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Prostaglandin-endoperoxide synthase 1 and 2 (COX-1 and COX-2) are the principal enzymes catalyzing the first step in prostanoid biosynthesis—the conversion of arachidonic acid into prostaglandin H2, via prostaglandin G2 as an intermediate. These enzymes possess both cyclooxygenase and peroxidase activities and are key targets for nonsteroidal anti-inflammatory drugs (NSAIDs). While COX-1 is constitutively expressed for physiological functions such as gastric mucosal protection and platelet aggregation, COX-2 is typically inducible at sites of inflammation and is the main mediator of pain and fever during tissue injury. Inhibition of these targets underpins the mechanism of action for NSAIDs, but therapeutic use must balance anti-inflammatory efficacy against potential risks such as gastrointestinal and cardiovascular toxicity.
Nonselective NSAIDs inhibit both COX-1 and COX-2, blocking prostaglandin synthesis. Selective COX-2 inhibitors block inflammatory prostaglandin production with reduced effect on gastric protection.
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