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Pharmacology: Etoricoxib is a nonsteroidal anti-inflammatory drug (NSAID) that exhibits anti-inflammatory, analgesic, and antipyretic activities. Etoricoxib is a potent, orally active, highly selective cyclooxygenase-2 (COX-2) inhibitor within and above the clinical dose range. Two isoforms of cyclooxygenase have been identified: cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2). COX-1 is responsible for prostaglandin-mediated normal physiologic functions such as gastric cytoprotection and platelet aggregation. Inhibition of COX-1 non-selective NSAIDs has been associated with gastric damage and platelet inhibition. COX-2 has been shown to be primarily responsible for the synthesis of prostanoid mediators of pain, inflammation, and fever. Selective inhibition of COX-2 by etoricoxib decreases these clinical signs and symptoms with decreased gastrointestinal toxicity and without effects on platelet function. Etoricoxib produced dose-dependent inhibition of COX-2 without inhibition of COX-1 at doses up to 150 mg daily.
Platelet function: Multiple doses of etoricoxib up to 150 mg administered daily up to nine days had no effect on bleeding time. Similarly, bleeding time was not altered in a single dose with etoricoxib 250 mg or 500 mg. There was no inhibition of ex-vivo arachidonic acid or collagen induced platelet aggregation at steady state with doses of etoricoxib up to 150 mg. These findings are consistent with the COX-2 selectivity of etoricoxib.
