Administration: oral, rectal. IV available under SAS
MOA: Inhibits COX1 irreversibly. This prevents conversion of arachadonic acid to thromboxane A2 after the platelet has been activated, which reduces activation of nearby platelets. Platelets have no nucleus, no cannot synthesize appreciable new COX1
A 50% OBA (large first pass)
D: Confined to circulating volume Vd ~0.1L/kg
M: Hepatically metabolized to salicylic acid, a reversible nonselective COX inhibitor
E: Aspirin and salicylate are both excreted in urine. Half life 20 minutes (aspirin), or 6 hours (salicylate)
Duration of effect: until platelets are replaced (~10 days, or until transfused new platelets)
Clopidogrel
Administration: oral
MOA: Irreversible noncompetitive antagonist of P2Y12 receptor (for ADP). Reduces platelet activation by ADP release from nearby degranulating platelets
Clopidogrel is a prodrug, hepatically activated by CYP2C19. The active metabolite is then hepatically inactivated, then excreted in urine and bile. The half-life of the parent drug is 6 hours.
Duration of effect: until platelets are replaced (~10 days, or until transfused new platelets)
Ticagrelor
Finally, a normal drug
Administration: oral
MOA: Reversible, noncompetative antagonist of P2Y12
Extensively metabolized, including to an active metabolite, mostly excreted in bile. Half-life ~8 hours