Repositioning Candidate Details
| Candidate ID: | R0212 |
| Source ID: | DB00605 |
| Source Type: | approved; investigational |
| Compound Type: | small molecule |
| Compound Name: | Sulindac |
| Synonyms: | (Z)-5-Fluoro-2-methyl-1-((p-(methylsulfinyl)phenyl)methylene)-1H-indene-3-acetic acid; cis-5-Fluoro-2-methyl-1-((4-(methylsulfinyl)phenyl)methylene)-1H-indene-3-acetic acid; cis-5-Fluoro-2-methyl-1-((p-methylsulfinyl)benzylidene)indene-3-acetic acid |
| Molecular Formula: | C20H17FO3S |
| SMILES: | CC1=C(CC(O)=O)C2=CC(F)=CC=C2\C1=C/C1=CC=C(C=C1)S(C)=O |
| Structure: |
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| DrugBank Description: | Sulindac is a nonsteroidal anti-inflammatory drug (NSAID) of the arylalkanoic acid class that is marketed by Merck under the brand name Clinoril. Like other NSAIDs, it may be used in the treatment of acute or chronic inflammatory conditions. Sulindac is a prodrug, derived from sulfinylindene, that is converted _in vivo_ to an active sulfide compound by liver enzymes. There is evidence from some studies that sulindac may be associated with fewer gastrointestinal side effects than other NSAIDs, except for the cyclooxygenase-2 (COX-2) inhibitor drug class. This may be due to the sulfide metabolite undergoing enterohepatic circulation thus maintaining constant blood levels of the compound without inducing gastrointestinal effects, where the drug is excreted in the bile and then reabsorbed from the intestines. While its full mechanism of action is not fully understood, sulindac is thought to primarily mediate its action by inhibiting prostaglandin synthesis by inhibiting COX-1 and COX-2. |
| CAS Number: | 38194-50-2 |
| Molecular Weight: | 356.411 |
| DrugBank Indication: | For acute or long-term use in the relief of signs and symptoms of osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, acute painful shoulder (acute subacromial bursitis/supraspinatus tendinitis), and acute gouty arthritis. |
| DrugBank Pharmacology: | Sulindac is a non-steroidal anti-inflammatory indene derivative, also possessing analgesic and antipyretic activities. |
| DrugBank MoA: | Sulindac's exact mechanism of action is unknown. Its antiinflammatory effects are believed to be due to inhibition of both COX-1 and COX-2 which leads to the inhibition of prostaglandin synthesis. Antipyretic effects may be due to action on the hypothalamus, resulting in an increased peripheral blood flow, vasodilation, and subsequent heat dissipation. |
| Targets: | Prostaglandin G/H synthase 2 inhibitor; Prostaglandin G/H synthase 1 inhibitor; Aldose reductase inhibitor; Mitogen-activated protein kinase 3 inhibitor; Peroxisome proliferator-activated receptor delta negative modulator; Prostaglandin D2 receptor 2 antagonist; Aldo-keto reductase family 1 member B10 inhibitor |
| Inclusion Criteria: | Therapeutic strategy associated |
| Strategy ID | Strategy | Synonyms | Related Targets | Related Drugs | |
|---|---|---|---|---|---|
| S05 | Anti-inflammatory | inflammatory | Bile acid; TNF-a inhibitor; Dual PPAR-α and -δ agonists; Toll-Like Receptor; (TLR)-4 antagonist; Caspase inhibitor; ASK-1 inhibitor | Ursodeoxycholic Acid; Pentoxifylline; Elafibranor; JKB-121; Emricasan; Selonsertib; | Details |
| Diseases ID | DO ID | Disease Name | Definition | Class | |
|---|---|---|---|---|---|
| I15 | 1290 | Bone disease | A connective tissue disease that affects the structure or development of bone or causes an impairment of normal bone function. http://en.wikipedia.org/wiki/Bone_disease | disease of anatomical entity/ musculoskeletal system disease/connective tissue disease | Details |