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Pharmacology

Antiplatelet drugs: aspirin, P2Y12 inhibitors and GP IIb/IIIa antagonists

How aspirin, clopidogrel, prasugrel, ticagrelor, dipyridamole and the GP IIb/IIIa antagonists act on platelet activation, and how irreversibility, prodrug activation, CYP2C19 and adenosine explain their timing, interactions and side effects.

Tier 2Medical sciences concept

Written with AI assistance and fact-checked against the sources below. For exam study, not clinical decisions. How notes are made

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At a glance

  • Platelets adhere via GP Ib-von Willebrand factor, activate, then aggregate when GP IIb/IIIa binds fibrinogen. Thromboxane A2 (TXA2) and ADP amplify activation.
  • Aspirin blocks TXA2 synthesis. P2Y12 inhibitors block the ADP receptor. GP IIb/IIIa antagonists block the final common pathway.
  • Irreversible drugs (aspirin, clopidogrel, prasugrel) act for the platelet's life. Ticagrelor is reversible, so its offset follows its half-life.

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Last updated
14 November 2026
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