alexa Vorapaxar: A New Antiplatelet Therapy
ISSN: 2329-6607

Cardiovascular Pharmacology: Open Access
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Review Article

Vorapaxar: A New Antiplatelet Therapy

Mehrnoosh Hashemzadeh1,2*, Mohammad Reza Movahed1,3 and Joseph M Arreguin1,2

1University of Arizona, USA

2Pima College, Tucson, AZ, USA

3Arizona Regional Cardiology Director CareMore, USA

*Corresponding Author:
Mehrnoosh Hashemzadeh
University of Arizona, Pima College
6119 north Pinchot, Tucson, az 85750, USA
Tel: +9493741501
E-mail: [email protected]

Received date: September 29, 2014; Accepted date: December 08, 2014; Published date: December 12, 2014

Citation: Hashemzadeh M, Movahed MR, Arreguin JM (2015) Vorapaxar: A New Antiplatelet Therapy. Cardiol Pharmacol 4:128. doi:10.4172/2329-6607.1000128

Copyright: © 2015 Hashemzadeh M et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.



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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