholipids that form the structures of the cell membranes and also serve as energy source. They form eicosanoids which are important signalling molecules with wide-ranging functions in the body's cardiovascular, pulmonary, immune and endocrine systems. DHA tends to exist in high concentrations in the retina, brain (via uptake by Mfsd2a as a transporter), and sperm.","Provided as daily supplements. Aa preparation of omega-3-acid ethyl esters is licensed in UK for prevention of recurrent events after myocardial infarction in addition to treatment of hypertriglyceridaemia.","PPARG ligand; PPARA activator","Hypolipidemic drug","Phase 2 completed (NCT00323414: PUFA provided no benefit over placebo in NASH patients with diabetes. The effects of PUFA on histology and insulin resistance were inferior to placebo. These data provide no support for PUFA supplements in NASH.)","Under clinical trials","2022-03-21"]
[259,"Omeprazole","OMEP; Omeprazole","Chemical drug","DB00338","Originally approved by the FDA in 1989, omeprazole is a _proton-pump inhibitor_, used to treat gastric acid-related disorders. These disorders may include gastroesophageal reflux disease (GERD), peptic ulcer disease, and other diseases characterized by the oversecretion of gastric acid.  This drug was the first clinical useful drug in its class, and its approval was followed by the formulation of many other proton pump inhibitor drugs . Omeprazole is generally effective and well-tolerated, promoting its popular use in children and adults .","4594","73590-58-6",true,"S(=O)(Cc1c(C)c(OC)c(cn1)C)c1nc2c([nH]1)ccc(c2)OC","SUBDBMMJDZJVOS-UHFFFAOYSA-N",345.424,"Potassium-transporting ATPase alpha chain 1 inhibitor; Aryl hydrocarbon receptor agonist","Hydrochloric acid (HCl) secretion into the gastric lumen is a process regulated mainly by the H(+)/K(+)-ATPase of the proton pump , expressed in high quantities by the parietal cells of the stomach. ATPase is an enzyme on the parietal cell membrane that facilitates hydrogen and potassium exchange through the cell, which normally results in the extrusion of potassium and formation of HCl (gastric acid) .\r\n\r\nOmeprazole is a member of a class of antisecretory compounds, the substituted _benzimidazoles_, that stop gastric acid secretion by selective inhibition of the _H+/K+ ATPase_ enzyme system. Proton-pump inhibitors such as omeprazole bind covalently to cysteine residues via disulfide bridges on the alpha subunit of the _H+/K+ ATPase_ pump, inhibiting gastric acid secretion for up to 36 hours .  This antisecretory effect is dose-related and leads to the inhibition of both basal and stimulated acid secretion, regardless of the stimulus .  \r\n\r\n**Mechanism of H. pylori eradication**\r\n\r\nPeptic ulcer disease (PUD) is frequently associated with _Helicobacter pylori_ bacterial infection (NSAIDs) . The treatment of H. pylori infection may include the addition of omeprazole or other proton pump inhibitors as part of the treatment regimen , . \r\n_H. pylori_ replicates most effectively at a neutral pH . Acid inhibition in H. pylori eradication therapy, including proton-pump inhibitors such as omeprazole, raises gastric pH, discouraging the growth of H.pylori . It is generally believed that proton pump inhibitors inhibit the _urease_ enzyme, which increases the pathogenesis of H. pylori in gastric-acid related conditions .","**Effects on gastric acid secretion**\r\n\r\nThis drug decreases gastric acid secretion . After oral administration, the onset of the antisecretory effect of omeprazole is usually achieved within one hour, with the maximum effect occurring by 2 hours after administration. The inhibitory effect of omeprazole on acid secretion increases with repeated once-daily dosing, reaching a plateau after four days .\r\n\r\n**Effects on serum gastrin**\r\n\r\nIn studies of 200 or more patients, serum gastrin levels increased during the first 1-2 weeks of daily administration of therapeutic doses of omeprazole. This occurred in a parallel fashion with the inhibition of acid secretion. No further increase in serum gastrin occurred with continued omeprazole administration. Increased gastrin causes enterochromaffin-like cell hyperplasia and increased serum Chromogranin A (CgA) levels. The increased CgA levels may lead to false positive results in diagnostic studies for neuroendocrine tumors .\r\n\r\n**Enterochromaffin-like (ECL) cell effects**\r\n\r\nHuman gastric biopsy samples have been obtained from more than 3000 pediatric and adult patients treated with omeprazole in long-term clinical studies. The incidence of enterochromaffin-like cell hyperplasia in these studies increased with time; however, no case of ECL cell carcinoids, dysplasia, or neoplasia have been identified in these patients. These studies, however, are of insufficient in power and duration to draw conclusions on the possible influence of long-term administration of omeprazole in the development of any premalignant or malignant conditions . \r\n\r\n**Other effects**\r\n\r\nSystemic effects of omeprazole in the central nervous system, cardiovascular and respiratory systems have not been found to date. Omeprazole, given in oral doses of 30 or 40 mg for 2-4 weeks, showed no effect on thyroid function, carbohydrate metabolism, or circulating levels of parathyroid hormone, cortisol, estradiol, testosterone, prolactin, cholecystokinin or secretin . \r\n\r\n\r","Omeprazole, according to the FDA label  is a proton pump inhibitor (PPI) used for the following purposes:\r\n\r\n• Treatment of active duodenal ulcer in adults \r\n\r\n• Eradication of Helicobacter pylori to reduce the risk of duodenal ulcer\r\nrecurrence in adults \r\n\r\n• Treatment of active benign gastric ulcer in adults \r\n\r\n• Treatment of symptomatic gastroesophageal reflux disease (GERD) in\r\npatients 1 year of age and older \r\n\r\n• Treatment of erosive esophagitis (EE) due to acid-mediated GERD in\r\npatients 1 month of age and older \r\n\r\n• Maintenance of healing of EE due to acid-mediated GERD in patients 1\r\nyear of age and older \r\n\r\n• Pathologic hypersecretory conditions in adults","AHR agonist",null,"Phase 2 completed  (NCT01876108)","Under clinical trials","2022-03-21"]
[260,"Orlistat","Xenical; (-)-Tetrahydrolipstatin; Orlipastat; Tetrahydrolipstatin","Chemical drug","DB01083","The global prevalence of obesity is increasing rapidly. Obesity-related complications lead to significant personal and economic burden by reducing quality of life and increasing the cost of healthcare.  In some individuals, diet and exercise are insufficient to maintain weight loss, and pharmacological or surgical intervention is required.\r\n\r\nOrlistat is a lipase inhibitor used in the treatment of obesity that works by inhibiting fat-metabolizing enzymes. It was approved by the FDA for use in combination with a reduced-calorie diet in 1999. This drug is a generally well-tolerated and effective weight-loss aid and is now available in both over-the-counter and prescription preparations, depending on the dosage quantity.","3034010","96829-58-2",true,"C([C@@H](OC(=O)[C@H](CC(C)C)NC=O)CCCCCCCCCCC)[C@H]1[C@H](CCCCCC)C(=O)O1","AHLBNYSZXLDEJQ-FWEHEUNISA-N",495.745,"Pancreatic triacylglycerol lipase inhibitor; Gastric triacylglycerol lipase inhibitor; Fatty acid synthase inhibitor","Orlistat is a potent and selective inhibitor of various lipase enzymes responsible for the metabolism of fat. It acts in the gastrointestinal (GI) tract via covalent binding to the serine residues located on the active site of both gastric and pancreatic lipase. When orlistat is taken with food containing fat, it partially inhibits the hydrolysis of triglycerides. This decreases absorption of monoaclglycerides and free fatty acids, contributing to weight maintenance and weight loss.","Orlistat helps with weight reduction and maintenance by inhibiting the absorption of dietary fats via the inhibition of lipase enzymes.","Orlistat is indicated for obesity management including weight loss and weight maintenance when used in combination with calorie reduction in overweight and obese adults; this indication applies to both the prescription formulation of 120 mg and the over the counter formulation of 60 mg. Orlistat in the 120 mg prescription formulation is also indicated to reduce the risk for weight regain following weight loss.","FASN inhibitor","Enhance lipid metabolism","Phase 4 completed  (NCT00160407: Orlistat did not enhance weight loss or improve liver enzymes, measures of insulin resistance, and histopathology. However, subjects who lost >or=5% of body weight over 9 months improved insulin resistance and steatosis, and those subjects who lost >or=9% also achieved improved hepatic histologic changes.)","Under clinical trials","2022-03-21"]
[261,"P2pal-18S",null,"Chemical drug",{"$nulls":3},"1918156-02-1",false,"[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)CCCCCCCCCCCCCCC)CCCNC(=N)N)CO)CO)C)CCSC)CC(=O)O)CCC(=O)O)CC(=O)N)CO)CCC(=O)O)CCCCN)CCCCN)(C(=O)N[C@H](C(=O)N[C@H](C(=O)N[C@H](C(=O)N[C@H](C(=O)N[C@@H](CCCCN)C(=O)N)[C@H](CC)C)C)CO)CCCCN)CCCNC(=N)N","WIVIEBFPYQHKBR-XJHBUOHHSA-N",2302.776,{"$nulls":7},"Under investigation","2022-03-21"]
[262,"Palatinose",null,"Chemical drug",null,null,"439559","13718-94-0",false,"O(C[C@H]([C@H]([C@@H](C(=O)CO)O)O)O)[C@H]1O[C@H](CO)[C@H]([C@@H]([C@H]1O)O)O","RJPPRBMGVWEZRR-WTZPKTTFSA-N",342.297,{"$nulls":6},"Clinical trial on-going (JPRN-UMIN000025866)","Under clinical trials","2022-03-21"]
[263,"Pancrelipase","Pancrealipase; Pancreatic extract pancrelipase; Pancreatic protease; Pancreatin; Pancrelipase; Pancrelipase (amylase;lipase;protease)","Biological drug","DB00085","Pancrelipase, in general, is composed of a mixture of pancreatic enzymes which include amylases, lipases, and proteases. These enzymes are extracted from porcine pancreatic glands. The pancrelipase mixture was developed by Ortho-McNeil-Janssen Pharmaceuticals, Inc and FDA approved on April 12, 2010. For further information on the components of this mixture please visit ,  and .",null,"53608-75-6",true,{"$nulls":3},"Dietary fat cleavage; Dietary protein cleavage; Dietary starch cleavage","Pancrelipase is used to replace the deficiency of pancreatic enzymes. As abovementioned, pancrelipase is formed by a mixture of lipase, protease, and amylase which are able to break down fat, protein, and starches, respectively, in the small intestine. For a more specific description of each mechanism of action, please visit ,  and .","The major maldigestion/malabsorption problems arise from incomplete fat digestion. In clinical trials, the administration of pancrelipase as a mixture of amylase, lipase, and protease demonstrated a significant improvement in the coefficient of fat absorption and nitrogen absorption. These effects are accompanied by increased in body weight and body mass index.","The use of pancrelipase amylase is part of the pancreatic enzyme replacement therapy. This therapy is indicated for the treatment of pancreatic insufficiency attributed to cystic fibrosis, chronic pancreatitis or any other medically defined pancreatic disease that might require it. Pancreatic diseases are associated with the deterioration of pancreatic parenchyma and of the dual physiological functions of the pancreas. Once established, pancreatic insufficiency results in malnutrition, weight loss, and steatorrhea.",null,null,"Clinical trial on-going (JPRN-UMIN000006841)","Under clinical trials","2022-03-21"]
[264,"Pantoprazole","Pantoprazole","Chemical drug","DB00213","Pantoprazole is a first-generation proton pump inhibitor (PPI) used for the management of gastroesophageal reflux disease (GERD), for gastric protection to prevent recurrence of stomach ulcers or gastric damage from chronic use of NSAIDs, and for the treatment of pathological hypersecretory conditions including Zollinger-Ellison (ZE) Syndrome. It can also be found in quadruple regimens for the treatment of _H. pylori_ infections along with other antibiotics including , , and , for example. Its efficacy is considered similar to other medications within the PPI class including , , , , and .\r\n\r\nPantoprazole exerts its stomach acid-suppressing effects by preventing the final step in gastric acid production by covalently binding to sulfhydryl groups of cysteines found on the (H+, K+)-ATPase enzyme at the secretory surface of gastric parietal cell. This effect leads to inhibition of both basal and stimulated gastric acid secretion, irrespective of the stimulus. As the binding of pantoprazole to the (H+, K+)-ATPase enzyme is irreversible and new enzyme needs to be expressed in order to resume acid secretion, pantoprazole's duration of antisecretory effect persists longer than 24 hours.\r\n\r\nDue to their good safety profile and as several PPIs are available over the counter without a prescription, their current use in North America is widespread. Long term use of PPIs such as pantoprazole have been associated with possible adverse effects, however, including increased susceptibility to bacterial infections (including gastrointestinal _C. difficile_), reduced absorption of micronutrients including iron and B12, and an increased risk of developing hypomagnesemia and hypocalcemia which may contribute to osteoporosis and bone fractures later in life.\r\n\r\nPPIs such as pantoprazole have also been shown to inhibit the activity of dimethylarginine dimethylaminohydrolase (DDAH), an enzyme necessary for cardiovascular health. DDAH inhibition causes a consequent accumulation of the nitric oxide synthase inhibitor asymmetric dimethylarginie (ADMA), which is thought to cause the association of PPIs with increased risk of cardiovascular events in patients with unstable coronary syndromes.\r\n\r\nPantoprazole doses should be slowly lowered, or tapered, before discontinuing as rapid discontinuation of PPIs such as pantoprazole may cause a rebound effect and a short term increase in hypersecretion.","4679","102625-70-7",true,"S(=O)(Cc1c(OC)c(OC)ccn1)c1nc2c([nH]1)cc(cc2)OC(F)F","IQPSEEYGBUAQFF-UHFFFAOYSA-N",383.376,"Potassium-transporting ATPase alpha chain 1 inhibitor; N(G),N(G)-dimethylarginine dimethylaminohydrolase 1 inhibitor","Hydrochloric acid (HCl) secretion into the gastric lumen is a process regulated mainly by the H(+)/K(+)-ATPase of the proton pump, expressed in high quantities by the parietal cells of the stomach. ATPase is an enzyme on the parietal cell membrane that facilitates hydrogen and potassium exchange through the cell, which normally results in the extrusion of potassium and formation of HCl (gastric acid). \r\n\r\nProton pump inhibitors such as pantoprazole are substituted _benzimidazole_ derivatives, weak bases, which accumulate in the acidic space of the parietal cell before being converted in the _canaliculi_  (small canal) of the gastric parietal cell, an acidic environment, to active _sulfenamide_ derivatives. This active form then makes disulfide bonds with important cysteines on the gastric acid pump, inhibiting its function. Specifically, pantoprazole binds to the _sulfhydryl group_ of H+, K+-ATPase, which is an enzyme implicated in accelerating the final step in the acid secretion pathway. The enzyme is inactivated, inhibiting gastric acid secretion. The inhibition of gastric acid secretion is stronger with proton pump inhibitors such as pantoprazole and lasts longer than with the H(2) antagonists.","This drug acts to decrease gastric acid secretion, which reduces stomach acidity. Pantoprazole administration leads to long-lasting inhibition of gastric acid secretion.\r\n\r\n**General Effects**\r\n\r\nPantoprazole has been shown to reduce acid reflux-related symptoms, heal inflammation of the esophagus, and improve patient quality of life more effectively than histamine-2 receptor antagonists (H2 blockers). This drug has an excellent safety profile and a low incidence of drug interactions. It can be used safely in various high-risk patient populations, including the elderly and those with renal failure or moderate hepatic dysfunction.\r\n\r\nDue to their good safety profile and as several PPIs are available over the counter without a prescription, their current use in North America is widespread. Long term use of PPIs such as pantoprazole have been associated with possible adverse effects, however, including increased susceptibility to bacterial infections (including gastrointestinal _C. difficile_), reduced absorption of micronutrients including iron and B12, and an increased risk of developing hypomagnesemia and hypocalcemia which may contribute to osteoporosis and bone fractures later in life.\r\n\r\nPPIs such as pantoprazole have also been shown to inhibit the activity of dimethylarginine dimethylaminohydrolase (DDAH), an enzyme necessary for cardiovascular health. DDAH inhibition causes a consequent accumulation of the nitric oxide synthase inhibitor asymmetric dimethylarginie (ADMA), which is thought to cause the association of PPIs with increased risk of cardiovascular events in patients with unstable coronary syndromes . \r\n\r\n**A note on laboratory testing abnormalities**\r\n\r\nDuring treatment with antisecretory medicinal products such as pantoprazole, serum gastrin (a peptide hormone that stimulates secretion of gastric acid) increases in response to the decreased acid secretion caused by proton pump inhibition. The increased gastrin level may interfere with investigations for neuroendocrine tumors. Published evidence suggests that proton pump inhibitors should be stopped 14 days before chromogranin A (CgA) measurements. This permits chromogranin A levels, that might be falsely elevated after proton pump inhibitor treatment, to return to the normal reference range. \r\n\r\nReports have been made of false-positive results in urine screening tests for tetrahydrocannabinol (THC) in patients receiving the majority of proton pump inhibitors, including pantoprazole. A confirmatory method should be used.","\r\n**Pantoprazole Injection**:\r\n\r\n**Treatment of gastroesophageal reflux disease associated with a history of erosive esophagitis**\r\n\r\nPantoprazole for injection is indicated for short-term treatment (7-10 days) of patients having gastroesophageal reflux disease (GERD) with a history of erosive esophagitis, as an alternative to oral medication in patients who are unable to continue taking pantoprazole delayed-release tablets. _Safety and efficacy of pantoprazole injection as the initial treatment of patients having GERD with a history of erosive esophagitis have not been demonstrated at this time_.\r\n\r\n**Pathological Hypersecretion Associated with Zollinger-Ellison Syndrome**\r\n\r\nPantoprazole for injection is indicated for the treatment of pathological hypersecretory conditions associated with Zollinger-Ellison Syndrome or other neoplastic conditions.\r\n\r\n**Pantoprazole delayed-release oral suspension**:\r\n\r\n**Short-Term Treatment of erosive esophagitis associated with gastroesophageal reflux disease (GERD)**\r\n\r\nIndicated in adults and pediatric patients five years of age and above for the short-term treatment (up to 8 weeks) in the healing and symptomatic relief of erosive esophagitis. For adult patients who have not healed after 8 weeks of treatment, an additional 8-week course of pantoprazole may be considered. Safety of treatment beyond 8 weeks in pediatric patients has not been determined.\r\n\r\n**Maintenance of healing of erosive esophagitis**\r\n\r\nIndicated for maintenance of healing of erosive esophagitis and reduction in relapse rates of daytime and nighttime heartburn symptoms in adult patients with GERD.\r\n\r\n**Pathological hypersecretory conditions including Zollinger-Ellison syndrome**\r\n\r\nIndicated for the long-term treatment of the above conditions.","gastric H-K-ATPase inhibitor; ATP4B inhibitor; ATP4A inhibitor","Gastrointestinal drug","Phase 4 on-going  (NCT04248335)","Under clinical trials","2022-03-21"]
[265,"Pemafibrate","Pemafibrate","Chemical drug","DB15212","Pemafibrate is under investigation in clinical trial NCT03350165 (A Study of Pemafibrate in Patients With Nonalcoholic Fatty Liver Disease (NAFLD)).","11526038","848259-27-8",false,"CC[C@](OC1=CC=CC(CN(C2=NC3=CC=CC=C3O2)CCCOC4=CC=C(OC)C=C4)=C1)([H])C(O)=O","ZHKNLJLMDFQVHJ-RUZDIDTESA-N",490.556,{"$nulls":4},"PPARA modulator","Anti-inflammatory","Phase 2 completed  (NCT03350165: Pemafibrate did not decrease liver fat content but had significant reduction in MRE-based liver stiffness. Pemafibrate may be a promising therapeutic agent for NAFLD/NASH, and also be a candidate for combination therapy with agents that reduce liver fat content.)","Under clinical trials","2022-03-21"]
[266,"Pentoxifylline","PTX; Oxpentifylline","Chemical drug","DB00806","Pentoxifylline (PTX) is a synthetic dimethylxanthine derivative that modulates the rheological properties of blood and also has both anti-oxidant and anti-inflammatory properties. Although originally developed to treat intermittent claudication, a form of exertion-induced leg pain common in patients with peripheral arterial disease, PTX has been investigated for its possible use in diverse conditions, including osteoradionecrosis, diabetic kidney disease, and generally any condition associated with fibrosis. More recently, PTX has been suggested as a possible treatment for COVID-19-induced pulmonary complications due to its ability to regulate the production of inflammatory cytokines.\r\n\r\nPentoxifylline has been marketed in Europe since 1972; PTX extended-release tablets sold under the trade name TRENTAL by US Pharm Holdings were first approved by the FDA on Aug 30, 1984, but have since been discontinued. A branded product, PENTOXIL, marketed by Upsher-Smith Laboratories, and generic forms marketed by Valeant Pharmaceuticals and APOTEX have been available since the late 1990s.","4740","6493-05-6",true,"O=c1c2c(n(c(=O)n1CCCCC(=O)C)C)ncn2C","BYPFEZZEUUWMEJ-UHFFFAOYSA-N",278.312,"Adenosine receptor A2a agonist; Phosphodiesterase enzymes inhibitor; Adenosine receptor A1; 5'-nucleotidase inhibitor","Patients with peripheral arterial disease (PAD) may suffer from intermittent claudication, exertional leg pain that resolves upon rest, which is underscored by a complex etiology including vascular dysfunction (reduced limb perfusion, angiogenesis, and microcirculatory flow), systemic inflammation, and skeletal muscle dysfunction. Pentoxifylline (PTX), (3,7-dimethyl-1-(5-oxohexyl)-3,7-dihydro-1H-purine-2,6-dione) or 1-(5-oxohexyl)-3,7-­dimethylxanthine, is a methyl-xanthine derivative that acts to lower blood viscosity by increasing erythrocyte flexibility, reducing plasma fibrinogen, inhibiting neutrophil activation, and suppressing erythrocyte/platelet aggregation; it also has antioxidant and anti-inflammatory effects. Although the precise mechanism of action has yet to be elucidated, numerous studies have suggested several effects of PTX.\r\n\r\nThe classical interpretation of PTX's broad effects is due to its ability to act, _in vitro_, as a non-specific cyclic-3',5'-phosphodiesterase (PDE) inhibitor at millimolar concentrations; specifically, it has been proposed that inhibition of PDE type III and IV isozymes leads to elevated cyclic adenosine monophosphate (cAMP) levels, which mediate diverse downstream effects. This view has been challenged, specifically by observing those plasma concentrations of PTX in routine clinical use are typically only around 1μM, far lower than those used to inhibit PDEs _in vitro_. Instead, several studies have suggested that PTX can modulate adenosine receptor function, specifically the Gα-coupled A2A receptor (A2AR). Whether PTX acts directly as an A2AR agonist is unclear, although it can clearly increase the response of A2AR to adenosine. A2AR activation activates adenylyl cyclase, which increases intracellular cAMP levels; this observation may explain PTX's ability to increase intracellular cAMP in a PDE-independent fashion.\r\n\r\nElevated cAMP levels have numerous downstream effects. cAMP-mediated activation of protein kinase A (PKA) suppresses nuclear translocation of NF-κB, which suppresses transcription of pro-inflammatory cytokines such as tumour necrosis factor (TNF-α), interleukin-1 (IL-1), and IL-6 as well as TNF-induced molecules such as adhesion molecules (ICAM1 and VCAM1) and the C-reactive protein (CRP). PTX has also been shown to prevent the downstream phosphorylation of p38 MAPK and ERK, which are responsible for assembling the NADPH oxidase involved in the neutrophil oxidative burst. This effect is due to a PKA-independent decrease in Akt phosphorylation and a PKA-dependent decrease in phosphorylation of p38 MAPK and ERK. This transcriptional regulation at least partially explains the anti-inflammatory and anti-oxidative properties of PTX.\r\n\r\nAlso, activated PKA can activate the cAMP response element-binding protein (CREB), which itself blocks SMAD-driven gene transcription, effectively disrupting transforming growth factor (TGF-β1) signalling. This results in lower levels of fibrinogenic molecules such as collagens, fibronectin, connective tissue growth factor, and alpha-smooth muscle actin. Hence, disruption of TGF-β1 signalling may explain the anti-fibrotic effects of PTX, including at least some of the decrease in blood viscosity.\r\n\r\nThe picture is complicated by the observation that PTX metabolites M1, M4, and M5 have been shown to inhibit C5 Des Arg- and formyl-methionylleucylphenylalanine-induced superoxide production in neutrophils and M1 and M5 significantly contribute to PTX's observed hemorheological effects. Overall, PTX administration is associated with decreased pro-inflammatory molecules, an increase in anti-inflammatory molecules such as IL-10, and decreased production of fibrinogenic and cellular adhesion molecules.","Pentoxifylline, a synthetic dimethylxanthine derivative structurally related to  and , exhibits hemorheological, anti-oxidative, and anti-inflammatory properties and is traditionally indicated in the treatment of peripheral arterial disease (PAD). In PAD patients with concurrent cerebrovascular and coronary artery diseases, pentoxifylline treatment has occasionally been associated with angina, arrhythmia, and hypotension. Concurrent use with  should be associated with more frequent monitoring of prothrombin times. Also, patients with risk factors complicated by hemorrhages, such as retinal bleeding, peptic ulceration, and recent surgery, should be monitored periodically for bleeding signs.","Pentoxifylline is indicated for the treatment of intermittent claudication in patients with chronic occlusive arterial disease. Pentoxifylline may improve limb function and reduce symptoms but cannot replace other therapies such as surgical bypass or removal of vascular obstructions.","ADORA2A antagonist; ADORA1 antagonist; PDE4A inhibitor; PDE3B inhibitor; PDE4B inhibitor; PDE5A inhibitor; PDE8A inhibitor; PDE4C inhibitor; PDE11A inhibitor; PDE7A inhibitor; PDE7B inhibitor; PDE4D inhibitor; PDE3A inhibitor","Anti-inflammatory; Cardiovascular drug","Phase 3 on-going (NCT05284448)","Under clinical trials","2022-03-21"]
[267,"Perindopril","(2S,3aS,7aS)-1-[(2S)-2-{[(2S)-1-ethoxy-1-oxopentan-2-yl]amino}propanoyl]octahydro-1H-indole-2-carboxylic acid; Perindopril","Chemical drug","DB00790","Perindopril is a nonsulfhydryl prodrug that belongs to the angiotensin-converting enzyme (ACE) inhibitor class of medications. It is rapidly metabolized in the liver to perindoprilat, its active metabolite, following oral administration. Perindoprilat is a potent, competitive inhibitor of ACE, the enzyme responsible for the conversion of angiotensin I (ATI) to angiotensin II (ATII). ATII regulates blood pressure and is a key component of the renin-angiotensin-aldosterone system (RAAS). Perindopril may be used to treat mild to moderate essential hypertension, mild to moderate congestive heart failure, and to reduce the cardiovascular risk of individuals with hypertension or post-myocardial infarction and stable coronary disease.","107807","82834-16-0",true,"C(=O)([C@@H](N[C@H](C(=O)OCC)CCC)C)N1[C@@H]2[C@H](C[C@H]1C(=O)O)CCCC2","IPVQLZZIHOAWMC-QXKUPLGCSA-N",368.474,"Angiotensin-converting enzyme inhibitor; Secreted frizzled-related protein 4 inhibitor","There are two isoforms of ACE: the somatic isoform, which exists as a glycoprotein comprised of a single polypeptide chain of 1277; and the testicular isoform, which has a lower molecular mass and is thought to play a role in sperm maturation and binding of sperm to the oviduct epithelium. Somatic ACE has two functionally active domains, N and C, which arise from tandem gene duplication. Although the two domains have high sequence similarity, they play distinct physiological roles. The C-domain is predominantly involved in blood pressure regulation while the N-domain plays a role in hematopoietic stem cell differentiation and proliferation. ACE inhibitors bind to and inhibit the activity of both domains, but have much greater affinity for and inhibitory activity against the C-domain. Perindoprilat, the active metabolite of perindopril, competes with ATI for binding to ACE and inhibits and enzymatic proteolysis of ATI to ATII. Decreasing ATII levels in the body decreases blood pressure by inhibiting the pressor effects of ATII as described in the Pharmacology section above. Perindopril also causes an increase in plasma renin activity likely due to a loss of feedback inhibition mediated by ATII on the release of renin and/or stimulation of reflex mechanisms via baroreceptors.","Perindopril is a nonsulfhydryl prodrug that is metabolized via first pass effect (62%) and systemic hydrolysis (38%) to perindoprilat, its active metabolite, following oral administration. Perindoprilat lowers blood pressure by antagonizing the effect of the RAAS. The RAAS is a homeostatic mechanism for regulating hemodynamics, water and electrolyte balance. During sympathetic stimulation or when renal blood pressure or blood flow is reduced, renin is released from the granular cells of the juxtaglomerular apparatus in the kidneys. In the blood stream, renin cleaves circulating angiotensinogen to ATI, which is subsequently cleaved to ATII by ACE. ATII increases blood pressure using a number of mechanisms. First, it stimulates the secretion of aldosterone from the adrenal cortex. Aldosterone travels to the distal convoluted tubule (DCT) and collecting tubule of nephrons where it increases sodium and water reabsorption by increasing the number of sodium channels and sodium-potassium ATPases on cell membranes. Second, ATII stimulates the secretion of vasopressin (also known as antidiuretic hormone or ADH) from the posterior pituitary gland. ADH stimulates further water reabsorption from the kidneys via insertion of aquaporin-2 channels on the apical surface of cells of the DCT and collecting tubules. Third, ATII increases blood pressure through direct arterial vasoconstriction. Stimulation of the Type 1 ATII receptor on vascular smooth muscle cells leads to a cascade of events resulting in myocyte contraction and vasoconstriction. In addition to these major effects, ATII induces the thirst response via stimulation of hypothalamic neurons. ACE inhibitors inhibit the rapid conversion of ATI to ATII and antagonize RAAS-induced increases in blood pressure. ACE (also known as kininase II) is also involved in the enzymatic deactivation of bradykinin, a vasodilator. Inhibiting the deactivation of bradykinin increases bradykinin levels and may sustain the effects of perindoprilat by causing increased vasodilation and decreased blood pressure.","For the treatment of mild to moderate essential hypertension, mild to moderate congestive heart failure, and to reduce the cardiovascular risk of individuals with hypertension or post-myocardial infarction and stable coronary disease.","ACE inhibitor","Antihypertensive drug","Clinical trial on-going (ChiCTR-TRC-14005028)","Under clinical trials","2022-03-21"]
[268,"PF-05221304",null,"Chemical drug",{"$nulls":3},"2248008-98-0",false,"O=C(O)C=1C=CC(=CC1)C2=NC(OC)=CC(=C2)C(=O)N3CCC4(CC(=O)C5=C(C=NN5C(C)C)C4)CC3","LXZMHBHEXAELHH-UHFFFAOYSA-N",502.56,{"$nulls":4},"ACC inhibitor","Enhance lipid metabolism","Phase 2 completed  (NCT03248882: AEs were reported for 10/28 (36%) patients after co-administered PF-05221304 and PF-06865571, with no discontinuations due to AEs, and the ACC inhibitor-mediated effect on serum triglycerides was mitigated, suggesting that PF-05221304 and PF-06865571 co-administration has the potential to address some of the limitations of ACC inhibition alone.)","Under clinical trials","2022-03-21"]
[269,"PF-06835919",null,"Chemical drug",{"$nulls":4},false,{"$nulls":7},"Ketohexokinase inhibitor","Enhance lipid metabolism","Phase 2 completed  (NCT04193436)","Under clinical trials","2022-03-21"]
[270,"PF-06865571",null,"Chemical drug",{"$nulls":4},false,{"$nulls":7},"DGAT2 inhibitor","Enhance lipid metabolism","Phase 2 completed  (NCT03776175: AEs were reported for 10/28 (36%) patients after co-administered PF-05221304 and PF-06865571, with no discontinuations due to AEs, and the ACC inhibitor-mediated effect on serum triglycerides was mitigated, suggesting that PF-05221304 and PF-06865571 co-administration has the potential to address some of the limitations of ACC inhibition alone.)","Under clinical trials","2022-03-21"]
[271,"Phentermine","alpha,alpha-Dimethylphenethylamine; Phentermine; Phentermine resin","Chemical drug","DB00191","Phentermine is a sympathomimetic amine anorectic agent and it was introduced in 1959 as part of an anti-obesity combination drug. It is chemically related to amphetamine and it is commonly referred to as an atypical amphetamine. Phentermine has not been reported an addictive potential which allows this agent to be classified under the Schedule IV drugs (low abuse potential).\r\n\r\nPhentermine was FDA approved for short-term weight management in 1959 and it became widely used in 1960. This initial product, formed by the combination of phentermine with  and  was discontinued after finding several reports of abnormal valves in nearly 30% of the consumers. Later on, phentermine was approved alone and in combination with topiramate in 2012 as a new alternative that required lower doses of phentermine to obtain the desired effect.","4771","122-09-8",true,"C(C(C)(C)N)c1ccccc1","DHHVAGZRUROJKS-UHFFFAOYSA-N",149.237,"Sodium-dependent noradrenaline transporter inhibitor; Sodium-dependent serotonin transporter inhibitor; Sodium-dependent dopamine transporter inhibitor; Amine oxidase [flavin-containing] A antagonist; Amine oxidase [flavin-containing] B antagonist; Pro-ne","Phentermine is an indirect-acting sympathomimetic agent that acts by releasing noradrenaline from the presynaptic vesicles in the lateral hypothalamus. This increase in noradrenaline concentration in the synaptic cleft results in the stimulation of beta2-adrenergic receptors. Phentermine is classified as an indirect sympathomimetic due to the increase in the level of norepinephrine, dopamine and its indirect effect towards serotonin. Some reports have indicated that phentermine inhibits the neuropeptide Y which is a principal signaling pathway for the induction of hunger. This combined effect produces a continuous flight-or-fight response in the body which reduces the hunger signal as this state is on the immediate need for energy.\r\n\r\nLastly, some reports have indicated that phentermine is a weak inhibitor of monoamine oxidase but this mechanism does not tend to produce a clinically significant response.","It is reported that the main mechanism of action of phentermine is the generation of appetite suppression, maybe due to the increase in leptin, but it is considered that other mechanisms should be involved. Some reports have indicated that the weight loss effect is mainly due to the increase in resting energy expenditure.\r\n\r\nIn clinical studies where phentermine was used as a monotherapy and as combination therapy, this drug has shown an average weight loss of 3.6 kg when compared with the placebo in 2-24 weeks. Patients treated with phentermine also showed increased maintenance of the weight after treatment discontinuation. As well, even though it is a derivative of the amphetamines, it has not been registered to produce any of the effects of amphetamine such as central nervous system stimulation, elevation of blood pressure, tachyphylaxis or QTc prolongation.","Phentermine is indicated, alone or in combination with topiramate, as a short-term adjunct, not pass a few weeks, in a regimen of weight reduction based on exercise, behavioral modifications and caloric restriction in the management of exogenous obesity for patients with an initial body mass index (BMI) greater than 30 kg/m2 or greater than 27 kg/m2 in presence of other risk factors such as controller hypertension, diabetes or hyperlipidemia.\r\n\r\nExogenous obesity is considered when the overweight is caused by consuming more food than the person activity level warrants. This condition commonly causes an increase in fat storage. It is an epidemic condition in the United States where over two-thirds of adults are overweight or obese and one in three Americans is obese. In the world, the incidence of obesity has nearly doubled.","MAOB antagonist; MAOA antagonist; SLC6A2 inhibitor; SLC6A3 inhibitor; SLC6A4 inhibitor; SLC6A2 stimulator; SLC6A3 stimulator","Anorexic; CNS stimulant","Phase 4 completed  (NCT03849729)","Under clinical trials","2022-03-21"]
