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["Target_ID","Target_Name","Synonyms","Target_GENE","Target_Action","Target_Class","Related_Drugs","UniProtKB_ID","UniProtKB_Entry_Name","Mechanism","Reference_PMIDs","ChEMBL_ID","Update"]
[1,"5'-AMP-activated protein kinase subunit beta-1","AMPK; AMPK subunit beta-1; PRKAB1; AMP-activated protein kinase, beta-1 subunit","PRKAB1","activator","Kinase","Metformin; Glucophage","Q9Y478","AAKB1_HUMAN","Liver-specific AMPK activation reprograms lipid metabolism, reduces liver steatosis, decreases expression of inflammation and fibrosis genes, and leads to significant therapeutic benefits in the context of diet-induced obesity. These findings further support AMPK as a target for the prevention and treatment of NAFLD.","30605676","CHEMBL3847","2022-03-21"]
[2,"Sodium/glucose cotransporter 2","SGLT2; Low affinity sodium-glucose cotransporter; Na(+)/glucose cotransporter 2; Solute carrier family 5 member 2; SLC5A2","SLC5A2","inhibitor","Transporter","Empagliflozin; Canagliflozin; Dapagliflozin","P31639","SC5A2_HUMAN","Sodium-glucose cotransporter 2 inhibitors (SGLT2i) are increasingly used antidiabetic drugs that increase urinary glucose excretion by inhibiting the reabsorption of glucose in the proximal tubule of the kidney. Inhibition of SGLT2 causes an additional 60 to 80 g of glucose per day to be excreted out of the body, which leads to caloric loss and weight reduction. There is a growing expectation that this mechanism of SGLT2i will assist in the improvement of NAFLD.","27531551; 21606218; 26380062","CHEMBL3884","2022-03-21"]
[3,"Peroxisome proliferator-activated receptor alpha","PPARA; PPAR-α; PPAR-alpha; NR1C1; Nuclear receptor subfamily 1 group C member 1","PPARA","agonist","Nuclear hormone receptor","Bezafibrate; DHA; Elafibranor; Epanova; Fenofibrate; Omega 3 PUFA; Rosiglitazone; Gemfibrozil","Q07869","PPARA_HUMAN","Peroxisome proliferator activated receptor-α (PPARα) activity is associated with increased energy burning and reduced fat storage in the liver. PPARα upregulates a number of genes that play roles in fatty acid oxidation and in phospholipid remodeling, and it inhibits hepatic inflammatory processes.","24524207","CHEMBL239","2022-03-21"]
[4,"Peroxisome proliferator-activated receptor delta","PPARD; PPAR-δ; PPAR-delta; NR1C2; NUC1; NUCI; Nuclear hormone receptor 1; Nuclear receptor subfamily 1 group C member 2; Peroxisome proliferator-activated receptor beta; PPAR-beta; PPARB; PPAR-β; PPAR β/δ","PPARD","agonist","Nuclear hormone receptor","Bezafibrate; Elafibranor; Rosiglitazone","Q03181","PPARD_HUMAN","Activation of PPARβ/δ promotes fatty acid metabolism and suppresses macrophage-mediated inflammation; Hepatic PPARβ/δ is involved in transforming potentially toxic lipids into less toxic molecules by regulating monounsaturated fatty acid synthesis and increasing AMP-activated protein kinase activity, thereby suppressing lipogenesis and glycogen synthesis, reducing gluconeogenesis, and increasing fatty acid oxidation. PPARβ/δ also stimulates anti-inflammatory responses in the liver.","35242173","CHEMBL3979","2022-03-21"]
[5,"Peroxisome proliferator-activated receptor gamma","PPARG; PPARG-γ; PPARG-gamma; NR1C3; Nuclear receptor subfamily 1 group C member 3","PPARG","agonist","Nuclear hormone receptor","Bezafibrate; Curcumin; DHA; Elafibranor; Epanova; Lobeglitazone; Omega 3 PUFA; Pioglitazone; Rosiglitazone; Telmisartan; Troglitazone","P37231","PPARG_HUMAN","The induction of PPARγ promotes the differentiation of large insulin-resistant pre-adipocytes into small, insulin-sensitive adipocytes.","8754811","CHEMBL235","2022-03-21"]
