This review summarizes the mechanism of action and rationale for using PAR-1 inhibitors like vorapaxar and atopaxar in patients with atherothrombosis.
PAR-1 inhibitors may broaden antiplatelet options in atherosclerosis; leaves open comparative efficacy and safety versus standard agents.
Protease-activated receptor (PAR)-1 inhibitors have recently become popular in the use of atherosclerosis among clinicians. Atherosclerosis can cause cardiovascular and cerebrovascular events leading to one of the major causes of mortality worldwide. Thrombin-mediated platelets can cause atherosclerotic plaques, and these platelets are activated by thrombin through the PAR-1. Vorapaxar and atopaxar are novel antiplatelet drugs that inhibit the thrombin-induced platelet activation by antagonizing the PAR-1. The objective of this article is to review the mechanism of action of vorapaxar and atopaxar and explain the rationale for using them in atherothrombosis patients including myocardial infarction, peripheral arterial disease, and stroke.
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Al-Khafaji et al. (2015) studied this question.
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