[272,"Phlebotomy",null,"Miscellany",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (IRCT20161205031252N4)","Under clinical trials","2022-03-21"]
[273,"Phosphatidylcholine","Lecithins; Phosphatidylcholine; Phospholutein","Chemical drug","DB15834","A complex mixture of phospholipids, glycolipids, triglycerides, phosphatidylcholines, phosphatidylethanolamines, and phosphatidylinositols.","6441487","27098-24-4",false,"P(=O)(OCC[N+](C)(C)C)(OC[C@H](OC(=O)CCCCCCC/C=C\\C/C=C\\CCCCC)COC(=O)CCCCCCCCCCCCCCCCC)[O-]","FORFDCPQKJHEBF-VPUSDGANSA-N",786.129,{"$nulls":6},"Phase 3 completed (NCT04411862)","Under clinical trials","2022-03-21"]
[274,"Phytosterol","Phytosterols; Plant Sterol","Supplement",null,null,"222284","949109-75-5",false,"O[C@@H]1CC2=CC[C@H]3[C@H]4[C@@]([C@H](CC4)[C@@H](CC[C@H](C(C)C)CC)C)(CC[C@@H]3[C@]2(CC1)C)C","KZJWDPNRJALLNS-VJSFXXLFSA-N",414.718,{"$nulls":5},"Hypolipidemic drug","Clinical trial on-going (NCT03627819)","Under clinical trials","2022-03-21"]
[275,"Pioglitazone","(±)-5-((4-(2-(5-ethyl-2-pyridinyl)ethoxy)phenyl)methyl)-2,4-thiazolidinedione; 5-{4-[2-(5-ethylpyridin-2-yl)ethoxy]benzyl}-1,3-thiazolidine-2,4-dione; Pioglitazone","Chemical drug","DB01132","Pioglitazone is an antihyperglycemic used as an adjunct to diet, exercise, and other antidiabetic medications to manage type 2 diabetes mellitus. It is administered as a racemic mixture, though there is no pharmacologic difference between the enantiomers and they appear to interconvert _in vivo_ with little consequence. The thiazolidinedione class of medications, which also includes  and , exerts its pharmacological effect primarily by promoting insulin sensitivity and the improved uptake of blood glucose via agonism at the peroxisome proliferator-activated receptor-gamma (PPARγ). PPARs are ligand-activated transcription factors that are involved in the expression of more than 100 genes and affect numerous metabolic processes, most notably lipid and glucose homeostasis.\r\n\r\nThiazolidinediones, including pioglitazone, have fallen out of favor in recent years due to the presence of multiple adverse effects and warnings regarding their use (e.g. congestive heart failure, bladder cancer) and the availability of safer and more effective alternatives for patients with type 2 diabetes mellitus.","4829","111025-46-8",true,"CCC1=CN=C(C=C1)CCOC2=CC=C(C=C2)C[C@@]3([H])SC(NC3=O)=O","HYAFETHFCAUJAY-QGZVFWFLSA-N",356.447,"Peroxisome proliferator-activated receptor gamma agonist; Amine oxidase [flavin-containing] B inhibitor","Pioglitazone is a selective agonist at peroxisome proliferator-activated receptor-gamma (PPARγ) in target tissues for insulin action such as adipose tissue, skeletal muscle, and liver. Activation of PPARγ increases the transcription of insulin-responsive genes involved in the control of glucose and lipid production, transport, and utilization. Through this mechanism, pioglitazone both enhances tissue sensitivity to insulin and reduces the hepatic production of glucose (i.e. gluconeogenesis) - insulin resistance associated with type 2 diabetes mellitus is therefore improved without an increase in insulin secretion by pancreatic beta cells.","Pioglitazone enhances cellular responsiveness to insulin, increases insulin-dependent glucose disposal, and improves impaired glucose homeostasis. In patients with type 2 diabetes mellitus, these effects result in lower plasma glucose concentrations, lower plasma insulin concentrations, and lower HbA1c values.\r\n \r\nSignificant fluid retention leading to the development/exacerbation of congestive heart failure has been reported with pioglitazone - avoid its use in patients in heart failure or at risk of developing heart failure. There is some evidence that pioglitazone may be associated with an increased risk of developing bladder cancer. Pioglitazone should not be used in patients with active bladder cancer and should be used with caution in patients with a history of bladder cancer.","Pioglitazone is indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. It is also available in combination with , , or  for the same indication.","PPARG agonist","Improve insulin resistance","Phase 3 completed (NCT00063622: Pioglitazone led to significant improvements in hepatic steatosis, inflammation, insulin resistance, and liver enzyme levels in the phase III.)","Advanced in clinical trials","2022-03-21"]
[276,"Piperine","Bioperine","Chemical drug","DB12582","Bioperine has been used in trials studying the treatment of Multiple Myeloma and Deglutition Disorders.","638024","94-62-2",false,"C(=C\\C=C\\C(=O)N1CCCCC1)/c1cc2c(cc1)OCO2","MXXWOMGUGJBKIW-YPCIICBESA-N",285.343,"Nuclear receptor subfamily 1 group I member 2",{"$nulls":3},"NR1I2",null,"Phase 3 on-going (IRCT20180802040678N2)","Under clinical trials","2022-03-21"]
[277,"Pitavastatin","Pitavastatin","Chemical drug","DB08860","Pitavastatin, also known as the brand name product Livalo, is a lipid-lowering drug belonging to the statin class of medications. By inhibiting the endogenous production of cholesterol within the liver, statins lower abnormal cholesterol and lipid levels and ultimately reduce the risk of cardiovascular disease. More specifically, statin medications competitively inhibit the enzyme hydroxymethylglutaryl-coenzyme A (HMG-CoA) Reductase, which catalyzes the conversion of HMG-CoA to mevalonic acid. This is the third step in a sequence of metabolic reactions involved in the production of several compounds involved in lipid metabolism and transport including cholesterol, low-density lipoprotein (LDL) (sometimes referred to as \"bad cholesterol\"), and very low-density lipoprotein (VLDL). Prescribing of statin medications is considered standard practice following any cardiovascular events and for people with a moderate to high risk of development of CVD, such as those with Type 2 Diabetes. The clear evidence of the benefit of statin use coupled with very minimal side effects or long term effects has resulted in this class becoming one of the most widely prescribed medications in North America.\r\n\r\nPitavastatin and other drugs from the statin class of medications including , , , , and  are considered first-line options for the treatment of dyslipidemia. Increasing use of the statin class of drugs is largely due to the fact that cardiovascular disease (CVD), which includes heart attack, atherosclerosis, angina, peripheral artery disease, and stroke, has become a leading cause of death in high-income countries and a major cause of morbidity around the world. Elevated cholesterol levels, and in particular, elevated low-density lipoprotein (LDL) levels, are an important risk factor for the development of CVD. Use of statins to target and reduce LDL levels has been shown in a number of landmark studies to significantly reduce the risk of development of CVD and all-cause mortality. Statins are considered a cost-effective treatment option for CVD due to their evidence of reducing all-cause mortality including fatal and non-fatal CVD as well as the need for surgical revascularization or angioplasty following a heart attack. Evidence has shown that even for low-risk individuals (with <10% risk of a major vascular event occurring within 5 years) statins cause a 20%-22% relative reduction in major cardiovascular events (heart attack, stroke, coronary revascularization, and coronary death) for every 1 mmol/L reduction in LDL without any significant side effects or risks.\r\n\r\nWhile all statin medications are considered equally effective from a clinical standpoint,  is considered the most potent; doses of 10 to 40mg  per day were found in clinical studies to result in a 45.8% to 54.6% decrease in LDL cholesterol levels. Study data has confirmed that pitavastatin's potency in lowering LDL-C is comparable to that of other statins but also has increased efficacy in increasing HDL-C (also known as \"good cholesterol\"). Despite these differences in potency, several trials have demonstrated only minimal differences in terms of clinical outcomes between statins.","5282452","147511-69-1",true,"C(=C\\[C@H](C[C@H](CC(=O)O)O)O)/c1c(c2c(nc1C1CC1)cccc2)c1ccc(cc1)F","VGYFMXBACGZSIL-MCBHFWOFSA-N",421.468,"3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor; Integrin alpha-L","Pitavastatin is a statin medication and a competitive inhibitor of the enzyme HMG-CoA (3-hydroxy-3-methylglutaryl coenzyme A) reductase, which catalyzes the conversion of HMG-CoA to mevalonate, an early rate-limiting step in cholesterol biosynthesis. Pitavastatin acts primarily in the liver, where decreased hepatic cholesterol concentrations stimulate the upregulation of hepatic low density lipoprotein (LDL) receptors which increase hepatic uptake of LDL, thereby reducing circulating LDL-C levels. \r\n\r\nIn vitro and in vivo animal studies also demonstrate that statins exert vasculoprotective effects independent of their lipid-lowering properties, also known as the pleiotropic effects of statins. This includes improvement in endothelial function, enhanced stability of atherosclerotic plaques, reduced oxidative stress and inflammation, and inhibition of the thrombogenic response.\r\n\r\nStatins have also been found to bind allosterically to β2 integrin function-associated antigen-1 (LFA-1), which plays an important role in leukocyte trafficking and in T cell activation.","Pitavastatin is an oral antilipemic agent which inhibits HMG-CoA reductase. It is used to lower total cholesterol, low density lipoprotein-cholesterol (LDL-C), apolipoprotein B (apoB), non-high density lipoprotein-cholesterol (non-HDL-C), and trigleride (TG) plasma concentrations while increasing HDL-C concentrations. High LDL-C, low HDL-C and high TG concentrations in the plasma are associated with increased risk of atherosclerosis and cardiovascular disease. The total cholesterol to HDL-C ratio is a strong predictor of coronary artery disease and high ratios are associated with higher risk of disease. Increased levels of HDL-C are associated with lower cardiovascular risk. By decreasing LDL-C and TG and increasing HDL-C, rosuvastatin reduces the risk of cardiovascular morbidity and mortality.\r\n\r\nElevated cholesterol levels, and in particular, elevated low-density lipoprotein (LDL) levels, are an important risk factor for the development of CVD. Use of statins to target and reduce LDL levels has been shown in a number of landmark studies to significantly reduce the risk of development of CVD and all-cause mortality. Statins are considered a cost-effective treatment option for CVD due to their evidence of reducing all-cause mortality including fatal and non-fatal CVD as well as the need for surgical revascularization or angioplasty following a heart attack. Evidence has shown that even for low-risk individuals (with <10% risk of a major vascular event occurring within 5 years) statins cause a 20%-22% relative reduction in major cardiovascular events (heart attack, stroke, coronary revascularization, and coronary death) for every 1 mmol/L reduction in LDL without any significant side effects or risks.\r\n\r\n**Skeletal Muscle Effects**\r\n\r\nPitavastatin may cause myopathy (muscle pain, tenderness, or weakness with creatine kinase (CK) above ten times the upper limit of normal) and rhabdomyolysis (with or without acute renal failure secondary to myoglobinuria). Rare fatalities have occurred as a result of rhabdomyolysis with statin use, including pitavastatin. Predisposing factors for myopathy include advanced age (≥65 years), female gender, uncontrolled hypothyroidism, and renal impairment. In most cases, muscle symptoms and CK increases resolved when treatment was promptly discontinued. As dosages of pitavastatin greater than 4mg per day were associated with an increased risk of severe myopathy, the product monograph recommends a maximum daily dose of 4mg once daily.\r\n\r\nThe risk of myopathy during treatment with pitavstatin may be increased with concurrent administration of interacting drugs such as , , , an d .  Cases of myopathy, including rhabdomyolysis, have been reported with HMG-CoA reductase inhibitors coadministered with , and caution should therefore be exercised when prescribing these two medications together.\r\n\r\nReal-world data from observational studies has suggested that 10-15% of people taking statins may experience muscle aches at some point during treatment.\r\n\r\n**Hepatic Dysfunction**\r\n\r\nIncreases in serum transaminases have been reported with pitavastatin. In most cases, the elevations were transient and either resolved or improved on continued therapy or after a brief interruption in therapy. There have been rare postmarketing reports of fatal and non-fatal hepatic failure in patients taking statins, including pitavastatin.\r\n\r\nPatients who consume substantial quantities of alcohol and/or have a history of liver disease may be at increased risk for hepatic injury.\r\n\r\n**Increases in HbA1c and Fasting Serum Glucose Levels**\r\n\r\nIncreases in HbA1c and fasting serum glucose levels have been reported with statins, including pitavastatin. Optimize lifestyle measures, including regular exercise, maintaining a healthy body weight, and making healthy food choices.\r\n\r\nAn in vitro study found that , , , and  exhibited a dose-dependent cytotoxic effect on human pancreas islet β cells, with reductions in cell viability of 32, 41, 34 and 29%, respectively, versus control. Moreover, insulin secretion rates were decreased by 34, 30, 27 and 19%, respectively, relative to control.","Pitavastatin is indicated for the treatment of adult patients with primary hyperlipidemia or mixed dyslipidemia to reduce elevated total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), apolipoprotein B (Apo B), triglycerides (TG), and to increase high-density lipoprotein cholesterol (HDL-C). It is also indicated for the treatment of pediatric patients aged 8 years and older with heterozygous familial hypercholesterolemia (HeFH) to reduce elevated TC, LDL-C, and Apo B.\r\n\r\nPrescribing of statin medications is considered standard practice following any cardiovascular events and for people with a moderate to high risk of development of CVD. Statin-indicated conditions include diabetes mellitus, clinical atherosclerosis (including myocardial infarction, acute coronary syndromes, stable angina, documented coronary artery disease, stroke, trans ischemic attack (TIA), documented carotid disease, peripheral artery disease, and claudication), abdominal aortic aneurysm, chronic kidney disease, and severely elevated LDL-C levels.","HMGCR inhibitor","Enhance lipid metabolism","Clinical trial completed (NCT02290106: Compared with placebo, pitavastatin did not affect hepatic or whole-body insulin sensitivity, and it did not reduce liver fat.)","Failed in clinical trials","2022-03-21"]
[278,"Plantago major seed",null,"Herbal medicine",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (IRCT20191006044993N1)","Under clinical trials","2022-03-21"]
[279,"Plantago Psyllium","Psyllium; Psyllium husk","Biological drug","DB11097","Platango seeds refer to the seeds collected from various species of plantago trees. It is found in some laxatives for treating occasional constipation and restoring regularity in bowel movements. Its potential benefit in maintaining remission in ulcerative colitis has been studied .\r\n\r\nRegardless, this agent is most predominantly used as a gentle laxative agent in many parts of the world that is more commonly referred as psyllium or psyllium husk.",null,"8063-16-9",false,{"$nulls":4},"Psyllium seeds are comprised of dietary fibre which, when mixed with water forms a gel-like mass that works as a mild laxative . This gel-like mass subsequently moves down a patient's digestive system and makes stools softer by increasing their water contents . At the same time psyllium seed lubricates the intestine, which improves the transit of stools . Moreover, as the presence of the gel-like mass increases the stool bulk it also increases the tension and/or the stretch stimulus in the bowel wall which serves to trigger bowel movements .\r\n\r\nThe dietary fibre of which psyllium husk is comprised is fermented to various degrees by bacteria in the colon, resulting in production of carbon dioxide, hydrogen, methane, water, and short chain fatty acids, which are absorbed and brought into the hepatic circulation . In humans, such fibre reaches the large bowel in a highly polymerized form that is fermented to a limited extent, resulting in increased fecal concentration and excretion of short chain fatty acids .","The active ingredient psyllium husk is comprised of the episperm and collapsed adjacent layers removed from the seeds of Plantago afar L. or Plantago indica L. . Psyllium husk is abundant in alimentary fibres and mucilages, with its mucilage content in particular being higher than that of other plantago species . Specifically, psyllium husk is capable of absorbing up to 40 times its own weight in water . Psyllium husk consists of 85% water-soluble fibre - it is subsequently partly fermentable (in vitro 72% unfermentable residue) and acts by hydration in the bowel .\r\n\r\nGastrointestinal tract motility and transit rate is capable of being modified by psyllium husk via mechanical stimulation of the gut wall as a result of the increase in intestinal bulk by water and the decrease in viscosity of the luminal contents . Taken with an adequate amount of liquid (at least 30 ml per 1 g of the agent), psyllium husk produces an increased volume of intestinal contents as a result of its highly bulking properties and therefore a stretch stimulus which triggers a defecation . Concurrently, the swollen mass of mucilage generates a lubricating layer that makes the transit of the intestinal contents easier .","Indications include the treatment of patients needing a high fibre regime, perhaps for: (a) the relief of constipation, including constipation in pregnancy and the maintenance of regularity; (b) the management of bowel function in patients with colostomy, ileostomy, hemorrhoids, anal fissure, chronic diarrhea with diverticular disease, irritable bowel syndrome, and ulcerative colitis .",{"$nulls":3},"Under investigation","2022-03-21"]
[280,"Pomegranate extract","Ae-pomegrante; Allergenic Extract- Pomegranate Punica Granatum; Dadima Fruit; Pomegranate Extract; Pomegranate Fruit; Pomegranate Fruit Polyphenol Extract; Pomegranates, Raw; Pomegranates,raw; Punica Granatum Fruit; Punica Granatum Fruit Extract; Shi Liu Fruit","Biological drug","DB14317","Pomegranate is a plant/plant extract used in some OTC (over-the-counter) products. It is not an approved drug.",null,"84961-57-9, 943248-40-6, 1377454-99-3",false,{"$nulls":9},"Clinical trial on-going (IRCT20140107016123N14)","Under clinical trials","2022-03-21"]
[281,"Prebiotic",null,"Supplement",{"$nulls":4},false,{"$nulls":9},"Clinical trial completed (NCT03184376: Independent of other lifestyle changes, prebiotic supplementation reduced histologically-confirmed steatosis in patients with NASH. Larger follow-up studies are warranted.)","Under clinical trials","2022-03-21"]
[282,"PRIM-DJ2727",null,"Supplement",{"$nulls":4},false,{"$nulls":9},"Phase 2 on-going (NCT04371653)","Under clinical trials","2022-03-21"]
[283,"Proanthocyanidin","Crofelemer","Chemical drug","DB04941","Crofelemer, previously known as the investigational drug SP-303, is a novel proanthocyanidin purified from the bark latex of the Amazonian Croton tree <i>Croton lechleri</i>. It is marketed under the brand name Fulyzaq and indicated for the symptomatic treatment of non-infectious diarrhea in adult patients with HIV/AIDS who are taking antiretroviral therapy.","108065","18206-61-6",true,"O[C@@H]1[C@H](c2c(O[C@@H]1c1ccc(cc1)O)cc(cc2O)O)c1c2c(C[C@H]([C@H](O2)c2cc(O)c(c(c2)O)OC)O)c(cc1O)O","JPFCOVZKLAXXOE-NFJBMHMQSA-N",592.553,"Cystic fibrosis transmembrane conductance regulator antagonist; Anoctamin-1 antagonist","Crofelemer is an inhibitor of the cystic fibrosis transmembrane regulator chloride channel (CFTR), as evidenced by its activity on cell cultures, single cell patch clamps, single CFTR channels, and elaboration of mouse intestinal fluid secretion. Crofelemer also inhibits calcium activated chloride channels (CaCC), which in combination with CFTR, are expressed on the luminal side of intestinal cells. Crofelemer inhibition of both of these channels prevents water loss from diarrhea by inhibiting chloride secretion.\r\n\r","Crofelemer is an inhibitor of secretory diarrhea via inhibition of the CFTR chloride transporter. Crofelemer is not an antimicrobial, and therefore does not drive the emergence of resistance; it does not inhibit motility, and therefore does not cause constipation or rebound diarrhea; and it is not systemically absorbed, reducing the potential for adverse drug interactions and toxicity.","For the symptomatic treatment of non-infectious diarrhea in adult patients with HIV/AIDS who are taking antiretroviral therapy.","CFTR antagonist",null,"Phase 2&3 on-going (ChiCTR-IPR-16008156)","Under clinical trials","2022-03-21"]
[284,"Probiotic",null,"Supplement",{"$nulls":3},"1830109-69-7",false,{"$nulls":9},"Phase 1&2 on-going (NCT04175392)","Under clinical trials","2022-03-21"]
[285,"Proglumide","Proglumide","Chemical drug","DB13431",null,"4922","6620-60-6",false,"C(C(=O)N(CCC)CCC)(NC(=O)c1ccccc1)CCC(=O)O","DGMKFQYCZXERLX-UHFFFAOYSA-N",334.416,{"$nulls":5},"Antiulcerative drug","Phase 1 on-going (NCT04152473)","Under clinical trials","2022-03-21"]
[286,"Propolis",null,"Biological extract",{"$nulls":3},"85665-41-4",false,{"$nulls":9},"Phase 3 on-going (IRCT20161023030445N2)","Under clinical trials","2022-03-21"]
[287,"Protandim",null,"Supplement",{"$nulls":3},"877143-83-4",false,{"$nulls":9},"Clinical trial completed (NCT00977730)","Under clinical trials","2022-03-21"]
[288,"ProWHEY 94 CFM",null,"Miscellany",{"$nulls":4},false,{"$nulls":9},"Clinical trial completed (NCT00870077: WPS improves hepatic steatosis and plasma lipid profiles in obese non diabetic patients, without adverse effects on glucose tolerance or creatinine clearance.)","Under clinical trials","2022-03-21"]
[289,"Purslane","Horse's Teeth Amaranth; Ma Chi Xian; Machixian; Portulaca Neglecta Top; Portulaca Oleracea Extract; Portulaca Oleracea Flower/leaf/stem Extract; Portulaca Oleracea Flowering Top; Portulaca Oleracea Top; Portulaca Retusa Top; Portulacae Herba; Purslane Herb; Purslane, Raw; Purslane,raw; Wild Portulaca Top","Biological drug","DB14327","Purslane is a plant/plant extract used in some OTC (over-the-counter) products. It is not an approved drug.",null,null,true,{"$nulls":9},"Phase 3 on-going (IRCT201701172709N44)","Under clinical trials","2022-03-21"]
[290,"Px-104",null,"Chemical drug","DB15416","PX-102 is under investigation in clinical trial NCT01998672 (Multiple Ascending Oral Dose Phase I Study With Px-102).","50943003","1268244-88-7",false,"Clc1c([C@H]2[C@@H](C2)c2ccc(cc2)C(=O)O)ccc(c1)OCc1c(noc1C1CC1)c1c(Cl)cccc1Cl","XBUXXJUEBFDQHD-SFTDATJTSA-N",554.857,{"$nulls":6},"Phase 2 completed  (NCT01999101)","Under clinical trials","2022-03-21"]
[291,"PXL065",null,"Chemical drug",{"$nulls":4},false,{"$nulls":7},"AMPK activator","Improve insulin resistance","Phase 2 on-going (NCT04321343)","Under clinical trials","2022-03-21"]
[292,"PXL770",null,"Chemical drug",{"$nulls":4},false,{"$nulls":7},"AMPK activator","Improve insulin resistance","Phase 2 completed  (NCT03763877: PXL770 treatment did not meet the primary outcome of liver fat improvement compared with placebo. Treatment was well tolerated. Given indications that metabolic features improved with PXL770 treatment, AMPK activation might be a promising pharmacological target for patients with type 2 diabetes and NAFLD, and could also be considered for further assessment in patients with non-alcoholic steatohepatitis.)","Under clinical trials","2022-03-21"]
[293,"Quercetin","2-(3,4-dihydroxyphenyl)-3,5,7-trihydroxy-4H-1-benzopyran-4-one; 3,3',4',5,7-pentahydroxyflavone; 3,5,7,3',4'-Pentahydroxyflavone; Sophoretin; Xanthaurine; Sigma quercetin","Supplement","DB04216","Quercetin is a flavonol widely distributed in plants. It is an antioxidant, like many other phenolic heterocyclic compounds. Glycosylated forms include RUTIN and quercetrin.","5280343","117-39-5",false,"O=c1c2c(oc(c1O)c1cc(O)c(cc1)O)cc(cc2O)O","REFJWTPEDVJJIY-UHFFFAOYSA-N",302.238,"Tyrosine-protein kinase HCK; Phosphatidylinositol 4,5-bisphosphate 3-kinase catalytic subunit gamma isoform; UDP-glucuronosyltransferase 3A1; ATP synthase subunit alpha, mitochondrial; ATP synthase subunit beta, mitochondrial; ATP synthase subunit gamma,","Quercetin is a specific quinone reductase 2 (QR2) inhibitor, an enzyme (along with the human QR1 homolog) which catalyzes metabolism of toxic quinolines. Inhibition of QR2 in plasmodium may potentially cause lethal oxidative stress. The inhibition of antioxidant activity in plasmodium may contribute to killing the malaria causing parasites.",null,null,"AHR; EIF3F; SF3B3; NR1I2 activator",null,"Clinical trial on-going (IRCT2016060628299N1)","Under clinical trials","2022-03-21"]
[294,"Quinidine","(+)-quinidine; (8R,9S)-Quinidine; (R)-(6-Methoxyquinolin-4-yl)((3S,4R,7S)-3-vinylquinuclidin-7-yl)methanol; (S)-(6-Methoxy-quinolin-4-yl)-((2R,5R)-5-vinyl-1-aza-bicyclo[2.2.2]oct-2-yl)-methanol; (S)-(6-Methoxyquinolin-4-yl)((2R,5R)-5-vinylquinuclidin-2-yl)methanol; 6-methoxy-α-(5-vinyl-2-quinuclidinyl)-4-quinolinemethanol; beta-Quinine; CIN-QUIN; Conchinin; Conquinine; Pitayine; α-(6-methoxy-4-quinolyl)-5-vinyl-2-quinuclidinemethanol; β-quinine","Chemical drug","DB00908","An optical isomer of , extracted from the bark of the Cinchona tree and similar plant species. This alkaloid dampens the excitability of cardiac and skeletal muscles by blocking sodium and potassium currents across cellular membranes. It prolongs cellular action potential, and decreases automaticity. Quinidine also blocks muscarinic and alpha-adrenergic neurotransmission.","441074","56-54-2",true,"[C@H](O)(c1c2c(ccc(c2)OC)ncc1)[C@@H]1N2C[C@@H]([C@H](C1)CC2)C=C","LOUPRKONTZGTKE-LHHVKLHASA-N",324.424,"Sodium channel protein type 5 subunit alpha inhibitor; Potassium channel subfamily K member 1 inhibitor; Potassium channel subfamily K member 6 inhibitor; Potassium voltage-gated channel subfamily H member 2 inhibitor; Alpha-1A adrenergic receptor antagon","Quinidine acts on sodium channels on the neuronal cell membrane, limiting the spread of seizure activity and reducing seizure propagation. The antiarrhythmic actions are mediated through effects on sodium channels in Purkinje fibers. Quinidine may also act on the slow inward calcium current (ICa), the rapid (IKr) and slow (IKs) components of the delayed potassium rectifier current, the inward potassium rectifier current (IKI), the ATP-sensitive potassium channel (IKATP) and Ito.","Quinidine, a hydantoin anticonvulsant, is used alone or with phenobarbital or other anticonvulsants to manage tonic-clonic seizures, psychomotor seizures, neuropathic pain syndromes including diabetic neuropathy, digitalis-induced cardiac arrhythmias, and cardiac arrhythmias associated with QT-interval prolongation.","For the treatment of ventricular pre-excitation and cardiac dysrhythmias","KCNH2 inhibitor","Antiadrenergic drug; Antiarrhythmic; Antiprotozoal drug; Cholinergic drug","Phase 2 completed (NCT03421431: Non-alcoholic fatty liver disease is a chronic hepatic disease that can progress to non-alcoholic steatohepatitis (NASH), which is associated with an increased risk of cirrhosis and liver cancer. Results from this phase II study support continued development of EDP-305, an oral farnesoid X receptor agonist, for the treatment of patients with NASH.)","Under clinical trials","2022-03-21"]
[295,"Qushi Huayu Decoction","Yin Chen, Hu Zhang, Jiang Huang, Tian Ji Huang, Zhi Zi","Traditional medicine",{"$nulls":4},false,{"$nulls":7},"AMPK activator","Improve insulin resistance","Clinical trial on-going (ChiCTR-IOR-17013491)","Under clinical trials","2022-03-21"]
[296,"Rabeprazol sodium",null,"Miscellany",{"$nulls":4},false,{"$nulls":9},"Phase 1 completed  (NCT03143166: The DE tablet demonstrated BE to the capsule; however, at high gastric pH, BA of the tablet was reduced by approximately 70%, which may lead to reduced efficacy. Data indicate the importance of examining not only BE under standard conditions, but relative BA at elevated gastric pH. Such investigations may avoid the reduced BA at elevated pH that is quite common in the target population (the elderly and/or patients treated with gastric-acid modifying co-medications), and therefore reduce treatment failure with DE.)","Under clinical trials","2022-03-21"]
[297,"Raltegravir","Raltegravir","Chemical drug","DB06817","Raltegravir is an antiretroviral drug produced by Merck & Co., used to treat HIV infection. It received approval by the U.S. Food and Drug Administration (FDA) on 12 October 2007, the first of a new class of HIV drugs, the integrase inhibitors, to receive such approval.","54671008","518048-05-0",true,"C(NC(=O)c1nnc(o1)C)(C)(C)c1nc(C(=O)NCc2ccc(cc2)F)c(c(=O)n1C)O","CZFFBEXEKNGXKS-UHFFFAOYSA-N",444.423,"Integrase inhibitor","Raltegravir inhibits HIV integrase to prevent the viral genome being incorporated into the human genome. Raltegravir is primarily metabolized by glucuronidation.",null,"For the treatment of HIV-1 infection in conjunction with other antiretrovirals.",null,"Anti-HIV drug","Clinical trial on-going (NCT02210715)","Under clinical trials","2022-03-21"]
[298,"Ranolazine","Ranolazine","Chemical drug","DB00243","Chronic angina is a common cardiovascular condition affecting millions worldwide and causes significant disability while interfering with daily activities. Ranolazine is a well-tolerated piperazine derivative used for the management of this condition, offering relief from uncomfortable and debilitating symptoms. With a mechanism of action different from drugs used to treat the same condition, ranolazine is a promising anti-anginal therapy. It was originally approved by the FDA in 2006.","56959","95635-55-5",true,"O(CC(CN1CCN(CC1)CC(=O)Nc1c(C)cccc1C)O)c1c(OC)cccc1","XKLMZUWKNUAPSZ-UHFFFAOYSA-N",427.545,"Sodium channel protein inhibitor; Inward rectifier potassium channel inhibitor; Voltage gated L-type calcium channel inhibitor; Alpha-1 adrenergic receptors antagonist; Beta-1 adrenergic receptor antagonist; Fatty acid other/unknown","Myocardial ischemia exerts effects on adenosine triphosphate flux, leading to a decrease in the energy available for contraction and relaxation of the heart muscle. Electrolyte balance of sodium and potassium is necessary for maintaining normal cardiac contraction and relaxation. Disruption of adequate sodium and potassium electrolyte balance leads to excessively high concentrations of sodium and calcium, which likely interferes with oxygen supply to the heart muscle. This imbalance eventually leads to angina symptoms of chest pain or pressure, nausea, and dizziness, among others.\r\n\r\nThe mechanism of action for ranolazine is not fully understood.  At therapeutic concentrations, it can inhibit the cardiac late sodium\r\n205 current (INa), which may affect the electrolyte balance in the myocardium, relieving angina symptoms. The clinical significance this inhibition in the treatment of angina symptoms is not yet confirmed.\r\n\r\nRanolazine inhibits sodium and potassium ion channel currents.  It has been shown to  exert weak activity on L-type calcium channels making it a weak direct vasodilator and exerts minimal direct effects on atrioventricular nodal conduction. Some additional mechanisms have been elucidated. Ranolazine exerts antagonistic activity towards the alpha 1 and beta 1 adrenergic receptors and inhibition of fatty acid oxidation.","Ranolazine exerts both antianginal and ischemic effects independent from lowering heart rate or blood pressure. It blocks IKr, the rapid portion of the delayed rectifier potassium current, and prolongs the QTc interval in a dose-dependent fashion. The Ikr is important for cardiac repolarization. Ranolazine exerts its therapeutic effects without negative chronotropic, dromotropic, or inotropic actions neither at rest, nor during exercise.","Ranolazine is indicated for the treatment of chronic angina. It can be used alone or in conjunction with nitrates, beta-blockers, angiotensin receptor blockers, anti-platelet drugs, calcium channel blockers, lipid-lowering drugs, and ACE inhibitors.\r\n\r\nRanolazine has also been used off-label for the treatment of certain arrhythmias, including ventricular tachycardia, however, this use is not strongly  supported by scientific evidence. Ranolazine has also been studied for the treatment of acute coronary syndrome, microvascular coronary dysfunction, arrhythmia, and glycemic control, which are not yet approved indications.",null,null,"Phase 4 on-going (CTRI/2019/06/019592)","Under clinical trials","2022-03-21"]
[299,"Remogliflozin",null,"Chemical drug",null,null,"136059718","329045-45-6",false,"C(c1c(O[C@@H]2O[C@H](CO)[C@H]([C@@H]([C@H]2O)O)O)nn(c1C)C(C)C)c1ccc(cc1)OC(C)C","GSINGUMRKGRYJP-VZWAGXQNSA-N",450.532,{"$nulls":6},"Phase 3 on-going (CTRI/2020/02/023250)","Under clinical trials","2022-03-21"]
[300,"Resmetirom","MGL-3196","Chemical drug","DB12914","MGL-3196 has been used in trials studying the treatment of Non-alcoholic steatohepatitis and Heterozygous Familial Hypercholesterolemia.","15981237","920509-32-6",false,"O=c1n(nc(c(=O)[nH]1)C#N)c1cc(Cl)c(c(c1)Cl)Oc1cc(C(C)C)c(=O)[nH]n1","FDBYIYFVSAHJLY-UHFFFAOYSA-N",435.227,{"$nulls":4},"THRB agonist","Anti-fibrosis","Phase 3 on-going (NCT04951219: Positive Topline Phase 3 MAESTRO-NAFLD-1 Data Demonstrate Resmetirom was Safe, Well-Tolerated and Provided Statistically Significant Improvements in Key Measures of Liver and Cardiovascular Health)","Advanced in clinical trials","2022-03-21"]
