Ticagrelor is a member of the chemical class cyclopentyltriazolopyrimidines (CPTP). It is a selective adenosine diphosphate (ADP) receptor antagonist acting on the P2Y12 ADP-receptor that can prevent ADP-mediated platelet activation and aggregation. Ticagrelor reversibly interacts with the platelet P2Y12 ADP-receptor. Ticagrelor does not interact with the ADP binding site itself, but interacts with platelet P2Y12 ADP-receptor to prevent signal transduction. Thus it prevents platelet activation & aggregation.
Absorption: Absorption of ticagrelor occurs with a median t-max of 1.5 hour (range 1.0-4.0). The formation of major circulating metabolite of ticagrelor occurs with a median tmax of 2.5 hours (range 1.5-5.0). Distribution: Ticagrelor and the active metabolite are extensively bound to human plasma proteins (> 99%). Metabolism: CYP3A4 is the major enzyme responsible for ticagrelor metabolism & the formation of its major active metabolite. Ticagrelor & its major active metabolite are weak P-glycoprotein substrates & inhibitors. Excretion: The primary route of ticagrelor elimination is hepatic metabolism. When radiolabeled ticagrelor is administered, the mean recovery of radioactivity is approximately 84% (58% in feces & 26% in urine).The primary route of elimination for the major metabolite of ticagrelor is most likely to be biliary secretion. The mean t1/2 is approximately 7 hours for ticagrelor & 9 hours for the active metabolite.