Abstract
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.
MeSH terms
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Atherosclerosis / complications
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Atherosclerosis / drug therapy*
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Blood Platelets / drug effects
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Blood Platelets / metabolism
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Clinical Trials as Topic
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Humans
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Imines / pharmacology
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Imines / therapeutic use
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Lactones / pharmacology
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Lactones / therapeutic use
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Myocardial Infarction / etiology
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Myocardial Infarction / prevention & control
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Peripheral Arterial Disease / etiology
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Peripheral Arterial Disease / prevention & control
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Platelet Activation / drug effects*
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Platelet Aggregation Inhibitors / pharmacology*
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Platelet Aggregation Inhibitors / therapeutic use
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Pyridines / pharmacology
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Pyridines / therapeutic use
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Receptor, PAR-1 / antagonists & inhibitors*
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Receptor, PAR-1 / metabolism
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Stroke / etiology
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Stroke / prevention & control
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Thrombin / metabolism
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Thrombosis / etiology
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Thrombosis / prevention & control*
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Treatment Outcome
Substances
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E 5555
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Imines
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Lactones
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Platelet Aggregation Inhibitors
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Pyridines
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Receptor, PAR-1
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Thrombin
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vorapaxar