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P2Y 12 receptors: structure and function
Author(s) -
Cattaneo M.
Publication year - 2015
Publication title -
journal of thrombosis and haemostasis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.947
H-Index - 178
eISSN - 1538-7836
pISSN - 1538-7933
DOI - 10.1111/jth.12952
Subject(s) - prasugrel , p2y12 , ticagrelor , clopidogrel , hemostasis , platelet , medicine , antithrombotic , adenosine diphosphate , pharmacology , thrombosis , receptor , aspirin , platelet aggregation
Summary The platelet P2Y 12 receptor (P2Y 12 R) for adenosine 5′diphosphate (ADP) plays a central role in platelet function, hemostasis, and thrombosis. Patients with inherited P2Y 12 R defects display mild‐to‐moderate bleeding diatheses. Defects of P2Y 12 R should be suspected when ADP, even at high concentrations (≥ 10 μ m ), is unable to induce full, irreversible platelet aggregation. P2Y 12 R also plays a role in inflammation: its role in the pathogenesis of allergic asthma has been well characterized. In addition, inhibition or genetic deficiency of P2Y 12 R has antitumor effects. Drugs inhibiting P2Y 12 R are potent antithrombotic drugs. Clopidogrel is the P2Y 12 R antagonist that is most widely used in the clinical setting. Its most important drawback is its inability to inhibit adequately P2Y 12 R‐dependent platelet function in about one‐third of patients. New drugs, such as prasugrel and ticagrelor, which effectively inhibit P2Y 12 R in the vast majority of patients, have proved to be more efficacious than clopdidogrel in preventing major adverse cardiovascular events.