Name: | Sulindac |
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PubChem Compound ID: | 11588179 |
Description: | A sulfinylindene derivative prodrug whose sulfinyl moiety is converted in vivo to an active NSAID analgesic. Specifically, the prodrug is converted by liver enzymes to a sulfide which is excreted in the bile and then reabsorbed from the intestine. This helps to maintain constant blood levels with reduced gastrointestinal side effects. |
Molecular formula: | C19H15FO3S |
Molecular weight: | 342.385 g/mol |
Name: | Sulindac |
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Name (isomeric): | DB00605 |
Drug Type: | small molecule |
Description: | A sulfinylindene derivative prodrug whose sulfinyl moiety is converted in vivo to an active NSAID analgesic. Specifically, the prodrug is converted by liver enzymes to a sulfide which is excreted in the bile and then reabsorbed from the intestine. This helps to maintain constant blood levels with reduced gastrointestinal side effects. |
Brand: | Clinoril |
Category: | Analgesics, Non-Narcotic, Antineoplastic Agents, Antipyretics, Cyclooxygenase Inhibitors, Analgesics, Anti-inflammatory Agents, Nonsteroidal Anti-inflammatory Agents (NSAIAs) |
CAS number: | 38194-50-2 |
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. |
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Pharmacology: | Sulindac is a non-steroidal anti-inflammatory indene derivative, also possessing analgesic and antipyretic activities. |
Mechanism of Action: |
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 dissipat...
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Absorption: | Approximately 90% absorbed in humans following oral administration. |
Protein binding: | At 1 mcg/ml concentrations, approximately 93% sulindac and 98% of its sulfide metabolite are bound to human serum albumin. |
Biotransformation: | Undergoes two major biotransformations: reversible reduction to the sulfide metabolite, and irreversible oxidation to the sulfone metabolite. Sulindac and its sulfide and sulfone metabolites undergo extensive enterohepatic circulation. Available evidence indicates that the biological activity resides with the sulfide metabolite. Side chain hydroxylation and hydration of the double bond also occur. |
Route of elimination: | Sulindac is excreted in rat milk; concentrations in milk were 10 to 20% of those levels in plasma. It is not known if sulindac is excreted in human milk. Approximately 50% of the administered dose of sulindac is excreted in the urine with the conjugated sulfone metabolite accounting for the major portion. Hepatic metabolism is an important elimination pathway. |
Half Life: | The mean half-life of sulindac is 7.8 hours while the mean half-life of the sulfide metabolite is 16.4 hours. |
Clearance: | Renal cl=68.12 +/- 27.56 mL/min [NORMAL (19-41 yrs)] |
Toxicity: | Acute oral toxicity (LD50) in rats is 264 mg/kg. Cases of overdose have been reported and rarely, deaths have occurred. The following signs and symptoms may be observed following overdose: stupor, coma, diminished urine output and hypotension. |
Affected organisms: | Humans and other mammals |
Drug interaction: |
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