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The **P2Y12 receptor** is a G protein-coupled purinergic receptor expressed primarily on the surface of blood platelets. It mediates platelet aggregation and stabilization of platelet plugs via response to adenosine diphosphate (ADP). Therapeutic blockade of P2Y12 is a major antiplatelet strategy in the prevention and treatment of cardiovascular events such as myocardial infarction and stroke. Clinically relevant P2Y12 inhibitors include thienopyridines (clopidogrel, prasugrel, ticlopidine) that irreversibly inhibit the receptor, and non-thienopyridines (ticagrelor, cangrelor) that do so reversibly. The term "adenosine diphosphate receptor" is less specific and refers to a class of receptors; in human platelets, the key ADP-responsive receptors are P2Y1 (initiating shape change and aggregation) and P2Y12 (amplification and stabilization of aggregation), with P2Y12 being the main therapeutic target for antiplatelet therapy[1][2][5][6][7][8]. **Note:** The user query uses “Adenosine diphosphate receptor,” which is imprecise, as platelets express more than one ADP (adenosine diphosphate) receptor—most importantly, **P2Y1** and **P2Y12**. However, in the context of pharmacology and therapeutic targeting, “adenosine diphosphate receptor” almost always refers to the P2Y12 receptor[2][5][7]. For later structured data handling, use P2Y12 receptor as the canonical form and note the ambiguity of the original query.
Inhibition of ADP-induced platelet aggregation via blockade of P2Y12 (reversible or irreversible); Inhibition of ADP binding (thereby blocking downstream platelet aggregation)
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