[6,"Glucagon-like peptide 1 receptor","GLP1R; GLP-1; GLP-1 receptor","GLP1R","agonist","GPCR","Dulaglutide; Exenatide; Glucagon; Liraglutide; Semaglutide","P43220","GLP1R_HUMAN","Glucagon-like peptide 1 (GLP-1) analogues have been reported to be involved in weight loss and systemic insulin resistance reduction, which may lead to improvements in NAFLD. GLP-1 analogues may also act directly on human hepatocytes to decrease de novo adipogenesis and increase fatty acid oxidation, thereby ameliorating NAFLD.","20225248","CHEMBL1784","2022-03-21"]
[7,"Bile acid receptor","BAR; Farnesoid X-activated receptor; Farnesol receptor HRR-1; FXR; HRR1; Nuclear receptor subfamily 1 group H member 4; Retinoid X receptor-interacting protein 14; RIP14; RXR-interacting protein 14; NR1H4","NR1H4","agonist","Nuclear hormone receptor","Obeticholic Acid; Tropifexor; Ursodeoxycholic acid","Q96RI1","NR1H4_HUMAN","Bile acids are natural ligands of the farnesoid X receptor (FXR). Together they regulate lipid and/or glucose homeostasis, promote insulin sensitivity, and potentially regulate liver fibrosis. FXR agonists have been shown to prevent the development of NASH and promote the resolution of NASH and fibrosis in rodent models.","25705637; 15860571; 25690590","CHEMBL2047","2022-03-21"]
[8,"Tumor necrosis factor","Cachectin; TNF-a; TNF-alpha; TNFA; TNFSF2; Tumor necrosis factor ligand superfamily member 2; TNF","TNF","inhibitor","Cytokine","Pentoxifylline","P01375","TNFA_HUMAN","TIPE2 suppresses NAFLD advancement by blocking TAK1-JNK/p38 pathway and is a promising target molecule for NAFLD therapy.","33768585","CHEMBL1825","2022-03-21"]
[9,"Toll-like receptor 4","TLR-4; hToll; TLR4","TLR4","antagonist","Membrane receptor","JKB-121","O00206","TLR4_HUMAN","Increased hepatocyte Jagged1 is the proximal hit for Notch-induced liver fibrosis in mice and suggest translational potential of Jagged1 inhibitors in patients with NASH.","34162749","CHEMBL5255","2022-03-21"]
[10,"Caspase-1","CASP-1; ICE; IL-1 beta-converting enzyme; IL-1BC; IL1BC; IL1BCE; Interleukin-1 beta convertase; Interleukin-1 beta-converting enzyme; p45; CASP1","CASP1","inhibitor","Enzyme","Emricasan","P29466","CASP1_HUMAN","Intervention with a caspase-1 inhibitor attenuated the development of NASH, liver fibrosis and insulin resistance. Data support the importance of inflammasome/caspase-1 in the development of NASH and demonstrate that therapeutic intervention in the already ongoing disease process is feasible.","27121255","CHEMBL4801","2022-03-21"]
[11,"Caspase-3","Apopain; CASP-3; CPP-32; CPP32; Cysteine protease CPP32; Protein Yama; SCA-1; SREBP cleavage activity 1; CASP3","CASP3","inhibitor","Enzyme","Emricasan","P42574","CASP3_HUMAN","Hepatocyte caspase 3 activation in NASH-related apoptosis, fibrogenesis and fibrosis which in part is mediated via CCR2-dependent infiltration of Ly6c positive monocytes.","24795036","CHEMBL2334","2022-03-21"]
[12,"Caspase-7","Apoptotic protease Mch-3; CASP-7; CMH-1; ICE-LAP3; ICE-like apoptotic protease 3; MCH3; CASP7","CASP7","inhibitor","Enzyme","Emricasan","P55210","CASP7_HUMAN","Activation of caspases, Bcl-2 family proteins, and c-Jun N-terminal kinase-induced hepatocyte apoptosis plays a role in the activation of NAFLD/NASH.","29991872","CHEMBL3468","2022-03-21"]
