Ticlopidine hydrochloride

China [CN]

Ticlopidine hydrochloride exerts its antithrombotic effects by specifically inhibiting multiple steps in platelet aggregation. Its mechanism differs from that of drugs like aspirin and is as follows:

Inhibition of platelet activation signaling pathways: Upon entry into the body, the drug selectively acts on ADP (adenosine diphosphate) receptors on the platelet membrane, blocking ADP-mediated platelet activation signaling, reducing calcium release and cyclic adenosine monophosphate (cAMP) concentration within platelets, thereby inhibiting platelet activation.

Interference with platelet aggregation: Inhibition of the activation and expression of platelet membrane glycoprotein IIb/IIIa receptors, which serve as a critical "bridge" for platelet-fibrinogen binding. Inhibition of these receptors prevents platelets from cross-linking and aggregating to form thrombi.

Prolongation of bleeding time: Through these actions, the drug significantly prolongs platelet aggregation and bleeding times, reducing the likelihood of thrombosis. The duration of action is long (platelet function recovery takes days to weeks after discontinuation of the drug).