Therapy with the murine monoclonal antibody 7E3 blocks the platelet glycoprotein IIb/IIIa receptor and may significantly improve outcomes in acute coronary thrombotic syndromes.
Does the murine monoclonal antibody 7E3 improve outcomes in acute coronary thrombotic syndromes?
The monoclonal antibody 7E3 shows promise as a potent platelet inhibitor for improving outcomes in acute coronary syndromes, though immunogenicity and thrombocytopenia are potential concerns.
The murine monoclonal antibody 7E3 blocks the platelet glycoprotein IIb/IIIa receptor, and is a potent inhibitor of platelet function in both animals and man. Animal models of the acute coronary syndromes suggest that 7E3 abolishes the in vivo formation of platelet thrombi, accelerates thrombolysis with tissue plasminogen activator, and prevents subsequent reocclusion. Human studies with 7E3 suggest that complete inhibition of platelet function may be safely undertaken for periods of up to 36 h, and preliminary studies indicate effectiveness in the therapy of clinical unstable angina. Potential problems with its use include immunogenicity and thrombocytopenia. The outcome of the acute coronary thrombotic syndromes, which include unstable angina, acute myocardial infarction and abrupt closure following coronary angioplasty, may be significantly improved with 7E3 therapy.
Bhattacharya et al. (Wed,) conducted a review in Acute coronary syndromes. Murine monoclonal antibody 7E3 was evaluated. Therapy with the murine monoclonal antibody 7E3 blocks the platelet glycoprotein IIb/IIIa receptor and may significantly improve outcomes in acute coronary thrombotic syndromes.
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