[13,"Apoptosis Signal-regulating Kinase 1","ASK1; ASK-1","ASK1","inhibitor","Enzyme","Selonsertib","Q99683","M3K5_HUMAN","In human livers of lean and obese subjects, ASK1 expression correlated negatively with liver fat content and NASH scores, but positively with markers for autophagy. Taken together, ASK1 may be a novel therapeutic target to tackle NAFLD and liver fibrosis.  Hepatocyte GSTM2 is an endogenous suppressor that protects against NASH progression by blocking ASK1 N-terminal dimerization and phosphorylation. Activating GSTM2 holds promise as a therapeutic strategy for NASH.","31595673; 34656650","CHEMBL5285","2022-03-21"]
[14,"Mitogen-activated protein kinase kinase kinase 5","MAP3K5; MAPK/ERK kinase kinase 5; MEK kinase 5; MEKK 5","MAP3K5","inhibitor","Enzyme","Selonsertib","Q99683","M3K5_HUMAN","CASP8 and FADD-like apoptosis regulator (CFLAR) as a key suppressor of steatohepatitis and indicate that the development of CFLAR-peptide-mimicking drugs and the screening of small-molecular inhibitors that specifically block ASK1 dimerization are new and feasible approaches for NASH treatment.","28218919","CHEMBL5285","2022-03-21"]
[15,"3-hydroxy-3-methylglutaryl-coenzyme A reductase","HMG-CoA reductase; HMGCR","HMGCR","inhibitor","Enzyme","Rosuvastatin; Pitavastatin; Atorvastatin","P04035","HMDH_HUMAN","Dicer1/miR-29/HMGCR axis contributes to hepatic free cholesterol accumulation in mouse NASH, and miR-29 may serve as an important regulator of hepatic cholesterol homeostasis. Thus, miR-29a could be utilized as a potential therapeutic target for the treatment of non-alcoholic fatty liver disease as well as for other liver diseases associated with FC accumulation","28112179","CHEMBL402","2022-03-21"]
[16,"Niemann-Pick C1-like protein 1","Niemann-Pick C1-like protein 1 precursor; \r\nNPC1L1","NPC1L1","inhibitor","Membrane other","Ezetimibe","Q9UHC9","NPCL1_HUMAN","Duodenal NPC1L1 expression was decreased in NAFLD and was negatively correlated with LXR expression in PMN cells. The livers of Ad‑L1 mice represent a more human‑like state for the study of hepatic autophagy. Hepatic expression of human NPC1L1 resulted in an inhibition of autophagy; it may contribute to alcoholic fatty liver disease in humans.","29466845; 31432115","CHEMBL2027","2022-03-21"]
[17,"Farnesoid X-activated receptor","FXR; Bile acid receptor","NR1H4","agonist","Nuclear hormone receptor","Obeticholic Acid; Tropifexor; Ursodeoxycholic acid","Q96RI1","NR1H4_HUMAN","Farnesoid X receptor (FXR), a nuclear receptor for bile acids, is widely expressed in the intestine, liver and kidneys, and is responsible for the homeostasis of cholesterol metabolism.","32552182; 28774887","CHEMBL2047","2022-03-21"]
[18,"Acetyl-CoA carboxylase 1","ACC; ACC1; ACCA; ACC-alpha; ACAC; ACACA","ACACA","inhibitor","Enzyme","Firsocostat","Q13085","ACACA_HUMAN","Acetyl-CoA carboxylases (ACCs) catalyse the committed step in DNL through the conversion of acetyl-CoA to malonyl-CoA. Furthermore, the product of this reaction, malonyl-CoA, is a signalling molecule that suppresses fatty acid oxidation through the inhibition of carnitine palmitoyltransferase 1. Thus, ACC inhibition could reduce hepatic lipid accumulation by suppressing DNL and stimulating fatty acid oxidation. ACC inhibitors improve hepatic steatosis and insulin sensitivity but increase plasma concentrations of triglyceride in mice, rats and humans.","28768177","CHEMBL3351","2022-03-21"]
[19,"Acetyl-CoA carboxylase 2","ACC-beta; ACC2; ACCB; ACACB","ACACB","inhibitor","Enzyme","Firsocostat","O00763","ACACB_HUMAN","Acetyl-CoA carboxylases (ACCs) catalyse the committed step in DNL through the conversion of acetyl-CoA to malonyl-CoA. Furthermore, the product of this reaction, malonyl-CoA, is a signalling molecule that suppresses fatty acid oxidation through the inhibition of carnitine palmitoyltransferase 1. Thus, ACC inhibition could reduce hepatic lipid accumulation by suppressing DNL and stimulating fatty acid oxidation. ACC inhibitors improve hepatic steatosis and insulin sensitivity but increase plasma concentrations of triglyceride in mice, rats and humans.","26976583","CHEMBL4829","2022-03-21"]