[301,"Resveratrol","(E)-5-(2-(4-hydroxyphenyl)ethenyl)-1,3-benzenediol(E)-5-(2-(4-hydroxyphenyl)ethenyl)-1,3-benzenediol; (E)-resveratrol; 3,4',5-trihydroxy-trans-stilbene; 3,4',5-trihydroxystilbene; 3,5,4'-trihydroxystilbene; 5-[(E)-2-(4-hydroxyphenyl)vinyl]benzene-1,3-diol; trans-resveratrol","Chemical drug","DB02709","Resveratrol (3,5,4'-trihydroxystilbene) is a polyphenolic phytoalexin. It is a stilbenoid, a derivate of stilbene, and is produced in plants with the help of the enzyme stilbene synthase. It exists as cis-(Z) and trans-(E) isomers. The trans- form can undergo isomerisation to the cis- form when heated or exposed to ultraviolet irradiation. In a 2004 issue of Science, Dr. Sinclair of Harvard University said resveratrol is not an easy molecule to protect from oxidation. It has been claimed that it is readily degraded by exposure to light, heat, and oxygen. However, studies find that Trans-resveratrol undergoes negligible oxidation in normal atmosphere at room temperature.","445154","501-36-0",false,"C(=C\\c1ccc(cc1)O)/c1cc(O)cc(c1)O","LUKBXSAWLPMMSZ-OWOJBTEDSA-N",228.247,"Ribosyldihydronicotinamide dehydrogenase [quinone]; Casein kinase II subunit alpha; Prostaglandin G/H synthase 1 inhibitor; Prostaglandin G/H synthase 2 inhibitor; Arachidonate 15-lipoxygenase; Arachidonate 5-lipoxygenase; Aryl hydrocarbon receptor; Phosp","Resveratrol suppresses NF-kappaB (NF-kappaB) activation in HSV infected cells. Reports have indicated that HSV activates NF-kappaB during productive infection and this may be an essential aspect of its replication scheme .","Resveratrol, a phytoalexin, has been found to inhibit herpes simplex virus types 1 and 2 (HSV-1 and HSV-2) replication in a dose-dependent, reversible manner, although this is only one of its many pharmaceutical properties. In some countries where there is higher consumption of red wine, there appears to be a lower incidence of heart disease. Other benefits of resveratrol include its anti-inflammatory and antioxidant effects. In preclinical studies, Resveratrol has been found to have potential anticancer properties.","Being investigated for the treatment of Herpes labialis infections (cold sores).","ALOX15; ALOX5; AHR; NR1I2; NR1I3","Anticancer agent","Phase 2&3 completed  (NCT02216552)","Under clinical trials","2022-03-21"]
[302,"RGMA001",null,"Miscellany",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (NCT01511523)","Under clinical trials","2022-03-21"]
[303,"Rifampicin","3-(((4-Methyl-1-piperazinyl)imino)methyl)rifamycin SV; RFP; Rifampicin; Rifampin","Chemical drug","DB01045","A semisynthetic antibiotic produced from Streptomyces mediterranei. It has a broad antibacterial spectrum, including activity against several forms of Mycobacterium. In susceptible organisms it inhibits DNA-dependent RNA polymerase activity by forming a stable complex with the enzyme. It thus suppresses the initiation of RNA synthesis. Rifampin is bactericidal, and acts on both intracellular and extracellular organisms. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p1160)","135398735","13292-46-1",true,"Oc1c2c3c4O[C@](C3=O)(C)O/C=C/[C@H](OC)[C@@H](C)[C@@H](OC(=O)C)[C@H](C)[C@@H]([C@@H]([C@H]([C@H](/C=C/C=C(\\C(=O)Nc(c1/C=N/N1CCN(CC1)C)c(c2c(c4C)O)O)/C)C)O)C)O","JQXXHWHPUNPDRT-WLSIYKJHSA-N",822.953,"DNA-directed RNA polymerase subunit beta inhibitor; Nuclear receptor subfamily 1 group I member 2 agonist","Rifampin acts via the inhibition of DNA-dependent RNA polymerase, leading to a suppression of RNA synthesis and cell death.","Rifampin is an antibiotic that inhibits DNA-dependent RNA polymerase activity in susceptible cells. Specifically, it interacts with bacterial RNA polymerase but does not inhibit the mammalian enzyme. It is bactericidal and has a very broad spectrum of activity against most gram-positive and gram-negative organisms (including <i>Pseudomonas aeruginosa</i>) and specifically <i>Mycobacterium tuberculosis</i>. Because of rapid emergence of resistant bacteria, use is restricted to treatment of mycobacterial infections and a few other indications. Rifampin is well absorbed when taken orally and is distributed widely in body tissues and fluids, including the CSF. It is metabolized in the liver and eliminated in bile and, to a much lesser extent, in urine, but dose adjustments are unnecessary with renal insufficiency.","For the treatment of Tuberculosis and Tuberculosis-related mycobacterial infections.","NR1I2 agonist","Antimycobacterial drug","Phase 4 completed  (NCT02329405)","Under clinical trials","2022-03-21"]
[304,"Rifaximin","Rifamycin L 105; Rifamycin L 105SV; Rifaxidin; Rifaximin","Chemical drug","DB01220","Rifaximin is a semisynthetic, rifamycin-based non-systemic antibiotic, meaning that the drug will not pass the gastrointestinal wall into the circulation as is common for other types of orally administered antibiotics. It has multiple indications and is used in treatment of traveller's diarrhea caused by E. coli; reduction in risk of overt hepatic encephalopathy recurrence; as well as diarrhea-predominant irritable bowel syndrome (IBS-D) in adult women and men. It is marketed under the brand name Xifaxan by Salix Pharmaceuticals.","6436173","80621-81-4",true,"O=C1c2c3c4c(n5c(n4)cc(cc5)C)c4c(c3c(c(c2O[C@]1(C)O/C=C/[C@H](OC)[C@@H](C)[C@@H](OC(=O)C)[C@H](C)[C@H](O)[C@H](C)[C@H]([C@H](/C=C/C=C(\\C(=O)N4)/C)C)O)C)O)O","NZCRJKRKKOLAOJ-XRCRFVBUSA-N",785.891,"DNA-directed RNA polymerase subunit beta inhibitor; Nuclear receptor subfamily 1 group I member 2 agonist","Rifaximin acts by inhibiting RNA synthesis in susceptible bacteria by binding to the beta-subunit of bacterial deoxyribonucleic acid (DNA)-dependent ribonucleic acid (RNA) polymerase enzyme. This binding blocks translocation, which stops transcription.","Rifaximin is a structural analog of rifampin and a non-systemic, gastrointestinal site-specific antibiotic. This non-systemic property of the drug is due to the addition of a pyridoimidazole ring, which renders it non-absorbable. Rifaximin acts by inhibiting bacterial ribonucleic acid (RNA) synthesis and contributes to restore intestinal microflora imbalance. Other studies have also shown rifaximin to be an pregnane X receptor (PXR) activator. As PXR is responsible for inhibiting the proinflammatory transcription factor NF-kappa B (NF-κB) and is inhibited in inflammatory bowel disease (IBD), rifaximin was proven to be effective for the treatment of IBS-D.","Rifaximin has multiple indications by the FDA: for the treatment of patients (≥12 years of age) with traveller's diarrhea caused by noninvasive strains of Escherichia coli; for the reduction of overt hepatic encephalopathy recurrence in patients ≥18 years of age; and in May 2015 it was approved for irritable bowel syndrome with diarrhea (IBS-D) treatment in adult men and women.","NR1I2 agonist","Antibiotic drug","Clinical trial on-going (IRCT20220104053626N1)","Under clinical trials","2022-03-21"]
[305,"Rimonabant","Rimonabant","Chemical drug","DB06155","Rimonabant is an anorectic anti-obesity drug produced and marketed by Sanofi-Aventis. It is an inverse agonist for the cannabinoid receptor CB1. Its main avenue of effect is reduction in appetite. Rimonabant is the first selective CB1 receptor blocker to be approved for use anywhere in the world. Rimonabant is approved in 38 countries including the E.U., Mexico, and Brazil. It was rejected for approval for use in the United States. This decision was made after a U.S. advisory panel recommended the medicine not be approved because it may increase suicidal thinking and depression.","104850","168273-06-1",true,"Cc1c(n(nc1C(=O)NN1CCCCC1)c1c(Cl)cc(cc1)Cl)c1ccc(cc1)Cl","JZCPYUJPEARBJL-UHFFFAOYSA-N",463.796,"Cannabinoid receptor 1 antagonist; G-protein coupled receptor 55","Rimonabant is a specific CB1 cannabinoid receptor antagonist. There is considerable evidence that the endocannabinoid (endogenous cannabinoid) system plays a significant role in appetitive drive and associated behaviours. It is therefore reasonable to hypothesize that the attenuation of the activity of this system would have therapeutic benefit in treating disorders that might have a component of excess appetitive drive or over-activity of the endocannabinoid system, such as obesity, ethanol and other drug abuse, and a variety of central nervous system and other disorders.","In the RIO-North America trial, 3040 patients were randomized to receive either placebo or one of two doses of rimonabant (5 mg or 20 mg per day). Patients taking 20 mg rimonabant had significant weigh loss, decrease in waist circumference, improved insulin sensitivity, and increases in HDL cholesterol, compared to patients on placebo.","For use in conjunction with diet and exercise for patients with a body mass index greater than 30 kg/m<sup>2</sup>, or patients wih a BMI greater than 27 kg/m<sup>2</sup> with associated risk factors, such as type 2 diabetes or dyslipidaemia.","CNR1 antagonist","Antialcoholic drug; CNS drug","Phase 3 terminated  (NCT00577148: Company decision taken in light of demands by certain national health authorities)","Under clinical trials","2022-03-21"]
[306,"RO5093151",null,"Biological drug",{"$nulls":4},false,{"$nulls":9},"Phase 1 completed  (NCT01277094: Inhibition of 11β-HSD1 by RO5093151 was effective and safe in reducing liver-fat content, suggesting that targeting of 11β-HSD1 might be a promising approach for the treatment of non-alcoholic fatty liver disease.)","Under clinical trials","2022-03-21"]
[307,"Roflumilast",null,"Chemical drug","DB01656","Roflumilast is a phosphodiesterase-4 (PDE-4) inhibitor. Due to its selective inhibition of the PDE4 isoenzyme in lung cells, roflumilast is indicated for the management of chronic obstrtuctive pulmonary disease (COPD) exacerbations. Treatment with Roflumilast is associated with an increase in psychiatric adverse reactions, including suicide and suicidal attempts.","449193","162401-32-3",true,"O(CC1CC1)c1c(OC(F)F)ccc(c1)C(=O)Nc1c(Cl)cncc1Cl","MNDBXUUTURYVHR-UHFFFAOYSA-N",403.212,"cAMP-specific 3',5'-cyclic phosphodiesterase 4D inhibitor; cAMP-specific 3',5'-cyclic phosphodiesterase 4A inhibitor; cAMP-specific 3',5'-cyclic phosphodiesterase 4B inhibitor; cAMP-specific 3',5'-cyclic phosphodiesterase 4C inhibitor","Roflumilast is a phosphodiesterase-4 (PDE-4) inhibitor which, due to its selective inhibition of the PDE4 isoenzyme, has potential antiinflammatory and antimodulatory effects in the pulmonary system. It is thought that the increased levels of intracellular cyclic AMP are responsible for the therapeutic actions of Roflumilast.","Roflumilast (and its active metabolite, roflumilast N-oxide) increases cyclic adenosine-3′, 5′-monophosphate (cAMP) in lung cells by inhibiting PDE4. Increased cAMP activates PKA, which inactivates transcription factors involved in inflammation. Romflumilast also decreases the amount of sputum neutrophils and eosinophils in COPD patients.","Roflumilast is indicated as a treatment to reduce the risk of COPD exacerbations in patients with severe COPD associated with chronic bronchitis and a history of exacerbations. Roflumilast is not a bronchodilator and is not indicated for the relief of acute bronchospasm.","PDE4C inhibitor; PDE4B inhibitor; Pde4 inhibitor; PDE4A inhibitor; PDE4D inhibitor","Antiasthmatic drug","Phase 2 terminated  (NCT01703260: Company decision; No safety or efficacy concerns.)","Under clinical trials","2022-03-21"]
[308,"Rosa canina",null,"Biological extract",{"$nulls":3},"84696-47-9",false,{"$nulls":9},"Clinical trial on-going (IRCT2017011514333N65)","Under clinical trials","2022-03-21"]
[309,"Rosa damascena",null,"Biological extract",{"$nulls":3},"90106-38-0",false,{"$nulls":9},"Clinical trial on-going (IRCT20191006044994N1)","Under clinical trials","2022-03-21"]
[310,"Rosemary","Allergenic Extract- Rosemary Rosmarinus Officinalis; Rosemary Herbs; Rosemary Leaf; Rosemary Leaf Extract; Rosemary, Fresh; Rosemary,dried; Rosemary,fresh; Rosmarini Folium; Rosmarinus Officinalis (Rosemary) Extract; Rosmarinus Officinalis (Rosemary) Leaf; Rosmarinus Officinalis (Rosemary) Leaf Extract; Rosmarinus Officinalis (Rosemary) Leaf Powder; Rosmarinus Officinalis Extract; Rosmarinus Officinalis Leaf; Rosmarinus Officinalis Leaf Dry Extract; Rosmarinus Officinalis Leaf Extract; Rosmarinus Officinalis Preparation; Spices, Rosemary, Dried","Biological drug","DB14272","Rosemary is a plant/plant extract used in some OTC (over-the-counter) products. It is not an approved drug.","10253785","97766-33-1",false,"O1[C@@H]([C@@H](O)[C@H](O)[C@@H](O)[C@@H]1Oc1cc(c2oc3c(c(=O)c2)c(O)cc(O)c3)ccc1O)C(=O)O","JDOFZOKGCYYUER-ZFORQUDYSA-N",462.363,{"$nulls":6},"Phase 2 on-going (IRCT20120415009472N20)","Under clinical trials","2022-03-21"]
[311,"Rosiglitazone","(±)-5-[p-[2-(methyl-2-pyridylamino)ethoxy]benzyl]-2,4-thiazolidinedione; (RS)-5-{4-[2-(Methyl-2-pyridylamino)ethoxy]benzyl}-2,4-thiazolidinedion; Rosiglitazone","Chemical drug","DB00412","Rosiglitazone is an anti-diabetic drug in the thiazolidinedione class of drugs. It is marketed by the pharmaceutical company GlaxoSmithKline as a stand-alone drug (Avandia) and in combination with metformin (Avandamet) or with glimepiride (Avandaryl). Like other thiazolidinediones, the mechanism of action of rosiglitazone is by activation of the intracellular receptor class of the peroxisome proliferator-activated receptors (PPARs), specifically PPARγ. Rosiglitazone is a selective ligand of PPARγ, and has no PPARα-binding action. Apart from its effect on insulin resistance, it appears to have an anti-inflammatory effect: nuclear factor kappa-B (NFκB) levels fall and inhibitor (IκB) levels increase in patients on rosiglitazone. Recent research has suggested that rosiglitazone may also be of benefit to a subset of patients with Alzheimer's disease not expressing the ApoE4 allele. This is the subject of a clinical trial currently underway.","77999","122320-73-4",true,"CN(CCOC1CCC(CC2SC(=O)NC2=O)CC1)C1CCCCN1","CZHAQHXDBPAXKQ-UHFFFAOYSA-N",357.435,"Peroxisome proliferator-activated receptor gamma agonist; Long-chain-fatty-acid--CoA ligase 4 inhibitor; Peroxisome proliferator-activated receptor alpha; Peroxisome proliferator-activated receptor delta; Retinoic acid receptor RXR-alpha; Retinoic acid re","Rosiglitazone acts as a highly selective and potent agonist at peroxisome proliferator activated receptors (PPAR) in target tissues for insulin action such as adipose tissue, skeletal muscle, and liver. Activation of PPAR-gamma receptors regulates the transcription of insulin-responsive genes involved in the control of glucose production, transport, and utilization. In this way, rosiglitazone enhances tissue sensitivity to insulin.","When rosiglitazone is used as monotherapy, it is associated with increases in total cholesterol, LDL, and HDL. It is also associated with decreases in free fatty acids. Increases in LDL occurred primarily during the first 1 to 2 months of therapy with AVANDIA and LDL levels remained elevated above baseline throughout the trials. In contrast, HDL continued to rise over time. As a result, the LDL/HDL ratio peaked after 2 months of therapy and then appeared to decrease over time.","Rosiglitazone is indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus.","PPARG agonist; PPARA; PPARD","Improve insulin resistance","Phase 2 completed (NCT00492700: Rosiglitazone has a substantial antisteatogenic effect in the first year of treatment without additional benefit with longer therapy despite a maintained effect on insulin sensitivity and transaminase levels. This suggests that improving insulin sensitivity might not be sufficient in NASH and that additional targets of therapy for liver injury should be explored.)","Failed in clinical trials","2022-03-21"]
[312,"Rosuvastatin","(3R,5S,6E)-7-(4-(4-fluorophenyl)-6-(1-methylethyl)-2-(ethyl(methylsulfonyl)amino)-5-pyrimidinyl)-3,5-dihydroxy-6-heptenoic acid; (3R,5S,6E)-7-{4-(4-fluorophenyl)-6-isopropyl-2-[methyl(methylsulfonyl)amino]pyrimidin-5-yl}-3,5-dihydroxyhept-6-enoic acid; Rosuvastatin","Chemical drug","DB01098","Rosuvastatin, also known as the brand name product Crestor, is a lipid-lowering drug that belongs to the statin class of medications, which are used to lower the risk of cardiovascular disease and manage elevated lipid levels by inhibiting the endogenous production of cholesterol in the liver. More specifically, statin medications competitively inhibit the enzyme hydroxymethylglutaryl-coenzyme A (HMG-CoA) Reductase, which catalyzes the conversion of HMG-CoA to mevalonic acid and is the third step in a sequence of metabolic reactions involved in the production of several compounds involved in lipid metabolism and transport including cholesterol, low-density lipoprotein (LDL) (sometimes referred to as \"bad cholesterol\"), and very low-density lipoprotein (VLDL). Prescribing of statin medications is considered standard practice following any cardiovascular events and for people with a moderate to high risk of development of CVD, such as those with Type 2 Diabetes. The clear evidence of the benefit of statin use coupled with very minimal side effects or long term effects has resulted in this class becoming one of the most widely prescribed medications in North America.\r\n\r\nRosuvastatin and other drugs from the statin class of medications including , , , , and  are considered first-line options for the treatment of dyslipidemia. This is largely due to the fact that cardiovascular disease (CVD), which includes heart attack, atherosclerosis, angina, peripheral artery disease, and stroke, has become a leading cause of death in high-income countries and a major cause of morbidity around the world. Elevated cholesterol levels, and in particular, elevated low-density lipoprotein (LDL) levels, are an important risk factor for the development of CVD. Use of statins to target and reduce LDL levels has been shown in a number of landmark studies to significantly reduce the risk of development of CVD and all-cause mortality. Statins are considered a cost-effective treatment option for CVD due to their evidence of reducing all-cause mortality including fatal and non-fatal CVD as well as the need for surgical revascularization or angioplasty following a heart attack. Evidence has shown that even for low-risk individuals (with <10% risk of a major vascular event occurring within 5 years) statins cause a 20%-22% relative reduction in major cardiovascular events (heart attack, stroke, coronary revascularization, and coronary death) for every 1 mmol/L reduction in LDL without any significant side effects or risks.\r\n\r\nWhile all statin medications are considered equally effective from a clinical standpoint, rosuvastatin is considered the most potent; doses of 10 to 40mg rosuvastatin per day were found in clinical studies to result in a 45.8% to 54.6% decreases in LDL cholesterol levels, which is about three-fold more potent than 's effects on LDL cholesterol. However, the results of the SATURN trial concluded that despite this difference in potency, there was no difference in their effect on the progression of coronary atherosclerosis.\r\n\r\nRosuvastatin is also a unique member of the class of statins due to its high hydrophilicity which increases hepatic uptake at the site of action, low bioavailability, and minimal metabolism via the Cytochrome P450 system. This last point results in less risk of drug-drug interactions compared to , , and , which are all extensively metabolized by Cytochrome P450 (CYP) 3A4, an enzyme involved in the metabolism of many commonly used drugs. Drugs such as , , and some antiretrovirals are more likely to interact with this statin through antagonism of OATP1B1 organic anion transporter protein 1B1-mediated hepatic uptake of rosuvastatin.","446157","287714-41-4",true,"C(=C\\[C@H](C[C@H](CC(=O)O)O)O)/c1c(nc(nc1C(C)C)N(S(=O)(=O)C)C)c1ccc(cc1)F","BPRHUIZQVSMCRT-VEUZHWNKSA-N",481.546,"3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor; Integrin alpha-L inhibitory allosteric modulator","Rosuvastatin is a statin medication and a competitive inhibitor of the enzyme HMG-CoA (3-hydroxy-3-methylglutaryl coenzyme A) reductase, which catalyzes the conversion of HMG-CoA to mevalonate, an early rate-limiting step in cholesterol biosynthesis. Rosuvastatin acts primarily in the liver, where decreased hepatic cholesterol concentrations stimulate the upregulation of hepatic low density lipoprotein (LDL) receptors which increases hepatic uptake of LDL. Rosuvastatin also inhibits hepatic synthesis of very low density lipoprotein (VLDL). The overall effect is a decrease in plasma LDL and VLDL. \r\n\r\nIn vitro and in vivo animal studies also demonstrate that rosuvastatin exerts vasculoprotective effects independent of its lipid-lowering properties, also known as the pleiotropic effects of statins. This includes improvement in endothelial function, enhanced stability of atherosclerotic plaques, reduced oxidative stress and inflammation, and inhibition of the thrombogenic response.\r\n\r\nStatins have also been found to bind allosterically to β2 integrin function-associated antigen-1 (LFA-1), which plays an important role in leukocyte trafficking and in T cell activation.\r\n\r\nRosuvastatin exerts an anti-inflammatory effect on rat mesenteric microvascular endothelium by attenuating leukocyte rolling, adherence and transmigration. The drug also modulates nitric oxide synthase (NOS) expression and reduces ischemic-reperfusion injuries in rat hearts. Rosuvastatin increases the bioavailability of nitric oxide by upregulating NOS and by increasing the stability of NOS through post-transcriptional polyadenylation. It is unclear as to how rosuvastatin brings about these effects though they may be due to decreased concentrations of mevalonic acid.","Rosuvastatin is a synthetic, enantiomerically pure antilipemic agent. It is used to lower total cholesterol, low density lipoprotein-cholesterol (LDL-C), apolipoprotein B (apoB), non-high density lipoprotein-cholesterol (non-HDL-C), and trigleride (TG) plasma concentrations while increasing HDL-C concentrations. High LDL-C, low HDL-C and high TG concentrations in the plasma are associated with increased risk of atherosclerosis and cardiovascular disease. The total cholesterol to HDL-C ratio is a strong predictor of coronary artery disease and high ratios are associated with higher risk of disease. Increased levels of HDL-C are associated with lower cardiovascular risk. By decreasing LDL-C and TG and increasing HDL-C, rosuvastatin reduces the risk of cardiovascular morbidity and mortality.\r\n\r\nElevated cholesterol levels, and in particular, elevated low-density lipoprotein (LDL) levels, are an important risk factor for the development of CVD. Use of statins to target and reduce LDL levels has been shown in a number of landmark studies to significantly reduce the risk of development of CVD and all-cause mortality. Statins are considered a cost-effective treatment option for CVD due to their evidence of reducing all-cause mortality including fatal and non-fatal CVD as well as the need for surgical revascularization or angioplasty following a heart attack. Evidence has shown that even for low-risk individuals (with <10% risk of a major vascular event occurring within 5 years) statins cause a 20%-22% relative reduction in major cardiovascular events (heart attack, stroke, coronary revascularization, and coronary death) for every 1 mmol/L reduction in LDL without any significant side effects or risks.\r\n\r\n**Skeletal Muscle Effects**\r\n\r\nCases of myopathy and rhabdomyolysis with acute renal failure secondary to myoglobinuria have been reported with HMG-CoA reductase inhibitors, including rosuvastatin. These risks can occur at any dose level, but are increased at the highest dose (40 mg). Rosuvastatin should be prescribed with caution in patients with predisposing factors for myopathy (e.g., age ≥ 65 years, inadequately treated hypothyroidism, renal impairment).\r\n\r\nThe risk of myopathy during treatment with rosuvastatin may be increased with concurrent administration of some other lipid-lowering therapies (such as fenofibrate or niacin), gemfibrozil, cyclosporine, atazanavir/ritonavir, lopinavir/ritonavir, or simeprevir.  Cases of myopathy, including rhabdomyolysis, have been reported with HMG-CoA reductase inhibitors, including rosuvastatin, coadministered with colchicine, and caution should therefore be exercised when prescribing these two medications together.\r\n\r\nReal-world data from observational studies has suggested that 10-15% of people taking statins may experience muscle aches at some point during treatment.\r\n\r\n**Liver Enzyme Abnormalities**\r\n\r\nIncreases in serum transaminases have been reported with HMG-CoA reductase inhibitors, including rosuvastatin. In most cases, the elevations were transient and resolved or improved on continued therapy or after a brief interruption in therapy. There were two cases of jaundice, for which a relationship to rosuvastatin therapy could not be determined, which resolved after discontinuation of therapy. There were no cases of liver failure or irreversible liver disease in these trials.\r\n\r\n**Endocrine Effects**\r\n\r\nIncreases in HbA1c and fasting serum glucose levels have been reported with HMG-CoA reductase inhibitors, including rosuvastatin calcium tablets. Based on clinical trial data with rosuvastatin, in some instances these increases may exceed the threshold for the diagnosis of diabetes mellitus.\r\n\r\nAn in vitro study found that atorvastatin, pravastatin, rosuvastatin, and pitavastatin exhibited a dose-dependent cytotoxic effect on human pancreas islet β cells, with reductions in cell viability of 32, 41, 34 and 29%, respectively, versus control]. Moreover, insulin secretion rates were decreased by 34, 30, 27 and 19%, respectively, relative to control.\r\n\r\nHMG-CoA reductase inhibitors interfere with cholesterol synthesis and lower cholesterol levels and, as such, might theoretically blunt adrenal or gonadal steroid hormone production. Rosuvastatin demonstrated no effect upon nonstimulated cortisol levels and no effect on thyroid metabolism as assessed by TSH plasma concentration. In rosuvastatin treated patients, there was no impairment of adrenocortical reserve and no reduction in plasma cortisol concentrations. Clinical studies with other HMG-CoA reductase inhibitors have suggested that these agents do not reduce plasma testosterone concentration. The effects of HMG-CoA reductase inhibitors on male fertility have not been studied. The effects, if any, on the pituitarygonadal axis in premenopausal women are unknown.\r\n\r\n**Cardiovascular**\r\n\r\nUbiquinone levels were not measured in rosuvastatin clinical trials, however significant decreases in circulating ubiquinone levels in patients treated with other statins have been observed. The clinical significance of a potential long-term statin-induced deficiency of ubiquinone has not been established. It has been reported that a decrease in myocardial ubiquinone levels could lead to impaired cardiac function in patients with borderline congestive heart failure.\r\n\r\n**Lipoprotein A**\r\n\r\nIn some patients, the beneficial effect of lowered total cholesterol and LDL-C levels may be partly blunted by a concomitant increase in the Lipoprotein(a) Lp(a) concentrations. Present knowledge suggests the importance of high Lp(a) levels as an emerging risk factor for coronary heart disease. It is thus desirable to maintain and reinforce lifestyle changes in high-risk patients placed on rosuvastatin therapy. Further studies have demonstrated statins affect Lp(a) levels differently in patients with dyslipidemia depending on their apo(a) phenotype; statins increase Lp(a) levels exclusively in patients with the low molecular weight apo(a) phenotype.","The FDA monograph states that rosuvastatin is indicated as an adjunct to diet in the treatment of triglyceridemia, Primary Dysbetalipoproteinemia (Type III Hyperlipoproteinemia), and Homozygous Familial Hypercholesterolemia.\r\n\r\nThe Health Canada monograph for rosuvastatin further specifies that rosuvastatin is indicated for the reduction of elevated total cholesterol (Total-C), LDL-C, ApoB, the Total-C/HDL-C ratio and triglycerides (TG) and for increasing HDL-C in hyperlipidemic and dyslipidemic conditions when response to diet and exercise alone has been inadequate. It is also indicated for the prevention of major cardiovascular events (including risk of myocardial infarction, nonfatal stroke, and coronary artery revascularization) in adult patients without documented history of cardiovascular or cerebrovascular events, but with at least two conventional risk factors for cardiovascular disease.\r\n\r\nPrescribing of statin medications is considered standard practice following any cardiovascular events and for people with a moderate to high risk of development of CVD. Statin-indicated conditions include diabetes mellitus, clinical atherosclerosis (including myocardial infarction, acute coronary syndromes, stable angina, documented coronary artery disease, stroke, trans ischemic attack (TIA), documented carotid disease, peripheral artery disease, and claudication), abdominal aortic aneurysm, chronic kidney disease, and severely elevated LDL-C levels.","HMGCR inhibitor","Enhance lipid metabolism","Phase 4 completed  (NCT03434613: Ezetimibe and rosuvastatin were found to be safe to treat participants with NAFLD. Furthermore, ezetimibe combined with rosuvastatin significantly reduced liver fat in this population.)","Under clinical trials","2022-03-21"]
[313,"Runihol",null,"Miscellany",{"$nulls":4},false,{"$nulls":9},"Phase 2 terminated  (NCT02930161: Low recruitment)","Under clinical trials","2022-03-21"]
[314,"RYI-018","Nimacimab","Biological drug","DB15115","Nimacimab is under investigation in clinical trial NCT03261739 (Safety Tolerability, and PK of RYI-018 After Repeat Dosing in Subjects With Non-Alcoholic Fatty Liver Disease (NAFLD)).",null,"2098636-09-8",false,{"$nulls":9},"Phase 1 completed  (NCT03261739)","Under clinical trials","2022-03-21"]
[315,"Saberry capsules","Phyllanthus emblica","Herbal medicine",{"$nulls":3},"2071610-60-9",false,{"$nulls":9},"Clinical trial on-going (CTRI/2016/04/006847)","Under clinical trials","2022-03-21"]
[316,"S-adenosyl-L-methionine","SAMe; Ademetionine; AdoMet; L-S-Adenosylmethionine; S-Adenosylmethionine; SAM; SAM-e; SAMe","Chemical drug","DB00118","Physiologic methyl radical donor involved in enzymatic transmethylation reactions and present in all living organisms. It possesses anti-inflammatory activity and has been used in treatment of chronic liver disease. (From Merck, 11th ed)","34755","29908-03-0",true,"O[C@H]1[C@H](n2c3c(nc2)c(N)ncn3)O[C@@H]([C@H]1O)C[S+](CC[C@@H](C(=O)[O-])N)C","MEFKEPWMEQBLKI-AIRLBKTGSA-N",398.445,"Glycine N-methyltransferase cofactor; S-adenosylmethionine decarboxylase proenzyme cofactor; S-adenosylmethionine synthase isoform type-2 cofactor; Cystathionine beta-synthase activator; S-adenosylmethionine synthase isoform type-1 cofactor; Catechol O-me","S-Adenosylmethionine (SAMe) is a natural substance present in the cells of the body. It is a direct metabolite of the essential amino acid L-methionine. SAMe plays a crucial biochemical role in the body by donating a one-carbon methyl group in a process called transmethylation. SAMe, formed from the reaction of L-methionine and adenosine triphosphate catalyzed by the enzyme S-adenosylmethionine synthetase, is the methyl-group donor in the biosynthesis of both DNA and RNA nucleic acids, phospholipids, proteins, epinephrine, melatonin, creatine and other molecules.","S-adenosylmethionine is an intermediate metabolite of methionine. Its involvement in methylation assists in cellular growth and repair, maintains the phospho-bilipid layer in cell membranes. It also helps in the maintenance of the action of several hormones and neurotransmitters that affect mood. Highest concentration are found in the brain and the liver.","S-Adenosylmethionine (SAMe) is used as a drug in Europe for the treatment of depression, liver disorders, fibromyalgia, and osteoarthritis. It has also been introduced into the United States market as a dietary supplement for the support of bone and joint health, as well as mood and emotional well being.","GNMT cofactor","Antiviral","Phase 3 on-going (DRKS00005767)","Under clinical trials","2022-03-21"]
[317,"Saffron","Crocus sativus","Herbal medicine",null,null,"5281233","89382-88-7",false,{"$nulls":9},"Phase 2 on-going (IRCT201610269472N11)","Under clinical trials","2022-03-21"]
[318,"Salsalate","2-Carboxyphenyl salicylate; Disalicylic acid; o-Salicylsalicylic acid; Salicylic acid bimolecular ester; Salicyloxysalicylic acid; Salicyloylsalicylic acid; Salicylsalicylic acid; Sasapyrin; Sasapyrine","Chemical drug","DB01399","Salsalate is a nonsteroidal anti-inflammatory agent for oral administration. Salsalate's mode of action as an anti-inflammatory and antirheumatic agent may be due to inhibition of synthesis and release of prostaglandins. The usefulness of salicylic acid, the active in vivo product of salsalate, in the treatment of arthritic disorders has been established. In contrast to aspirin, salsalate causes no greater fecal gastrointestinal blood loss than placebo. Salsalate is readily soluble in the small intestine where it is partially hydrolyzed to two molecules of salicylic acid. A significant portion of the parent compound is absorbed unchanged and undergoes rapid esterase hydrolysis in the body. The parent compound has an elimination half-life of about 1 hour. Salicylic acid (the active metabolite) biotransformation is saturated at anti-inflammatory doses of salsalate. Such capacity limited biotransformation results in an increase in the half-life of salicylic acid from 3.5 to 16 or more hours.","5161","552-94-3",true,"O(C(=O)c1c(O)cccc1)c1c(C(=O)O)cccc1","WVYADZUPLLSGPU-UHFFFAOYSA-N",258.229,"Prostaglandin G/H synthase 2 inhibitor; Prostaglandin G/H synthase 1 inhibitor","The mode of anti-inflammatory action of salsalate and other nonsteroidal anti-inflammatory drugs is not fully defined, but appears to be primarily associated with inhibition of prostaglandin synthesis. This inhibition of prostaglandin synthesis is done through the inactivation of cyclooxygenase-1 (COX-1) and COX-2, which are reponsible for catalyzing the formation of prostaglandins in the arachidonic acid pathway. Although salicylic acid (the primary metabolite of salsalate) is a weak inhibitor of prostaglandin synthesis in vitro, salsalate appears to selectively inhibit prostaglandin synthesis in vivo, providing anti-inflammatory activity equivalent to aspirin and indomethacin. Unlike aspirin, salsalate does not inhibit platelet aggregation.","Salsalate is a nonsteroidal anti-inflammatory agent for oral administration. Salsalate's mode of action as an anti-inflammatory and antirheumatic agent may be due to inhibition of synthesis and release of prostaglandins. The usefulness of salicylic acid, the active in vivo product of salsalate, in the treatment of arthritic disorders has been established. In contrast to aspirin, salsalate causes no greater fecal gastrointestinal blood loss than placebo.","For relief of the signs and symptoms of rheumatoid arthritis, osteoarthritis and related rheumatic disorders.","PTGS2 inhibitor; PTGS1 inhibitor","NSAID","Phase 4 completed  (NCT03222206)","Under clinical trials","2022-03-21"]
[319,"Sancailianmei Particle",null,"Traditional medicine",{"$nulls":4},false,{"$nulls":9},"Phase 0 on-going (ChiCTR2000033099)","Under clinical trials","2022-03-21"]
[320,"SAR425899",null,"Chemical drug",{"$nulls":4},false,{"$nulls":9},"Phase 2 withdrawn (NCT03437720: Sponsor decision to cancel TRIAL, not related to safety concern.)","Under clinical trials","2022-03-21"]
[321,"Saroglitazar",null,"Chemical drug","DB13115","Saroglitazar has been investigated for the treatment of Fatty Liver.","60151560","495399-09-2",false,"CCO[C@@H](CC1=CC=C(OCCN2C(C)=CC=C2C2=CC=C(SC)C=C2)C=C1)C(O)=O","MRWFZSLZNUJVQW-DEOSSOPVSA-N",439.577,{"$nulls":4},"PPARA agonist; PPARG agonist","Antidiabetic drug","Phase 2 completed (NCT03061721: Saroglitazar 4 mg significantly improved ALT, LFC, insulin resistance, and atherogenic dyslipidemia in participants with NAFLD/NASH.)\r\nPhase 3 on-going (NCT03639623)","Approved in India","2022-03-21"]
