Company InfoNewsInvestor InformationResearchDevelopmentCareersBusiness DevelopmentResourcesDrugs databaseBack to the home pageSearch  
Drugs database
Drugs A-Z

Brands A-Z

Drugs by categories

Drugs by manufacturer

Drugs by packager

Antibiotics for sale

Online Viagra bestellen in Nederland

Home / Drugs / Starting with S / Sulindac
 
Sulindac
 

Sulindac is a nonsteroidal anti-inflammatory agent (NSAIA) of the arylalkanoic acid class that is marketed in the U.S. by Merck as Clinoril. Like other NSAIAs, 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. The sulfide metabolite then undergoes enterohepatic circulation; it is excreted in the bile and then reabsorbed from the intestine. This is thought to help maintain constant blood levels with reduced gastrointestinal side effects. Some studies have shown sulindac to be relatively less irritating to the stomach than other NSAIA's except for drugs of the cyclooxygenase-2 (COX-2) inhibitor class. The exact mechanism of its NSAIA properties is unknown, but it is thought to act on enzymes COX-1 and COX-2, inhibiting prostaglandin synthesis.
BrandsClinoril
CategoriesAntineoplastic Agents
Anti-inflammatory Agents
Cyclooxygenase Inhibitors
Analgesics
Analgesics, Non-Narcotic
Antipyretics
Nonsteroidal Anti-inflammatory Agents (NSAIAs)
ManufacturersMerck research laboratories div merck co inc
Epic pharma llc
Heritage pharmaceuticals inc
Mutual pharmaceutical co inc
Mylan pharmaceuticals inc
Sandoz inc
Teva pharmaceuticals usa inc
Watson laboratories inc
PackagersA-S Medication Solutions LLC
Avkare Incorporated
Bryant Ranch Prepack
Dept Health Central Pharmacy
DHHS Program Support Center Supply Service Center
Direct Dispensing Inc.
Dispensing Solutions
Diversified Healthcare Services Inc.
Endo Pharmaceuticals Inc.
Epic Pharma LLC
Golden State Medical Supply Inc.
Group Health Cooperative
H.J. Harkins Co. Inc.
Heartland Repack Services LLC
Heritage Pharmaceuticals
Innoviant Pharmacy Inc.
Kaiser Foundation Hospital
Keltman Pharmaceuticals Inc.
Major Pharmaceuticals
Merck & Co.
Murfreesboro Pharmaceutical Nursing Supply
Mutual Pharmaceutical Co.
Mylan
Nucare Pharmaceuticals Inc.
PD-Rx Pharmaceuticals Inc.
Pharmedix
Physicians Total Care Inc.
Prepackage Specialists
Prepak Systems Inc.
Prescription Dispensing Service Inc.
Qualitest
Richmond Pharmacy
Southwood Pharmaceuticals
Spectrum Pharmaceuticals
St Mary's Medical Park Pharmacy
Stat Rx Usa
Tya Pharmaceuticals
UDL Laboratories
Va Cmop Dallas
Watson Pharmaceuticals

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.

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 dissipation.

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.

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.

absorption

Approximately 90% absorbed in humans following oral administration.

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.

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.

drug interactions

Acenocoumarol: The NSAID, sulindac, may increase the anticoagulant effect of acenocoumarol. Consider alternate therapy or monitor for signs and symptoms of bleeding during concomitant therapy.

Acetylsalicylic acid: Risk of additive toxicity (e.g. bleed risk). Acetylsalicylic acid may decrease the serum concentration of sulindac. Sulindac may counteract the cardioprotective effects of acetylsalicylic acid. Consider alternate therapy or monitor for changes in the therapeutic and adverse effects of both agents if the interacting agent is initiated, discontinued or dose changed.

Aminosalicylic Acid: Risk of additive toxicity (e.g. bleed risk). Aminosalicylic acid may decrease the serum concentration of sulindac. Consider alternate therapy or monitor for changes in the therapeutic effects of sulindac and adverse effects of both agents if the interacting agent is initiated, discontinued or dose changed.

Bumetanide: The NSAID, sulindac, decreases the diuretic and antihypertensive effects of the loop diuretic, bumetanide.

