Differential inhibition of COX-1 and COX-2 in vitro and pharmacological profile in vivo of NSAIDs

Non-steroid antiinflammatory drugs (NSAIDs) are among the most commonly prescribed medicines. However, their therapeutic use is limited by significant adverse effects on the gastrointestinal (GI) tract1,2 and the kidneys3,4. Since the demonstration by Vane5 that inhibition of prostanoid synthesis through cyclooxygenase blockade is the mechanism of action of aspirin and related NSAIDs, it has been widely accepted that the mechanisms underlying both the therapeutic (i.e. anti-inflammatory) actions and the side effects of NSAIDs on the gastric mucosa, renal function and platelet aggregation are closely related.