[New therapy with monoclonal antibodies--abciximab, chimeric anti-GP IIb/IIIa antibody]

Platelet aggregation is now believed to be mediated by fibrinogen binding to activated GP IIb/IIIa. Antigen binding site of mouse anti-human GP IIb/IIIa monoclonal antibody 7E3, which can inhibit fibrinogen binding to activated human platelet GP IIb/IIIa, was combined with constant region of human IgG to reduce immunogenicity. Monovalent Fab of this mouse-human chimeric antibody named abciximab effectively reduced the onset of cardiovascular accidents when administered in combination with heparin and aspirin in patients undergoing coronary interventions. Although several anti-GP IIb/IIIa other than monoclonal antibodies were developed, clinical efficiency of abciximab is still superior to other agents while its effects on preventing myocardial infarction in unstable angina patients are uncertain.