[20,"Fatty acid synthase","FAS; FASN","FASN","inhibitor","Enzyme","TVB-2640","P49327","FAS_HUMAN","Fatty acid synthase (FAS) is a critical enzyme in the DNL pathway that uses malonyl-CoA, synthesized by ACC, to form saturated long-chain fatty acids. The hepatic expression and activity of FAS are upregulated in NAFLD and preclinical studies in obese mice demonstrate that FAS inhibition lowers liver levels of triglycerides and improves insulin sensitivity.","21389266","CHEMBL4158","2022-03-21"]
[21,"Diacylglycerol O-acyltransferase 2","DGAT2; Acyl-CoA retinol O-fatty-acyltransferase; ARAT; Diglyceride acyltransferase 2; Retinol O-fatty-acyltransferase","DGAT2","inhibitor","Enzyme","IONIS-DGAT2rx","Q96PD7","DGAT2_HUMAN","The final step in triglyceride synthesis, esterifying a fatty acyl-CoA moiety to diacylglycerol, is catalysed by diacylglycerol acyltransferase (DGAT). Two isoforms of this enzyme have been identified, DGAT1 and DGAT2, which have distinct patterns of expression and substrate specificity.","18757836","CHEMBL5853","2022-03-21"]
[22,"Stearoyl-CoA desaturase","SCD FADS5; SCD1; SCDOS; SCD","SCD","inhibitor","Enzyme","Aramchol","O00767","SCD_HUMAN","Stearoyl-CoA desaturase 1 (SCD1) is a fatty acid desaturase, highly expressed in lipogenic tissues, such as adipose and liver, that converts saturated fatty acids, such as palmitate and stearate, to monounsaturated fatty acids.","29089222","CHEMBL5555","2022-03-21"]
[23,"Type-1 angiotensin II receptor","AGTR1A; AGTR1B; Angiotensin II type-1 receptor; AT1; AT1AR; AT1BR; AT2R1; AT2R1B; Angiotensin Receptor; AGTR1","AGTR1","antagonist","GPCR","Losartan; Telmisartan","P30556","AGTR1_HUMAN","Treatment with angiotensin II type I receptor blocker attenuated the progression of hepatic steatosis, activation of hepatic stellate cells, expression of transforming growth factor beta 1, and liver fibrosis in the rat methione-choline-deficient diet model of nonalcoholic steatohepatitis.","17518368","CHEMBL227","2022-03-21"]
[24,"C-C chemokine receptor type 2","C-C CKR-2; CMKBR2; MCP-1-R; Monocyte chemoattractant protein 1 receptor; CCR2","CCR2","antagonist","GPCR","Cenicriviroc","P41597","CCR2_HUMAN","C-C motif chemokine receptor (CCR) type 2 plays a role in the recruitment, migration and infiltration of proinflammatory monocytes and macrophages at the site of liver injury. C motif chemokine receptor types 2 and 5 are both involved in the inflammatory and fibrogenic pathways.","32381514","CHEMBL4015","2022-03-21"]
[25,"C-C chemokine receptor type 5","C-C CKR-5; CHEMR13; CMKBR5; HIV-1 fusion coreceptor; CCR5","CCR5","antagonist","GPCR","Cenicriviroc","P51681","CCR5_HUMAN","CCR5 in the activation and proliferation of collagen-producing activated hepatic stellate cells/myofibroblasts. C motif chemokine receptor types 2 and 5 are both involved in the inflammatory and fibrogenic pathways.","32381514","CHEMBL274","2022-03-21"]
[26,"Thyroid hormone receptor beta","c-erbA-2; c-erbA-beta; ERBA2; NR1A2; Nuclear receptor subfamily 1 group A member 2; THR1; Thyroid receptor β; THRB","THRB","agonist","Nuclear hormone receptor","Levothyroxine; VK-2809; MGL-3196; Resmetirom","P10828","THB_HUMAN","Thyroid hormones are involved in the regulation of hepatic triglyceride and cholesterol metabolism. Thyroid hormones reduce serum cholesterol by affecting cholesterol synthesis, LDL clearance, and reverse cholesterol transport. In this respect, thyroid hormone receptor-β (THR-β), which is mainly expressed in the liver, could be a target for NAFLD treatment.","31389309","CHEMBL1947","2022-03-21"]
