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Newer agents in antiplatelet therapy: a review

Authors Yeung J, Holinstat M

Received 1 May 2012

Accepted for publication 17 May 2012

Published 25 June 2012 Volume 2012:3 Pages 33—42

DOI https://doi.org/10.2147/JBM.S25421

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 3


Jennifer Yeung, Michael Holinstat

Cardeza Foundation for Hematologic Research, Department of Medicine, Thomas Jefferson University, Philadelphia, PA, USA

Abstract: Antiplatelet therapy remains the mainstay in preventing aberrant platelet activation in pathophysiological conditions such as myocardial infarction, ischemia, and stroke. Although there has been significant advancement in antiplatelet therapeutic approaches, aspirin still remains the gold standard treatment in the clinical setting. Limitations in safety, efficacy, and tolerability have precluded many of the antiplatelet inhibitors from use in patients. Unforeseen incidences of increased bleeding risk and recurrent arterial thrombosis observed in patients have hampered the development of superior next generation antiplatelet therapies. The pharmacokinetic and pharmacodynamic profiles have also limited the effectiveness of a number of antiplatelet inhibitors currently in use due to variability in metabolism, time to onset, and reversibility. A focused effort in the development of newer antiplatelet therapies to address some of these shortcomings has resulted in a significant number of potential antiplatelet drugs which target enzymes (phosphodiesterase, cyclooxygenase), receptors (purinergic, prostaglandins, protease-activated receptors, thromboxane), and glycoproteins (αIIbß3, GPVI, vWF, GPIb) in the platelet. The validation and search for newer antiplatelet therapeutic approaches proven to be superior to aspirin is still ongoing and should yield a better pharmacodynamic profile with fewer untoward side-effects to what is currently in use today.

Keywords: platelet aggregation inhibitors, blood platelets, purinergic P2Y receptor antagonists, receptor, PAR-1, platelet glycoprotein GPIIb-IIIa, thrombosis

Erratum for this paper has been published.

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