[322,"Sebelipase Alfa","SBC-102; SBC-102; Sebelipase alfa","Biological drug","DB11563","The lysosomal acid lipase (LAL) enzyme is found in lysosomes and is primarily responsible for the metabolism of lipids, and its absence or deficiency results in the accumulation of lipids in various organs. This lipid accumulation can lead to end-organ damage in the form of liver dysfunction or malabsorption secondary to intestinal dysfunction. In addition, patients with LAL deficiency typically develop dyslipidemia, which itself contributes to a number of adverse cardiovascular outcomes.\r\n\r\nSebelipase alfa is a recombinant form LAL approved for the treatment of LAL deficiency. It was first approved by both the FDA and EMA in 2015 and is marketed under the brand name Kanuma (Alexion Pharmaceuticals).",null,"1276027-63-4",true,{"$nulls":4},"Lysosomal acid lipase (LAL) deficiency is an inherited storage disorder caused by a genetic defect that results in a marked decrease or loss in activity of the LAL enzyme. Endogenous LAL is found in the lysosome and is responsible for the breakdown of lipids - a deficiency of these enzymes results in the accumulation of cholesteryl esters and triglycerides, which lead to a number of downstream consequences such as progressive liver disease, malabsorption, and growth failure. Dyslipidemia associated with LAL deficiency may also result in the typical cardiovascular effects associated with elevated lipid levels.\r\n\r\nSebelipase alfa is a recombinant form of human lysosomal acid lipase (rhLAL) which binds to cell surface receptors via glycans expressed on the protein and is subsequently internalized into lysosomes. From within the lysosome, sebelipase alfa catalyzes the lysosomal hydrolysis of cholesteryl esters and triglycerides to free cholesterol, glycerol and free fatty acids.","Sebelipase alfa serves as a replacement enzyme for patients deficient in lysosomal acid lipase (LAL) caused by a genetic defect. As it is produced using recombinant DNA technology in the eggs of genetically engineered chickens, it should be used with caution in patients with a known history of egg allergy. Hypersensitivity reactions, including anaphylaxis, have also been observed in patients without egg allergy - for this reason, appropriate therapy for the treatment of hypersensitivity reactions should be readily available during its administration.\r","Sebelipase alfa is a hydrolytic lysosomal cholesteryl ester and triacylglycerol-specific enzyme indicated for the treatment of patients with a diagnosis of Lysosomal Acid Lipase (LAL) deficiency.",null,"Enzyme replacement therapy","Phase 2&3 completed  (NCT01371825: Sebelipase alfa markedly improved survival with substantial clinically meaningful improvements in growth and other key disease manifestations in infants with rapidly progressive lysosomal acid lipase deficiency.)","Under clinical trials","2022-03-21"]
[323,"Secukinumab","Secukinumab","Biological drug","DB09029","Secukinumab (Cosentyx) is a human monoclonal antibody designed for the treatment of uveitis, rheumatoid arthritis, ankylosing spondylitis, and psoriasis. Secukinumab is an interleukin-17A (IL-17A) inhibitor marketed by Novartis. IL-17 is a group of proinflammatory cytokines released by cells of the immune system and and exist in higher levels in many immune conditions associated with chronic inflammation. By targeting IL-17A, secukinumab has shown excellent efficacy in psoriasis by normalizing skin histology and was approved by the United States Food and Drug Administration on January 21, 2015 to treat adults with moderate-to-severe plaque psoriasis.",null,"1229022-83-6",true,{"$nulls":3},"Interleukin-17A antagonist","Secukinumab is a human monoclonal antibody that targets IL-17A cytokine to downregulate inflammation in psoriasis, an autoimmune dermatological disease. The pathophysiology of psoriasis has not been fully established, however it is known that dysregulation of innate and adaptive immune responses plays part in the chronic inflammation associated with the disease. IL-17 represents is a six-membered family (IL-17A to F) of pleiotropic pro-inflammatory cytokines, expression of which is found to be elevated in psoriatic skin.  These cytokines act on many different cell types and provide defense against different extracellular pathogens causing fungal or bacterial infections. IL-17 cytokines are produced by many cells involved in immune system defense, such as Th17, mast cells, neutrophils, and dendritic cells - all implicated in promoting inflammation. There is evidence linking IL-17 to pathogenesis of multiple autoimmune diseases including rheumatoid arthritis, spondyloarthritis, psoriasis, Crohn's disease, multiple sclerosis, and even atherosclerosis.",null,"For the treatment of moderate to severe plaque psoriasis in patients that are candidates for systemic therapy or phototherapy.","IL17A antagonist; antibody","Immunomodulator","Phase 3 completed  (NCT04237116)","Under clinical trials","2022-03-21"]
[324,"Seladelpar","MBX-8025","Chemical drug","DB12390","Seladelpar (MBX-8025) has been used in trials studying the treatment of Hyperlipidemia.","11236126","851528-79-5",false,"CCO[C@H](COC1=CC=C(C=C1)C(F)(F)F)CSC1=CC(C)=C(OCC(O)=O)C=C1","JWHYSEDOYMYMNM-QGZVFWFLSA-N",444.471,{"$nulls":6},"Phase 2 terminated (NCT03551522: unexpected histological findings)","Failed in clinical trials","2022-03-21"]
[325,"Selimarine",null,"Miscellany",{"$nulls":4},false,{"$nulls":9},"Phase 2&3 on-going (IRCT138902253933N1)","Under clinical trials","2022-03-21"]
[326,"Selonsertib","GS-4997; Selonsertib","Chemical drug","DB14916","Selonsertib is under investigation in clinical trial NCT03053050 (Safety and Efficacy of Selonsertib in Adults With Nonalcoholic Steatohepatitis (NASH) and Bridging (F3) Fibrosis).","71245288","1448428-04-3",false,"Cc1c(cc(c(c1)F)C(=O)Nc1nc(ccc1)c1n(C(C)C)cnn1)n1cc(nc1)C1CC1","YIDDLAAKOYYGJG-UHFFFAOYSA-N",445.502,{"$nulls":4},"MAP3K5 inhibitor; ASK1 inhibitor","Anti-oxidative stress; Anticancer agent","Phase 3 on-going (NCT03053050; NCT03053063: Forty-eight weeks of selonsertib monotherapy had no antifibrotic effect in patients with bridging fibrosis or compensated cirrhosis due to NASH.)","Failed in clinical trials","2022-03-21"]
[327,"Semaglutide","Semaglutide","Chemical drug","DB13928","Semaglutide is a glucagon-like peptide 1 (GLP-1) analog used to manage type 2 diabetes along with lifestyle changes, such as dietary restrictions and increased physical activity. Other members of this drug class include  and . Semaglutide was developed by Novo Nordisk and approved by the FDA for subcutaneous injection in December 2017. The tablet formulation was approved for oral administration in September 2019. Semaglutide works by binding to and activating the GLP-1 receptor, thereby stimulating insulin secretion and reducing blood glucose.\r\n\r\nThe subcutaneous injection is administered once weekly and the tablet is administered once a day. Semaglutide offers a competitive advantage over other drugs used to manage diabetes, which may require several daily doses. Clinical trials have determined that this drug reduces glycosylated hemoglobin (HbA1c) levels and reduces body weight, proving to be effective for patients with type 2 diabetes. In June 2021, semaglutide was approved by the FDA for chronic weight management in adults with general obesity or overweight who have at least one weight-related condition: this marks semaglutide as the first approved drug for such use since 2014. Health Canada also approved semaglutide in November 2021 for the treatment of adults with obesity.","56843331","910463-68-2",true,"O=C(N[C@@H](C(C)C)C(=O)N[C@@H](CCCNC(=N)N)C(=O)NCC(=O)N[C@@H](CCCNC(=N)N)C(=O)NCC(=O)O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)CNC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)CNC(=O)[C@@H](NC(=O)C(NC(=O)[C@@H](N)Cc1[nH]cnc1)(C)C)CCC(=O)O)[C@H](O)C)Cc1ccccc1)[C@H](O)C)CO)CC(=O)O)C(C)C)CO)CO)Cc1ccc(O)cc1)CC(C)C)CCC(=O)O)CCC(=O)N)C)C)CCCCNC(=O)COCCOCCNC(=O)COCCOCCNC(=O)CC[C@@H](NC(=O)CCCCCCCCCCCCCCCCC(=O)O)C(=O)O)CCC(=O)O)Cc1ccccc1)[C@H](CC)C)C)Cc1c2c([nH]c1)cccc2)CC(C)C","DLSWIYLPEUIQAV-CCUURXOWSA-N",4113.641,"Glucagon-like peptide 1 receptor agonist","**Mechanism of glycemic control**\r\n\r\nGLP-1 is a physiological hormone that promotes glycemic control via several different mechanisms, including insulin secretion, slowing gastric emptying, and reducing postprandial glucagon secretion. The homeostasis of glucose is dependent on hormones such as insulin and amylin, which are secreted by the beta cells of the pancreas.  Semaglutide is 94% similar to human GLP-1. Analogs of this hormone such as semaglutide stimulate the synthesis of insulin by stimulating pancreatic islet cells and reducing glucagon secretion.  They directly bind with selectivity to the GLP-1 receptor, causing various beneficial downstream effects that reduce blood glucose in a glucose-dependent fashion. \r\n\r\n**Mechanism of cardiovascular benefit and weight loss**\r\n\r\n In hypercholesterolemia, semaglutide is believed to reduce the progression of atherosclerosis via decreased gut permeability and decreased inflammation. Weight loss is believed to occur via the reduction of appetite and food cravings after semaglutide administration.","Semaglutide reduces HbA1c, systolic blood pressure, and body weight. After 12 weeks of treatment, semaglutide decreased fasting and postprandial glucose by increasing insulin production and decreasing glucagon secretion (which is normally associated with increases in blood sugar). Semaglutide also lowers fasting triglycerides and VLDL cholesterol, exerting beneficial effects on cardiovascular health.\r\n\r\nSemaglutide has been shown to cause medullary thyroid cell carcinoma in rodents. While its clinical relevance to humans is unknown, the FDA advises not to administer this drug in those with a personal or family history of medullary thyroid carcinoma.  Semaglutide also poses a risk of pancreatitis and dehydration. Patients must be adequately hydrated while on semaglutide and are advised to seek medical attention immediately in cases of abdominal pain radiating to the back. Because this drug delays gastric emptying, it is important to monitor for the efficacy or adverse effects of other drugs that are administered orally.","Semaglutide is indicated to improve glycemic control in adults diagnosed with type 2 diabetes mellitus, and is used as an adjunct to diet and exercise. However, semaglutide is not a suitable first-line drug for diabetes that has not been controlled by diet and exercise. In addition, it has not been studied in patients with pancreatitis.  Semaglutide is not intended for use in patients with type 1 diabetes or to treat diabetic ketoacidosis.\r\n\r\nSemaglutide is indicated for chronic weight management in adults with obesity or overweight with at least one weight-related condition (such as high blood pressure, type 2 diabetes, or high cholesterol), for use in addition to a reduced-calorie diet and increased physical activity.","GLP1R agonist","Antidiabetic drug","Phase 2 completed (This phase 2 trial involving patients with NASH showed that treatment with semaglutide resulted in a significantly higher percentage of patients with NASH resolution than placebo. However, the trial did not show a significant between-group difference in the percentage of patients with an improvement in fibrosis stage. (Funded by Novo Nordisk; ClinicalTrials.gov number, NCT02970942.).)","Under clinical trials","2022-03-21"]
[328,"Serine","(S)-2-Amino-3-hydroxypropanoic acid; (S)-Serine; alpha-Amino-beta-hydroxypropionic acid; beta-Hydroxyalanine; L-Serine; Ser; Serine","Chemical drug","DB00133","A non-essential amino acid occurring in natural form as the L-isomer. It is synthesized from glycine or threonine. It is involved in the biosynthesis of purines; pyrimidines; and other amino acids.","5951","302-84-1",false,"C(C(=O)O)(CO)N","MTCFGRXMJLQNBG-UHFFFAOYSA-N",105.093,"Cystathionine beta-synthase; L-serine dehydratase/L-threonine deaminase; Serine racemase; Serine palmitoyltransferase 2; Serine palmitoyltransferase 1; Serine--tRNA ligase, cytoplasmic; Serine--pyruvate aminotransferase","L-Serine plays a role in cell growth and development (cellular proliferation). The conversion of L-serine to glycine by serine hydroxymethyltransferase results in the formation of the one-carbon units necessary for the synthesis of the purine bases, adenine and guanine. These bases when linked to the phosphate ester of pentose sugars are essential components of DNA and RNA and the end products of energy producing metabolic pathways, ATP and GTP. In addition, L-serine conversion to glycine via this same enzyme provides the one-carbon units necessary for production of the pyrimidine nucleotide, deoxythymidine monophosphate, also an essential component of DNA.","Serine is classified as a nutritionally non-essential amino acid. Serine is critical for the production of the body's proteins, enzymes and muscle tissue. Serine is needed for the proper metabolism of fats and fatty acids. It also helps in the production of antibodies. Serine is used as a natural moisturizing agent in some cosmetics and skin care products. The main source of essential amino acids is from the diet, non-essential amino acids are normally synthesize by humans and other mammals from common intermediates.","Used as a natural moisturizing agent in some cosmetics and skin care products.","SRR","Improve insulin resistance","Phase 1&2 completed  (NCT02599038)","Under clinical trials","2022-03-21"]
[329,"SGM-1019",null,"Chemical drug",{"$nulls":4},false,{"$nulls":9},"Phase 2 terminated  (NCT03676231: Study terminated due to a safety event which rendered the risk-benefit profile in NASH to no longer be adequately favorable)","Failed in clinical trials","2022-03-21"]
[330,"Shan Zha Xiao Zhi capsule",null,"Traditional medicine",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (ChiCTR-IPR-15006694)","Under clinical trials","2022-03-21"]
[331,"Shizazi thyme","Thymus vulgaris","Herbal medicine",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (IRCT2015120925447N1)","Under clinical trials","2022-03-21"]
[332,"Volixibat","Volixibat potassium; Volixibat; SHP626","Chemical drug","DB13914","Volixibat, also known as SHP626 or LUM002, is an investigational drug that will potentially be used for the treatment of Non-Alcoholic Steatohepatitis (NASH). If approved for use, it will be the first available agent for the treatment of NASH.\r\n\r\nVolixibat is a selective inhibitor of the apical sodium-dependent bile acid transporter (ASBT), a transmembrane protein primarily expressed by enterocytes of the ileum. Also known as the ileal bile acid transporter (IBAT), ASBT is primarily responsible for the enterohepatic recirculation of bile acids and ultimately for hepatic lipid and glucose metabolism . Inhibiting this enzyme results in a decrease of bile acids returning to the liver, which is helpful for the treatment of NASH as abnormal cholesterol metabolism and accumulation of free cholesterol in the liver have been implicated in its pathogenesis. \r\n\r\nAccording to Shire, the pharmaceutical manufacturer of Volixibat, it has been granted fast track status by the Food and Drug Administration due to promising initial results and a need for therapeutic treatments for NASH.",null,"1025216-57-2",false,"O[C@@H]1[C@@H](c2c(S(=O)(=O)C[C@]1(CCCC)CC)ccc(c2)N(C)C)c1cc(NC(=O)N[C@H]2[C@H](O)[C@@H](OCc3ccccc3)[C@@H]([C@H](O2)COS(=O)(=O)O)O)ccc1","ULVBLFBUTQMAGZ-RTNCXNSASA-N",805.969,"Ileal sodium/bile acid cotransporter inhibitor","Volixibat is a selective inhibitor of the apical sodium-dependent bile acid transporter (ASBT), a transmembrane protein primarily expressed by enterocytes of the ileum. ASBT is primarily responsible for the recirculation of bile acids and therefore for hepatic lipid and glucose metabolism. Inhibiting this enzyme results in a decrease of bile acids returning to the liver, which is helpful for the treatment of NASH as abnormal cholesterol metabolism and accumulation of free cholesterol in the liver have been implicated in its pathogenesis.",null,"Volixibat is an investigational drug that has not been approved for use in any conditions.","SLC10A2 inhibitor; ASBT inhibitor","Lipid regulating agents","Phase 3 terminated  (NCT02787304: Volixibat did not reduce the amount of fat in the liver, nor did it have any other beneficial effect on liver injury. Participants in the study generally tolerated the side effects of volixibat and, as in previous studies, the main side effect was diarrhoea. These results show that volixibat is not an effective treatment for people with fatty liver disease.)","Failed in clinical trials","2022-03-21"]
[333,"Sibutramine","Sibutramine","Chemical drug","DB01105","Sibutramine (trade name Meridia in the USA, Reductil in Europe and other countries), usually as sibutramide hydrochloride monohydrate, is an orally administered agent for the treatment of obesity. It is a centrally acting stimulant chemically related to amphetamines thus it is classified as a Schedule IV controlled substance in the United States. In October 2010, Sibutramine was withdrawn from Canadian and U.S. markets due to concerns that the drug increases the risk of heart attack and stroke in patients with a history of heart disease.","5210","106650-56-0",true,"C(CC(C)C)(N(C)C)C1(CCC1)c1ccc(cc1)Cl","UNAANXDKBXWMLN-UHFFFAOYSA-N",279.855,"Sodium-dependent noradrenaline transporter inhibitor; Sodium-dependent serotonin transporter inhibitor; Sodium-dependent dopamine transporter inhibitor","Sibutramine produces its therapeutic effects by inhibition of norepinephrine (NE), serotonin (5-hydroxytryptamine, 5-HT), and to a lesser extent, dopamine reuptake at the neuronal synapse. By inhibiting the reuptake of these neurotransmitters, sibutramine promotes a sense of satiety and decrease in appetite, thereby reducing food intake. Data from animal studies also suggest that sibutramine may also increase energy expenditure through thermogenic effects in both the basal and fed states, but this has not been confirmed in humans. Sibutramine and its major pharmacologically active metabolites (M1 and M2) do not act via release of monoamines.","Sibutramine is an orally administered agent for the treatment of obesity. Sibutramine exerts its pharmacological actions predominantly via its secondary (M1) and primary (M2) amine metabolites. The parent compound, sibutramine, is a potent inhibitor of serotonin and norepinephrine reuptake <i>in vivo</i>, but not <i>in vitro</i>. However, metabolites M1 and M2 inhibit the reuptake of these neurotransmitters both <i>in vitro</i> and <i>in vivo</i>. In human brain tissue, M1 and M2 also inhibit dopamine reuptake <i>in vitro</i>, but with ~3-fold lower potency than for the reuptake inhibition of serotonin or norepinephrine. Sibutramine, M1 and M2 exhibit no evidence of anticholinergic or antihistaminergic actions. In addition, receptor binding profiles show that sibutramine, M1 and M2 have low affinity for serotonin (5-HT<sub>1</sub>, 5-HT<sub>1A</sub>, 5-HT<sub>1B</sub>, 5-HT<sub>2A</sub>, 5-HT<sub>2C</sub>), norepinephrine (b, b1, b3, a1 and a2), dopamine (D1 and D2), benzodiazepine, and glutamate (NMDA) receptors. These compounds also lack monoamine oxidase inhibitory activity <i>in vitro</i> and <i>in vivo</i>.","For the treatment of obesity.",null,null,"Clinical trial on-going (IRCT201012275483N1)","Under clinical trials","2022-03-21"]
[334,"Siliphos-Selenium-Methionine-Alpha Lipoic Acid","IdB 1016","Miscellany",{"$nulls":4},false,{"$nulls":8},"Antiviral","Phase 4 completed  (NCT01650181)","Under clinical trials","2022-03-21"]
[335,"Silybum marianum",null,"Herbal medicine",null,null,"1548994",null,false,{"$nulls":9},"Phase 3 on-going (IRCT2017042824198N2)","Under clinical trials","2022-03-21"]
[336,"Silymarin","822i9lej7s; Cardui Mariae Fructus; Carduus Marianus; Carduus Marianus Preparation; Carduus Marianus Seed; Fruit of Silybum Marianum; Holy Thistle Seed; Lady's Thistle Seed; Mariana Mariana Seed; Mary's Thistle Seed; Milk Thistle Extract; Milk Thistle Fruit; Milk Thistle Seed; Milk Thistle Seed Extract; Milk Thistle Silymarin; Milkthistle Fruit (Silybum Marianum L. Gaertner); Saint Mary's Thistle Extract; Shuifeiji; Silybi Fructus; Silybi Mariani Fructus (Silybum Marianum L. Gaertner); Silybum Marianum Dry Fruit; Silybum Marianum Dry Fruit Extract; Silybum Marianum Extract; Silybum Marianum Fruit; Silybum Marianum Fruit Extract; Silybum Marianum Seed; Silybum Marianum Seed Extract","Biological drug","DB14375","Milk thistle is a plant/plant extract used in some OTC (over-the-counter) products. It is not an approved drug.","5213","65666-07-1",false,"O1C(C(Oc2c1cc(C1Oc3c(C(=O)C1O)c(O)cc(O)c3)cc2)CO)c1cc(OC)c(O)cc1","SEBFKMXJBCUCAI-UHFFFAOYSA-N",482.441,{"$nulls":5},"Antiviral; Antioxidant; Antifibrotic; Anti-inflammatory","Phase 3 on-going (IRCT20081110001444N6)","Under clinical trials","2022-03-21"]
[337,"Simtuzumab","SIM, GS-6624; GS-6624; Simtuzumab","Biological drug","DB12152","Simtuzumab has been used in trials studying the treatment and basic science of Myelofibrosis, Pancreatic Cancer, Colorectal Cancer, and Idiopathic Pulmonary Fibrosis.",null,"1318075-13-6",false,{"$nulls":7},"LOXL2; antibody","Anti-fibrosis; Anticancer agent; Immunomodulator;","Phase 2 terminated (In two phase 2b trials of patients with bridging fibrosis or compensated cirrhosis associated with nonalcoholic steatohepatitis, simtuzumab was ineffective in decreasing hepatic collagen content or hepatic venous pressure gradient, respectively. Clinicaltrials.govNCT01672866 and NCT01672879.)","Failed in clinical trials","2022-03-21"]
[338,"Sitagliptin","Sitagliptin","Chemical drug","DB01261","Sitagliptin is an oral dipeptidyl peptidase-4 (DPP-4) inhibitor used in conjunction with diet and exercise to improve glycemic control in patients with type 2 diabetes mellitus. The effect of this medication leads to glucose dependent increases in insulin and decreases in glucagon to improve control of blood sugar. Sitagliptin was granted FDA approval on October 16, 2006.","4369359","486460-32-6",true,"FC(F)(F)c1n2CCN(Cc2nn1)C(=O)C[C@H](N)Cc1c(F)cc(F)c(F)c1","MFFMDFFZMYYVKS-SECBINFHSA-N",407.318,"Dipeptidyl peptidase 4 inhibitor","Inhibition of DPP-4 by sitagliptin slows DPP-4 mediated inactivation of incretins like GLP-1 and GIP. Incretins are released throughout the day and upregulated in response to meals as part of glucose homeostasis. Reduced inhibition of incretins increase insulin synthesis and decrease glucagon release in a manner dependant on glucose concentrations. These effects lead to an overall increase in blood glucose control which is demonstrated by reduced glycosylated hemoglobin (HbA1c).","Sitagliptin inhibits DPP-4 which leads to increased levels of glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide(GIP), decreased levels of glucagon, and a stronger insulin response to glucose.","Sitagliptin is indicated for the management of glycemic control in type 2 diabetes mellitus along with diet and exercise.","DPP4 inhibitor","Antidiabetic drug","Phase 4 on-going (NCT05195944)","Under clinical trials","2022-03-21"]
[339,"Smectite",null,"Miscellany",null,null,"517273","12199-37-0",false,{"$nulls":9},"Clinical trial completed (NCT03614039)","Under clinical trials","2022-03-21"]
[340,"SNP-610",null,"Biological drug",{"$nulls":3},"206137-85-1",false,{"$nulls":9},"Phase 2 on-going (NCT03468556)","Under clinical trials","2022-03-21"]
[341,"SNP-612",null,"Miscellany",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (NCT03868566)","Under clinical trials","2022-03-21"]
[342,"Solithromycin","Solithromycin","Chemical drug","DB09308","Solithromycin is a ketolide antibiotic undergoing clinical development for the treatment of community-acquired pneumonia (CAP) and other infections.","25242512","760981-83-7",false,"F[C@]1(C(=O)[C@@H]([C@@H](O[C@@H]2O[C@@H](C[C@H](N(C)C)[C@H]2O)C)[C@](OC)(C[C@H](C(=O)[C@@H]([C@H]2N(C(=O)O[C@@]2([C@H](OC1=O)CC)C)CCCCn1nnc(c1)c1cc(N)ccc1)C)C)C)C)C","IXXFZUPTQVDPPK-ZAWHAJPISA-N",845.023,{"$nulls":3},"Investigated for the treatment of community-acquired pneumonia (CAP).","NF-kB inhibitor","Antibiotic drug, anti-inflammatory","Phase 2 completed  (NCT02510599)","Under clinical trials","2022-03-21"]
[343,"Somatropin","Growth hormone; Growth hormone (human); hGH; Human growth hormone; Recombinant human growth hormone; rhGH; Somatotropin (human); Somatotropin human; Somatotropin human growth hormone; Somatropin; Somatropin (rDNA origin); Somatropin (recombinant DNA origin); Somatropin [rDNA origin]; Somatropin recombinant; Somatropin(recombinant DNA origin)","Biological drug","DB00052","Human growth hormone (HGH), also known as somatotropin, is a peptide hormone that is synthesized and secreted by the somatotropic cells of the anterior pituitary gland. Growth hormone plays an essential role in growth regulation during childhood as well as other basal metabolic functions, muscle and fat mass regulation, blood glucose level regulation, and lipid regulation in both children and adults. Synthesized in a strain of _Escherichia coli_, recombinant HGH is a polypeptide hormone that contains 191 amino acid residues with a molecular weight of 22 kDa. It has an identical primary protein structure to endogenous human growth hormone. Recombinant HGH has been commercially available since 1985 after its development by Genentech.  was the first available recombinant HGH and was largely replaced by somatropin, another form of recombinant HGH. \r\n\r\nGrowth hormone therapy is approved for various disorders of growth hormone deficiency, growth failure, or short stature including Turner syndrome, chronic renal insufficiency before transplantation, Prader-Willi syndrome, a history of fetal growth restriction, short stature homeobox (SHOX) haploinsufficiency, Noonan syndrome, idiopathic short stature, and adult- or childhood-onset growth hormone deficiency. Recombinant growth hormone is available as a subcutaneous injection for children and adults under a wide variety of brand names.",null,"12629-01-5",true,{"$nulls":3},"Growth hormone receptor ligand; Prolactin receptor ligand","In conditions of growth failure, growth hormone deficiency, low body mass, and malnutrition, somatotropin treatment acts to mimic and restore the actions of endogenous growth hormone of stimulating linear bone growth, increasing bone mass, increasing muscle and reduced fat mass, and regulating blood glucose and lipid levels. Somatotropin mediates its effects both directly by somatotropin and indirectly by insulin-like growth factor-1 (IGF-1), which is upregulated by growth hormone. It binds to the human growth hormone receptor (GHR), which is a dimeric receptor expressed in target cells in the liver and cartilage. Upon binding of growth hormone, GHR dimerizes and interacts with Janus kinase 2 (JAK2), subsequently leading to tyrosine phosphorylation of JAK2 and the GH receptor. The signal transducer activator of transcription (STAT) pathway is initiated, where transcription factors such as STAT1, STAT3, and STAT5 are translocated into the nucleus to stimulate target gene transcription. \r\n\r\nAt the epiphysis or growth plate, growth hormone increases linear growth by promoting differentiation of prechondrocytes and expansion of osteoblasts. Growth hormone binding to its receptor in the liver and cartilage promotes the production of IGF-1, which acts on type 1 IGF receptors to also stimulate linear growth. In the liver, activated growth hormone receptor signalling leads to increased production of IGF binding protein-3 (IGFBP-3) and acid-labile subunit (ALS), which are proteins that bind to IGF-1 in a ternary complex to increase its half-life.","Somatotropin induces growth in nearly every tissue and organ in the body. It stimulates linear growth and cartilaginous growth of long bones. In children with short stature, growth hormone increases both the number and size of muscle cells. It also promotes the growth of internal organs, and it also increases red cell mass. By promoting nitrogen retention, growth hormone increases cellular protein synthesis. Growth hormone also retains potassium and phosphorus in the serum, which may be the result of cell growth. Growth hormone stimulates the synthesis of chondroitin sulfate and collagen and increases the urinary excretion of hydroxyproline. It has negligible effects on serum calcium levels. Although increased calcium excretion in the urine is observed, calcium absorption from the intestine is simultaneously enhanced. In end-stage renal disease, growth hormone was shown to improve several nutritional parameters, such as increases in serum insulin-like growth factor-I (IGF-I), serum albumin, and transferrin, as well as a reduction in blood urea nitrogen.\r\n\r\nThe metabolic effects of growth hormone are caused by the upregulation of insulin-like growth factor-1. Generally, growth hormone leads cells to enter an anabolic protein state with increased amino acid uptake, protein synthesis, and decreased catabolism of proteins. The diabetogenic effect of larger doses of growth hormone is well documented in the literature: somatotropin antagonizes insulin action _in vivo_, causing insulin resistance and glucose intolerance. It increases glucose production through gluconeogenesis and glycogenolysis from the liver and kidney  and suppresses glucose uptake in the adipose tissue. In mice, growth hormone increased mRNA expression of 2 major gluconeogenic genes, phosphoenolpyruvate carboxy-kinase and glucose-6-phosphatase. The risk for impaired glucose tolerance and reduced insulin sensitivity may be increased in susceptible patients, especially in those with risk factors for diabetes mellitus, such as obesity, Turner syndrome, or a family history of diabetes mellitus. The development of new-onset type 2 Diabetes Mellitus was observed in patients receiving somatotropin treatment. \r\n\r\nGrowth hormone stimulates lipolysis via activation of the hormone-sensitive lipase in the adipose tissue, thereby increasing circulating levels of free fatty acids and triglycerides in the plasma. It also leads to a reduction of fat stores and decreased serum levels of low-density lipoprotein (LDL) cholesterol. In contrast to the effects seen in the adipose tissue, growth hormone promotes cellular uptake of free fatty acids in skeletal muscle by increasing the activity of lipoprotein lipase. Growth hormone may cause hyperinsulinism following beta-cell compensation for insulin resistance; however, there is some evidence that growth hormone directly promotes beta-cell proliferation and glucose-stimulated insulin secretion.","Somatotropin is indicated for the treatment of pediatric patients who have growth failure due to an inadequate secretion of endogenous growth hormone, short stature associated with Turner syndrome, Prader-Willi syndrome (PWS), idiopathic short stature (ISS), short stature or growth failure in short stature homeobox-containing gene (SHOX) deficiency, and short stature born small for gestational age (SGA). It is indicated for the treatment of growth failure in children associated with chronic kidney disease up to the time of renal transplantation.\r\n\r\nIt is also indicated for adults with adult-onset growth hormone deficiency, either alone or associated with multiple hormone deficiencies (hypopituitarism), as a result of pituitary disease, hypothalamic disease, surgery, radiation therapy, or trauma. It is also used to treat childhood-onset growth hormone deficiency in adults due to congenital, genetic, acquired, or idiopathic causes.\r\n\r\nSomatotropin is indicated for the treatment of wasting or cachexia in patients with human immunodeficiency virus (HIV) who are receiving antiretroviral therapy to increase lean body mass and body weight and improve physical endurance.\r\n\r\nSomatotropin is indicated for the treatment of short bowel syndrome in adult patients receiving specialized nutritional support.","GHR ligand; PRLR ligand","Hormone replacement drug","Early phase 1 completed  (NCT02726542)","Under clinical trials","2022-03-21"]
[344,"Spironolactone","Spironolattone","Chemical drug","DB00421","Spironolactone is a potassium sparing diuretic like  that competitively inhibits mineralocorticoid receptors in the distal convoluted tubule to promote sodium and water excretion and potassium retention.. Spironolactone was originally developed purely for this ability before other pharmacodynamic properties of the drug were discovered. It is indicated to treat a number of conditions including heart failure, deem, hyperaldosteronism, adrenal hyperplasia, hypertension, and nephrotic syndrome. Off label uses of spironolactone involving its antiandrogenic activity include hirsutism, female pattern hair loss, and adult acne vulgaris. Spironolactone is also frequently used in medical gender transition.\r\n\r\nSpironolactone was developed in 1957, marketed in 1959, and approved by the FDA on January 21, 1960.","5833","52-01-7",true,"C[C@@]12[C@]3(CC[C@H]1[C@H]1[C@H](CC2)[C@]2(C)C(=CC(=O)CC2)C[C@H]1SC(=O)C)OC(=O)CC3","LXMSZDCAJNLERA-ZHYRCANASA-N",416.583,"Mineralocorticoid receptor antagonist; Androgen receptor antagonist; Progesterone receptor agonist; Glucocorticoid receptor antagonist; Cytochrome P450 11B2, mitochondrial antagonist; Steroid 17-alpha-hydroxylase/17,20 lyase antagonist; 3-oxo-5-alpha-ster","Spironolactone competitively inhibits aldosterone dependant sodium potassium exchange channels in the distal convoluted tubule. This action leads to increased sodium and water excretion, but more potassium retention. The increased excretion of water leads to diuretic and also antihypertensive effects.","Originally spironolactone was only studied for its potassium sparing diuretic effect. Spironolactone competitively inhibits mineralocorticoid receptors in the distal convoluted tubule to promote sodium and water excretion and potassium retention.. Inhibition of this receptor leads to increased renin and aldosterone levels.\r\n\r\nSpironolactone is structurally similar to progesterone and as a result is associated with progestogenic and antiandrogenic effects.","Spironolactone is indicated for the treatment of New York Heart Association Class III-IV heart failure, management of edema in cirrhotic adults not responsive to fluid and sodium restrictions, primary hyperaldosteronism short-term preoperatively, primary hyperaldosteronism long-term in patients with aldosterone producing adrenal adenomas that are not candidates for surgery or patients with bilarteral micro/macronodular adrenal hyperplasia, as an add-on therapy in hypertension, and in nephrotic syndrome when treatment of the disease as well as fluid and sodium restriction with other diuretics is inadequate.\r\n\r\nSpironolactone has antiandrogenic activity which leads to many of its off label uses. Spironolactone is used off label in the treatment of hirsutism, female pattern hair loss, and adult acne vulgaris.\r\n\r\nSpironolactone is also frequently used for its antiandrogenic effects in transgender female patients due to its low cost and reducing male-pattern hair growth.","AR antagonist; PGR agonist; NR1I2","Diuretic drug","Phase 1&2 on-going (NCT03576755)","Under clinical trials","2022-03-21"]
[345,"Spirulina","Arthrospira platensis; Arthrospira platensis whole; Oscillatoria platensis; Spirulina; Spirulina (arthrospira platensis); Spirulina platensis; Spirulina platensis whole","Biological drug","DB14744",null,"91864513","1087037-76-0",false,"O([C@@H](/C=C/C(=C/C=C/C(=C/C=C/C(=C/C=C/C=C(/C=C/C=C(/C=C/C1=C(C)C[C@H](CC1(C)C)O)\\C)\\C)/C)/C)/C)C(C)(C)O)[C@H]1[C@H](O)[C@H](O)[C@H]([C@@H](O1)C)O","MUCOHWBULSBLLZ-ALZSAHPVSA-N",731.027,{"$nulls":5},"Prebiotics","Clinical trial on-going (IRCT20200304046692N1)","Under clinical trials","2022-03-21"]
[346,"SponserR",null,"Miscellany",{"$nulls":4},false,{"$nulls":9},"Clinical trial completed (NCT00870077: WPS improves hepatic steatosis and plasma lipid profiles in obese non diabetic patients, without adverse effects on glucose tolerance or creatinine clearance.)","Under clinical trials","2022-03-21"]
[347,"SPP-1",null,"Chemical drug",null,null,"139063835 ","26063-22-9",false,"C(=C)C","QQONPFPTGQHPMA-UHFFFAOYSA-N",42.081,{"$nulls":6},"Phase 2 on-going (NCT04308980)","Under clinical trials","2022-03-21"]
