Sulindac
2-[6-fluoro-2-methyl-3- [(4-methylsulfinylphenyl)methylidene]inden-1-yl]- acetic acid

本品為非固醇類抗炎劑，同時有鎮痛、解熱作用，其治療作用，為抑制Prostaglandin Synthesis，本劑及其Sulfide代謝產物均有抗炎作用。

Absorption
T max is 3 to 4 h. Approximately 90% of the drug is absorbed after oral administration.

Distribution
93% bound to plasma proteins. Sulindac does penetrate the blood-brain and placental barriers.

Metabolism
Recirculation of sulindac and its sulfone metabolite is more active and extensive than that of the active sulfide metabolite.

Elimination
The t ½ is 7.8 h. The main route of excretion is via the urine. Approximately 25% is found in feces, primarily as the sulfone and sulfide metabolites. Renal clearance is 68 to 74 mL/min.

Special Populations
Renal Function Impairment
A lower daily dose should be anticipated to avoid excessive drug accumulation.

Hepatic Function Impairment
Plasma concentrations have been reported to be higher in patients with alcoholic liver disease; patients with acute and chronic hepatic disease may require reduced doses.

ACE inhibitors (eg, captopril), angiotensin II antagonists (eg, losartan)
The antihypertensive effect may be decreased by sulindac.

Anticoagulants
May increase effect of anticoagulants because of decreased plasma protein binding. May increase risk of gastric erosion and bleeding.

Aspirin
Risk of GI adverse reactions may be increased; plasma levels of active sulindac metabolite may be reduced.

Bile acid sequestrants (eg, cholestyramine)
Plasma levels of sulindac may be reduced.

Cimetidine
Sulindac has increased cimetidine bioavailability.

Cyclosporine
Risk of cyclosporine toxicity may be increased.

Diflunisal
Plasma level of active sulindac metabolite may be reduced.

Dimethyl sulfoxide
Dimethyl sulfoxide may decrease formation of active metabolite of sulindac, possibly resulting in decreased therapeutic effect. Also, topical dimethyl sulfoxide with sulindac has resulted in severe peripheral neuropathy.

Diuretics
Decreased diuresis may result.

Lithium
May decrease lithium clearance.

Methotrexate
May increase methotrexate levels.

NSAIDs (eg, ibuprofen)
Coadministration with other NSAIDs may increase the risk of GI toxicity.

Probenecid
Sulindac plasma levels may be elevated.

Ranitidine
Sulindac has increased ranitidine bioavailability.