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Antiplatelet therapy plays an integral role in the treatment of ischemic heart disease, the leading cause of death in most Western Countries. Previously, the classes of antiplatelet drugs that proved effective included aspirin, thienopyridines (e.g.ticlopidine, clopidogrel, prasugrel), a non-thienopyridine (ticagrelor), and glycoprotein (GP) IIb/IIIa receptor antagonists (e.g. abciximab, eptifibatide, tirofiban). Administration of antiplatelet therapy typically included dosages of acetylsalicylic acid alongside either a thienopyridine or non-thienopyridine ADP receptor inhibitor. Particular combinations within this dual antiplatelet therapy were contingent on specific needs and occurrences of patients. Inherent limitations of these antiplatelet drugs, however, lead inevitably to the development of new agents that not only conquer said limitations but also possess new, more efficient mechanistic modes of action. Vorapaxar functions as a thrombin receptor antagonist, working against the protease activated receptor PAR-1 to inhibit platelet aggregation without affecting hemostasis.
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