Pharmacology · Class
Antiplatelet drugs !
Medicines that stop platelets from sticking together, the first step of an arterial clot. Used after heart attacks, stents and strokes.
Updated 2026-11-01
What they are
Drugs that block platelet activation or aggregation at different points: the ADP receptor P2Y12, the final fibrinogen receptor (glycoprotein IIb/IIIa), cyclooxygenase (aspirin) or the cAMP-breaking phosphodiesterases.
Mechanism of action
Platelets are activated by ADP, thromboxane A2 and thrombin, and then link to each other through fibrinogen bridges on the glycoprotein IIb/IIIa receptor. P2Y12 blockers stop ADP from switching platelets on; glycoprotein IIb/IIIa blockers stop the final bridging step; phosphodiesterase inhibitors raise cAMP inside the platelet, which keeps it at rest. Aspirin (on the NSAID page) blocks thromboxane A2 production. Because arterial clots are platelet-rich, these drugs protect mainly arteries: coronary, cerebral and peripheral.
Target: P2Y12 receptor, glycoprotein IIb/IIIa (integrin αIIbβ3) or phosphodiesterase
Drugs in this class
- ClopidogrelAn oral antiplatelet drug that blocks the platelet ADP receptor P2Y12 for the platelet's whole life. It must be…P2Y12 ADP receptor on platelets
- TicagrelorAn oral antiplatelet drug that blocks P2Y12 directly and reversibly, with no liver activation. Shortness of breath is…P2Y12 ADP receptor on platelets
- PrasugrelAn oral thienopyridine that blocks P2Y12 irreversibly, more strongly than clopidogrel. Not used after a stroke or…P2Y12 ADP receptor on platelets
- CilostazolAn oral phosphodiesterase III inhibitor that relaxes leg arteries and calms platelets. It increases walking distance…Phosphodiesterase 3 (PDE3)
- EptifibatideAn intravenous cyclic peptide that blocks the platelet fibrinogen receptor (glycoprotein IIb/IIIa), the final step of…Glycoprotein IIb/IIIa (integrin αIIbβ3)
- TirofibanAn intravenous non-peptide blocker of the platelet glycoprotein IIb/IIIa receptor, used in acute coronary syndromes…Glycoprotein IIb/IIIa (integrin αIIbβ3)
- DipyridamoleAn oral antiplatelet and vasodilator that raises adenosine around platelets. It is combined with warfarin after heart…Equilibrative nucleoside transporter 1 (adenosine uptake), and phosphodiesterases
- AbciximabAn antibody fragment given by vein that blocks the platelet glycoprotein IIb/IIIa receptor during coronary…Glycoprotein IIb/IIIa (integrin αIIbβ3)
Others in the class
- ticlopidine
- cangrelor
- vorapaxar
- acetylsalicylic acid (NSAID page)
Test yourself
Think of the answer, then tap the question to see it.
Why does clopidogrel work less well in some people?
It is a prodrug activated mainly by CYP2C19. People with two loss-of-function CYP2C19 alleles make less active metabolite, and so get less platelet inhibition.
How does ticagrelor differ from clopidogrel in how it binds P2Y12?
Ticagrelor binds P2Y12 directly and reversibly, without activation. The active metabolite of clopidogrel binds irreversibly, for the life of the platelet.
Why do antiplatelet drugs protect mainly the arteries?
Arterial clots form under high flow and are rich in platelets, so blocking platelets prevents them; venous clots are fibrin-rich and respond better to anticoagulants.
Educational content on how drugs work; not a prescribing guide and no substitute for a health professional's advice. No doses are given.
Sources: DailyMed - CLOPIDOGREL BISULFATE tablet (DailyMed (U.S. National Library of Medicine), 2026); DailyMed - TICAGRELOR tablet, film coated (DailyMed (U.S. National Library of Medicine), 2026); DailyMed - PRASUGREL tablet, film coated (DailyMed (U.S. National Library of Medicine), 2026); ATCDDD - ATC/DDD Index (WHO Collaborating Centre for Drug Statistics Methodology, 2026).
Spotted a mistake?We are always improving for the community. Tell us what is wrong and our team will review it.Report a mistake
Representative model, for educational purposes only.