[348,"Stanol",null,"Biological extract",{"$nulls":3},"127121-08-8",false,{"$nulls":9},"Clinical trial on-going (NCT03627819)","Under clinical trials","2022-03-21"]
[349,"Statins",null,"Miscellany",{"$nulls":4},false,{"$nulls":9},"Phase 2 on-going (NCT04679376)","Under clinical trials","2022-03-21"]
[350,"Stevia","Stevia Dry Leaves","Chemical drug","DB15136","Rebaudioside A is under investigation in clinical trial NCT03510624 (Acute Effect of Rebaudioside A on Glucose Excursion During an Oral Glucose Tolerance Test in Type 2 Diabetes Mellitus).","6918840","58543-16-1",false,"C[C@]12[C@H]3[C@]4(C[C@@](CC3)(C(=C)C4)O[C@H]3[C@H](O[C@@H]4O[C@H](CO)[C@H]([C@@H]([C@H]4O)O)O)[C@@H](O[C@@H]4O[C@H](CO)[C@H]([C@@H]([C@H]4O)O)O)[C@@H]([C@H](O3)CO)O)CC[C@@H]1[C@@](C(=O)O[C@@H]1O[C@H](CO)[C@H]([C@@H]([C@H]1O)O)O)(C)CCC2","HELXLJCILKEWJH-NCGAPWICSA-N",967.021,{"$nulls":6},"Phase 3 on-going (IRCT20181119041701N1)","Under clinical trials","2022-03-21"]
[351,"Stronger Neo-Minophagen C","SNMC","Traditional medicine",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (JPRN-UMIN000012336)","Under clinical trials","2022-03-21"]
[352,"Sublimated mares milk","Sublimated mare's milk","Supplement",{"$nulls":4},false,{"$nulls":9},"Clinical trial completed (NCT03664596:  The study showed benefits of the fast weight loss method improving in steatosis/fibrosis and biochemical/metabolic outcomes in patients with severe NASH and T2D.)","Under clinical trials","2022-03-21"]
[353,"Sulfonylurea",null,"Chemical drug",null,null,"140987867",null,false,"S(=O)(=O)=NC(=O)N.S(=O)(=O)=NC(=O)N","YDMLDADNVSAMLD-UHFFFAOYSA-N",244.21,{"$nulls":6},"Phase 4 completed  (NCT02649465)","Under clinical trials","2022-03-21"]
[354,"Sulforaphane","(-)-sulforaphane; (R)-sulforaphane; 4-methylsulfinylbutyl isothiocyanate","Chemical drug","DB12422","Sulforaphane is under investigation for the treatment of Autism Spectrum Disorder. It is a naturally occurring isothiocyanate found in high concentration in a variety of broccoli.","5350","4478-93-7",false,"C(CCN=C=S)CS(=O)C","SUVMJBTUFCVSAD-UHFFFAOYSA-N",177.294,{"$nulls":5},"Anticarcinogenic, Antineoplastic, Antioxidant","Clinical trial on-going (NCT04364360)","Under clinical trials","2022-03-21"]
[355,"Sumac","Toxicodendron vernicifluum (Stokes) F. A. Barkl.","Biological extract",{"$nulls":3},"93686-19-2",false,{"$nulls":9},"Clinical trial on-going (IRCT20191009045043N1)","Under clinical trials","2022-03-21"]
[356,"Symbiotic",null,"Biological drug",{"$nulls":4},false,{"$nulls":9},"Phase 2&3 on-going (NCT02530138)","Under clinical trials","2022-03-21"]
[357,"Synbiotic","Synbiotics","Supplement",{"$nulls":3},"1678556-56-3, 943828-05-5",false,{"$nulls":9},"Clinical trial on-going (SLCTR/2018/042)","Under clinical trials","2022-03-21"]
[358,"TAF","Tenofovir alafenamide","Chemical drug","DB09299","Tenofovir alafenamide is a novel  prodrug developed in order to improve renal safety when compared to the counterpart . Both of these prodrugs were first created to cover the polar phosphonic acid group on tenofovir by using a novel oxycarbonyloxymethyl linkers to improve the oral bioavailability and intestinal diffusion. Tenofovir alafenamide is an alanine ester form characterized for presenting low systemic levels but high intracellular concentration. It has been reported to produce a large antiviral efficacy at doses ten times lower than tenofovir disoproxil. Tenofovir alafenamide is indicated to treat chronic hepatitis B, treat HIV-1, and prevent HIV-1 infections.\r\n\r\nTenofovir alafenamide was developed by Gilead Sciences Inc and granted FDA approval on 5 November 2015.",null,null,true,"S1C[C@H](O[C@H]1CO)n1cc(F)c(nc1=O)N.[P@@](=O)(Oc1ccccc1)(N[C@@H](C)C(=O)OC(C)C)CO[C@@H](Cn1c2ncnc(N)c2nc1)C.N(c1c(cc(cc1C)/C=C/C#N)C)c1nc(Nc2ccc(cc2)C#N)ncc1","GHWBYIZAYFIRPA-PPEAAZTNSA-N",1090.153,"Reverse transcriptase/RNaseH inhibitor; Reverse transcriptase inhibitor; DNA polymerase inhibitor","Tenofovir alafenamide presents 91% lower plasma concentration with an intracellular presence of about 20-fold higher when compared to . This is due to its prolonged systemic exposure and its higher intracellular accumulation of the active metabolite tenofovir diphosphate.\r\n\r\nTenofovir alafenamide accumulates more in peripheral blood mononuclear cells compared to red blood cells.\r\n\r\nOnce activated, tenofovir acts with different mechanisms including the inhibition of viral polymerase, causing chain termination and the inhibition of viral synthesis. To know more about the specific mechanism of action of the active form, please visit the drug entry of .","Tenofovir alafenamide has been shown to be a potent inhibitor of hepatitis B viral replication.\r\n\r\nTenofovir alafenamide presents a better renal tolerance when compared with the counterpart . This improved safety profile seems to be related to a lower plasma concentration of tenofovir.\r\n\r\nIn clinical trials, tenofovir alafenamide was shown to present 5-fold more potent antiviral activity against HIV-1 when compared to tenofovir disoproxil.","Tenofovir alafenamide is indicated for the treatment of chronic hepatitis B in adult patients with compensated liver disease.\r\n\r\nIn combination with  and other antiretrovirals, it is indicated for the treatment of HIV-1 infection in adolescent and adult patients with a weight higher than 35 kg. This combination is also indicated to prevent HIV-1 infections in high risk adolescent and adult patients, excluding patients at risk from receptive vaginal sex. When combined with antiretrovirals other than protease inhibitors that require a CYP3A inhibitor, it can be used to treat pediatric patients weighing 25-35 kg.\r\n\r\nIn the combination product with emtricitabine and , tenofovir alafenamide is considered as a complete regimen for the treatment of HIV-1 infection in treatment-naive patients or in patients virologically suppressed for at least 3 months with no history of treatment failure. \r\n\r\nAdditionally, the combination product including , , emtricitabine and tenofovir alafenamide and the combination product including emtricitabine,  and tenofovir alafenamide can be used in the treatment of HIV-1 infection in patients older than 12 years with no previous antiretroviral therapy history or who are virologically suppressed for at least 6 months with no history of treatment failure.\r\n\r\nThe combination product including , cobicistat, emtricitabine, and tenofovir alafenamide is indicated for the treatment of HIV-1 infection in adults without prior antiretroviral therapy or in patients virologically suppressed for 6 months and no reported resistance to darunavir or tenofovir.",null,null,"Phase 4 on-going (ChiCTR1900023153)","Under clinical trials","2022-03-21"]
[359,"Taraxacum officinale extract",null,"Biological extract",{"$nulls":4},false,{"$nulls":9},"Phase 2&3 on-going (IRCT20170430033730N2)","Under clinical trials","2022-03-21"]
[360,"Telmisartan","4'-((1,4'-dimethyl-2'-propyl(2,6'-bi-1H-benzimidazol)-1'-yl)methyl)-(1,1'-biphenyl)-2-carboxylic acid; 4'-((4-methyl-6-(1-methyl-2-benzimidazolyl)-2-propyl-1-benzimidazolyl)methyl)-2-biphenylcarboxylic acid; 4'-[(1,4'-dimethyl-2'propyl[2,6'-bi-1H-benzimidazol]-1'-yl)methyl]-[1,1'-biphenyl]-2-carboxylic acid; 4'-[(1,7'-dimethyl-2'-propyl-1H,3'H-2,5'-bibenzimidazol-3'-yl)methyl]biphenyl-2-carboxylic acid; Telmisartan","Chemical drug","DB00966","Telmisartan is an angiotensin II receptor antagonist (ARB) used in the management of hypertension. Generally, angiotensin II receptor blockers (ARBs) such as telmisartan bind to the angiotensin II type 1 (AT1) receptors with high affinity, causing inhibition of the action of angiotensin II on vascular smooth muscle, ultimately leading to a reduction in arterial blood pressure. Recent studies suggest that telmisartan may also have PPAR-gamma agonistic properties that could potentially confer beneficial metabolic effects.","65999","144701-48-4",true,"CCCC1=NC2=C(N1CC3=CC=C(C4=CC=CC=C4C(O)=O)C=C3)C=C(C5=NC6=CC=CC=C6N5C)C=C2C","RMMXLENWKUUMAY-UHFFFAOYSA-N",514.629,"Type-1 angiotensin II receptor antagonist; Peroxisome proliferator-activated receptor gamma partial agonist","Telmisartan interferes with the binding of angiotensin II to the angiotensin II AT<sub>1</sub>-receptor by binding reversibly and selectively to the receptors in vascular smooth muscle and the adrenal gland. As angiotensin II is a vasoconstrictor, which also stimulates the synthesis and release of aldosterone, blockage of its effects results in decreases in systemic vascular resistance. Telmisartan does not inhibit the angiotensin converting enzyme, other hormone receptors, or ion channels. Studies also suggest that telmisartan is a partial agonist of PPAR&gamma;, which is an established target for antidiabetic drugs. This suggests that telmisartan can improve carbohydrate and lipid metabolism, as well as control insulin resistance without causing the side effects that are associated with full PPAR&gamma; activators.","Telmisartan is an orally active nonpeptide angiotensin II antagonist that acts on the AT<sub>1</sub> receptor subtype. It has the highest affinity for the AT<sub>1</sub> receptor among commercially available ARBS and has minimal affinity for the AT<sub>2</sub> receptor. New studies suggest that telmisartan may also have PPAR&gamma; agonistic properties that could potentially confer beneficial metabolic effects, as PPAR&gamma; is a nuclear receptor that regulates specific gene transcription, and whose target genes are involved in the regulation of glucose and lipid metabolism, as well as anti-inflammatory responses. This observation is currently being explored in clinical trials. Angiotensin II is formed from angiotensin I in a reaction catalyzed by angiotensin-converting enzyme (ACE, kininase II). Angiotensin II is the principal pressor agent of the renin-angiotensin system, with effects that include vasoconstriction, stimulation of synthesis and release of aldosterone, cardiac stimulation, and renal reabsorption of sodium. Telmisartan works by blocking the vasoconstrictor and aldosterone secretory effects of angiotensin II.","Used alone or in combination with other classes of antihypertensives for the treatment of hypertension. Also used in the treatment of diabetic nephropathy in hypertensive patients with type 2 diabetes mellitus, as well as the treatment of congestive heart failure (only in patients who cannot tolerate ACE inhibitors).","PPARG partial agonist","Improve insulin resistance","Clinical trial on-going (NCT02213224)","Under clinical trials","2022-03-21"]
[361,"Teneligliptin","Teneligliptin","Chemical drug","DB11950","Teneligliptin has been investigated for the treatment of Type 2 Diabetes Mellitus.","11949652","760937-92-6",false,"Cc1cc(n(n1)c1ccccc1)N1CCN(CC1)[C@H]1C[C@H](NC1)C(=O)N1CCSC1","WGRQANOPCQRCME-PMACEKPBSA-N",426.59,{"$nulls":4},"DPP4 inhibitor",null,"Clinical trial on-going (JPRN-UMIN000013048)","Under clinical trials","2022-03-21"]
[362,"TERN-101",null,"Chemical drug","DB16045","TERN-101 is under investigation in clinical trial NCT04328077 (LIFT Study: A Safety, Tolerability, Efficacy, and Pharmacokinetics Study of TERN-101 in Subjects With Non-cirrhotic Non-alcoholic Steatohepatitis (NASH)).","25204767","1103500-20-4",false,"C(OC1CCN(CC1)c1cc2c(cc1)c(cn2C)C(=O)O)c1c(noc1C1CC1)c1c(Cl)cccc1Cl","RPVDFHPBGBMWID-UHFFFAOYSA-N",540.447,{"$nulls":4},"FXR agonist","Enhance lipid metabolism","Phase 2 completed  (NCT04328077)","Under clinical trials","2022-03-21"]
[363,"Tesamorelin","GHRH(1-44); N-[(3E)-1-oxo-3-hexenyl]Somatoliberin (human pancreatic islet); Tesamorelin","Chemical drug","DB08869","Tesamorelin is a stabilized synthetic peptide analogue of the hypothalamic peptide, Growth Hormone Releasing Hormone (GHRH) indicated for the reduction of excess abdominal fat in HIV-infected patients with lipodystrophy. Lipodystrophy is a metabolic condition characterized by insulin resistance, fat redistribution, and hyperlipidemia associated with antiretroviral therapy for HIV infection.","16137828","218949-48-5",true,"S(CC[C@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)CNC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)C/C=C/CC)Cc1ccc(O)cc1)C)CC(=O)O)C)[C@H](CC)C)Cc1ccccc1)[C@H](O)C)CC(=O)N)CO)Cc1ccc(O)cc1)CCCNC(=N)N)CCCCN)C(C)C)CC(C)C)CCC(=O)N)CC(C)C)CO)C)CCCNC(=N)N)CCCCN)CC(C)C)CC(C)C)CCC(=O)N)CC(=O)O)[C@H](CC)C)C(=O)N[C@H](C(=O)N[C@@H](CCCNC(=N)N)C(=O)N[C@@H](CCC(=O)N)C(=O)N[C@@H](CCC(=O)N)C(=O)NCC(=O)N[C@@H](CCC(=O)O)C(=O)N[C@H](C(=O)N[C@H](C(=O)N[C@@H](CCC(=O)N)C(=O)N[C@@H](CCC(=O)O)C(=O)N[C@@H](CCCNC(=N)N)C(=O)NCC(=O)N[C@H](C(=O)N[C@@H](CCCNC(=N)N)C(=O)N[C@H](C(=O)N[C@@H](CCCNC(=N)N)C(=O)N[C@@H](CC(C)C)C(=O)N)C)C)CC(=O)N)CO)CO)C","QBEPNUQJQWDYKU-BMGKTWPMSA-N",5135.863,"Growth hormone-releasing hormone receptor binder","By acting on the pituitary cells in the brain, tesamorelin stimulates production and release of the endogenous hormone (hGRF). Tesamorelin therapy predisposes the patient to glucose intolerance and can also increase the risk of type 2 diabetes, so the drug is contraindicated in pregnancy.","Tesamorelin stimulates growth hormone secretion, and subsequently increases IGF-1 and IGFBP-3 levels.","Tesamorelin acetate is a synthetic analogue of human hypothalamic Growth Hormone Releasing Factor (hGRF) indicated to induce and maintain a reduction of excess abdominal fat in HIV-infected patients with lipodystrophy.","GHRHR agonist;GHRHR binder","Growth stimulant","Phase 2 on-going (NCT03375788)","Under clinical trials","2022-03-21"]
[364,"Testosterone Undecanoate","Testosterone undecanoate; Testosterone undeconate; Testosterone undecylate","Chemical drug","DB13946","Testosterone undecanoate is the ester prodrug of testosterone and has a midchain fatty acid at the 17Beta position.   It is available as an intramuscular injection and as an oral capsule, and is indicated for treatment of testosterone deficiency.   It should be noted that testosterone undecanoate is only indicated for treatment of hypogonadal conditions with structural or genetic etiologies and should not be used to manage \"age-related hypogonadism\".","65157","5949-44-0",true,"C[C@@]12[C@@H]3[C@H]([C@H]4[C@@](CC3)(C)[C@H](CC4)OC(=O)CCCCCCCCCC)CCC1=CC(=O)CC2","UDSFVOAUHKGBEK-CNQKSJKFSA-N",456.711,"Androgen receptor agonist; Estrogen receptor alpha; Mineralocorticoid receptor","Testosterone is produced by Leydig cells and exerts it's effects by binding to androgen receptors throughout the body.   Testosterone affects the voice, genitalia, mood, and influences muscle growth and protein expression.   Accordingly, males with low levels of testosterone often experience decreased libido, fatigue, mood changes and dysphoria.   Exogenous sources of testosterone are designed to mimic the effects of endogenous testosterone.","Testosterone plays a key role in male sexual differentiation and is involved in regulation of hematopoiesis, body composition, and bone metabolism.  As a result, testosterone replacement therapy in males with hypogonadism can result in improved sexual function, increased lean body mass, bone density, erythropoiesis, prostate size, and changes in lipid profiles.","Testosterone undecanoate is indicated for replacement therapy in adult males with conditions that are linked with an absence or deficiency in endogenous testosterone production.","AR agonist","Hormone replacement drug","Phase 3 on-going (ACTRN12619000701123)","Under clinical trials","2022-03-21"]
[365,"TEV-45478",null,"Biological drug",{"$nulls":4},false,{"$nulls":3},"FXR",{"$nulls":5},"Phase 2 withdrawn (NCT02769091:  Business decision)","Under clinical trials","2022-03-21"]
[366,"Thiazolidinediones","TZD; Thiazolidinedione","Chemical drug","DB11898","Thiazolidinedione has been investigated for the treatment of Type 2 Diabetes, Diabetes Mellitus, and DIABETES MELLITUS, TYPE 2.","5437","2295-31-0",false,"O=C1NC(=O)SC1","ZOBPZXTWZATXDG-UHFFFAOYSA-N",117.129,{"$nulls":6},"Phase 4 on-going (NCT03646292)","Under clinical trials","2022-03-21"]
[367,"Thioctic acid","(+)-alpha-Lipoic acid; (R)-(+)-Lipoate; (R)-(+)-lipoic acid; (R)-1,2-Dithiolane-3-pentanoic acid; (R)-1,2-dithiolane-3-valeric acid; (R)-6,8-thioctic acid; (R)-lipoic acid; Alpha lipoic acid; alpha-Lipoic acid; D-thioctic acid; Lipoic acid; R-(+)-thioctic acid; R-alpha-lipoic acid; Thioctic acid; Thioctic acid D-form; α-lipoic acid","Chemical drug","DB00166","A vitamin-like antioxidant.","864","1077-28-7",true,"C(CCCC(=O)O)C1CCSS1","AGBQKNBQESQNJD-UHFFFAOYSA-N",206.332,"Lipoyltransferase 1, mitochondrial; Lipoyl synthase, mitochondrial; Sodium-dependent multivitamin transporter","Lipoic Acid is generally involved in oxidative decarboxylations of keto acids and is presented as a growth factor for some organisms. Lipoic acid exists as two enantiomers, the R-enantiomer and the S-enantiomer. Normally only the R-enantiomer of an amino acid is biologically active, but for lipoic acid the S-enantiomer assists in the reduction of the R-enantiomer when a racemic mixture is given. Some recent studies have suggested that the S-enantiomer in fact has an inhibiting effect on the R-enantiomer, reducing its biological activity substantially and actually adding to oxidative stress rather than reducing it. Furthermore, the S-enantiomer has been found to reduce the expression of GLUT-4s in cells, responsible for glucose uptake, and hence reduce insulin sensitivity.","Lipoic acid (or &alpha;-lipoic acid) is able to pass the blood-brain barrier and is putatively used for detoxification of mercury attached to the brain cells. It can mobilise bound mercury into the blood stream as it is a mercaptan (sulfur compound which readily binds to the mercury). In the blood stream, another chelator such as dimercaptosuccinic acid (DMSA) or methylsulfonylmethane (MSM) is used to transfer mercury safely into the urine for excretion. Neither DMSA nor MSM can cross the blood-brain barrier, which is why both lipoic acid and DMSA are used. It is hypothesized that this treatment-along with carnitine, dimethylglycine (DMG), Vitamin B6, folic acid, and magnesium&mdash;could be used to treat autism and amalgam poisoning. In this hypothesis, the reason why autism is difficult to treat is that mercury is attached to the brain cells and most medicines and vitamin supplements do not penetrate the blood-brain barrier. However, &alpha;-lipoic acid and perhaps vitamin B12 could making it possible for other chelators to remove mercury safely out of the body and could perhaps one day be used as a treatment for autism. Because lipoic acid is related to cellular uptake of glucose and it is both soluble in water and fat, it is being used for treatment in diabetes. It may be helpful for people with Alzheimer's disease or Parkinson's disease.","For nutritional supplementation, also for treating dietary shortage or imbalance.",null,"Vitamin source drug","Phase 4 terminated  (NCT01406704: Because of withdrawal of Avandia sale due to its risks outweigh its benefits)","Under clinical trials","2022-03-21"]
[368,"Thriphala choorna","Trifolium pratense","Herbal medicine",{"$nulls":4},false,{"$nulls":9},"Phase 1&2 on-going (CTRI/2019/07/020021)","Under clinical trials","2022-03-21"]
[369,"Thyme","Garden thyme","Biological drug","DB10983","Thyme allergenic extract is used in allergenic testing.","6850745","8007-46-3",true,"OC1(C2C(C2)(CC1)C(C)C)C.OC(C1CCC(=CC1)C)(C)C.OC(CCC=C(C)C)(C)C=C.Oc1c(C(C)C)ccc(c1)C.C(c1ccc(cc1)C)(C)C","VOHUWOUGEDDNDQ-UHFFFAOYSA-N",747.202,{"$nulls":5},"Antibiotic drug, antifungal drug","Clinical trial completed (NCT02983669)","Under clinical trials","2022-03-21"]
[370,"Tirzepatide","Tirzepatide","Biological drug","DB15171","Tirzepatide is under investigation in clinical trial NCT03311724 (A Study of Tirzepatide (LY3298176) in Participants With Type 2 Diabetes).",null,"2023788-19-2",false,{"$nulls":7},"GIP agonist; GLP-1 receptor agonist","Improve insulin resistance","Phase 3 completed (In patients with type 2 diabetes, tirzepatide was noninferior and superior to semaglutide with respect to the mean change in the glycated hemoglobin level from baseline to 40 weeks. (Funded by Eli Lilly; SURPASS-2 ClinicalTrials.gov number, NCT03987919.).)","Under clinical trials","2022-03-21"]
[371,"Tocotrienol",null,"Chemical drug","DB12647","Tocotrienol has been investigated for the treatment of Cholesterol Lowering.","9929901","6829-55-6",false,"C(CC=C(CCC=C(CCC=C(C)C)C)C)C1(C)Oc2c(CC1)cc(cc2)O","GJJVAFUKOBZPCB-UHFFFAOYSA-N",382.588,{"$nulls":4},"HMG-CoA inhibitor","Enhance lipid metabolism","Phase 2 on-going (NCT04704063)","Under clinical trials","2022-03-21"]
[372,"Tofogliflozin","Tofogliflozin; Tofogliflozin anhydrous","Chemical drug","DB11824","Tofogliflozin has been used in trials studying the treatment and prevention of Diabetes Mellitus Type 2.","46908929","903565-83-3",false,"O[C@H]1[C@]2(c3c(CO2)ccc(c3)Cc2ccc(cc2)CC)O[C@@H]([C@H]([C@@H]1O)O)CO","VWVKUNOPTJGDOB-BDHVOXNPSA-N",386.444,{"$nulls":4},"SGLT2 inhibitor","Improve insulin resistance","Clinical trial completed (JPRN-jRCTs031190040: SGLT2 inhibitors tended to reduce liver fat content and liver hardness compared to the control drug metformin, but the number of samples was small, individual differences were large, and statistically significant differences were not observed. Regarding safety, no serious adverse events were observed, and there was no need to change other therapeutic agents.)","Under clinical trials","2022-03-21"]
[373,"Tranilast","N-(3,4-Dimethoxycinnamoyl)anthranilic acid","Chemical drug","DB07615","Tranilast is an antiallergic drug developed by Kissei Pharmaceuticals. In 1982, it was approved in Japan and South Korea for the management of bronchial asthma. Indications for keloid and hypertrophic scar were added in 1993. It has been used for the treatment of allergic disorders such as asthma, allergic rhinitis and atopic dermatitis.","5282230","53902-12-8",false,"N(C(=O)C=Cc1cc(OC)c(cc1)OC)c1c(C(=O)O)cccc1","NZHGWWWHIYHZNX-UHFFFAOYSA-N",327.336,"Hematopoietic prostaglandin D synthase inhibitor",null,null,"For the treatment of bronchial asthma, keloid and hypertrophic scar, and allergic disorders such as asthma, allergic rhinitis and atopic dermatitis.","HPGDS inhibitor",null,"Clinical trial on-going (JPRN-UMIN000001670)","Under clinical trials","2022-03-21"]
[374,"Trehalose","Cabaletta","Chemical drug","DB12310","Cabaletta has been used in trials studying the treatment of Oculopharyngeal Muscular Dystrophy.","7427","99-20-7",false,"O([C@H]1O[C@H](CO)[C@H]([C@@H]([C@H]1O)O)O)[C@H]1O[C@H](CO)[C@H]([C@@H]([C@H]1O)O)O","HDTRYLNUVZCQOY-LIZSDCNHSA-N",342.297,{"$nulls":6},"Clinical trial completed (NCT03738358)","Under clinical trials","2022-03-21"]
[375,"Trikatu Kajjali Tablet","Sunthi; Marich; Pippali; Kajjali","Traditional medicine",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (CTRI/2020/02/023426)","Under clinical trials","2022-03-21"]
[376,"Trimada Kajjali Tablet",null,"Traditional medicine",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (CTRI/2020/02/023426)","Under clinical trials","2022-03-21"]
[377,"TRO19622",null,"Chemical drug","DB05185","TRO19622 is a cholesterol-like small molecule that has demonstrated a remarkable neuroprotective profile in a battery of both in vitro and in vivo preclinical models. For example, it has demonstrated the ability to prevent neurodegeneration, enhance nerve function and accelerate neuroregeneration following nerve trauma.","9930827","66538-08-7",false,"C[C@]12[C@H]([C@H]3[C@H](CC2)[C@]2(C)C(=C/C(=N/O)/CC2)CC3)CC[C@@H]1[C@@H](CCCC(C)C)C","QNTASHOAVRSLMD-SIWSWZRQSA-N",399.663,null,"TRO19622 interacts with a physiologically relevant target: the mitochondrial permeability transition pore (mPTP).\r\nMitochondria are central mediators of cell death and are implicated in most if not all neurodegenerative diseases regardless of the initiating factor: genetic mutations,\r\nexcitotoxicity, reactive oxygen species, ischemia, chemical toxicity, etc. Mitochondria play diverse roles in all cells.\r\nIn neurons, especially near synaptic sites, mitochondria are essential calcium-buffering organelles in areas where membrane excitability leads to large influx of calcium through calcium channels. Mitochondria also produce the ATP necessary for microtubule-based axoplasmic transport and maintaining the activity of ion and nutrient transporters. If a neuron fails to establish or maintain its functional role, mitochondria are responsible for eliminating it\r\nby releasing apoptotic factors. TRO19622, by interacting with protein components of the mPTP, prevents the release of\r\nthese apoptotic factors and therefore protects the neuron. This mechanism of action may lead to a general neuroprotective activity with utility in other therapeutic indications.\r",null,"Investigated for use/treatment in neurologic disorders.","mPTP",null,"Phase 2 completed  (NCT00666016)","Under clinical trials","2022-03-21"]
[378,"Troglitazone","Troglitazone","Chemical drug","DB00197","Troglitazone was withdrawn in 2000 due to risk of hepatotoxicity. It was superseded by  and .","5591","97322-87-7",true,"CC(C(C)=C1OC(COC2=CC=C(C=C2)CC(C(N3)=O)SC3=O)(C)CCC1=C4C)=C4O","GXPHKUHSUJUWKP-UHFFFAOYSA-N",441.549,"Peroxisome proliferator-activated receptor gamma agonist; Long-chain-fatty-acid--CoA ligase 4 inhibitor; Plasminogen activator inhibitor 1 antagonist; Equilibrative nucleoside transporter 1 inhibitor; Estrogen-related receptor gamma inverse agonist; Stero","Troglitazone is a thiazolidinedione antidiabetic agent that lowers blood glucose by improving target cell response to insulin. It has a unique mechanism of action that is dependent on the presence of insulin for activity. Troglitazone decreases hepatic glucose output and increases insulin dependent glucose disposal in skeletal muscle. Its mechanism of action is thought to involve binding to nuclear receptors (PPAR) that regulate the transcription of a number of insulin responsive genes critical for the control of glucose and lipid metabolism. Troglitazone is a ligand to both PPARα and PPARγ, with a highter affinity for PPARγ. The drug also contains an α-tocopheroyl moiety, potentially giving it vitamin E-like activity. Troglitazone has been shown to reduce inflammation, and is associated with a decrase in nuclear factor kappa-B (NF-κB) and a concomitant increase in its inhibitor (IκB). Unlike sulfonylureas, troglitazone is not an insulin secretagogue.","Troglitazone is an oral antihyperglycemic agent which acts primarily by decreasing insulin resistance. Troglitazone is used in the management of type II diabetes (noninsulin-dependent diabetes mellitus (NIDDM) also known as adult-onset diabetes). It improves sensitivity to insulin in muscle and adipose tissue and inhibits hepatic gluconeogenesis. Troglitazone is not chemically or functionally related to either the sulfonylureas, the biguanides, or the g-glucosidase inhibitors. Troglitazone may be used concomitantly with a sulfonylurea or insulin to improve glycemic control.","For the treatment of Type II diabetes mellitus. It is used alone or in combination with a sulfonylurea, metformin, or insulin as an adjunct to diet and exercise.","PPARG agonist; PPARD; PPARA","Improve insulin resistance",null,"Under investigation","2022-03-21"]
[379,"Tropifexor","LJN452","Chemical drug","DB16343","Tropifexor is under investigation in clinical trial NCT02516605 (A Multi-part, Double Blind Study to Assess Safety, Tolerability and Efficacy of Tropifexor (LJN452) in PBC Patients).","121418176","1383816-29-2",false,"O(Cc1c(noc1C1CC1)c1c(OC(F)(F)F)cccc1)[C@@H]1C[C@H]2N([C@@H](C1)CC2)c1nc2c(s1)cc(cc2F)C(=O)O","VYLOOGHLKSNNEK-PIIMJCKOSA-N",603.594,"Bile acid receptor agonist&binder",{"$nulls":3},"FXR agonist","Enhance lipid metabolism","Phase 2 terminated  (NCT04147195: Sponsor Decision)","Under clinical trials","2022-03-21"]
[380,"TVB-2640","FASN Inhibitor","Chemical drug",null,null,"66548316","1987917-56-5",false,"O=C(N1CCC(CC1)c1ccc(cc1)C#N)c1c(cc(C2CCC2)c(c1)c1nc([nH]n1)C)C","BBGOSBDSLYHMRA-UHFFFAOYSA-N",439.563,{"$nulls":4},"FASN inhibitor","Enhance lipid metabolism; Anticancer agent","Phase 2 on-going (NCT04906421); Phase 2 completed  (NCT03938246: TVB-2640 significantly reduced liver fat and improved biochemical, inflammatory, and fibrotic biomarkers after 12 weeks, in a dose-dependent manner in patients with nonalcoholic steatohepatitis. )","Under clinical trials","2022-03-21"]
[381,"Ursodeoxycholic acid","(3alpha,5beta,7beta)-3,7-dihydroxycholan-24-oic acid; (3α,5β,7β)-3,7-dihydroxycholan-24-oic acid; 3alpha,7beta-Dihydroxy-5beta-cholan-24-oic acid; UDCA; Ursodeoxycholate; Ursodeoxycholic acid; Ursodiol","Chemical drug","DB01586","Ursodeoxycholic acid is an epimer of . It is a mammalian bile acid found first in the bear and is apparently either a precursor or a product of chenodeoxycholate. Its administration changes the composition of bile and may dissolve gallstones. It is used as a cholagogue and choleretic.","31401","128-13-2",true,"C[C@]12[C@H]([C@H]3[C@H](CC2)[C@]2(C)[C@H](C[C@@H]3O)C[C@@H](CC2)O)CC[C@@H]1[C@@H](CCC(=O)O)C","RUDATBOHQWOJDD-UZVSRGJWSA-N",392.58,"Aldo-keto reductase family 1 member C2 inducer; Bile acid receptor","Ursodeoxycholic acid reduces elevated liver enzyme levels by facilitating bile flow through the liver and protecting liver cells.\r\nThe main mechanism if anticholelithic. Although the exact process of ursodiol's anticholelithic action is not completely understood, it is thought that the drug is concentrated in bile and decreases biliary cholesterol by suppressing hepatic synthesis and secretion of cholesterol and by inhibiting its intestinal absorption. The reduced cholesterol saturation permits the gradual solubilization of cholesterol from gallstones, resulting in their eventual dissolution.\r\n\r\n\r","Ursodiol (commonly known as ursodeoxycholic acid) is a product of metabolism of bacteria in the intestine.  It is considered a secondary bile acid. The other type of bile acid, primary bile acids, are produced hepatically and subsequently stored in the gallbladder. When primary bile acids are secreted into the large intestine, they can be broken down into secondary bile acids by bacteria present in the intestine. Both types of bile acids assist in the metabolism of dietary fat. Ursodeoxycholic acid regulates cholesterol levels by slowing the rate at which the intestine is able to absorb cholesterol and also acts to break down micelles, which contain cholesterol. Because of this property, ursodeoxycholic acid is used to treat gall stones non-surgically.","The drug decreases the absorption of cholesterol and is used to dissolve (cholesterol) gallstones in patients as an alternative to a surgical procedure to remove the gallstones.","AKR1C2 inducer","Anti-inflammatory","Phase 2 on-going (NCT05083390)","Under clinical trials","2022-03-21"]
[382,"Vigabatrin","4-Amino-5-hexenoic acid; Gamma vinyl GABA; gamma-Vinyl GABA; gamma-Vinyl-gamma-aminobutyric acid; GVG; Vigabatrin; Vinyl gamma-aminobutyric acid","Chemical drug","DB01080","Vigabatrin is an analog of gamma-aminobutyric acid (), the main inhibitory neurotransmitter in the central nervous system, used in the treatment of refractory seizures and infantile spasms. It irreversibly inhibits the enzyme responsible for GABA metabolism, thereby increasing levels of circulating GABA. Although administered as a racemic mixture, only the S(+) enantiomer is pharmacologically active.\r\n\r\nIt was first introduced as an antiepileptic agent in the United Kingdom in 1989 and was used extensively until 1997, when an association with vision loss became apparent. Its use is now generally reserved for patients who have failed alternative therapies, and its US approval by the FDA in 2009 mandated the creation of a drug registry to monitor patients for visual deficits.","5665","68506-86-5",true,"C(CCC(=O)O)(C=C)N","PJDFLNIOAUIZSL-UHFFFAOYSA-N",129.159,"4-aminobutyrate aminotransferase, mitochondrial inhibitor","Gamma-aminobutyric acid (GABA) is the major inhibitory transmitter throughout the central nervous system, and the potentiation of GABAergic neurotransmission is therefore a crucial mechanism through which antiepileptic agents may combat the pathologic excitatory neurotransmission seen in epilepsy. Vigabatrin increases concentrations of GABA in the central nervous system by irreversibly inhibiting the enzymes responsible for its metabolism to succinic semialdehyde: gamma-aminobutyric acid transaminase (GABA-T).","Vigabatrin is an antiepileptic agent chemically unrelated to other anticonvulsants. Vigabatrin prevents the metabolism of GABA by irreversibly inhibiting GABA transaminase (GABA-T). As vigabatrin is an irreversible inhibitor of gamma-aminobutyric acid transaminase (GABA-T), its duration of effect is thought to be dependent on the rate of GABA-T re-synthesis rather than on the rate of drug elimination.\r","Vigabatrin is indicated as adjunctive therapy in the treatment of refractory complex partial seizures in patients 2 years of age and older who have had inadequate responses to multiple previous treatments (i.e. not to be used for first-line therapy). It is also indicated as monotherapy in the treatment of infantile spasms in patients between 1 month and 2 years of age for whom the potential benefits outweigh the risk of vision loss.","GABBR1 agonist; ABAT inhibitor","Antiepileptic drug","Phase 2 on-going (NCT04321395)","Under clinical trials","2022-03-21"]
[383,"Vildagliptin","Vitagliptin; Galvus; Jalra; Xiliarx","Chemical drug","DB04876","Vildagliptin (LAF237) is an orally active antihyperglycemic agent that selectively inhibits the dipeptidyl peptidase-4 (DPP-4) enzyme. It is used to manage type II diabetes mellitus, where GLP-1 secretion and insulinotropic effects are impaired. By inhibiting DPP-4, vildagliptin prevents the degradation of glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which are incretin hormones that promote insulin secretion and regulate blood glucose levels. Elevated levels of GLP-1 and GIP consequently results in improved glycemic control. In clinical trials, vildagliptin has a relatively low risk of hypoglycemia.\r\n\r\nOral vildagliptin was approved by the European Medicines Agency in 2008 for the treatment of type II diabetes mellitus in adults as monotherapy or in combination with , a sulfonylurea, or a thiazolidinedione in patients with inadequate glycemic control following monotherapy. It is marketed as Galvus. Vildagliptin is also available as Eucreas, a fixed-dose formulation with metformin for adults in who do not adequately glycemic control from monotherapy. Vildagliptin is currently under investigation in the US.","6918537","274901-16-5",true,"N(CC(=O)N1[C@H](C#N)CCC1)C12CC3(O)CC(C2)CC(C1)C3","SYOKIDBDQMKNDQ-XWTIBIIYSA-N",303.406,"Dipeptidyl peptidase 4 inhibitor","Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) are incretin hormones that regulate blood glucose levels and maintain glucose homeostasis. It is estimated that the activity of GLP-1 and GIP contribute more than 70% to the insulin response to an oral glucose challenge. They stimulate insulin secretion in a glucose-dependent manner via G-protein-coupled GIP and GLP-1 receptor signalling. In addition to their effects on insulin secretion, GLP-1 is also involved in promoting islet neogenesis and differentiation, as well as attenuating pancreatic beta-cell apoptosis. Incretin hormones also exert extra-pancreatic effects, such as lipogenesis and myocardial function. In type II diabetes mellitus, GLP-1 secretion is impaired, and the insulinotropic effect of GIP is significantly diminished.\r\n\r\nVildagliptin exerts its blood glucose-lowering effects by selectively inhibiting dipeptidyl peptidase-4 (DPP-4), an enzyme that rapidly truncates and inactivates GLP-1 and GIP upon their release from the intestinal cells. DPP-4 cleaves oligopeptides after the second amino acid from the N-terminal end. Inhibition of DPP-4 substantially prolongs the half-life of GLP-1 and GIP, increasing the levels of active circulating incretin hormones. The duration of DPP-4 inhibition by vildagliptin is dose-dependent. Vildagliptin reduces fasting and prandial glucose and HbA1c. It enhances the glucose sensitivity of alpha- and beta-cells and augments glucose-dependent insulin secretion. Fasting and postprandial glucose levels are decreased, and postprandial lipid and lipoprotein metabolism are also improved.","Vildagliptin works to improve glycemic control in type II diabetes mellitus by enhancing the glucose sensitivity of beta-cells (β-cells) in pancreatic islets and promoting glucose-dependent insulin secretion. Increased GLP-1 levels leads to enhanced sensitivity of alpha cells to glucose, promoting glucagon secretion. Vildagliptin causes an increase in the insulin to glucagon ratio by increasing incretin hormone levels: this results in a decrease in fasting and postprandial hepatic glucose production. Vildagliptin does not affect gastric emptying. It also has no effects on insulin secretion or blood glucose levels in individuals with normal glycemic control.\r\n\r\nIn clinical trials, treatment with vildagliptin 50-100 mg daily in patients with type 2 diabetes significantly improved markers of beta-cells, proinsulin to insulin ratio, and measures of beta-cell responsiveness from the frequently-sampled meal tolerance test.  Vildagliptin has improves glycated hemoglobin (HbA1c) and fasting plasma glucose (FPG) levels.","Vildagliptin is indicated in the treatment of type II diabetes mellitus in adults. As monotherapy, vildagliptin is indicated in adults inadequately controlled by diet and exercise alone and for whom metformin is inappropriate due to contraindications or intolerance. It is also indicated as dual therapy in combination with metformin, a sulphonylurea, or a thiazolidinedione in adults patients with insufficient glycemic control despite maximal tolerated dose of monotherapy. \r\n\r\nVildagliptin is also marketed in a combination product with  for the treatment of adults with type II diabetes mellitus who inadequately respond to either monotherapy of vildagliptin or metformin. This fixed-dose formulation can be used in combination with a sulphonylurea or insulin (i.e., triple therapy) as an adjunct to diet and exercise in adults who do not achieve adequate glycemic control with monotherapy or dual therapy.","DPP4 inhibitor","Antidiabetic drug","Phase 3 on-going (NCT03925701)","Under clinical trials","2022-03-21"]
