tcsc1882 Clopidogrel (hydrogen sulfate)

S-(+)-Clopidogrel Hydrogen Sulfate is the S enantiomer of clopidogrel and a P2Y12 receptor inhibitor.

Target: P2Y Receptor

Clopidogrel is an effective antiplatelet agent useful for the treatment of ischemic cerebrovascular, cardiac, and peripheral arterial disease. Clopidogrel abolishes the inhibitory P2Y(AC) receptor-mediated ADP effects on prostaglandin E(1)-stimulated, cAMP-dependent phosphorylation of VASP without affecting epinephrine, thrombin, and thromboxane signaling. VASP phosphorylation is known to be closely correlated with the inhibition of platelet and fibrinogen receptor (glycoprotein IIb/IIIa) activation. Therefore, inhibition of the platelet P2Y(AC) ADP receptor and its intracellular signaling, including decreased VASP phosphorylation, is suggested as a molecular mechanism of clopidogrel action [1]. Clopidogrel ingestion reduced the thrombus volume significantly (p < 0.05) at 100 and 2600 s-1 (39 and 51% respectively). clopidogrel reduced significantly the fibrinopeptide A plasma levels and the fibrin deposition at shear rates below 650 s-1 [2]. Clopidogrel therapy resulted in a significant reduction in soluble CD40 ligand (p=0.03), a pro-thrombotic and pro-inflammatory molecule derived mainly from activated platelets. However, clopidogrel therapy had no effect on endothelial function, arterial stiffness, inflammatory and oxidative stress markers, or progenitor cells [3].

Clinical indications: Acute coronary syndrome; Peripheral vascular disease; Thromboembolism