Reopro 2mg/1ml 5ml Injection (Abciximab)
Reopro 2mg/1ml 5ml Injection (Abciximab) is the Fab fragment of the chimeric human-murine , monoclonal antibody 7E3. Abciximab binds to the glycoprotein (GP) IIb/IIIa receptor of human platelets and inhibits platelet aggregation.
Abciximab binds to the intact platelet GPIIb/IIIa receptor, which is a member of the integrin family of adhesion receptors and the major platelet surface receptor involved in platelet aggregation. Abciximab inhibits platelet aggregation by preventing the binding of fibrinogen, von Willebrand factor, and other adhesive molecules to
GPIIb/IIIa receptor sites on activated platelets. The mechanism of action is thought to involve steric hindrance and/or conformational effects to block access of large molecules to the receptor rather than direct interaction with the RGD (arginine-glycine-aspartic acid) binding site of GPIIb/IIIa.
Following intravenous bolus administration, free plasma concentrations of Abciximab decrease rapidly with an initial half-life of less than 10 minutes and a second phase half-life of about 30 minutes, probably related to rapid binding to the platelet GPIIb/IIIa receptors. Platelet function generally recovers over the course of 48 hours (1,2), although Abciximab remains in the circulation for 15 days or more in a platelet-bound state. Intravenous administration of a 0.25 mg/kg bolus dose of Abciximab followed by continuous infusion of 10 ,ug/min (or a weight-adjusted infusion of 0.125 l.tg/kg/min to a maximum of 10 pg/min) produces approximately constant free plasma concentrations throughout the infusion. At the termination of the infusion period, free plasma concentrations fall rapidly for approximately six hours then decline at a slower rate
Because Abciximab may increase the risk of bleedin,, 0 Abciximab is contraindicated in the following clinical
Active internal bleeding
Recent (within six weeks) gastrointestinal (GI) or genitourinary (GU) bleeding of clinical significance.
History of cerebrovascular accident (CVA) within two years, or CVA with a significant residual neurological
Administration of oral anticoagulants within seven days unless prothrombin time is I 1.2 times control
Thrombocytopenia (< 100,000 cells/pL)
Recent (within six weeks) major surgery or trauma
Intracranial neoplasm, arteriovenous malformation, or aneurysm
Severe uncontrolled hypertension
Presumed or documented history of vasculitis
Use of intravenous dextran before percutaneous coronary intervention, or intent to use it during an