Aspirin exerts its antithrombotic effect by irreversibly inhibiting COX-1 and reducing TXA2 production, despite a short plasma half-life of 20 minutes.
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May support once-daily aspirin regimens despite brief exposure; leaves open dosing optimization across populations.
Cyclooxygenase-1 [COX-1, prostaglandin synthase] catalyses the transformation of arachidonic acid to the unstable intermediate prostaglandin PGH 2 . Subsequently, thromboxane synthase acts on PGH 2 to form TXA 2 , a transient biological product that induces platelet aggregation and is a powerful vasoconstrictor. Aspirin acts primarily by interfering with the biosynthesis of cyclic prostanoids: TXA 2 , prostacyclin, and other prostaglandins. It irreversibly inhibits COX-1 by acetylation of serine-530 and induces a long-lasting functional defect in the platelets. The resultant decrease in production of prostaglandins and TXA 2 probably accounts for much of aspirin's antithrombotic effect [ 1 , 2 ]. The plasma half-life of aspirin is only 20 min in circulating blood. It is rapidly deacetylated and converted to salicylate in vivo. Salicylate does not affect COX-1 or COX-2 activity [ 3 ].
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Altman et al. (2004) studied this question.
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