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Clopidogrel is an antiplatelet drug that irreversibly binds to the platelet purinergic P2Y12 receptor and inhibits ADP-induced stimulation of the GPIIb/IIIa receptor complex. It is widely used for management of atherothrombotic disease in patients who have experienced severe vascular events such as stroke or myocardial infarction or with peripheral artery disease. The current data, however, show that about 5% to 44% of patients treated with conventional doses of clopidogrel do not display adequate antiplatelet response and result in a high risk of recurrent atherothrombotic events. There are several factors that can affect clopidogrel response such as genetic polymorphisms of drug metabolizing enzymes (i.e. CES1, CYP2C19, and PON1), genetic polymorphisms of P2Y12 receptors, drug formulations, and drug-drug interaction. Identification of factors affecting clopidogrel response is needed to improve the antiplatelet effect and reduce risks for cardiovascular events. The purpose of this review is to discuss the contribution of individual factors responsible for variations of action and clopidogrel efficacy. This information will be very useful for physicians, pharmacists, and healthcare personnel for considering and increasing the safety and efficacy of clopidogrel therapy.
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