[384,"Vitamin B12","Cyanocob(III)alamin; Cyanocobalamin; Vitamin B12; Vitamin B12 complex; Vitamin B12 NOS","Supplement","DB00115","Cyanocobalamin (commonly known as Vitamin B12) is a highly complex, essential vitamin, owing its name to the fact that it contains the mineral, cobalt. This vitamin is produced naturally by bacteria , and is necessary for DNA synthesis and cellular energy production. Vitamin B12 has many forms, including the cyano-, methyl-, deoxyadenosyl- and hydroxy-cobalamin forms. The _cyano_ form, is the most widely used form in supplements and prescription drugs , .  Several pharmaceutical forms of cyanocobalamin have been developed, including the tablet, injection, and nasal spray forms , , .  This drug was initially approved by the FDA in 1942 .","5311498","68-19-9",true,"[CH-](#N)[Co+3]1234N5=C6[C@H]([C@@]([C@@]5([C@@H]5[N-]1C(=C(C1=N3C(=CC3=N2C(=C6C)[C@]([C@@H]3CCC(=O)N)(CC(=O)N)C)C([C@@H]1CCC(=O)N)(C)C)C)[C@]([C@H]5CC(=O)N)(C)CCC(=O)NC[C@H](OP(=O)(O[C@H]1C([C@@H](N2C=N4c3c2cc(c(c3)C)C)O[C@@H]1CO)O)[O-])C)C)(CC(=O)N)C)CCC(=O)N",null,-666,"Methionine synthase cofactor; Methylmalonyl-CoA mutase, mitochondrial cofactor; Methionine synthase reductase cofactor; Methylmalonic aciduria type A protein, mitochondrial binder; Methylmalonic aciduria and homocystinuria type C protein cofactor; Methyle","Vitamin B12 serves as a cofactor for _methionine synthase_ and _L-methylmalonyl-CoA mutase_ enzymes. Methionine synthase is essential for the synthesis of purines and pyrimidines that form DNA. L-methylmalonyl-CoA mutase converts L-methylmalonyl-CoA to _succinyl-CoA_ in the degradation of propionate , an important reaction required for both fat and protein metabolism. It is a lack of vitamin B12 cofactor in the above reaction and the resulting accumulation of methylmalonyl CoA that is believed to be responsible for the neurological manifestations of B12 deficiency . Succinyl-CoA is also necessary for the synthesis of hemoglobin . \r\n\r\nIn tissues, vitamin B12 is required for the synthesis of _methionine_ from homocysteine.   Methionine is required for the formation of S-adenosylmethionine, a methyl donor for nearly 100 substrates, comprised of DNA, RNA, hormones, proteins, as well as lipids . Without vitamin B12, tetrahydrofolate cannot be regenerated from 5-methyltetrahydrofolate, and this can lead to functional folate deficiency , . \r\nThis reaction is dependent on methylcobalamin (vitamin B12) as a co-factor and is also dependent on folate, in which the methyl group of methyltetrahydrofolate is transferred to homocysteine to form _methionine_ and _tetrahydrofolate_. Vitamin B12 incorporates into circulating folic acid into growing red blood cells; retaining the folate in these cells . A deficiency of vitamin B12 and the interruption of this reaction leads to the development of megaloblastic anemia.","\r\n**General effects**\r\n\r\nCyanocobalamin corrects vitamin B12 deficiency and improves the symptoms and laboratory abnormalities associated with pernicious anemia (megaloblastic indices, gastrointestinal lesions, and neurologic damage). This drug aids in growth, cell reproduction, hematopoiesis, nucleoprotein, and myelin synthesis.  It also plays an important role in fat metabolism, carbohydrate metabolism, as well as protein synthesis. Cells that undergo rapid division (for example, epithelial cells, bone marrow, and myeloid cells) have a high demand for vitamin B12 . \r\n \r\n**Parenteral cyanocobalamin effects**\r\n\r\nThe parenteral administration of vitamin B12 rapidly and completely reverses the megaloblastic anemia and gastrointestinal symptoms of vitamin B12 deficiency. Rapid parenteral administration of vitamin B12 in deficiency related neurological damage prevents the progression of this condition . \r\n\r\n**Nasal spray effects**\r\n\r\nIn 24 vitamin B12 deficient patients who were already stabilized on intramuscular (IM) vitamin B12 therapy, single daily doses of intranasal cyanocobalamin for 8 weeks lead to serum vitamin B12 concentrations that were within the target therapeutic range (>200 ng/L) .\r","\r\n**Nasal spray**\r\n\r\nThe cyanocobalamin nasal spray is indicated for the maintenance of vitamin B12 concentrations after normalization with intramuscular vitamin B12 therapy in patients with deficiency of this vitamin who have no nervous system involvement .\r\n\r\nNote:  CaloMist , the nasal spray form, has not been evaluated for the treatment of newly diagnosed vitamin B12 deficiency.\r\n\r\n**Injection forms (subcutaneous, intramuscular)**\r\n\r\nThese forms are indicated for vitamin B12 deficiencies due to various causes, with or without neurologic manifestations .  Vitamin B12 deficiency is frequently caused by malabsorption, which is often associated with the following conditions :\r\n\r\nAddisonian (pernicious) anemia\r\n\r\nGastrointestinal pathology, dysfunction, or surgery, including gluten enteropathy or sprue, small bowel bacterial overgrowth, total or partial gastrectomy\r\n\r\nFish tapeworm infestation\r\n\r\nMalignancy of the pancreas or bowel\r\n\r\nFolic acid deficiency\r\n\r\n\r\n**Oral forms**\r\n\r\nVitamin B12 supplements are widely available and indicated in patients who require supplementation for various reasons.  Dose requirements for vitamin B12 which are higher than normal (caused by pregnancy, thyrotoxicosis, hemolytic anemia, hemorrhage, malignancy, hepatic and renal disease) can usually be achieved with oral supplementation .   Oral products of vitamin B12 are not recommended in patients with malabsorption, as these forms are primarily absorbed in the gastrointestinal tract .","MTHFR cofactor",null,"Phase 3 on-going (IRCT20120718010333N5)","Under clinical trials","2022-03-21"]
[385,"Vitamin B6","2-methyl-3-hydroxy-4,5-dihydroxymethylpyridine; 3-hydroxy-4,5-bis(hydroxymethyl)-2-methylpyridine; 3-hydroxy-4,5-dimethylol-α-picoline; 5-hydroxy-6-methyl-3,4-pyridinedimethanol; Pyridoxine; Pyridoxol; Vitamin B6","Supplement","DB00165","Pyridoxine is the 4-methanol form of vitamin B6, an important water-soluble vitamin that is naturally present in many foods. As its classification as a vitamin implies, Vitamin B6 (and pyridoxine) are essential nutrients required for normal functioning of many biological systems within the body. While many plants and microorganisms are able to synthesize pyridoxine through endogenous biological processes, animals must obtain it through their diet. \r\n\r\nMore specifically, pyridoxine is converted to pyridoxal 5-phosphate in the body, which is an important coenzyme for synthesis of amino acids, neurotransmitters (serotonin, norepinephrine), sphingolipids, and aminolevulinic acid. It's important to note that Vitamin B6 is the collective term for a group of three related compounds, pyridoxine, pyridoxal, and pyridoxamine, and their phosphorylated derivatives, pyridoxine 5'-phosphate, pyridoxal 5'-phosphate and pyridoxamine 5'-phosphate. Although all six of these compounds should technically be referred to as vitamin B6, the term vitamin B6 is commonly used interchangeably with just one of them, pyridoxine . \r\n\r\nVitamin B6, principally in its biologically active coenzyme form pyridoxal 5'-phosphate, is involved in a wide range of biochemical reactions, including the metabolism of amino acids and glycogen, the synthesis of nucleic acids, hemogloblin, sphingomyelin and other sphingolipids, and the synthesis of the neurotransmitters serotonin, dopamine, norepinephrine and gamma-aminobutyric acid (GABA) . \r\n\r\nPyridoxine is used medically for the treatment of vitamin B6 deficiency and for the prophylaxis of isoniazid-induced peripheral neuropathy (due to 's mechanism of action which competitively inhibits the action of pyridoxine in the above-mentioned metabolic functions). It is also used in combination with  (as the commercially available product Diclectin) for the treatment of nausea and vomiting in pregnancy.","1054","65-23-6",true,"C(O)c1c(CO)cnc(c1O)C","LXNHXLLTXMVWPM-UHFFFAOYSA-N",169.18,"Pyridoxal kinase ligand","Vitamin B6 is the collective term for a group of three related compounds, pyridoxine (PN), pyridoxal (PL) and pyridoxamine (PM), and their phosphorylated derivatives, pyridoxine 5'-phosphate (PNP), pyridoxal 5'-phosphate (PLP) and pyridoxamine 5'-phosphate (PMP). Although all six of these compounds should technically be referred to as vitamin B6, the term vitamin B6 is commonly used interchangeably with just one of them, pyridoxine. Vitamin B6, principally in its biologically active coenzyme form pyridoxal 5'-phosphate, is involved in a wide range of biochemical reactions, including the metabolism of amino acids and glycogen, the synthesis of nucleic acids, hemogloblin, sphingomyelin and other sphingolipids, and the synthesis of the neurotransmitters serotonin, dopamine, norepinephrine and gamma-aminobutyric acid (GABA).","Vitamin B6 (pyridoxine) is a water-soluble vitamin used in the prophylaxis and treatment of vitamin B6 deficiency and peripheral neuropathy in those receiving isoniazid (isonicotinic acid hydrazide, INH). Vitamin B6 has been found to lower systolic and diastolic blood pressure in a small group of subjects with essential hypertension. Hypertension is another risk factor for atherosclerosis and coronary heart disease. Another study showed pyridoxine hydrochloride to inhibit ADP- or epinephrine-induced platelet aggregation and to lower total cholesterol levels and increase HDL-cholesterol levels, again in a small group of subjects. Vitamin B6, in the form of pyridoxal 5'-phosphate, was found to protect vascular endothelial cells in culture from injury by activated platelets. Endothelial injury and dysfunction are critical initiating events in the pathogenesis of atherosclerosis. Human studies have demonstrated that vitamin B6 deficiency affects cellular and humoral responses of the immune system. Vitamin B6 deficiency results in altered lymphocyte differentiation and maturation, reduced delayed-type hypersensitivity (DTH) responses, impaired antibody production, decreased lymphocyte proliferation and decreased interleukin (IL)-2 production, among other immunologic activities.","Pyridoxine is indicated for the treatment of vitamin B6 deficiency and for the prophylaxis of -induced peripheral neuropathy. It is also approved by Health Canada for the treatment of nausea and vomiting in pregnancy in a combination product with  (as the commercially available product Diclectin).","PDXK ligand",null,"Clinical trial on-going (JPRN-UMIN000032611)","Under clinical trials","2022-03-21"]
[386,"Vitamin C","Ascorbate; Ascorbic acid; L-(+)-ascorbic acid; L-Ascorbate; L-Ascorbic Acid; Vitamin C","Supplement","DB00126","A six carbon compound related to glucose. It is found naturally in citrus fruits and many vegetables. Ascorbic acid is an essential nutrient in human diets, and necessary to maintain connective tissue and bone. Its biologically active form, vitamin C, functions as a reducing agent and coenzyme in several metabolic pathways. Vitamin C is considered an antioxidant.","54670067","50-81-7",true,"[C@@H](CO)(O)[C@@H]1C(=C(C(=O)O1)O)O","CIWBSHSKHKDKBQ-JLAZNSOCSA-N",176.124,"Hyaluronate lyase inhibitor; DNA cleavage; Xylose isomerase substrate; Procollagen-lysine,2-oxoglutarate 5-dioxygenase 2 cofactor; Phytanoyl-CoA dioxygenase, peroxisomal cofactor; Procollagen-lysine,2-oxoglutarate 5-dioxygenase 3 cofactor; Gamma-butyrobet","In humans, an exogenous source of ascorbic acid is required for collagen formation and tissue repair by acting as a cofactor in the posttranslational formation of 4-hydroxyproline in -Xaa-Pro-Gly- sequences in collagens and other proteins. Ascorbic acid is reversibly oxidized to dehydroascorbic acid in the body. These two forms of the vitamin are believed to be important in oxidation-reduction reactions. The vitamin is involved in tyrosine metabolism, conversion of folic acid to folinic acid, carbohydrate metabolism, synthesis of lipids and proteins, iron metabolism, resistance to infections, and cellular respiration.","Ascorbic Acid (vitamin C) is a water-soluble vitamin indicated for the prevention and treatment of scurvy, as ascorbic acid deficiency results in scurvy. Collagenous structures are primarily affected, and lesions develop in bones and blood vessels. Administration of ascorbic acid completely reverses the symptoms of ascorbic acid deficiency.","Used to treat vitamin C deficiency, scurvy, delayed wound and bone healing, urine acidification, and in general as an antioxidant. It has also been suggested to be an effective antiviral agent.","PLOD2 cofactor; PLOD3 cofactor; DBH cofactor; P3H1 cofactor; P3H2 cofactor; P3H3 cofactor; PLOD1 cofactor",null,"Phase 0 on-going (ChiCTR2000033171)","Under clinical trials","2022-03-21"]
[387,"Vitamin D","Calciferol; Vitamin D NOS; Vitamin D, unspecified form","Supplement","DB11094","Vitamin D ultimately comprises a group of lipid-soluble secosteroids responsible for a variety of biological effects, some of which include increasing the intestinal absorption of calcium, magnesium, and phosphate. With reference to human use, there are 2 main forms of vitamin D - vitamin D3 (cholecalciferol) and vitamin D2 (ergocalciferol). When non-specific references are made about 'vitamin d', the references are usually about the use of vitamin D3 and/or D2.\r\n\r\nVitamin D3 and D2 require hydroxylation in order to become biologically active in the human body. Since vitamin D can be endogenously synthesized in adequate amounts by most mammals exposed to sufficient quantities of sunlight, vitamin D functions like a hormone on vitamin D receptors to regulate calcium in opposition to parathyroid hormone. Vitamin D plays an essential physiological role in maintaining calcium homeostasis and metabolism. There are several different vitamin D supplements that are given to treat or to prevent osteomalacia and rickets, or to meet the daily criteria of vitamin D consumption.","5280795","67-97-0",true,"C[C@]12[C@H](/C(=C/C=C/3\\C(=C)CC[C@@H](C3)O)/CCC2)CC[C@@H]1[C@@H](CCCC(C)C)C","QYSXJUFSXHHAJI-YRZJJWOYSA-N",384.648,"Vitamin D3 receptor; Vitamin D-binding protein","Most individuals naturally generate adequate amounts of vitamin D through ordinary dietary intake of vitamin D (in some foods like eggs, fish, and cheese) and natural photochemical conversion of the vitamin D3 precursor 7-dehydrocholesterol in the skin via exposure to sunlight.\r\n\r\nConversely, vitamin D deficiency can often occur from a combination of insufficient exposure to sunlight, inadequate dietary intake of vitamin D, genetic defects with endogenous vitamin D receptor, or even severe liver or kidney disease . Such deficiency is known for resulting in conditions like rickets or osteomalacia, all of which reflect inadequate mineralization of bone, enhanced compensatory skeletal demineralization, resultant decreased calcium ion blood concentrations, and increases in the production and secretion of parathyroid hormone . Increases in parathyroid hormone stimulates the mobilization of skeletal calcium and the renal excretion of phosphorus . This enhanced mobilization of skeletal calcium leads towards porotic bone conditions .\r\n\r\nOrdinarily, while vitamin D3 is made naturally via photochemical processes in the skin, both itself and vitamin D2 can be found in various food and pharmaceutical sources as dietary supplements. The principal biological function of vitamin D is the maintenance of normal levels of serum calcium and phosphorus in the bloodstream by enhancing the efficacy of the small intestine to absorb these minerals from the diet . At the liver, vitamin D3 or D2 is hydroxylated to 25-hydroxyvitamin D and then finally to the primary active metabolite 1,25-dihydroxyvitamin D in the kidney via further hydroxylation . This final metabolite binds to endogenous vitamin d receptors, which results in a variety of regulatory roles - including maintaining  calcium balance, the regulation of parathyroid hormone, the promotion of the renal reabsorption of calcium, increased intestinal absorption of calcium and phosphorus, and increased calcium and phosphorus mobilization of calcium and phosphorus from bone to plasma to maintain balanced levels of each in bone and the plasma .","The in vivo synthesis of the predominant two biologically active metabolites of vitamin D occurs in two steps. The first hydroxylation of vitamin D3 or D2 occurs in the liver to yield 25-hydroxyvitamin D while the second hydroxylation happens in the kidneys to give 1, 25-dihydroxyvitamin D . These vitamin D metabolites subsequently facilitate the active absorption of calcium and phosphorus in the small intestine, serving to increase serum calcium and phosphate levels sufficiently to allow bone mineralization . Conversely, these vitamin D metabolites also assist in mobilizing calcium and phosphate from bone and likely increase the reabsorption of calcium and perhaps also of phosphate via the renal tubules . There exists a period of 10 to 24 hours between the administration of vitamin D and the initiation of its action in the body due to the necessity of synthesis of the active vitamin D metabolites in the liver and kidneys . It is parathyroid hormone that is responsible for the regulation of such metabolism at the level of the kidneys .","Vitamin D is indicated for use in the treatment of hypoparathyroidism, refractory rickets (also known as vitamin D resistant rickets), and familial hypophosphatemia .",null,"Vitamin source drug","Clinical trial on-going (IRCT20190701044062N2)","Under clinical trials","2022-03-21"]
[388,"Vitamin E","(+)-α-tocopherol; (2R,4'R,8'R)-α-tocopherol; (R,R,R)-α-tocopherol; 5,7,8-trimethyltocol; alpha-tocopherol; d-α-tocopherol","Supplement","DB00163","In 1922, vitamin E was demonstrated to be an essential nutrient. Vitamin E is a term used to describe 8 different fat soluble tocopherols and tocotrienols, alpha-tocopherol being the most biologically active. Vitamin E acts as an antioxidant, protecting cell membranes from oxidative damage. The antioxidant effects are currently being researched for use in the treatment of diseases causing bone loss, cardiovascular diseases, diabetes mellitus and associated comorbidities, eye diseases, inflammatory diseases (including skin conditions), lipid disorders, neurological diseases, and radiation damage. Though this research is so far inconclusive, vitamin E remains a popular supplement and is generally considered safe by the FDA.","14985","59-02-9",true,"Cc1c2c(CC[C@](O2)(CCC[C@@H](CCC[C@@H](CCCC(C)C)C)C)C)c(c(c1C)O)C","GVJHHUAWPYXKBD-IEOSBIPESA-N",430.717,"Nuclear receptor subfamily 1 group I member 2; Protein kinase C beta type; Arachidonate 5-lipoxygenase; Protein kinase C alpha type; Diacylglycerol kinase alpha; Serine/threonine-protein phosphatase 2A catalytic subunit beta isoform; Serine/threonine-prot","The mechanism of action for most of vitamin E's effects are still unknown. Vitamin E is an antioxidant, preventing free radical reactions with cell membranes. Though in some cases vitamin E has been shown to have pro-oxidant activity.\r\n\r\nOne mechanism of vitamin E's antioxidant effect is in the termination of lipid peroxidation. Vitamin E reacts with unstable lipid radicals, producing stable lipids and a relatively stable vitamin E radical. The vitamin E radical is then reduced back to stable vitamin E by reaction with ascorbate or glutathione.","Vitamin E is a collective term used to describe 8 separate fat soluble antioxidants, most commonly alpha-tocopherol. Vitamin E acts to protect cells against the effects of free radicals, which are potentially damaging by-products of the body's metabolism. Vitamin E deficiency is seen in persons with abetalipoproteinemia, premature, very low birth weight infants (birth weights less than 1500 grams, or 3&frac12; pounds), cystic fibrosis, and cholestasis and severe liver disease. Preliminary research suggests vitamin E may help prevent or delay coronary heart disease and protect against the damaging effects of free radicals, which may contribute to the development of chronic diseases such as cancer. It also protects other fat-soluble vitamins (A and B group vitamins) from destruction by oxygen. Low levels of vitamin E have been linked to increased incidence of breast and colon cancer.","Vitamin E supplementation is indicated for treatment of vitamin E deficiency which can occur in cystic fibrosis, cholestasis and severe liver disease, abetalipoproteinemia or simply poor diet.","NR1I2; ALOX5; DGKA","Anti-inflammatory","Phase 3 completed (Vitamin E was superior to placebo for the treatment of nonalcoholic steatohepatitis in adults without diabetes. There was no benefit of pioglitazone over placebo for the primary outcome; however, significant benefits of pioglitazone were observed for some of the secondary outcomes. NCT00063622); Phase 2 on-going (NCT04198805)","Under clinical trials","2022-03-21"]
[389,"Viusid",null,"Supplement",{"$nulls":3},"943241-73-4",false,{"$nulls":8},"Antioxidant drug","Phase 3 completed  (NCT00509418: Our results suggest that triple therapy with Viusid, IFN alpha-2b and ribavirin was well tolerated and may have a beneficial effect on histologic and biochemical variables. The intensity of anemia is reduced in patients treated with Viusid.)","Under clinical trials","2022-03-21"]
[390,"VK-2809","MB-07811; VK 2809","Chemical drug","DB15137","VK-2809 is under investigation in clinical trial NCT02927184 (Safety and Tolerability of VK2809 in Patients With Primary Hypercholesterolemia and Non-Alcoholic Fatty Liver Disease).","15942005","852948-13-1",false,"C(Oc1cc(C)c(c(c1)C)Cc1cc(C(C)C)c(cc1)O)P1(=O)O[C@@H](CCO1)c1cc(Cl)ccc1","LGGPZDRLTDGYSQ-GYKKGXIBSA-N",514.986,{"$nulls":4},"THR agonist","Anti-fibrosis","Phase 2 completed (NCT02927184)","Under clinical trials","2022-03-21"]
[391,"VSL#3",null,"Biological drug",{"$nulls":3},"742088-29-5",false,{"$nulls":7},"TCPTP activator","Probiotics","Phase 1&2 terminated  (NCT03511365: IRB haulted the study there was no evidence that the probiotic would benefit the patient)","Failed in clinical trials","2022-03-21"]
[392,"Yaq-001",null,"Miscellany",{"$nulls":4},false,{"$nulls":9},"Clinical trial withdrawn (NCT03962608: Study was not approved by Health Authorities until get the results of the previous study)","Under clinical trials","2022-03-21"]
[393,"YiQiSanJu","Huangqi, Huanglian, Yinchen etc.","Herbal medicine",{"$nulls":4},false,{"$nulls":9},"Phase 1 completed  (NCT01677325)","Under clinical trials","2022-03-21"]
[394,"CJHR","Cirsii Japonici Herba Radix; Cirsium japonicum","Herbal medicine",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (NCT03375580)","Under clinical trials","2022-03-21"]
[395,"Zinc","Zinc, chelated; Zinc, elemental; Zincum metallicum; Zn","Chemical drug","DB01593","A metallic element of atomic number 30 and atomic weight 65.38. It is a necessary trace element in the diet, forming an essential part of many enzymes, and playing an important role in protein synthesis and in cell division. Zinc deficiency is associated with anemia, short stature, hypogonadism, impaired wound healing, and geophagia. It is identified by the symbol _Zn_ .\r\n\r\nA newer study suggests implies that an imbalance of zinc is associated with the neuronal damage associated with traumatic brain injury, stroke, and seizures .\r\n\r\n Understanding the mechanisms that control brain zinc homeostasis is, therefore, imperative to the development of preventive and treatment regimens for these and other neurological disorders .\r\n\r\nIn addition to the above, recent review articles have already demonstrated the important role of zinc in the pathophysiology and treatment of affective disorders, plus discussed the potential value of zinc as a marker of these diseases .  Most recently, research has shown that polymorphism of the common polymorphism in zinc transporter _SLC30A8/ZnT8_ may increase susceptibility to type 2 diabetes provided novel insights into the role of zinc in diabetes .","23994","7440-66-6",true,"[Zn]","HCHKCACWOHOZIP-UHFFFAOYSA-N",65.39,"B1 bradykinin receptor; Methylated-DNA--protein-cysteine methyltransferase; Fructose-bisphosphate aldolase A; Elongation factor 1-alpha 1; Alpha-enolase; Glyceraldehyde-3-phosphate dehydrogenase, testis-specific; Nucleoside diphosphate kinase A; Protein d","**Zinc has three primary biological roles**: _catalytic_, _structural_, and _regulatory_. The catalytic and structural role of zinc is well established, and there are various noteworthy reviews on these functions. For example, zinc is a structural constituent in numerous proteins, inclusive of growth factors, cytokines, receptors, enzymes, and transcription factors for different cellular signaling pathways. It is implicated in numerous cellular processes as a cofactor for approximately 3000 human proteins including enzymes, nuclear factors, and hormones .\r\n\r\nZinc promotes resistance to epithelial apoptosis through cell protection (cytoprotection) against reactive oxygen species and bacterial toxins, likely through the antioxidant activity of the cysteine-rich metallothioneins .\r\n\r\nIn HL-60 cells (promyelocytic leukemia cell line), zinc enhances the up-regulation of A20 mRNA, which, via TRAF pathway, decreases NF-kappaB activation, leading to decreased gene expression and generation of tumor necrosis factor-alpha (TNF-alpha), IL-1beta, and IL-8 .\r\n\r\nThere are several mechanisms of action of zinc on acute diarrhea. Various mechanisms are specific to the gastrointestinal system: zinc restores mucosal barrier integrity and enterocyte brush-border enzyme activity, it promotes the production of antibodies and circulating lymphocytes against intestinal pathogens, and has a direct effect on ion channels, acting as a potassium channel blocker of adenosine 3-5-cyclic monophosphate-mediated chlorine secretion. Cochrane researchers examined the evidence available up to 30 September 2016 .\r\n\r\nZinc deficiency in humans decreases the activity of serum _thymulin_ (a hormone of the thymus), which is necessary for the maturation of T-helper cells. T-helper 1 (Th(1)) cytokines are decreased but T-helper 2 (Th(2)) cytokines are not affected by zinc deficiency in humans .\r\n\r\nThe change of _Th(1)_ to _Th(2)_ function leads to cell-mediated immune dysfunction. Because IL-2 production (Th(1) cytokine) is decreased, this causes decreased activity of natural-killer-cell (NK cell) and T cytolytic cells, normally involved in killing viruses, bacteria, and malignant cells . \r\n\r\nIn humans, zinc deficiency may lead to the generation of new CD4+ T cells, produced in the thymus. In cell culture studies (HUT-78, a Th(0) human malignant lymphoblastoid cell line), as a result of zinc deficiency, nuclear factor-kappaB (NF-kappaB) activation, phosphorylation of IkappaB, and binding of NF-kappaB to DNA are decreased and this results in decreased Th(1) cytokine production .\r\n\r\nIn another study, zinc supplementation in human subjects suppressed the gene expression and production of pro-inflammatory cytokines and decreased oxidative stress markers . In HL-60 cells (a human pro-myelocytic leukemia cell line), zinc deficiency increased the levels of TNF-alpha, IL-1beta, and IL-8 cytokines and mRNA. In such cells, zinc was found to induce A20, a zinc finger protein that inhibited NF-kappaB activation by the tumor necrosis factor receptor-associated factor pathway. This process decreased gene expression of pro-inflammatory cytokines and oxidative stress markers .\r\n\r\nThe exact mechanism of zinc in acne treatment is poorly understood. However, zinc is considered to act directly on microbial inflammatory equilibrium and facilitate antibiotic absorption when used in combination with other agents. Topical zinc alone as well as in combination with other agents may be efficacious because of its anti-inflammatory activity and ability to reduce P. acnes bacteria by the inhibition of P. acnes lipases and free fatty acid levels .","Zinc is involved in various aspects of cellular metabolism. It has been estimated that approximately 10% of human proteins may bind zinc, in addition to hundreds of proteins that transport and traffic zinc. It is required for the catalytic activity of more than 200 enzymes, and it plays a role in immune function wound healing, protein synthesis, DNA synthesis, and cell division. Zinc is an essential element for a proper sense of taste and smell and supports normal growth and development during pregnancy, childhood, and adolescence. It is thought to have antioxidant properties, which may be protective against accelerated aging and helps to speed up the healing process after an injury; however, studies differ as to its effectiveness. Zinc ions are effective antimicrobial agents even if administered in low concentrations .\r\n\r\nStudies on oral zinc for specific conditions shows the following evidence in various conditions :\r\n\r\n**Colds:** Evidence suggests that if zinc lozenges or syrup are taken within 24 hours after cold symptoms start, the supplement may shorten the length of colds. The use intranasal zinc has been associated with the loss of the sense of smell, in some cases long-term or permanently .\r\n\r\n**Wound healing:** Patients with skin ulcers and decreased levels of zinc may benefit from oral zinc supplements . \r\n\r\n**Diahrrea**: Oral zinc supplements can reduce the symptoms of diarrhea in children with low levels of zinc, especially in cases of malnutrition .\r","Zinc can be used for the treatment and prevention of zinc deficiency/its consequences, including stunted growth and acute diarrhea in children, and slowed wound healing. It is also utilized for boosting the immune system, treating the common cold and recurrent ear infections, as well as preventing lower respiratory tract infections .  \r\n\r","PSPH; CCS; HDAC1 cofactor; HDAC4 cofactor; INS; UTRN; ASPA cofactor; TP73 cofactor; A2M; AGT; APOBR; APOE; APOL1; C3; C5; CFB; CFH; CFI; CLU; CP; CPN2; DSP; F12; F13B; FGA; GSN; HBB; HPR; JUP; SELENOP; TTR; VTN",null,"Phase 3 on-going (IRCT20200531047614N1)","Under clinical trials","2022-03-21"]
[396,"ZSP0678",null,"Chemical drug",{"$nulls":4},false,{"$nulls":8},"Hepatoprotectants","Phase 1 completed  (NCT04137055)","Under clinical trials","2022-03-21"]
[397,"ZSP1601",null,"Chemical drug",{"$nulls":4},false,{"$nulls":7},"PDE inhibitor","Hepatoprotectants","Phase 1&2 completed  (NCT04140123)","Under clinical trials","2022-03-21"]
[398,"Zucchini",null,"Chemical drug",null,null,"131751591","246248-10-2",true,"C[C@@]12C3=CC[C@@H]4[C@](C3=CC[C@@]1(C)[C@H]1[C@](CC2)(C)CC[C@](C1)(COC(=O)c1ccccc1)C)(C)CC[C@H](C4(C)C)OC(=O)c1ccc(cc1)N","VKNUHXUEPNYSDN-GJSTXJOSSA-N",663.943,{"$nulls":6},"Clinical trial on-going (IRCT20200419047137N1)","Under clinical trials","2022-03-21"]
[399,"β-glucan",null,"Chemical drug",null,null,"439262","9041-22-9",false,null,null,504.438,{"$nulls":4},"Cr3 modulator","Anticancer agent","Clinical trial on-going (NCT02178839)","Under clinical trials","2022-03-21"]
[400,"Eltrombopag","Eltrombopag","Chemical drug","DB06210","Eltrombopag is used to treat low blood platelet counts in adults with chronic immune (idiopathic) thrombocytopenia (ITP), when certain other medicines, or surgery to remove the spleen, have not worked well enough. ITP is a condition that may cause unusual bruising or bleeding due to an abnormally low number of platelets in the blood. Eltrombopag has also been recently approved (late 2012) for the treatment of thrombocytopenia (low blood platelet counts) in patients with chronic hepatitis C to allow them to initiate and maintain interferon-based therapy.",null,"496775-61-2",true,"CC1=NN(C(=O)\\C1=N/NC1=CC=CC(C2=CC=CC(=C2)C(O)=O)=C1O)C1=CC=C(C)C(C)=C1","XDXWLKQMMKQXPV-QYQHSDTDSA-N",442.467,"Thrombopoietin receptor agonist","Eltrombopag is an orally bioavailable, small-molecule TPO-receptor agonist that interacts with the transmembrane domain of the human TPO-receptor. Eltrombopag is a stimulator of STAT and JAK phosphorylation. Unlike recombinant TPO or romiplostim, Eltrombopag does not activate the AKT pathway in any way. It should be noted that when given to patients with aplastic anemia, other lineages besides platelet count were increased, suggesting that either eltrombopag enhanced the effect of TPO in vivo; or there is a yet uncovered mechanism of action at work.",null,"Thrombopoietin receptor agonists are pharmaceutical agents that stimulate platelet production in the bone marrow. In this, they differ from the previously discussed agents that act by attempting to curtail platelet destruction.",null,null,"Phase 3 terminated  (NCT00678587: GSK decision)","Under clinical trials","2022-03-21"]
[401,"A mixture of Huangqi, Huanglian, Zexie, Yujin, Zhidahuang, Shanzha, Maiya, Zhizhi, Huangqin and Yincheng","Astragalus memeranaceus; Coptis chinensis; Alisma plantago-aquatica; Curcuma rcenyujin;  Crataegus pinnatifida; Hordeurn vulgare; Scutellaria baicalensis; Artemisia capillaris","Herbal medicine",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (ChiCTR-TRC-11001661)","Under clinical trials","2022-03-21"]
[402,"A mixture of Anethum graveolens, Citrus bigardia, Cynara scolymus, Portulaca oleracea, and Silybum marianum",null,"Herbal medicine",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (IRCT2015123025772N1)","Under clinical trials","2022-03-21"]
[403,"Avandia",null,"Chemical drug",{"$nulls":3},"155141-29-0",false,"O=C(O)C=CC(=O)O.O=C1SC(C(=O)N1)CC2=CC=C(OCCN(C3=NC=CC=C3)C)C=C2","SUFUKZSWUHZXAV-BTJKTKAUSA-N",473.5,{"$nulls":6},"Phase 2 on-going (NCT00699036)","Under clinical trials","2022-03-21"]
[404,"Chlorella Vulgaris",null,"Supplement",{"$nulls":4},false,{"$nulls":8},"Prebiotics","Clinical trial on-going (IRCT2014121620345N1)","Under clinical trials","2022-03-21"]
