Abstract

Aspirin (ASP) inhibits H cyclo-oxygenase (COX) irreversibly and hence thromboxane A2 (TXA2) to prevent platelet aggregation. Orally administered ASP requires high and frequent dosing because it undergoes extensive presystemic hydrolysis in the gut and the liver into salicylic acid (SAL) which is devoid of antiplatelet activity. Continuous exposure of new platelets to ASP is necessary to achieve prolonged inhibition of platelet aggregation. We developed a matrix type transdermal patch of ASP using polyvinyl alcohol (with and without hydrolysis Inhibitor and a penetration enhancer). The transdermal flux of ASP, in rat skin was 11.85 and 52.92μg/cm2.h without and with penetration enhancer respectively. Transdermal administration in human volunteers resulted in a significant reduction in serum lipid peroxides (MDA levels: 0.998±0.899 to 0.236±0.076 nM/ml) and inhibition of platelet aggregation.