Note aspirin is included under COX inhibitors.

Classification of Antiplatelet Agents

Antiplatelet agents can be classified by which stage of platelet function they affect:

  • Adhesion
    • vWF inhibitors
      e.g. Dextran 70.
  • Activation
    • Prostacyclins
      e.g. Epoprostenol.
    • Phosphodiesterase inhibition
      e.g. Dipyridamole.
    • COX inhibitors
      Prevent thromboxane A2 production, e.g. aspirin.
  • Aggregation
    • ADP receptor antagonists
      Prevent activation of GP IIb/IIIa receptors, e.g. clopidogrel.
    • GP IIb/IIIa receptor antagonists
      Prevent platelet aggregation via fibrin linkages between GP IIb/IIIa receptors, e.g. tirofiban.

Comparison of Common Antiplatelet Agents

Property Clopidogrel Dipyridamole Tirofiban Prasugrel Ticagrelor
Class ADP antagonist Phosphodiesterase inhibitor GP IIb/IIa antagonists ADP receptor antagonist/thienopyridine P2Y12-receptor antagonist
Uses PVD, STEMI, NSTEMI, stent prophylaxis CVA UA, NSTEMI ACS ACS
Route of Administration PO only PO/IV IV only PO PO PO
Mechanism of Action Irreversibly prevents ADP from binding to its receptor on the platelet, preventing activation of the IIb/IIIa receptor Inhibits platelet adhesion to walls, potentiates prostacyclin activity and increases platelet cAMP, ↓ Ca2+ and inhibiting platelet aggregation and deformation. Also acts as a coronary vasodilator. Reversible antagonism of IIb/IIIa receptor, preventing platelet aggregation Irreversibly binds to P2Y12, preventing platelet activation and aggregation. Greater potency than clopidogrel. Reversible, non-competitive binding to P2Y12-receptor
Dosing 300mg load, 75mg daily thereafter 200mg BD for CVA Load 25, maintenance 60mg load, then 10mg daily 180mng load, then 90mg BD
Absorption Rapid absorption and onset within 2 hours Variable depending on oral intake IV only. Onset within 10 minutes PO absorption within 2-4 hours
Distribution Highly protein-bound drug and metabolites Highly protein bound 65% protein bound 99% protein bound
Metabolism Prodrug. Majority hydrolysed by esterases to inactive drug, with a small proportion hepatically metabolised by CYP450 to active form. Half-life ~8 hours, however prolonged duration of action (5-7 days) due to irreversible effect on platelets Partial hepatic to inactive metabolites Not metabolised. Prodrug, hepatic by CYP 3A4 and 2B6. Irreversible binding gives same duration of action as clopidogrel. Not a prodrug; extensive metabolism with active metabolites with elimintation t1/2 ~ 8 hours. Clinical effect persists despite this for somet ime: ~60% activity at 24 hours and 10% activity at 5 days.
Elimination Urinary and faecal Renal and faecal Urinary as unchanged drug. Platelet aggregation returns to baseline within 4-8 hours Majority eliminated in urine Majority eliminated in faeces, minimal renal elimination
CVS Vasodilatation may drop CPP in AS and recent MI Coronary artery dissection Fewer cardiovascular adverse events (stent thrombosis, revascularisation, MI) compared with clopidogrel
GIT Mucosal irritation
Haeme Haemorrhage Thrombocytopaenia and haemorrhage Haemorrhage Greater risk of bleeding compared with clopidogrel
Other Many pharmacokinetic interactions, including genetic variability. Previously thought to kinetically interact with omeprazole - more recently disproved. Greater benefit in diabetic patients compared with clopidogrel or ticagrelor


  1. Peck TE, Hill SA. Pharmacology for Anaesthesia and Intensive Care. 4th Ed. Cambridge University Press. 2014.
  2. Rang HP, Dale MM, Ritter JM, Flower RJ. Rang and Dale's Pharmacology. 6th Ed. Churchill Livingstone.
  3. Australian Prescriber. Prasugrel. National Prescriber. 2010.
  4. Dobesh PP, Oestreich JH. Ticagrelor: Pharmacokinetics, Pharmacodynamics, Clinical Efficacy, and Safety. Pharmacotherapy. 2014 Oct;34(10):1077–90.
Last updated 2019-11-24

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