[405,"Evoglitin",null,"Chemical drug",{"$nulls":3},"1222102-29-5",false,"O=C1NCCN(C(=O)CC(N)CC2=CC(F)=C(F)C=C2F)C1COC(C)(C)C","LCDDAGSJHKEABN-MLGOLLRUSA-N",401.42,{"$nulls":4},"DPP-4 inhibitor",null,"Phase 4 completed  (NCT03910361)","Under clinical trials","2022-03-21"]
[406,"Gemfibrozil","2,2-Dimethyl-5-(2,5-xylyloxy)valeric acid; Gemfibrozil","Chemical drug","DB01241","Gemfibrozil is a fibric acid agent, similar to , used to treat Type IIb, IV, and V hyperlipidemias. Gemfibrozil is not a first line treatment and is prescribed to patients who have not responded adequately to weight loss, diet, exercise, and other medications.\r\n\r\nGemfibrozil was granted FDA approval on 21 December 1981.",null,"25812-30-0",true,"CC1=CC(OCCCC(C)(C)C(O)=O)=C(C)C=C1","HEMJJKBWTPKOJG-UHFFFAOYSA-N",250.3334,"Peroxisome proliferator-activated receptor alpha agonist; Solute carrier organic anion transporter family member 1B1 inhibitor; Solute carrier family 22 member 8 inhibitor; Solute carrier organic anion transporter family member 2B1 inhibitor","Gemfibrozil activates peroxisome proliferator-activated receptor-α (PPARα), which alters lipid metabolism. This activation leads to increased HDL, apo AI, apo AII, lipoprotein lipase (LPL), inhibition of apo B synthesis, peripheral lipolysis, decreased removal of free fatty acids by the liver, and increased clearance of apoB.\r\n\r\nUpregulated LPL reduces plasma triglyceride levels. Decreased hepatic removal of fatty acids decreases the production of triglycerides. The effects on apoB synthesis and clearance decrease VLDL production which also reduce plasma triglyceride levels.\r\n\r\nGemfibrozil's glucuronide metabolite is also an inhibitor of CYP2C8.","Gemfibrozil alters lipid metabolism to treat patients with hyperlipidemia. The duration of action requires twice daily dosing as the mean residence time of gemfibrozil is up to 9.6h in patients with chronic renal failure. Gemfibrozil has a wide therapeutic index as trials with twice the standard dose were not associated with severe side effects. Patients taking gemfibrozil may be at an increased risk of developing cholelithiasis and cholecystitis, as seen in patients taking .","Gemfibrozil is indicated to treat patients with Types IV and V hyperlipidemia who have elevated serum triglycerides (usually above 2000mg/dL), elevated VLDL cholesterol, fasting chylomicrons, are at risk of developing pancreatitis, and do not adequately respond to dietary restrictions. Gemfibrozil is also indicated to reduce the risk of developing coronary heart disease in patients with Type IIb hyperlipidemia without history or symptoms of coronary heart disease; who do not adequately respond to weight loss, diet, exercise, and other medications; and have low HDL, raised LDL, and raised triglycerides.","PPARA agonist; SLCO1B1 inhibitor; SLC22A8 inhibitor; SLCO2B1 inhibitor; SLCO1B3 inhibitor","Hypolipidemic drug",null,"Under investigation","2022-03-21"]
[407,"H.Pylori Eradication","Omeprazole, Amoxicillin, Bismuth subcitrate, Azithromycin","Chemical drug",{"$nulls":3},"73590-58-6",false,{"$nulls":9},"Phase 2 completed  (NCT01876108)","Under clinical trials","2022-03-21"]
[408,"IMM-H014",null,"Miscellany",{"$nulls":4},false,{"$nulls":7},"Nrf2 activator; PDE4D inhibitor",null,null,"Under investigation","2022-03-21"]
[409,"Intraconazole",null,"Chemical drug",{"$nulls":3},"84625-61-6",false,"VHVPQPYKVGDNFY-WGEGMAFPNA-N","O=C1N(N=CN1C2=CC=C(C=C2)N3CCN(C4=CC=C(OCC5OC(OC5)(C6=CC=C(Cl)C=C6Cl)CN7N=CN=C7)C=C4)CC3)C(C)CC",705.63,{"$nulls":4},"P450 inhibitor","Antimycotic drug","Phase 2 completed (NCT03421431 LAY SUMMARY: Non-alcoholic fatty liver disease is a chronic hepatic disease that can progress to non-alcoholic steatohepatitis (NASH), which is associated with an increased risk of cirrhosis and liver cancer. Results from this phase II study support continued development of EDP-305, an oral farnesoid X receptor agonist, for the treatment of patients with NASH.)","Under clinical trials","2022-03-21"]
[410,"MF4637",null,"Miscellany",{"$nulls":4},false,{"$nulls":9},"Clinical trial completed (NCT02923804)","Under clinical trials","2022-03-21"]
[411,"Propofol tenofovir",null,"Chemical drug",{"$nulls":4},false,{"$nulls":9},"Phase 4 on-going (ChiCTR1900023153)","Under clinical trials","2022-03-21"]
[412,"Saroglitazar Magnesium",null,"Chemical drug",{"$nulls":3},"1639792-20-3",false,"O=C1[O-][Mg+2]2([O-]C(=O)C(O2CC)CC3=CC=C(OCCN4C(=CC=C4C)C=5C=CC(SC)=CC5)C=C3)O(CC)C1CC6=CC=C(OCCN7C(=CC=C7C)C=8C=CC(SC)=CC8)C=C6","UJYFZCVPOSZDMK-UHFFFAOYSA-L",901.43,{"$nulls":6},"Phase 2 completed  (NCT03863574)","Under clinical trials","2022-03-21"]
[413,"Zhenzhu Tiaozhi Capsule","composed of Ligustri Lucidi Fructus (LLF), Salviae Miltiorrhizae Radix et Rhizoma (SMR), Coptidis Rhizoma (CR),Notoginseng Radix et Rhizoma (NRR), Atractylodis Macrocephalae Rhizoma (AMR), Cirsii Japonici Herba Radix (CJHR), Citri Sarcodactylis Fructus (CSF) and Eucommiae Cortex (EC)","Traditional medicine",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (NCT03375580)","Under clinical trials","2022-03-21"]
[414,"Efruxifermin","AKR-001; AMG-876; EFX; Fc-FGF21(RGE)","Biological drug",{"$nulls":4},false,{"$nulls":7},"Fibroblast growth factor receptor agonist","anti-fibrotic, improves metabolic status","Phase 2 completed (NCT03976401: Treatment with efruxifermin significantly reduced HFF in patients with F1-F3 stage NASH, with an acceptable safety profile.)","Under clinical trials","2022-03-30"]
[415,"Tropifexor plus Licogliflozin",null,"Combinatory",{"$nulls":4},false,{"$nulls":7},"FXR agonist & SGLTs inhibitor",null,"Phase 2 on-going (NCT04065841)","Under clinical trials","2022-03-30"]
[416,"Tropifexor plus Cenicriviroc",null,"Combinatory",{"$nulls":4},false,{"$nulls":7},"FXR agonist & CCR2/5 antagonist",null,"Phase 2 on-going (NCT03517540)","Under clinical trials","2022-03-30"]
[417,"Tropifexor plus LYS006",null,"Combinatory",{"$nulls":4},false,{"$nulls":7},"FXR agonist & leukotriene A4 hydrolase inhibitor",null,"Phase 2 on-going (NCT04147195)","Under clinical trials","2022-03-30"]
[418,"MET409 plus Empagliflozin",null,"Combinatory",{"$nulls":4},false,{"$nulls":7},"FXR agonist & Sodium-glucose cotransporter 2 inhibitors (SGLT2i)",null,"Phase 2 on-going (NCT04702490)","Under clinical trials","2022-03-30"]
[443,"Pioglitazone plus Empagliflozin",null,"Combinatory",{"$nulls":4},false,{"$nulls":7},"Thiazolidinediones (TZD) & SGLT2i",null,"Phase 2 on-going (NCT03646292)","Under clinical trials","2022-03-30"]
[444,"Obeticholic acid plus Atorvastatin",null,"Combinatory",{"$nulls":4},false,{"$nulls":7},"FXR agonist & HMG CoA reductase inhibitor",null,"Phase 2 on-going (NCT02633956)","Under clinical trials","2022-03-30"]
[445,"PF-06865571 plus PF-05221304",null,"Combinatory",{"$nulls":4},false,{"$nulls":7},"Diacylglycerol acyltransferase 2 (DGAT2) inhibitor & acetyl CoA carboxylase (ACC) inhibitor",null,"Phase 2 on-going (NCT03776175)","Under clinical trials","2022-03-30"]
[446,"PF-06865571 plus PF-05221304",null,"Combinatory",{"$nulls":4},false,{"$nulls":7},"DGAT2 inhibitor & ACC inhibitor",null,"Phase 2 on-going (NCT04399538)","Under clinical trials","2022-03-30"]
[447,"PF-06865571 plus PF-05221304",null,"Combinatory",{"$nulls":4},false,{"$nulls":7},"DGAT2 inhibitor & ACC inhibitor",null,"Phase 2 on-going (NCT04321031)","Under clinical trials","2022-03-30"]
[448,"Semaglutide + Cilofexor + Firsocostat",null,"Combinatory",{"$nulls":4},false,{"$nulls":7},"GLP1 receptor agonist & FXR agonist & ACC inhibitor",null,"Phase 2 on-going (NCT03987074)","Under clinical trials","2022-03-30"]
[449,"Semaglutide + (Cilofexor or/and Firsocostat)",null,"Combinatory",{"$nulls":4},false,{"$nulls":7},"GLP1 receptor agonist & FXR agonist & ACC inhibitor",null,"Phase 2 on-going (NCT04971785)","Under clinical trials","2022-03-30"]
[450,"Selonsertib + Firsocostat + Cilofexor",null,"Combinatory",{"$nulls":4},false,{"$nulls":7},"ASK1 inhibitor & ACC inhibitor & FXR agonist",null,"Phase 2 on-going (NCT03449446)","Under clinical trials","2022-03-30"]
[451,"Selonsertib + Firsocostat, Cilofexor, Fenofibrate or Vascepa",null,"Combinatory",{"$nulls":4},false,{"$nulls":7},"ASK1 inhibitor & ACC inhibitor & FXR agonist & PPAR-α activator & icosapent ethyl",null,"Phase 2 on-going (NCT02781584)","Under clinical trials","2022-03-30"]
[452,"Elobixibat + Cholestyramine",null,"Combinatory",{"$nulls":4},false,{"$nulls":7},"Ileal bile acid transporter (IBAT) inhibitor & bile acid sequestrant",null,"Phase 2 on-going (NCT04235205)","Under clinical trials","2022-03-30"]
[453,"Vitamin E + Omega-3 fatty acid",null,"Combinatory",{"$nulls":4},false,{"$nulls":8},"Antioxidant","Phase 2 on-going (NCT04198805)","Under clinical trials","2022-03-30"]
[454,"Vitamin E + Saraglitazar + Lifestyle Changes",null,"Combinatory",{"$nulls":4},false,{"$nulls":7},"PPARα/γ agonist","Antioxidant","Phase 2 on-going (NCT04193982)","Under clinical trials","2022-03-30"]
[455,"NNC0194 0499 + Semaglutide + NNC0174 0833",null,"Combinatory",{"$nulls":4},false,{"$nulls":7},"GLP1 receptor agonist & islet amyloid polypeptide (IAPP) analogue",null,"Phase 2 on-going (NCT05016882)","Under clinical trials","2022-03-30"]
[456,"Probiotics and Glutamine, Quercetin, Vitamin E, Curcumin, Silybin, Pectin",null,"Combinatory",{"$nulls":4},false,{"$nulls":8},"Complex","Phase 2 on-going (NCT04781933)","Under clinical trials","2022-03-30"]
[458,"Breviscapine","scutellarin; Erigeron breviscapus","Biological extract",{"$nulls":4},false,{"$nulls":10},"Under investigation","2022-04-03"]
[459,"ECC0509",null,"Chemical drug",{"$nulls":4},false,{"$nulls":7},"semicarbazide-sensitive amine oxidase (SSAO) inhibitor; vascular adhesion protein-1 (VAP-1) inhibitor",null,"Phase 1 on-going (NCT05012423)","Under clinical trials","2022-04-05"]
[460,"HU6",null,"Biological drug",{"$nulls":4},false,{"$nulls":8},"Controlled Metabolic Accelerators","Phase 2 completed (NCT04874233)","Under clinical trials","2022-04-05"]
[461,"ALG-055009","ALG055009","Chemical drug",{"$nulls":4},false,{"$nulls":7},"Thyroid hormone receptor beta agonist",null,"Phase 1 on-going (NCT05090111)","Under clinical trials","2022-04-05"]
[462,"ALN-HSD",null,"Biological drug",{"$nulls":4},false,{"$nulls":9},"Phase 1 on-going (NCT04565717)","Under clinical trials","2022-04-05"]
[463,"Alphalipoic acid","(R)-lipoic acid; Alpha lipoic acid; alpha-Lipoic acid; D-thioctic acid; Lipoic acid; R-alpha-lipoic acid; Thioctic acid; Thioctic acid D-form","Chemical drug","DB00166","A vitamin-like antioxidant",null,null,true,"OC(=O)CCCC[C@@H]1CCSS1","AGBQKNBQESQNJD-SSDOTTSWSA-N",206.326,"Sodium-dependent multivitamin transporter; Lipoyl synthase, mitochondrial; Lipoyltransferase 1, mitochondrial","Lipoic Acid is generally involved in oxidative decarboxylations of keto acids and is presented as a growth factor for some organisms. Lipoic acid exists as two enantiomers, the R-enantiomer and the S-enantiomer. Normally only the R-enantiomer of an amino acid is biologically active, but for lipoic acid the S-enantiomer assists in the reduction of the R-enantiomer when a racemic mixture is given. Some recent studies have suggested that the S-enantiomer in fact has an inhibiting effect on the R-enantiomer, reducing its biological activity substantially and actually adding to oxidative stress rather than reducing it. Furthermore, the S-enantiomer has been found to reduce the expression of GLUT-4s in cells, responsible for glucose uptake, and hence reduce insulin sensitivity.","Lipoic acid (or α-lipoic acid) is able to pass the blood-brain barrier and is putatively used for detoxification of mercury attached to the brain cells. It can mobilise bound mercury into the blood stream as it is a mercaptan (sulfur compound which readily binds to the mercury). In the blood stream, another chelator such as dimercaptosuccinic acid (DMSA) or methylsulfonylmethane (MSM) is used to transfer mercury safely into the urine for excretion. Neither DMSA nor MSM can cross the blood-brain barrier, which is why both lipoic acid and DMSA are used. It is hypothesized that this treatment-along with carnitine, dimethylglycine (DMG), Vitamin B6, folic acid, and magnesium—could be used to treat autism and amalgam poisoning. In this hypothesis, the reason why autism is difficult to treat is that mercury is attached to the brain cells and most medicines and vitamin supplements do not penetrate the blood-brain barrier. However, α-lipoic acid and perhaps vitamin B12 could making it possible for other chelators to remove mercury safely out of the body and could perhaps one day be used as a treatment for autism. Because lipoic acid is related to cellular uptake of glucose and it is both soluble in water and fat, it is being used for treatment in diabetes. It may be helpful for people with Alzheimer's disease or Parkinson's disease.","For nutritional supplementation, also for treating dietary shortage or imbalance.",null,null,"Phase 4 on-going (NCT04475276)","Under clinical trials","2022-04-05"]
[464,"AMG 609",null,"Biological drug",{"$nulls":4},false,{"$nulls":9},"Phase 1 on-going (NCT04857606)","Under clinical trials","2022-04-05"]
[465,"Amlexanox","Amlexanox; Amoxanox","Chemical drug","DB01025","Amlexanox is an antiallergic drug, clinically effective for atopic diseases, especially allergic asthma and rhinitis. Amlexanox as a topical paste is a well tolerated treatment of recurrent aphthous ulcers. Recurrent aphthous ulcer (RAU) is the most prevalent oral mucosal disease in humans, estimated to affect between 5% and 50% of the general population.",null,null,true,"CC(C)C1=CC2=C(OC3=NC(N)=C(C=C3C2=O)C(O)=O)C=C1","SGRYPYWGNKJSDL-UHFFFAOYSA-N",298.2934,"Protein S100-A12\t antagonist; Protein S100-A13 \tantagonist; Interleukin-3\t antagonist; Fibroblast growth factor 1 \tinhibitor","As a benzopyrano-bipyridine carboxylic acid derivative, amlexanox has anti-inflammatory and antiallergic properties. It inhibits chemical mediatory release of the slow-reacting substance of anaphylaxis (SRS-A) and may have antagonistic effects on interleukin-3. When cells are under stress, they release an inactive form of human fibroblast growth factor 1 (FGF-1), a potent mitogen (entity that causes mitosis). Amlexanox binds to FGF1, increasing its conformational stability, sterically blocking Cu(2+) induced oxidation which normally leads to activation of FGF-1.","Amlexanox is a mucoadhesive oral paste which has been clinically proven to abort the onset, accelerate healing and resolve the pain of aphthous ulcers (canker sores). It decreases the time ulcers take to heal. Because amlexanox decreases the healing time, it also decreases the pain you feel. Recent studies have also shown that the majority of ulcers can be prevented by application of the paste during the prodromal (pre-ulcerative) phase of the disease. Recurrent Aphthous Ulcers (RAU) also known as Recurrent Aphthous Stomatitis (RAS) is recognized as the most common oral mucosal disease known to man. Estimates suggest that 20% - 25% of the general population suffer at least one incidence of aphthous ulcers each year. Amlexanox is also being investigated for its anti-allergenic and anti-inflammatory properties.","Used as a paste in the mouth to treat aphthous ulcers (canker sores).",null,null,"Phase 2 completed (NCT01975935)","Under clinical trials","2022-04-05"]
[466,"ASC41",null,"Chemical drug",{"$nulls":4},false,{"$nulls":7},"THR-beta agonist",null,"Phase 2 on-going (NCT05118360)","Under clinical trials","2022-04-05"]
[467,"ASC40",null,"Chemical drug",{"$nulls":4},false,{"$nulls":7},"Fatty Acid Synthase inhibitor",null,null,"Under investigation","2022-04-05"]
[468,"AZD2693","IONIS-AZ6-2.5-LRx","Chemical drug",{"$nulls":4},false,{"$nulls":9},"Phase 1 completed (NCT04142424)","Under clinical trials","2022-04-05"]
[469,"AZD7503",null,"Chemical drug",{"$nulls":4},false,{"$nulls":9},"Phase 1 on-going (NCT05143905)","Under clinical trials","2022-04-05"]
[470,"BAR502",null,"Chemical drug",{"$nulls":3},"1612191-86-2",false,null,null,392.62,{"$nulls":4},"dual GPBAR1 and FXR agonist",null,"Phase 1 on-going (NCT05203367)","Under clinical trials","2022-04-05"]
[471,"BI456906","BI-456906; BI 456906","Chemical drug",{"$nulls":4},false,{"$nulls":7},"GLP-1 agonist; GCG agonist",null,"Phase 2 on-going (NCT04771273)","Under clinical trials","2022-04-05"]
[472,"BOS-580",null,"Chemical drug",{"$nulls":4},false,{"$nulls":9},"Phase 2 on-going (NCT04880031)","Under clinical trials","2022-04-05"]
[474,"Cilostazol","Cilostazol; Cilostazole","Chemical drug","DB01166","Cilostazol is a quinolinone derivative and antiplatelet agent with vasodilating properties that has been used in the symptomatic treatment of intermittent claudication in patients with peripheral ischaemia. It is marketed under the brand name Pletal by Otsuka Pharmaceutical Co.. Cilostazol works by inhibiting both primary and secondary aggregation and reducing calcium-induced contractions.",null,"73963-72-1",true,"O=C1CCC2=C(N1)C=CC(OCCCCC1=NN=NN1C1CCCCC1)=C2","RRGUKTPIGVIEKM-UHFFFAOYSA-N",369.4607,"cGMP-inhibited 3',5'-cyclic phosphodiesterase A \tinhibitor","Cilostazol and several of its metabolites are cyclic AMP (cAMP) phosphodiesterase III inhibitors (PDE III inhibitors), inhibiting phosphodiesterase activity and suppressing cAMP degradation with a resultant increase in cAMP in platelets and blood vessels, leading to inhibition of platelet aggregation and vasodilation.","Cilostazol reduces the symptoms of intermittent claudication, as indicated by an increased walking distance. Intermittent claudication is pain in the legs that occurs with walking and disappears with rest. The pain occurs due to reduced blood flow to the legs.","Indicated for the alleviation of symptoms of intermittent claudication (pain in the legs that occurs with walking and disappears with rest).",null,null,"Phase 2 on-going (NCT04761848)","Under clinical trials","2022-04-05"]
[475,"DD01",null,"Chemical drug",{"$nulls":4},false,{"$nulls":7},"GLP-1R agonist; GCGR agonist",null,"Phase 1 on-going (NCT04812262)","Under clinical trials","2022-04-06"]
[476,"Estradiol","17beta oestradiol; beta-Estradiol; cis-Estradiol;","Chemical drug","DB00783","Estradiol is an estrogenic steroid used to treat vasomotor symptoms of vulvar and vaginal atrophy in menopause, hypoestrogenism, prevention of postmenopausal osteoporosis, treatment of breast cancer, and advanced androgen-dependent carcinoma of the prostate.",null,"35380-71-3",true,"[H][C@@]12CC[C@H](O)[C@@]1(C)CC[C@]1([H])C3=C(CC[C@@]21[H])C=C(O)C=C3","VOXZDWNPVJITMN-ZBRFXRBCSA-N",272.382,"Estrogen receptor alpha agonist; Estrogen receptor beta agonist; Nuclear receptor subfamily 1 group I member 2 binder; Neuronal acetylcholine receptor subunit alpha-4 binder; G-protein coupled estrogen receptor 1 binder; ATP synthase subunit a inhibitor; Beclin-1 binder","Estrogen is found in the the breast, uterine, ovarian, skin, prostate, bone, fat, and brain tissues. The main source of estrogen in adult women during the reproductive period of life is the ovarian follicle, which secretes 70 to 500 mcg of estradiol each day. After menopause, however, the majority of endogenous estrogen is produced by transformation of androstenedione (which is secreted by the adrenal cortex) to estrone in the peripheral tissues. Both estrone and its sulphate conjugated form, estrone sulphate, represent the most abundant estrogens found in postmenopausal women.\r\n\r\nEstradiol, however, is considerably more potent than estrone and estriol at the estrogen receptor (ER). As a result, the higher estrone concentration in postmenopausal population, can cause various undesirable effects. These effects may include hot flashes, chills, vaginal dryness, mood swings, irregular menstruation, and chills, in addition to sleep problems.\r\n\r\nEstradiol workings by binding to subtypes of the estrogen receptor: estrogen receptor alpha (ERα) and estrogen receptor beta (ERβ). It also exerts potent agonism of G Protein-coupled estrogen receptor (GPER), which is recognized an important regulator of this drug's rapid effects. Once the estrogen receptor has bound to its ligand, it enters the nucleus of the target cell, regulating gene transcription and formation of of messenger RNA. This mRNA makes contact with ribosomes producing specific proteins that express the effect of estradiol upon the target cell. Agonism of estrogen receptors increases pro-estrogenic effects, leading to the relief of vasomotor and urogenital symptoms of a postmenopausal or low estradiol state.","Estradiol acts on the on the estrogen receptors to relieve vasomotor systems (such as hot flashes) and urogenital symptoms (such as vaginal dryness and dyspareunia).\r\n\r\nEstradiol has also been shown to exert favorable effects on bone density by inhibiting bone resorption. Estrogen appears to inhibit bone resorption and may have beneficial effects on the plasma lipid profile. Estrogens cause an increase in hepatic synthesis of various proteins, which include sex hormone binding globulin (SHBG), and thyroid-binding globulin (TBG). Estrogens are known to suppress the formation of follicle-stimulating hormone (FSH) in the anterior pituitary gland.\r\n\r\nA note on hyper-coagulable state, cardiovascular health, and blood pressure\r\n\r\nEstradiol may cause an increased risk of cardiovascular disease, DVT, and stroke, and its use should be avoided in patients at high risk of these conditions. Estrogen induces a hyper-coagulable state, which is also associated with both estrogen-containing oral contraceptive (OC) use and pregnancy. Although estrogen causes an increase in levels of plasma renin and angiotensin. Estrogen-induced increases in angiotensin, causing sodium retention, which is likely to be the mechanism causing hypertension after oral contraceptive treatment.","Estradiol is indicated in various preparations for the treatment of moderate to severe vasomotor symptoms and vulvar and vaginal atrophy due to menopause, for the treatment of hypoestrogenism due to hypogonadism, castration, or primary ovarian failure, and for the prevention of postmenopausal osteoporosis. It is also used for the treatment of breast cancer (only for palliation therapy) in certain men or women with metastatic disease, and for the treatment of androgen-dependent prostate cancer (only for palliation therapy). It is also used in combination with other hormones as a component of oral contraceptive pills for preventing pregnancy (most commonly as Ethinylestradiol, a synthetic form of estradiol).\r\n\r\nA note on duration of treatment\r\n\r\nRecommendations for treatment of menopausal symptoms changed drastically following the release of results and early termination of the Women's Health Initiative (WHI) studies in 2002 as concerns were raised regarding estrogen use. Specifically, the combined estrogen–progestin group was discontinued after about 5 years of follow up due to a statistically significant increase in invasive breast cancer and in cardiovascular events.\r\n\r\nFollowing extensive critique of the WHI results, Hormone Replacement Therapy (HRT) is now recommended to be used only for a short period (for 3-5 years postmenopause) in low doses, and in women without a history of breast cancer or increased risk of cardiovascular or thromboembolic disease. Estrogen for postmenopausal symptoms should always be given with a progestin component due to estrogen's stimulatory effects on the endometrium; in women with an intact uterus, unopposed estrogen has been shown to promote the growth of the endometrium which can lead to endometrial hyperplasia and possibly cancer over the long-term.",null,null,"Phase 3 on-going (NCT04833140)","Under clinical trials","2022-04-06"]
[477,"FM101",null,"Chemical drug",{"$nulls":4},false,{"$nulls":7},"A3 adenosine receptor modulator",null,"Phase 2 on-going (NCT04710524)","Under clinical trials","2022-04-06"]
[478,"GFT505",null,"Chemical drug",{"$nulls":4},false,{"$nulls":9},"Phase 2 completed (NCT01694849)","Under clinical trials","2022-04-06"]
[480,"Guanabenz",null,"Chemical drug","DB00629","Guanabenz is an alpha-2 adrenergic agonist used to treat hypertension.",null,"5051-62-7",true,"NC(N)=NN=CC1=C(Cl)C=CC=C1Cl","WDZVGELJXXEGPV-YIXHJXPBSA-N",231.082,"Alpha-2A adrenergic receptor agonist; Alpha-2B adrenergic receptor binder","Guanabenz's antihypertensive effect is thought to be due to central alpha-adrenergic stimulation, which results in a decreased sympathetic outflow to the heart, kidneys, and peripheral vasculature in addition to a decreased systolic and diastolic blood pressure and a slight slowing of pulse rate. Chronic administration of guanabenz also causes a decrease in peripheral vascular resistance.","Guanabenz, a centrally acting α-2 adrenergic agonist, is indicated for treatment of hypertension.","For management of High blood pressure.",null,null,"Phase 2 on-going (NCT05084404)","Under clinical trials","2022-04-06"]
[481,"HEC88473",null,"Chemical drug",{"$nulls":4},false,{"$nulls":7},"GLP-1 agonist; FGF21 agonist",null,"Phase 1 on-going (NCT04829123)","Under clinical trials","2022-04-06"]
[482,"Heme Oxygenase",null,"Biological drug",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (NCT00842205)","Under clinical trials","2022-04-06"]
[484,"Idebenone",null,"Chemical drug","DB09081","Idebenone is an analogue of ubiquinone used for the treatment of visual impairment in adolescent and adult patients with Leber’s Hereditary Optic Neuropathy (LHON).",null,"58186-27-9",true,"COC1=C(OC)C(=O)C(CCCCCCCCCCCCO)=C(C)C1=O","VMHWZDULLBLUMS-UHFFFAOYSA-N",366.498,null,"Idebenone is a synthetic analogue of ubiquinone (also known as Coenzyme Q10), a vital cell antioxidant and essential component of the Electron Transport Chain (ETC). It has been proposed that by interacting with the ETC, idebenone increases ATP production required for mitochondrial function, reduces free radicals, inhibits lipid peroxidation, and consequently protects the lipid membrane and mitochondria from oxidative damage. More specifically, idebenone is thought to transfer electrons directly to complex III of the mitochondrial ETC, thereby circumventing complex I and restoring cellular energy (ATP) generation.",null,"Idebenone is indicated for use by the European Medicines Agency (EMA) for the treatment of visual impairment in adolescent and adult patients with Leber’s Hereditary Optic Neuropathy (LHON). It is not currently approved for use by either the Food and Drug Administration (USA) or Health Canada.",null,null,"Phase 1&2 on-going (NCT04669158)","Under clinical trials","2022-04-06"]
[485,"IMM 124-E","Bovine Colostrum","Supplement",{"$nulls":4},false,{"$nulls":9},"Phase 2 withdrawn (NCT01466894: Sponsor administrative decision)","Under clinical trials","2022-04-06"]
[488,"LB-P6",null,"Chemical drug",{"$nulls":4},false,{"$nulls":9},"Phase 1 on-going (NCT05053165)","Under clinical trials","2022-04-06"]
[489,"Leronlimab",null,"Biological drug","DB05941","Leronlimab is a humanized monoclonal antibody being investigated",null,null,false,{"$nulls":3},"C-C chemokine receptor type 5 antagonist","CCR5 is a helical protein with multiple extracellular regions with adjacent G proteins.1,3 When a chemokine binds CCR5, the Gαβγ trimer phosphorylates GDP to GTP and Gα dissociates. Activated Gα activates adenylate cyclase, and increasing levels of cyclic AMP activate cytosolic protein kinase A. Further downstream effects of CCR5 signalling include activation of NF-κB and IL-6, as well as effects on cell proliferation, migration, and survival.\r\n\r\nHIV enters cells expressing CD4 and a fusion coreceptor such as CCR5 and CXCR4. Leronlimab is a monoclonal antibody which binds to multiple extracellular regions of the CCR5 receptor, preventing the entry of HIV into the cell.\r\n\r\nLeronlimab's blocking of CCR5 is being investigated in cancer treatment, for it's effect on the cell cycle and immuno-modulation.\r\n\r\nLeronlimab is also being investigated as a treatment for patients severely ill with COVID-19 due to it's effects on mitigating the cytokine storm and preventing immune-mediated injury.","Leronlimab is a humanized monoclonal antibody that binds CCR5 being investigated for it's anti-HIV, immunomodulatory, and anti-cancer effects.","Leronlimab is currently being investigated for the treatment of a number of cancers and HIV. \r\nRecently leronlimab has begun a phase II clinical trial in severely ill COVID-19 patients. Preliminary data shows a reduction in the 'cytokine storm', particularly IL-6, as well as a normalization of the CD4/CD8 T-cell ratio. These results may mitigate immune mediate injury seen in severely ill COVID-19 patients",null,null,"Phase 2 on-going (NCT04521114)","Under clinical trials","2022-04-06"]
[491,"Methyl-D9-choline",null,"Chemical drug","DB12628","Methyl-D9-choline is under investigation in clinical trial NCT01807910 (ER Stress in NAFLD).",null,"50673-41-1",false,"[2H]C([2H])([2H])[N+](CCO)(C([2H])([2H])[2H])C([2H])([2H])[2H]","OEYIOHPDSNJKLS-GQALSZNTSA-N",113.227,{"$nulls":6},"Phase 1 withdrawn (NCT01807910: The study was not funded)","Under clinical trials","2022-04-06"]
[492,"EDP-297",null,"Chemical drug",{"$nulls":4},false,{"$nulls":7},"FXR agonist","Anti-fibrotic effects","Phase 1 completed (NCT04559126)","Under clinical trials","2022-04-06"]
[493,"MET642",null,"Chemical drug",{"$nulls":4},false,{"$nulls":7},"FXR agonist",null,"Phase 2 on-going (NCT04773964)","Under clinical trials","2022-04-06"]
[494,"Mitoquinone mesylate","MitoQ","Chemical drug",{"$nulls":4},false,{"$nulls":9},"Phase 2 terminated (NCT01167088: This study has been terminated due to poor participant recruitment)","Under clinical trials","2022-04-06"]
[495,"MK-3655",null,"Chemical drug",{"$nulls":4},false,{"$nulls":7},"β-Klotho/FGFR1c agonist",null,"Phase 2 on-going (NCT04583423)","Under clinical trials","2022-04-06"]
[496,"Montelukast",null,"Chemical drug","DB00471","Montelukast is a leukotriene receptor antagonist used as part of an asthma therapy regimen, to prevent exercise induced bronchoconstriction, and to treat seasonal allergic rhinitis.",null,"158966-92-8",true,"OC(=O)CC1(CC1)CS[C@H](CCC1=CC=CC=C1C(O)©C)C1=CC=CC(\\C=C\\C2=NC3=C(C=CC(Cl)=C3)C=C2)=C1","UCHDWCPVSPXUMX-TZIWLTJVSA-N",586.183,null,"Cysteinyl leukotrienes (CysLT) like LTC4, LTD4, and LTE4, among others, are eicosanoids released by a variety of cells like mast cells and eosinophils. When such CysLT bind to corresponding CysLT receptors like CysLT type-1 receptors located on respiratory airway smooth muscle cells, airway macrophages, and on various pro-inflammatory cells like eosinophils and some specific myeloid stem cells activities that facilitate the pathophysiology of asthma and allergic rhinitis are stimulated.\r\n\r\nIn particular, CysLT-mediated airway bronchoconstriction, occluding mucous secretion, vascular permeability, and eosinophil recruitment are all types of effects that facilitate asthma. Alternatively, in allergic rhinitis, CysLTs are released by the nasal mucosa when exposed to allergens during both early and late phase reactions and participate in eliciting symptoms of allergic rhinitis like a congested nose and airway.\r\n\r\nSubsequently, montelukast is a leukotriene receptor antagonist that binds with high affinity and selectivity to the CysLT type 1 receptor, which consequently assists in inhibiting any physiological actions of CysLTs like LTC4, LTD4, and LTE4 at the receptor that may facilitate asthma or allergic rhinitis.","Montelukast is a leukotriene receptor antagonist that demonstrates a marked affinity and selectivity to the cysteinyl leukotriene receptor type-1 in preference to many other crucial airway receptors like the prostanoid, cholinergic, or beta-adrenergic receptors. As a consequence, the agent can elicit substantial blockage of LTD4 leukotriene-mediated bronchoconstriction with doses as low as 5 mg. Moreover, a placebo-controlled, crossover study (n=12) demonstrated that montelukast is capable of inhibiting early and late phase bronchoconstriction caused by antigen challenge by 75% and 57% respectively.\r\n\r\nIn particular, it has been documented that montelukast can cause bronchodilation as soon as within 2 hours of oral administration. This action can also be additive to the bronchodilation caused by the concomitant use of a beta agonist. Nevertheless, clinical investigations performed with adults 15 years of age and older revealed that no additional clinical benefit is obtained when doses of montelukast greater than 10 mg a day are used.\r\n\r\nAdditionally, in clinical trials with adults and pediatric asthmatic patients aged 6 to 14 years, it was also determined that montelukast can reduce mean peripheral blood eosinophils by about 13% to 15% from baseline in comparison to placebo during double-blind treatment periods. At the same time, in patients aged 15 years and older who were experiencing seasonal allergic rhinitis, the use of montelukast caused a median reduction of 13% in peripheral blood eosinophil counts when compared to placebo as well.","Montelukast is indicated for:\r\n(a) the prophylaxis and chronic treatment of asthma in adults and pediatric patients who are 12 months of age and older3, although other regional health authorities specifically note this indication for adults and adolescents who are 15 years and older and also include indications for preventing day and night-time symptoms, and the treatment of acetylsalicylic acid-sensitive asthma;\r\n(b) the prevention of exercise-induced bronchoconstriction (EIB) in patients who are 6 years of age and older, although other regional health authorities specifically note this indication for adults and adolescents who are 15 years and older; and\r\n(c) the relief of symptoms of seasonal allergic rhinitis in patients 2 years of age and older and perennial allergic rhinitis in patients 6 months of age and older, although other regional health authorities specifically note the relief of seasonal allergic rhinitis symptoms for adults and adolescents who are 15 years and older.\r\nFurthermore, some formulations like chewable montelukast tablets may also be specifically indicated by particular regulatory bodies for the prophylaxis and chronic treatment of asthma, including the prevention of day and night-time symptoms, the treatment of acetylsalicylic acid based asthma, and the prevention of exercise-induced bronchoconstriction in adult and pediatric patients aged 2 and older, between the ages 2 and 57, or between the ages of 6 and 14 years.\r\nMoreover, when employed for such indications montelukast is considered effective as monotherapy or when combined with other medications indicated for the maintenance treatment of chronic asthma. For instance, montelukast and inhaled corticosteroids can be used concomitantly to demonstrate additive effects to control asthma or to decrease the necessary inhaled corticosteroid dose while still maintaining clinical stability.\r\nAdditionally, in patients who continue to experience asthma symptoms, montelukast can also be combined with an 'as required' short-acting beta-agonist, an inhaled corticosteroid, or inhaled corticosteroid paired with a long-acting beta-agonist.",null,null,"Phase 1&2 completed (NCT04080947: Treatment with montelukast may represent a promising therapeutic strategy for patients with non-alcoholic steatohepatitis secondary to its efficacy and safety.)","Under clinical trials","2022-04-06"]
[497,"Namodenoson","CF102; 2-Cl-IB-MECA; CF102","Chemical drug",{"$nulls":3},"163042-96-4",false,"CNC(=O)[C@H]1O[C@@H](n2cnc3c(NCc4cccc(I)c4)nc(Cl)nc32)[C@H](O)[C@@H]1O","IPSYPUKKXMNCNQ-PFHKOEEOSA-N",544.74,{"$nulls":4},"A3 adenosine receptor agonist","Anti-inflammatory","Phase 2 on-going (NCT04697810)","Under clinical trials","2022-04-06"]
[498,"NNC0194-0499",null,"Chemical drug",{"$nulls":4},false,{"$nulls":9},"Phase 1 completed (NCT04722653)","Under clinical trials","2022-04-06"]
[499,"NS-0200","Leu-Met-Sil; Leucine-Metformin-Sildenafil Combination","Combinatory",{"$nulls":4},false,{"$nulls":9},"Phase 2 completed (NCT02546609)","Under clinical trials","2022-04-06"]
