Abstract
Clinical trials have shown that abciximab, a chimeric Fab fragment of monoclonal antibody against glycoprotein (GP) IIb/IIIa, prevents acute thrombotic occlusion of coronary arteries after interventions.1 Although the main antithrombotic effects of abciximab is believed to depend on its inhibitory effect on platelet aggregation due to inhibition of fibrinogen binding to activated GP IIb/IIIa, the in-vivo antithrombotic effects of abciximab seem superior to that of other anti-GP IIb/IIIa agents.2 The reason why is unknown although some investigators suggest that the irreversible binding of abciximab to GP IIb/IIIa or inhibition of vitronectin binding to integrin αvβ3 as reasons for its superior in-vivo antithrombotic effects.
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