ADP Receptor (P2Y12 Receptor) Inhibitors

This version of the course is no longer available.
Need multiple seats for your university or lab? Get a quote
The page below is a sample from the LabCE course . Access the complete course and earn ASCLS P.A.C.E.-approved continuing education credits by subscribing online.

Learn more about (online CE course)
ADP Receptor (P2Y12 Receptor) Inhibitors

  • Examples: Clopidogrel, prasugrel, ticagrelor and ticlopidine are drugs in the ADP receptor (also known as P2Y12 receptor) inhibitor class.
  • Mechanism of action: As discussed earlier, ADP is a substance released from platelets that activates other platelets and results in platelet aggregation. The drugs of this class irreversibly inhibit the ADP receptor on platelets, making them unresponsive to ADP. This results in decreased platelet aggregation.
  • Use: Ticlopidine is used for prevention of strokes in those who are unable to take aspirin, while clopidogrel is used to prevent thrombosis after a patient has coronary angioplasty to open an occluded coronary artery.
  • Laboratory measurement: Like with aspirin, there are platelet aggregation tests that assess the ability of platelets to aggregate in vitro. A normal response to clopidogrel therapy (or therapy with the other drugs in this class) would be decreased platelet aggregation when a patient's platelets are exposed to platelet aggregation agonists. Genetic testing can be performed for CYP2C19, an enzyme involved in the metabolism of clopidogrel. This enzyme is needed to metabolize the ingested clopidogrel into its active form. This test may be ordered to determine if a patient who is not responding to clopidogrel testing has a genetic variant of the CYP2C19 enzyme.
  • Toxicity: Ticlopidine causes bone marrow suppression with neutropenia and thrombocytopenia and the values for those analytes must be monitored. Clopidogrel produces gastrointestinal symptoms similar to aspirin and doesn't have the bone marrow suppression of ticlopidine.