[28,"Fibroblast growth factor 21","FGF21; FGF-21","FGF21","analogue","Secreted","Pegbelfermin","Q9NSA1","FGF21_HUMAN","FGF21 is a key regulator of whole-body and individual organ metabolism. It activates a cell membrane co-receptor complex of β-klotho and one of its cognate FGF receptors (FGFRs), FGFR1c, FGFR2c or FGFR3c. FGF21 and its analogs improve metabolic status in preclinical models of obesity, diabetes and NASH, suggesting promise as a therapeutic for NASH. FGF-21 plays a central role in regulating energy metabolism.","33381084; 32764725; 26567701",null,"2022-03-21"]
[29,"Fibroblast growth factor 19","FGF-19; FGF19","FGF19","variant","Secreted","NGM282","O95750","FGF19_HUMAN","Human FGF19 is a gastrointestinal hormone that regulates bile acid synthesis, glucose metabolism and hepatic fatty acid oxidation, and is known to be a target of FXR; Fibroblast growth factor 19 (FGF-19) plays a central role in regulating bile acids and energy metabolism in the liver via FGF receptor 4.","32781086; 26567701",null,"2022-03-21"]
[30,"Lysyl oxidase homolog 2","LOXL2; LOXL-2","LOXL2","antibody","Enzyme","Simtuzumab","Q9Y4K0","LOXL2_HUMAN","The mechanism entails a cross-talk between enhanced lipotoxicity in insulin resistant HEPs and Loxl2 production by HSCs, which was confirmed in patients with diabetes, thereby facilitating extracellular matrix (ECM) stabilization.","28468951","CHEMBL3714029","2022-03-21"]
[31,"Galectin-3","Galectin 3; 35 kDa lectin; Carbohydrate-binding protein 35; CBP 35; Gal-3; Galactose-specific lectin 3; Galactoside-binding protein; GALBP; IgE-binding protein; L-31; Laminin-binding protein; Lectin L-29; Mac-2 antigen; MAC2; LGALS3","LGALS3","inhibitor","Enzyme","GR-MD-02; Belapectin","P17931","LEG3_HUMAN","The present study confirmed the roles of Gal3 in hepatic lipid metabolism in both in vitro and in vivo studies and revealed that Gal3 is a secretory protein that promotes hepatic steatosis through the PPARγ-CD36-dependent pathway, suggesting that targeting Gal3 may represent a potential therapeutic approach for the treatment of NAFLD and related metabolic disorders.","33991615","CHEMBL4531","2022-03-21"]
[32,"Ketohexokinase","KHK","KHK","inhibitor","Enzyme","PF-06835919","P50053","KHK_HUMAN","Ketohexokinase is an enzyme that catalyses the phosphorylation of fructose to fructose-1-phosphate, an important step in fructose metabolism. Fructose overconsumption leads to elevated ketohexokinase expression, impaired fatty acid oxidation, increased DNL, hepatic steatosis and impaired insulin signalling, but this effect can be mitigated by the liver-specific deletion of ketohexokinase in high fructose-fed mice.","32694791; 32502381","CHEMBL1275212","2022-03-31"]
[33,"Mitochondrial pyruvate carrier 1","MPC1","MPC1","inhibitor","Enzyme","MSDC-0602K","Q9Y5U8","MPC1_HUMAN","In the past decade, the mitochondrial pyruvate carrier (MPC) was identified as a heterodimeric complex of two proteins, MPC1 and MPC2, which functions to transport pyruvate from the cytosol across the inner mitochondrial membrane. This is a required step in the conversion of carbohydrate to fatty acids via DNL.","22628558",null,"2022-03-31"]