Cholestyramine: The bile acid sequestrant, cholestyramine, may decrease the absorption of the NSAID, sulindac. Monitor for changes in the therapeutic and adverse effects of sulindac if cholestyramine is initiated, discontinued or dose changed. Administering the two agents 2 or more hours apart may reduce, but not eliminate, the risk of this interactions.

Colesevelam: The bile acid sequestrant, colesevelam, may decrease the absorption of the NSAID, sulindac. Sulindac should be administered at least 1 hour before or 4 hours after colesevelam. Monitor for changes in the therapeutic and adverse effects of sulindac if colesevelam is initiated, discontinued or dose changed.

Colestipol: The bile acid sequestrant, colestipol, may decrease the absorption of the NSAID, sulindac. Monitor for changes in the therapeutic and adverse effects of sulindac if colestipol is initiated, discontinued or dose changed. Administering the two agents 2 or more hours apart may reduce, but not eliminate, the risk of this interactions.

Cyclosporine: The NSAID, sulindac, may increase the nephrotoxic effect of cyclosporine. Sulindac may increase the serum concentration of cyclosporine. Consider alternate therapy or monitor for increased cyclosporine levels and nephrotoxicity during concomitant therapy.

Ethacrynic acid: The NSAID, sulindac, may decrease the diuretic and antihypertensive effects of the loop diuretic, ethacryninc acid.

Furosemide: The NSAID, sulindac, may decrease the diuretic and antihypertensive effects of the loop diuretic, furosemide.

Ginkgo biloba: Ginkgo biloba may enhance the anticoagulant effect of sulindac. Increased risk of bleeding, bruising and altered mental status due to CNS bleeds. Concomitant therapy should be avoided.

Ginseng: Ginseng may enhance the anticoagulant effect of sulindac. Increased risk of bleeding, bruising and altered mental status due to CNS bleeds. Concomitant therapy should be avoided.

Ketorolac: May cause additive or synergistic NSAID toxicities (e.g. GI bleeding, renal dysfunction, etc.). Concomitant therapy is contraindicated.

Methotrexate: The NSAID, sulindac, may decrease the clearance methotrexate. Consider alternate therapy, especially in patients receiving high antineoplastic doses of methotrexate. Otherwise, monitor for hematologic and renal toxicities.

Pemetrexed: The NSAID, sulindac, may increase the serum concentration of pemetrexed by decreasing its elimination. This interaction more prevalent in patients with mild to moderate renal insufficiency. Consider alternate therapy or monitor for pemetrexed toxicity during concomitant therapy.

S-Adenosylmethionine: S-adenosylmethionine may enhance the anticoagulant effect of sulindac. Increased risk of bleeding, bruising and altered mental status due to CNS bleeds. Concomitant therapy should be avoided.

Salicylate-sodium: Risk of additive toxicity (e.g. bleed risk). Salicylate-sodium may decrease the serum concentration of sulindac. Consider alternate therapy or monitor for changes in the therapeutic effects of sulindac and adverse effects of both agents if the interacting agent is initiated, discontinued or dose changed.

Salsalate: Risk of additive toxicity (e.g. bleed risk). Salsalate may decrease the serum concentration of sulindac. Consider alternate therapy or monitor for changes in the therapeutic effects of sulindac and adverse effects of both agents if the interacting agent is initiated, discontinued or dose changed.

Telmisartan: Concomitant use of Telmisartan and Sulindac may increase the risk of acute renal failure and hyperkalemia. Monitor renal function at the beginning and during treatment.

Timolol: The NSAID, Sulindac, may antagonize the antihypertensive effect of Timolol.

Trandolapril: The NSAID, Sulindac, may reduce the antihypertensive effect of Trandolapril. Consider alternate therapy or monitor for changes in Trandolapril efficacy if Sulindac is initiated, discontinued or dose changed.

Treprostinil: The prostacyclin analogue, Treprostinil, may increase the risk of bleeding when combined with the NSAID, Sulindac. Monitor for increased bleeding during concomitant thearpy.

Warfarin: The antiplatelet effects of sulindac may increase the bleed risk associated with warfarin. Consider alternate therapy or monitor for signs and symptoms of bleeding during concomitant therapy.