[500,"Ornithine Aspartic Acid Granules",null,"Biological drug",{"$nulls":4},false,{"$nulls":9},"Phase 4 on-going (NCT05042245)","Under clinical trials","2022-04-06"]
[502,"PF-07202954",null,"Chemical drug",{"$nulls":4},false,{"$nulls":9},"Phase 1 completed (NCT04857437)","Under clinical trials","2022-04-06"]
[503,"Silybin-phospholipids complex",null,"Combinatory",{"$nulls":4},false,{"$nulls":9},"Clinical trial completed (NCT04640324: The wild-type treated group showed a significant improvement of FPG, insulinemia, HOMA-IR, ALT, CRP, and TBARS (p < 0.05), whereas no improvements were recorded in the other two study groups.)","Under clinical trials","2022-04-06"]
[504,"Polyunsaturated Fatty Acids","Opti-EPA; PUFA","Supplement",{"$nulls":4},false,{"$nulls":9},"Phase 2 completed (NCT00323414: PUFA provided no benefit over placebo in NASH patients with diabetes. The effects of PUFA on histology and insulin resistance were inferior to placebo. These data provide no support for PUFA supplements in NASH.)","Under clinical trials","2022-04-06"]
[505,"RXC007",null,"Chemical drug",{"$nulls":4},false,{"$nulls":9},"Phase 1 on-going (NCT04931147)","Under clinical trials","2022-04-06"]
[506,"SNP-630",null,"Chemical drug",{"$nulls":4},false,{"$nulls":9},"Phase 1 completed (NCT04808154)","Under clinical trials","2022-04-06"]
[507,"Tilmanocept","Tc99m-Tilmanocept; (99m)Tc-Tilmanocept","Chemical drug","DB15373","Tilmanocep is under investigation in clinical trial NCT03241446 (Pharmacokinetics and Dosimetry of Tc 99m Tilmanocept Following a Single Intravenous Dose Administration in Male and Female Subjects Diagnosed With Rheumatoid Arthritis (RA)).",null,"1185986-76-8",false,{"$nulls":9},"Phase 1 completed (NCT03332940: Characteristics of agents such as tilmanocept that exploit the natural history of diseases with remarkably high specificity are the expectations for the future of patient- and disease-centered diagnosis and therapy.)","Under clinical trials","2022-04-06"]
[508,"Technetium Tc 99M Mebrofenin","(99m)Technetium-mebrofenin; (99m)Tc-mebrofenin","Chemical drug",{"$nulls":4},false,{"$nulls":9},"Phase 1 completed (NCT02235233: These in vitro data supported conclusions from modeling/simulation that ritonavir inhibited (99m)Tc-mebrofenin hepatic uptake, but not biliary excretion, at clinically relevant concentrations.)","Under clinical trials","2022-04-06"]
[510,"Trigonella Foenum-graecum Seed Extract",null,"Biological extract",{"$nulls":4},false,{"$nulls":9},"Phase 2&3 completed (NCT02303314)","Under clinical trials","2022-04-06"]
[512,"VK2735",null,"Chemical drug",{"$nulls":4},false,{"$nulls":9},"Phase 1 on-going (NCT05203237)","Under clinical trials","2022-04-06"]
[513,"VK2809",null,"Chemical drug","DB15137","VK-2809 is under investigation in clinical trial NCT02927184 (Safety and Tolerability of VK2809 in Patients With Primary Hypercholesterolemia and Non-Alcoholic Fatty Liver Disease).",null,"852948-13-1",false,"CC(C)C1=CC(CC2=C(C)C=C(OC[P@@]3(=O)OCC[C@H](O3)C3=CC=CC(Cl)=C3)C=C2C)=CC=C1O","LGGPZDRLTDGYSQ-JADSYQMUSA-N",514.98,{"$nulls":4},"THR-β agonist",null,"Phase 2 completed (NCT02927184)","Under clinical trials","2022-04-06"]
[514,"XW003",null,"Biological drug",{"$nulls":4},false,{"$nulls":9},"Phase 1 completed (NCT04389775)","Under clinical trials","2022-04-06"]
[515,"XZP-5610",null,"Chemical drug",{"$nulls":4},false,{"$nulls":7},"FXR agonist",null,"Phase 1 on-going (NCT04913090)","Under clinical trials","2022-04-06"]
[516,"XZP-6019",null,"Chemical drug",{"$nulls":4},false,{"$nulls":9},"Phase 1 on-going (NCT05063968)","Under clinical trials","2022-04-06"]
[517,"LB-P8",null,"Chemical drug",{"$nulls":4},false,{"$nulls":9},"Phase 1 on-going (NCT05053165)","Under clinical trials","2022-04-06"]
[518,"ALT-801",null,"Biological drug","DB15386",null,null,"1188450-53-4",false,{"$nulls":9},"Phase 1 on-going (NCT05006885)","Under clinical trials","2022-04-07"]
[519,"AstraZeneca","A Novel AstraZeneca Compound;  AZ compound","Chemical drug",{"$nulls":4},false,{"$nulls":9},"Phase 2 terminated (NCT02605616: Astra Zeneca notified Dr. Rita Basu that they will not manufacture new drug due to business reasons and study was stopped.)","Under clinical trials","2022-04-07"]
[520,"BMS-963272",null,"Chemical drug",{"$nulls":4},false,{"$nulls":9},"Phase 1 terminated (NCT04766476: Business objectives have changed)","Under clinical trials","2022-04-07"]
[521,"BMS-986171","PEGylated FGF21; BMS986171","Chemical drug",{"$nulls":4},false,{"$nulls":7},"Fibroblast growth factor replacements","Antifibrotics; Fibroblast growth factors; Hepatoprotectants","Phase 1 completed (NCT02538874)","Under clinical trials","2022-04-07"]
[522,"Caffeic acid","Cinnamates","Chemical drug",{"$nulls":4},false,{"$nulls":7},"STAT3 transcription factor inhibitor",null,"Phase 0 on-going (ChiCTR2000035899)","Under clinical trials","2022-04-07"]
[523,"Capparis Spinosa Fruit pickle",null,"Herbal medicine",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (IRCT2015122425686N1)","Under clinical trials","2022-04-07"]
[524,"Carom copticum","C.copticum","Herbal medicine",{"$nulls":4},false,{"$nulls":9},"Phase 3 on-going (ChiCTR2000035899)","Under clinical trials","2022-04-07"]
[525,"Dava AL-balgham","The equal proportions of Nigella Sativa ,Zataria Multiflora, Trachyspermum ammi, Pistacia lentiscus","Traditional medicine",{"$nulls":4},false,{"$nulls":8},"anti-inflammatory; Anti Atherogenic; antioxidants","Clinical trial on-going (IRCT2017073135415N1)","Under clinical trials","2022-04-07"]
[526,"DUR-928","25HC3S; DUR-928; DUR-928 sodium - DURECT Corporation; DV-928; Larsucosterol sodium - DURECT Corporation","Chemical drug",{"$nulls":4},false,{"$nulls":7},"DNA methylation inhibitors; Inflammation mediator modulators; Lipid modulators","Anti-inflammatories; Antipsoriatics; Hepatoprotectants","Phase 1 on-going (ACTRN12615001355561)","Under clinical trials","2022-04-07"]
[527,"EPA/DHA","omega-3 fatty acid","Supplement","DB11133","Omega-3 fatty acids is an ingredient found in a variety of supplements and vitamins.",null,"329042-31-1",false,{"$nulls":3},"Peroxisome proliferator-activated receptor gamma ligand; Peroxisome proliferator-activated receptor alpha activator; Sterol regulatory element-binding protein 1 inhibitor","Omega-3 fatty acids mediate anti-inflammatory effects and increased levels of EPA or DHA has shown to decrease the levels of PGE2 and 4 series-LT. Eicosapentaenoic acids compete with constitutive levels of arachidonic acid in cell membranes for the same desaturation enzymes and produce 3-series prostaglandins and thromboxanes, and 5-series leukotrienes which have low pro-inflammatory potential. The alteration in leukotriene biosynthesis due to higher concentration of omega-3 fatty acids compared to arachidonic acid underlies the anti-inflammatory effects. EPA and DHA also give rise to resolvins and related lipid signalling molecules such as protectins via cyclooxygenase and lipoxygenase pathways, which have anti-inflammatory effects. They inhibit transendothelial migration of neutrophils and inhibit TNF and IL-1β production. Omega-3 fatty acids also decrease adhesion molecule expression on leukocytes and on endothelial cells and decrease intercellular adhesive interactions. Omega-3 (or n-3) polyunsaturated fatty acids (PUFAs) and their metabolites are natural ligands for peroxisome proliferator-activated receptor (PPAR) gamma that regulates inflammatory gene expression and NFκB activation. PPAR alpha activation is also associated with induction of COX-2 expression. The role of EPA and DHA in reducing triglyceride levels include inhibition of acyl-CoA:1,2-diacylglycerol acyltransferase, increased mitochondrial and peroxisomal-beta-oxidation in the liver, decreased lipogenesis in the liver, and increased plasma lipoprotein lipase activity. They also may reduce triglyceride synthesis because they are poor substrates for the enzymes responsible for TG synthesis, and EPA and DHA inhibit esterification of other fatty acids.","Omega-3 fatty acids are triglycerides that get broken down into smaller fatty acid units. They act to reduce plasma triglyceride levels however increase the cholesterol levels and are thought to possess potent antiarrythmic effects. Polyunsaturated fatty acids including eicosapentaenoic and docosahexaenoic acid mediate important cellular function such as inhibition of platelet function, prolongation of bleeding time, anti-inflammatory effects and reduction of plasma fibrinogen. Polyunsaturated fatty acids are components of the phospholipids that form the structures of the cell membranes and also serve as energy source. They form eicosanoids which are important signalling molecules with wide-ranging functions in the body's cardiovascular, pulmonary, immune and endocrine systems. DHA tends to exist in high concentrations in the retina, brain (via uptake by Mfsd2a as a transporter), and sperm.","Provided as daily supplements. Aa preparation of omega-3-acid ethyl esters is licensed in UK for prevention of recurrent events after myocardial infarction in addition to treatment of hypertriglyceridaemia.",null,null,"Clinical trial on-going (JPRN-UMIN000012886)","Under clinical trials","2022-04-07"]
[529,"Gan-Jiang Ling-Zhu decoction",null,"Traditional medicine",{"$nulls":4},false,{"$nulls":9},"Phase 0 on-going (ChiCTR2000035798)","Under clinical trials","2022-04-07"]
[530,"GDD3898","GDD-3898","Chemical drug",{"$nulls":4},false,{"$nulls":8},"Hepatoprotectants; Obesity therapies","Phase 1 on-going (ACTRN12622000171718)","Under clinical trials","2022-04-07"]
[531,"GLP-1 analogue",null,"Biological drug",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (JPRN-UMIN000004512)","Under clinical trials","2022-04-07"]
[532,"Kashoos herbal syrup",null,"Herbal medicine",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (IRCT2014120320197N1)","Under clinical trials","2022-04-07"]
[533,"Lisinopril","Prinivil; Qbrelis; Zestoretic; Zestril","Chemical drug","DB00722","Lisinopril is an ACE inhibitor used to treat hypertension, heart failure, and acute myocardial infarction.",null,"76547-98-3",true,"NCCCC[C@H](N[C@@H](CCC1=CC=CC=C1)C(O)=O)C(=O)N1CCC[C@H]1C(O)=O","RLAWWYSOJDYHDC-BZSNNMDCSA-N",405.4879,"Angiotensin-converting enzyme inhibitor; Renin inhibitor","Angiotensin II constricts coronary blood vessels and is positively inotropic, which under normal circumstances, would increase vascular resistance and oxygen consumption. This action can eventually lead to myocyte hypertrophy and vascular smooth muscle cell proliferation.\r\n\r\nLisinopril is an angiotensin converting enzyme inhibitor (ACEI), preventing the conversion of angiotensin I to angiotensin II. This action prevents myocyte hypertrophy and vascular smooth muscle cell proliferation seen in untreated patients. Increased levels of bradykinin also exhibit vasodilating effects for patients taking ACEIs. Lisinopril also inhibits renin's conversion of angiotensin to angiotensin I.","Lisinopril is an angiotensin converting enzyme inhibitor used to treat hypertension, heart failure, and myocardial infarction. Lisinopril is not a prodrug, and functions by inhibition of angiotensin converting enzyme as well as the renin angiotensin aldosterone system. It has a wide therapeutic index and a long duration of action as patients are generally given 10-80mg daily.","Lisinopril is indicated for the treatment of acute myocardial infarction, hypertension in patients ≥6 years, and as an adjunct therapy for heart failure. A combination product with hydrochlorothiazide is indicated for the treatment of hypertension.","ACE inhibitor",null,"Phase 2 on-going (NCT04550481)","Under clinical trials","2022-04-07"]
[534,"Lepicol probiotic","Lepicol probiotic & prebiotic formula","Supplement",{"$nulls":4},false,{"$nulls":9},"Clinical trial completed (NCT00870012: Probiotics treatment may reduce liver fat and AST level in NASH patients. The therapeutic potential of probiotics in NASH should be tested in larger studies.)","Under clinical trials","2022-04-07"]
[535,"LM011","LM-011; LM 011","Chemical drug",{"$nulls":4},false,{"$nulls":8},"Hepatoprotectants","Phase 2 on-going (ACTRN12619000610134)","Under clinical trials","2022-04-07"]
[536,"Lycium barbarum polysaccharide supplementation",null,"Supplement",{"$nulls":4},false,{"$nulls":9},"Phase 0 on-going (ChiCTR2000034740)","Under clinical trials","2022-04-07"]
[537,"Lycopene supplementation",null,"Supplement",{"$nulls":4},false,{"$nulls":9},"Phase 0 on-going (ChiCTR2000035261)","Under clinical trials","2022-04-07"]
[538,"Mazindol","Sanorex","Chemical drug","DB00579","Mazindol is a sympathomimetic used to treat obesity in combination with lifestyle modifications.",null,"22232-71-9",true,"OC1(N2CCN=C2C2=CC=CC=C12)C1=CC=C(Cl)C=C1","ZPXSCAKFGYXMGA-UHFFFAOYSA-N",284.74,"Sodium-dependent noradrenaline transporter inhibitor; Sodium-dependent dopamine transporter inhibitor; Sodium-dependent serotonin transporter inhibitor; Synaptic vesicular amine transporter","Unlike other sympathomimetic appetite suppressants such as phentermine, mazindol is thought to inhibit the reuptake of norepinephrine rather than to cause its release.","Mazindol is a sympathomimetic amine that stimulates the central nervous system (nerves and brain), leading to increased your heart rate and blood pressure, and decreased appetite. Since the appetite-suppressing effect of the drug tends to decrease after few weeks of treatment, sympathomimetic appetite suppressants are typically used short-term weight-loss program.","Used in short-term (a few weeks) treatment of exogenous obesity in conjunction with a regimen of weight reduction based on caloric restriction, exercise, and behavior modification in patients with a body mass index of 30 kg of body weight per height in meters squared (kg/m2) or in patients with a body mass index of 27 kg/m2 in the presence of risk factors such as hypertension, diabetes, or hyperlipidemia.",null,null,"Clinical trial on-going (JPRN-UMIN000022879)","Under clinical trials","2022-04-07"]
[539,"N-Acetylsyctein",null,"Chemical drug",{"$nulls":4},false,{"$nulls":9},"Phase 3 on-going (IRCT201309188308N3)","Under clinical trials","2022-04-07"]
[540,"ninjin'yoeito","rehmannia root, Japanese angelica root, atractylodes rhizome, poria sclerotium, ginseng, cinnamon bark, polygala root, peony root, citrus unshiu peel, astragalus root, glycyrrhiza, and Schisandra fruit","Herbal medicine",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (JPRN-jRCTs071200113)","Under clinical trials","2022-04-07"]
[541,"Olmesartan","Olmesartan is an angiotensin receptor blocker (ARB) used in the treatment of hypertension.","Chemical drug","DB00275",null,null,"144689-24-7",true,"CCCC1=NC(=C(N1CC1=CC=C(C=C1)C1=C(C=CC=C1)C1=NN=NN1)C(O)=O)C©©O","VTRAEEWXHOVJFV-UHFFFAOYSA-N",446.5016,"Type-1 angiotensin II receptor antagonist","Olmesartan belongs to the angiotensin II receptor blocker (ARB) family of drugs, which also includes telmisartan, candesartan, losartan, valsartan, and irbesartan. ARBs selectively bind to angiotensin receptor 1 (AT1) and prevent the protein angiotensin II from binding and exerting its hypertensive effects. As the principal pressor agent of the renin-angiotensin system, Angiotensin II causes vasoconstriction, stimulation of synthesis and release of aldosterone, cardiac stimulation and renal reabsorption of sodium. Olmesartan blocks the vasoconstrictor effects of angiotensin II by selectively blocking the binding of angiotensin II to the AT1 receptor in vascular smooth muscle. Its action is, therefore, independent of the pathways for angiotensin II synthesis. Overall, olmesartan's physiologic effects lead to reduced blood pressure, lower aldosterone levels, reduced cardiac activity, and increased excretion of sodium.\r\nOlmesartan also effects on the renin-angiotensin aldosterone system (RAAS) plays an important role in hemostasis and regulation of kidney, vascular, and cardiac functions. Pharmacological blockade of RAAS via AT1 receptor blockade inhibits negative regulatory feedback within RAAS, which is a contributing factor to the pathogenesis and progression of cardiovascular disease, heart failure, and renal disease. In particular, heart failure is associated with chronic activation of RAAS, leading to inappropriate fluid retention, vasoconstriction, and ultimately a further decline in left ventricular function. ARBs have been shown to have a protective effect on the heart by improving cardiac function, reducing afterload, increasing cardiac output and preventing ventricular hypertrophy and remodelling.","Overall, olmesartan's physiologic effects lead to reduced blood pressure, lower aldosterone levels, reduced cardiac activity, and increased excretion of sodium.\r\nHypotension in Volume- or Salt-Depleted Patients\r\nIn patients with an activated renin-angiotensin aldosterone system, such as volume-and/or salt-depleted patients (e.g., those being treated with high doses of diuretics), symptomatic hypotension may be anticipated after initiation of treatment with olmesartan. Initiate treatment under close medical supervision. If hypotension does occur, place the patient in the supine position and, if necessary, give an intravenous infusion of normal saline. A transient hypotensive response is not a contraindication to further treatment, which usually can be continued without difficulty once the blood pressure has stabilized.\r\nValvular Stenosis: there is concern on theoretical grounds that patients with aortic stenosis might be at a particular risk of decreased coronary perfusion, because they do not develop as much afterload reduction.\r\nImpaired Renal Function\r\nAs a consequence of inhibiting the renin-angiotensin-aldosterone system, changes in renal function may be anticipated in susceptible individuals treated with olmesartan. In patients whose renal function may depend upon the activity of the renin-angiotensin- aldosterone system (e.g., patients with severe congestive heart failure), treatment with angiotensin converting enzyme (ACE) inhibitors and angiotensin receptor antagonists has been associated with oliguria and/or progressive azotemia and rarely with acute renal failure and/or death. Similar results may be anticipated in patients treated with olmesartan.\r\nIn studies of ACE inhibitors in patients with unilateral or bilateral renal artery stenosis, increases in serum creatinine or blood urea nitrogen (BUN) have been reported. There has been no long-term use of olmesartan medoxomil in patients with unilateral or bilateral renal artery stenosis, but similar results may be expected.\r\nSprue-like Enteropathy\r\nSevere, chronic diarrhea with substantial weight loss has been reported in patients taking olmesartan months to years after drug initiation. Intestinal biopsies of patients often demonstrated villous atrophy. If a patient develops these symptoms during treatment with olmesartan, exclude other etiologies. Consider discontinuation of olmesartan medoxomil in cases where no other etiology is identified.\r\nElectrolyte Imbalances\r\nOlmesartan medoxomil contains olmesartan, a drug that inhibits the renin-angiotensin system (RAS). Drugs that inhibit the RAS can cause hyperkalemia. Monitor serum electrolytes periodically.","Olmesartan is indicated for the treatment of hypertension either alone or in combination with other antihypertensive agents.\r\nOlmesartan is also used off-label for the management Type 2 Diabetes-associated nephropathy, heart failure, and post-myocardial infarction, particularly in patients who are unable to tolerate ACE inhibitor ARBs such as olmesartan have been shown in a number of large-scale clinical outcomes trials to improve cardiovascular outcomes including reducing risk of myocardial infarction, stroke, the progression of heart failure, and hospitalization. Like other ARBs, olmesartan blockade of RAAS slows the progression of diabetic nephropathy due to its renoprotective effects.",null,null,"Clinical trial on-going (JPRN-UMIN000001587)","Under clinical trials","2022-04-07"]
[542,"Olmesartan Medoxomil",null,"Chemical drug",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (JPRN-UMIN000005409)","Under clinical trials","2022-04-07"]
[543,"Plantago Psyllium and Ocimum Basilicum seeds",null,"Herbal medicine",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (IRCT2014101811763N17)","Under clinical trials","2022-04-07"]
[544,"Pomegranate peel extract","Punica granatum L.","Biological extract",{"$nulls":4},false,{"$nulls":9},"Phase 3 on-going (IRCT20091114002709N58)","Under clinical trials","2022-04-07"]
[545,"Pig placenta extract","PPE","Biological extract",{"$nulls":4},false,{"$nulls":9},"Phase 1 on-going (JPRN-jRCTs041210149)","Under clinical trials","2022-04-07"]
[546,"Proanthocyanidins",null,"Biological extract",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (ChiCTR-IPR-16008156)","Under clinical trials","2022-04-07"]
[547,"Qinghua Decoction",null,"Traditional medicine",{"$nulls":4},false,{"$nulls":9},"Phase 0 on-going (ChiCTR2000036225)","Under clinical trials","2022-04-07"]
[548,"Rilpivirine","Complera; Edurant; Juluca; Odefsey","Chemical drug","DB08864","Rilpivirine is a non-nucleoside reverse transcriptase inhibitor (NNRTI) used in combination with other antiretrovirals to specifically treat human immunodeficiency virus type 1 (HIV-1).",null,"500287-72-9",true,"CC1=CC(\\C=C\\C#N)=CC©=C1NC1=CC=NC(NC2=CC=C(C=C2)C#N)=N1","YIBOMRUWOWDFLG-ONEGZZNKSA-N",366.4185,"Reverse transcriptase/RNaseH inhibitor; Nuclear receptor subfamily 1 group I member 2 agonist","Rilpivirine is a non-competitive NNRTI that binds to reverse transcriptase.9 Its binding results in the blockage of RNA and DNA- dependent DNA polymerase activities, like HIV-1 replication. It does not present activity against human DNA polymerases α, β and γ. Rilpivirine's flexible structure around the aromatic rings allows the adaptation to changes in the non-nucleoside RT binding pocket, reducing the likelihood of viral mutations conferring resistance.","Rilpivirine is a non-nucleoside reverse transcriptase inhibitor that inhibits the replication of HIV-1. It has a long duration of action as the oral tablet is given daily and the intramuscular suspension is given monthly. Patients should be counselled regarding the risk of hypersensitivity reactions, hepatotoxicity, depressive disorders, and the redistribution or accumulation of body fat.","Rilpivirine, in combination with other agents, is indicated for the treatment of HIV-1 infections in antiretroviral treatment-naive patients with HIV-1 RNA ≤100,000 copies/mL and CD4+ cell count >200 cells/mm3.6 The FDA combination therapy approval of rilpivirine and dolutegravir is indicated for adults and adolescents 12 years of age and older weighing at least 35 kg with HIV-1 infections whose virus is currently suppressed (< 50 copies/ml) on a stable regimen for at least six months, without a history of treatment failure and no known substitutions associated to resistance to any of the two components of the therapy.\r\nRilpivirine in combination with cabotegravir is indicated as a complete regimen for the treatment of HIV-1 infection in adults to replace the current antiretroviral regimen in those who are virologically suppressed (HIV-1 RNA <50 copies/mL) on a stable antiretroviral regimen with no history of treatment failure and with no known or suspected resistance to either cabotegravir or rilpivirine.",null,null,"Phase 4 on-going (TCTR20210403003)","Under clinical trials","2022-04-07"]
[549,"SGLT2 inhibitor",null,"Chemical drug",{"$nulls":4},false,{"$nulls":7},"SGLT2 inhibitor",null,"Clinical trial on-going (JPRN-UMIN000027362)","Under clinical trials","2022-04-07"]
[550,"DPP4 inhibitor",null,"Chemical drug",{"$nulls":4},false,{"$nulls":7},"DPP4 inhibitor",null,"Clinical trial on-going (JPRN-UMIN000027304)","Under clinical trials","2022-04-07"]
[551,"Sijunzi Decoction",null,"Traditional medicine",{"$nulls":4},false,{"$nulls":9},"Phase 0 on-going (ChiCTR2000036224)","Under clinical trials","2022-04-07"]
[552,"TERN-201","TERN 201","Chemical drug",{"$nulls":4},false,{"$nulls":7},"AOC3 protein inhibitor","Hepatoprotectants","Phase 1 on-going (NCT04897594)","Under clinical trials","2022-04-07"]
[553,"TQA3526","TQA-3526","Chemical drug",{"$nulls":4},false,{"$nulls":7},"Farnesoid X-activated receptor agonist","Hepatoprotectants","Phase 1 on-going (ChiCTR1800019570)","Under clinical trials","2022-04-07"]
[554,"Turmeric and Chicory seeds","Turmeric seed; Curcuma longa L.; Cichorium intybus L.","Herbal medicine",{"$nulls":4},false,{"$nulls":9},"Phase 2 on-going (IRCT201406183664N12)","Under clinical trials","2022-04-07"]
[555,"Vitamin Bs",null,"Supplement",{"$nulls":4},false,{"$nulls":9},"Phase 3 on-going (IRCT20180908040972N1)","Under clinical trials","2022-04-07"]
[556,"Wuwei Baogan Pill",null,"Traditional medicine",{"$nulls":4},false,{"$nulls":9},"Phase 1 on-going (ChiCTR2000036882)","Under clinical trials","2022-04-07"]
[557,"Yinchen Linggui decoction",null,"Traditional medicine",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (ChiCTR2000036882)","Under clinical trials","2022-04-07"]
[558,"Yinchenhao decoction","Artemisia capillaris Thunb.","Traditional medicine",{"$nulls":4},false,{"$nulls":9},"Phase 0 on-going (ChiCTR2000034868)","Under clinical trials","2022-04-07"]
[559,"Cynarol",null,"Chemical drug",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (IRCT2015122125641N1)","Under clinical trials","2022-04-07"]
[560,"Grape seed polyphenols","Vitis vinifera L.","Biological extract",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (ChiCTR1800018428)","Under clinical trials","2022-04-07"]
[561,"Korea Red Ginseng","Panax schinseng","Herbal medicine",{"$nulls":4},false,{"$nulls":9},"Phase 4 completed (NCT02331589)","Under clinical trials","2022-04-07"]
[562,"Levocarnitine Chloride",null,"Chemical drug",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (JPRN-UMIN000013760)","Under clinical trials","2022-04-07"]
[563,"Purslane seeds","Portulaca oleracea L.","Herbal medicine",{"$nulls":4},false,{"$nulls":9},"Phase 3 on-going (IRCT2014090210826N14)","Under clinical trials","2022-04-07"]
[564,"Rice Bran Nutritional Supplement","RBAC; Oryza sativa L.","Biological extract",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (NCT02568787)","Under clinical trials","2022-04-07"]
[565,"TurmXtra 60N","Water dispersible Turmeric extract","Biological extract",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (CTRI/2020/03/023814)","Under clinical trials","2022-04-07"]
[566,"Zataria multiflora Boiss.",null,"Herbal medicine",{"$nulls":4},false,{"$nulls":9},"Clinical trial on-going (IRCT2015120925447N1)","Under clinical trials","2022-04-07"]
[567,"IMA-1",null,"Chemical drug",{"$nulls":4},false,{"$nulls":7},"12-lipoxygenase (ALOX12)–acetyl-CoA carboxylase 1 (ACC1)  inhibitor",null,null,"Under investigation","2022-05-06"]
[568,"ML355","ML-355; VLX-1005","Chemical drug",{"$nulls":4},false,{"$nulls":7},"12-lipoxygenase inhibitor","Platelet aggregation inhibitor",null,"Under investigation","2022-05-06"]
[570,"INI-678","INI 678","Chemical drug",{"$nulls":4},false,{"$nulls":7},"17-hydroxysteroid dehydrogenase modulators","Antifibrotics; Hepatoprotectants",null,"Under investigation","2022-05-06"]
[571,"GW7647",null,"Miscellany",{"$nulls":4},false,{"$nulls":7},"PPARα agonist","Anti-diabetic drugs",null,"Under investigation","2022-05-06"]
[572,"GLP1/2-Fc fusion",null,"Miscellany",{"$nulls":4},false,{"$nulls":7},"GLP-1/GLP-2R dual agonist","Anti-diabetic drugs",null,"Under investigation","2022-05-06"]
[573,"Oxyntomodulin analogue","OXM analogue","Miscellany",{"$nulls":4},false,{"$nulls":7},"Glucagon like peptide 1 receptor agonists; Glucagon receptor agonists","Anti-diabetic drugs",null,"Under investigation","2022-05-06"]
[574,"ND-654","ND-630; ND-646","Chemical drug",{"$nulls":4},false,{"$nulls":7},"Acetyl-CoA carboxylase inhibitor","Enhance lipid metabolism",null,"Under investigation","2022-05-06"]
[575,"WZ66",null,"Miscellany",{"$nulls":4},false,{"$nulls":7},"ACC inhibitor","Enhance lipid metabolism",null,"Under investigation","2022-05-06"]
[576,"Hydroxy citrate",null,"Chemical drug",{"$nulls":4},false,{"$nulls":7},"ACLY iinhibitor","Enhance lipid metabolism",null,"Under investigation","2022-05-06"]
[577,"Bempedoic acid","ETC-1002","Chemical drug",{"$nulls":4},false,{"$nulls":7},"ACLY iinhibitor","Enhance lipid metabolism",null,"Under investigation","2022-05-06"]
[578,"25-HL",null,"Miscellany",{"$nulls":4},false,{"$nulls":7},"SREBP inhibitor","Enhance lipid metabolism",null,"Under investigation","2022-05-06"]
[579,"Emfilermin","AM 424; Leukaemia inhibitory factor; Leukemia inhibitory factor; LIF; recombinant leukaemia inhibitory factor","Miscellany",{"$nulls":4},false,{"$nulls":7},"adipocytes","Enhance lipid metabolism",null,"Under investigation","2022-05-06"]
[580,"Tiliamsoine",null,"Miscellany",{"$nulls":4},false,{"$nulls":7},"FXR agonist","Enhance lipid metabolism",null,"Under investigation","2022-05-06"]
[581,"sobetirome","GC-1; NV 1205; QRX-431","Chemical drug",{"$nulls":4},false,{"$nulls":7},"Thyroid hormone receptor beta agonists","Enhance lipid metabolism",null,"Under investigation","2022-05-06"]
[582,"EPB-53",null,"Miscellany",{"$nulls":4},false,{"$nulls":7},"FGF21 agonist","Enhance lipid metabolism",null,"Under investigation","2022-05-06"]
[583,"Doxorubicin","SA 033; SA 083","Chemical drug",{"$nulls":4},false,{"$nulls":7},"DNA intercalators; Type II DNA topoisomerase inhibitors","Enhance lipid metabolism",null,"Under investigation","2022-05-06"]
[584,"shRNA-mediated knockdown of Sms1",null,"Miscellany",{"$nulls":4},false,{"$nulls":10},"Under investigation","2022-05-06"]
[585,"Overexpression of RASSF4",null,"Miscellany",{"$nulls":4},false,{"$nulls":7},"Ras-association domain family 4 (RASSF4) agonists",null,null,"Under investigation","2022-05-06"]
[586,"CGS21680","CGS 21680C","Miscellany",{"$nulls":4},false,{"$nulls":7},"Adenosine A2 receptor agonists","Antiepileptic drugs; Antihypertensives; Antiparkinsonians; Anxiolytics; Neuroprotectants",null,"Under investigation","2022-05-06"]
[587,"Fecal microbiota transplantation","FMT","Miscellany",{"$nulls":4},false,{"$nulls":10},"Under investigation","2022-05-06"]
[588,"Momelotinib","CYT-387; GS-0387; Momelotinib dihydrochloride","Chemical drug",{"$nulls":4},false,{"$nulls":7},"ACVR1 protein inhibitors; Janus kinase 1 inhibitors; Janus kinase-2 inhibitors","Antineoplastics; Antirheumatics",null,"Under investigation","2022-05-06"]
[589,"Minor allele-specific small interfering RNA","siRNA","Miscellany",{"$nulls":4},false,{"$nulls":7},"PNPLA3-rs738409 (I148M) variant inhibitor",null,null,"Under investigation","2022-05-06"]
[590,"Polaprezinc","Aprozinate; Aprozinato; Promac; Z 103; ZC 103; Zinc L-carnosine","Chemical drug",{"$nulls":4},false,{"$nulls":7},"Lipid peroxidation inhibitors","Anti-oxidative stress",null,"Under investigation","2022-05-06"]
[591,"Matrine",null,"Miscellany",{"$nulls":4},false,{"$nulls":8},"Anti-oxidative stress",null,"Under investigation","2022-05-06"]
[592,"Ncst ASO",null,"Miscellany",{"$nulls":4},false,{"$nulls":7},"Notch inhibitor","Anti-fibrosis",null,"Under investigation","2022-05-06"]
[593,"GSI",null,"Miscellany",{"$nulls":4},false,{"$nulls":7},"Notch inhibitor","Anti-fibrosis",null,"Under investigation","2022-05-06"]
[594,"GalNAc-siTAZ",null,"Miscellany",{"$nulls":4},false,{"$nulls":7},"TAZ inhibitor","Anti-fibrosis",null,"Under investigation","2022-05-06"]
[595,"AAV8-ALB-hHNF 4α",null,"Miscellany",{"$nulls":4},false,{"$nulls":8},"Anti-fibrosis",null,"Under investigation","2022-05-06"]
[596,"Emodin","Emodol","Chemical drug",{"$nulls":4},false,{"$nulls":7},"DNA synthesis inhibitors; Protein synthesis inhibitors; Protein tyrosine kinase inhibitors; RNA synthesis inhibitors","Anti-fibrosis",null,"Under investigation","2022-05-06"]
[597,"Yellow loosestrife","Lysimachia vulgaris var. davurica","Herbal medicine",{"$nulls":4},false,{"$nulls":8},"Anti-fibrosis",null,"Under investigation","2022-05-06"]
[598,"Tetrodecadazinone",null,"Chemical drug",{"$nulls":4},false,{"$nulls":8},"Anti-fibrosis",null,"Under investigation","2022-05-06"]
[599,"TIPE2",null,"Miscellany",{"$nulls":4},false,{"$nulls":8},"Anti-fibrosis",null,"Under investigation","2022-05-06"]
[600,"Oxy210","Oxy-210","Chemical drug",{"$nulls":4},false,{"$nulls":7},"Hedgehog cell-signalling pathway inhibitors; Transforming growth factor beta inhibitors; Virus replication inhibitors","Anti-fibrosis",null,"Under investigation","2022-05-06"]
[601,"SP-1154",null,"Miscellany",{"$nulls":4},false,{"$nulls":8},"Anti-fibrosis",null,"Under investigation","2022-05-06"]
[602,"IGF-I",null,"Miscellany",{"$nulls":4},false,{"$nulls":7},"P53 activitor","Anti-fibrosis",null,"Under investigation","2022-05-06"]
[603,"Ravoxertinib","GD0 994; GDC-0994; RG-7842","Chemical drug",{"$nulls":4},false,{"$nulls":7},"Extracellular signal-regulated MAP kinase inhibitors; Mitogen activated protein kinase 3 inhibitors; Mitogen-activated protein kinase 1 inhibitors","Anti-inflammatory",null,"Under investigation","2022-05-06"]
[604,"FR180204",null,"Miscellany",{"$nulls":4},false,{"$nulls":8},"Anti-inflammatory",null,"Under investigation","2022-05-06"]
[605,"Sulforaphen","SFN","Miscellany",{"$nulls":4},false,{"$nulls":7},"NLRP3 inhibitor","Anti-inflammatory",null,"Under investigation","2022-05-06"]
[606,"Sparstolonin B","SsnB","Miscellany",{"$nulls":4},false,{"$nulls":7},"TLR4 antagonist","Anti-inflammatory",null,"Under investigation","2022-05-06"]
[607,"Anti-IL11","X203","Biological drug",{"$nulls":4},false,{"$nulls":7},"IL11 antibody","Anti-inflammatory",null,"Under investigation","2022-05-06"]
[608,"anti-IL11RA","X209","Biological drug",{"$nulls":4},false,{"$nulls":7},"IL11 antibody","Anti-inflammatory",null,"Under investigation","2022-05-06"]
[609,"Annexin A5","ANXA5","Miscellany",{"$nulls":4},false,{"$nulls":8},"Anti-inflammatory",null,"Under investigation","2022-05-06"]
[610,"Thalidomide",null,"Chemical drug",{"$nulls":4},false,{"$nulls":7},"Tumour necrosis factor inhibitors","Antifibrotics; Antileprotics; Antineoplastics; Anti-inflammatory",null,"Under investigation","2022-05-06"]
[611,"Infliximab","GS 071; NI-071","Biological drug",{"$nulls":4},false,{"$nulls":7},"Tumour necrosis factor alpha inhibitors","Anti-inflammatories",null,"Under investigation","2022-05-06"]
[612,"Rapamycin","AY 22989; CYPHER; CYPHER SELECT PLus; HYFTOR; NEVO; NPC-12; NPC-12G; NPC-12T; NSC 226080; NSC 606698; Rapalimus; Rapamune; Sirolimus","Miscellany",{"$nulls":4},false,{"$nulls":7},"Immunosuppressants; Methylmalonyl CoA mutase stimulants; MTOR protein inhibitors; T lymphocyte inhibitors",null,null,"Under investigation","2022-05-06"]
[613,"shRNA against ATG3",null,"Biological drug",{"$nulls":4},false,{"$nulls":7},"ATG3 inhibitor",null,null,"Under investigation","2022-05-06"]
[614,"Flavopiridol","Alvocidib hydrochloride; DSP-2033; Flavopiridol; Flavopiridol hydrochloride; HL-275; HMR 1275; IND 46211; L-86-8275; MDL-107826A; NSC 649890","Chemical drug",{"$nulls":4},false,{"$nulls":7},"Cyclin dependent kinase 9 inhibitors","Antineoplastics",null,"Under investigation","2022-05-06"]
[615,"PD-0332991","Palbociclib; Ibrance; Iburance; Parvociclib; PD-0332991; PD-332991; PD-991","Chemical drug",{"$nulls":4},false,{"$nulls":7},"Cyclin-dependent kinase 4 inhibitors; Cyclin-dependent kinase 6 inhibitors",null,null,"Under investigation","2022-05-06"]
[616,"ECH1",null,"Miscellany",{"$nulls":4},false,{"$nulls":7},"Ferroptosis inhibitor","Anti-apoptosis",null,"Under investigation","2022-05-06"]
[617,"Glutathione S-transferase Mu 2","GSTM2","Miscellany",{"$nulls":4},false,{"$nulls":7},"ASK1 inhibitor","Anti-apoptosis",null,"Under investigation","2022-05-06"]
[618,"Adeno-associated virus 8 (AAV8)-TNFAIP3 injection",null,"Miscellany",{"$nulls":4},false,{"$nulls":7},"ASK1 inhibitor","Anti-apoptosis",null,"Under investigation","2022-05-06"]
[619,"Peptide fragment of CFLAR","CFLAR(S1)","Biological drug",{"$nulls":4},false,{"$nulls":7},"ASK1 inhibitor","Anti-apoptosis",null,"Under investigation","2022-05-06"]