[34,"Mitochondrial pyruvate carrier 2","MPC2","MPC2","inhibitor","Enzyme","MSDC-0602K","O95563","MPC2_HUMAN","In the past decade, the mitochondrial pyruvate carrier (MPC) was identified as a heterodimeric complex of two proteins, MPC1 and MPC2, which functions to transport pyruvate from the cytosol across the inner mitochondrial membrane. This is a required step in the conversion of carbohydrate to fatty acids via DNL.","22628558","CHEMBL4295686","2022-03-31"]
[35,"Platelet glycoprotein Ib alpha","Platelet GPIbα; GP-Ib alpha; GPIb-alpha; GPIbA; Glycoprotein Ibalpha","GP1BA","inhibitor","Enzyme","aspirin/clopidogrel; ticagrelor","P07359","GP1BA_HUMAN","Platelet-derived GPIbα proved critical for development of NASH and subsequent HCC, independent of its reported cognate ligands vWF, P-selectin or Mac-1, offering a potential target against NASH.","30936549","CHEMBL4630891","2022-03-31"]
[36,"Caspase-6","Caspase-6; CASP-6; CSP-6","CASP6","inhibitor","Enzyme",null,"P55212","CASP6_HUMAN","Active caspase-6 cleaved Bid to induce cytochrome c release, generating a feedforward loop that leads to hepatocyte death. Thus, the AMPK-caspase-6 axis regulates liver damage in NASH, implicating AMPK and caspase-6 as therapeutic targets.","32029622","CHEMBL3308","2022-03-31"]
[37,"Caspase-2","Caspase-2; CASP-2","CASP2","inhibitor","Enzyme",null,"P42575","CASP2_HUMAN","Caspase-2 inhibition offers a specific and effective strategy for preventing or treating stress-driven fatty liver diseases, whereas caspase-2-generated S1P proteolytic fragments, which enter the secretory pathway, are potential NASH biomarkers.","30220454","CHEMBL4884","2022-03-31"]
[38,"Caspase-4","Caspase-4; CASP-4; Caspase-11; CASP-11","Casp4","inhibitor","Enzyme",null,"P49662","CASP4_HUMAN","Upregulated caspase-11 was detected in liver of mice with NASH. MCD-treated caspase-11-deficient mice had significantly decreased liver injury, fibrosis, and inflammation. The activation of gasdermin D and interleukin-1β was inhibited in caspase-11-deficient mice after MCD treatment. Overexpression of caspase-11 promoted steatohepatitis. Caspase-11-mediated hepatocytic pyroptosis promotes the progression of NASH.","33894425","CHEMBL2226","2022-03-31"]
[39,"Glutathione S-transferase Mu 2","GSTM2; GST4","GSTM2","agonist","Enzyme",null,"P28161","GSTM2_HUMAN","These data demonstrated that hepatocyte GSTM2 is an endogenous suppressor that protects against NASH progression by blocking ASK1 N-terminal dimerization and phosphorylation. Activating GSTM2 holds promise as a therapeutic strategy for NASH.","34656650","CHEMBL4589","2022-04-03"]
[40,"N-formyl peptide receptor 2","Formyl peptide receptor; FMLP-related receptor I, FMLP-R-I; Formyl peptide receptor-like 1;  HM63; Lipoxin A4 receptor, LXA4 receptor; RFP","FPR2","inhibitor","Enzyme",null,"P25090","FPR2_HUMAN","FPR2 has anti-inflammatory roles in the liver and that its sex-specific expression is closely related to sex disparities in NAFLD/NASH development. Higher expression of FPR2 in female mice than in male mice makes females more resistant to NAFLD development and progression, and severe injury in FPR2-depleted female mice supports the protective effect of FPR2 in the livers of female mice. Estrogen directly regulates FPR2 expression, which is related to estrogen-mediated protection against NAFLD.","35102146","CHEMBL4227","2022-04-03"]
[41,"X-box-binding protein 1","XBP-1; XBP1; Tax-responsive element-binding protein 5, TREB-5","XBP1","inhibitor","Protein",null,"P17861","XBP1_HUMAN","The severity of liver disease in patients with NASH was positively correlated with XBP1 expression. Macrophage XBP1 exacerbates the development of steatohepatitis by increasing M1 macrophage transition and pro-inflammatory cytokines secretion, which promote lipid accumulation and inflammatory response in hepatocyte. Macrophage Xbp1 depletion inhibits fibrogenesis and hepatic stellate cells activation. Hepatocyte XBP1 aggravates the development of steatohepatitis by promoting lipid accumulation via enhancing lipogenesis and inhibiting lipolysis. Pharmacological XBP1 inhibitors might bring light to the treatment of steatohepatitis.","35292349","CHEMBL1741176","2022-04-03"]
