Table 1.

Mechanisms of Abciximab

IIb/IIIa platelet glycoprotein blockade determining platelet aggregation inhibition; active thrombolytic effect by means of partial displacement of platelet-bound fibrinogen; inhibition of platelet-induced generation of thrombin reducing granule release: it results in reduced levels of platelet-derived inhibition of fibrinolysis such as PAI-1 and α2-anti-plasmin; Blokade of the binding of the factor XIIIa to platelets, thereby diminishing crosslinking of both fibrin strands and α2-anti-plasmin to fibrin and reduction of clot retraction; blockade of the activated Mac-1 on monocytes and Mac-1-expressing THP-1 cells; inhibition of fibrinogen binding to Mac-1 preventing formation of leukocyte/leukocyte or leukocyte/platelet aggregates; inhibition of Mac-1-mediated monocyte adhesion on ICAM-1; inhibition of factor X binding to Mac-1 and Mac-1-mediated conversion of factor X to Xa; blockade of αVb3 vitronectin receptor preventing smooth muscle cells migration and intimal hyperplasia following vascular injury, inhibition of platelet adhesion to osteopontin in atherosclerotic plaque and platelet-mediated thrombin generation via blokade of αVb3 receptor.

After Romagnoli et al. [41].