Case study Topic: Ticagrelor

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Ticagrelor

Brand Names: Brilinta™

Pharmacologic Category: Antiplatelet Agent; Antiplatelet Agent, Cyclopentyltriazolopyrimidine

Mechanism of Action

Reversibly and noncompetitively binds the adenosine diphosphate (ADP) P2Y12 receptor on the platelet surface which prevents ADP-mediated activation of the GPIIb/IIIa receptor complex thereby reducing platelet aggregation. Due to the reversible antagonism of the P2Y12 receptor, recovery of platelet function is likely to depend on serum concentrations of ticagrelor and its active metabolite.

Pharmacodynamics/Kinetics

Onset of inhibition of platelet aggregation (IPA): 180 mg loading dose: ~41% within 30 minutes (similar to clopidogrel 600 mg at 8 hours)

Peak effect: Time to maximal IPA: 180 mg loading dose: IPA ~88% at 2 hours post administration

Duration of IPA: 180 mg loading dose: 87% to 89% maintained from 2-8 hours; 24 hours after the last maintenance dose, IPA is 58% (similar to maintenance clopidogrel)

Time after discontinuation when IPA is 30%: ~56 hours; IPA 10%: ~110 hours (Gurbel, 2009). Mean IPA observed with ticagrelor at 3 days post-discontinuation was comparable to that observed with clopidogrel at 5 days post discontinuation.

Absorption: Rapid

Distribution: 88 L

Protein binding: >99% (parent drug and active metabolite)

Metabolism: Hepatic via CYP3A4/5 to active metabolite (AR-C124910XX)

Bioavailability: ~36% (range: 30% to 42%)

Half-life elimination: Parent drug: ~7 hours; active metabolite: ~9 hours

Time to peak: Parent drug: ~1.5 hours; active metabolite (AR-C124910XX): ~2.5 hours

Excretion: Feces (58%); urine (26%); actual amount of parent drug and active metabolite excreted in urine was <1% of total dose administered

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