[42,"Serine/threonine-protein kinase 17B","DAP kinase-related apoptosis-inducing protein kinase 2; death-associated protein kinase-related apoptosis-inducing kinase-2 (DRAK2)","STK17B","inhibitor","Kinase",null,"O94768","ST17B_HUMAN","novel therapeutic targets for the treatment of this pandemic disease.","34614409","CHEMBL3980","2022-04-03"]
[43,"TGF-beta-activated kinase 1 and MAP3K7-binding protein 1","Mitogen-activated protein kinase kinase kinase 7-interacting protein 1; TGF-beta-activated kinase 1-binding protein 1, TAK1-binding protein 1; TGF-β-activated kinase; TAK1","TAB1","inhibitor","Kinase",null,"Q15750","TAB1_HUMAN","RNA-sequencing and multiomics analyses further indicated that the key mechanism linking the anti-NASH effects of breviscapine was inhibition of TGF-β-activated kinase 1 (TAK1) phosphorylation and the subsequent mitogen-activated protein kinase signaling cascade. Treatment with the TAK1 inhibitor 5Z-7-oxozeaenol abrogated breviscapine-mediated hepatoprotection under metabolic stress. Molecular docking illustrated that breviscapine directly bound to TAK1.","34717002","CHEMBL5605","2022-04-03"]
[44,"Amine oxidase, copper containing","semicarbazide-sensitive amine oxidase (SSAO); vascular adhesion protein-1 (VAP-1); AOC3; Copper amine oxidase; HPAO; Membrane primary amine oxidase; Semicarbazide-sensitive amine oxidase; SSAO; VAP1; VAP-1; Vascular adhesion protein 1","AOC3","inhibitor","Enzyme","ECC0509","Q16853","AOC3_HUMAN","The elevations in hepatic VAP-1 expression reported in nonalcoholic steatohepatitis can contribute to steatosis, metabolic disturbance and inflammation. This suggests that targeting the semicarbazide sensitive amine oxidase capacity of VAP-1 may represent a useful adjunct to other therapeutic strategies in NAFLD.","33312420","CHEMBL3437","2022-04-05"]
[45,"Arachidonate 12-lipoxygenase","12LO; 12S-lipoxygenase; 12S-LOX; ALOX12; Arachidonate (12S)-lipoxygenase; Arachidonate (15S)-lipoxygenase; Linoleate (13S)-lipoxygenase; Lipoxin synthase 12-LO; LOG12; Platelet-type lipoxygenase 12; Polyunsaturated fatty acid lipoxygenase ALOX12","ALOX12","inhibitor","Enzyme","IMA-1","P18054","LOX12_HUMAN","ALOX12 was shown to induce NASH by directly targeting acetyl-CoA carboxylase 1 (ACC1) via a lysosomal degradation mechanism. Overall, our findings reveal a key molecular driver of NASH pathogenesis and suggest that ALOX12-ACC1 interaction may be a therapeutic target in NASH.","34910546","CHEMBL3687","2022-05-06"]
[46,"ATP-citrate synthase","ACL; ACLY; ATP-citrate (pro-S-)-lyase; ATP-citrate synthase; Citrate cleavage enzyme","ACLY","inhibitor","Transferase","Bempedoic acid (ETC-1002)","P53396","ACLY_HUMAN","ATP citrate lyase (ACLY) is a cytoplasmic enzyme that responsible for the generation of acetyl coenzyme A (acetyl-CoA) in de novo lipogenesis and cholesterol synthesis. ACLY inhibitor, alleviates high-fat diet (HFD) induced NASH in male C57BL6/N mice, including decreased body weight gain, improved glycemic control, reduced hepatic TG and total cholesterol (TC), lowered mRNA expression of inflammatory and fibrotic genes (Ccl2, Timp1 and Col1a1), and improvement in NAS score.5","34909677; 28153881","CHEMBL3720","2022-05-06"]