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Abciximab (ReoPro): Drug Monograph

    Brand Names
    • ReoPro
    Drug Class
    • GPIIaIIIb Receptor Blocker
      • Note the ending of the name abcixi-mab.  "Mab" stands for monoclonal antibody (technically it is a Fab fragment of the chimeric human-murine monoclonal antibody 7E3).
    • As an adjunct to percutaneous coronary intervention (PCI) for the prevention of cardiac ischemic complications in patients undergoing PCI
    • Unstable angina not responding to conventional medical therapy when PCI is planned within 24 hours.
    • Note:
      • Safety and efficacy of abciximab use in patients not undergoing PCI have not been established.
      • Intended for use with aspirin and heparin and has been studied only in that setting.
    • PCI: 
      • 0.25 mg/kg IV bolus over 10-60 minutes before the start of PCI, followed by a continuous IV infusion of 0.125 mg/kg/min (to a maximum of 10 mg/min) for 12 hours.
        • Renal or Hepatic impairment: No dosage adjustment provided by manufacturer
    • Unstable Angina or NSETMI (not responding to standard medical therapy and who are planning to get PCI within 24 hours):
      • 0.25 mg/kg IV bolus followed by an 18- to 24-hour IV infusion of 10 μg/min, concluding one hour after the PCI.
        • Renal or Hepatic Impairment:  No dosage adjustment provided by manufacturer
    Renal Dosing
    • No dosage adjustment provided by manufacturer
    Hepatic Dosing
    • No dosage adjustment provided by manufacturer
    Dosage Forms
    • 5 mL vials for injection: 10 mg

    Due to the increased risk of bleeding, contraindicated in the following clinical situations:

    • Active internal bleeding
    • Gastrointestinal (GI) or genitourinary (GU) bleeding of clinical significance within preceding 6 weeks
    • History of stroke within two years, or CVA with a significant residual neurological deficit
    • Bleeding diathesis
    • Administration of oral anticoagulants within seven days unless prothrombin time is ≤ 1.2 times control
    • Thrombocytopenia (< 100,000 cells/μL)
    • 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 IV dextran before PCI, or intent to use it during an intervention

    In patients with known hypersensitivity to any component of this product or to murine proteins.

    • Bleeding events - especially with the use of anticoagulation, e.g., from heparin, other anticoagulants, or thrombolytics.
    • Allergic reactions - including anaphylaxis
    • Thrombocytopenia
    Adverse Reactions
    • Bleeding
    • Thrombocytopenia
    • Allergic reactions
    • No experience of overdosage in human clinical trials
    Drug Interactions
    • Abciximab does not undergo any metabolism via CYP450 enzymes, phase 2 conjugative enzymes or movement via cell membrane transporters.
    Pregnancy Rating

    Pregnancy Category C

    • Use caution as it is unknown if excreted in human milk or absorbed systemically after ingestion.
    Mechanism of Action
    • Abciximab binds to the platelet GPIIb/IIIa receptor, which is the major platelet surface receptor involved in platelet aggregation and prevents the binding of fibrinogen, von Willebrand factor, and other adhesive molecules to GPIIb/IIIa receptor sites on activated platelets.
    • The maximum degree of inhibition of platelet aggregation was observed when ≥ 80% of GPIIb/IIIa receptors were blocked by abciximab. In non-human primates, abciximab bolus doses of 0.25 mg/kg generally achieved a blockade of at least 80% of platelet receptors and fully inhibited platelet aggregation. Inhibition of platelet function was temporary following a bolus dose, but receptor blockade could be sustained at ≥ 80% by continuous intravenous infusion. The inhibitory effects of abciximab were substantially reversed by the transfusion of platelets in monkeys.
    • Doses of the murine version of 7E3 or abciximab sufficient to produce high-grade (≥ 80%) GPIIb/IIIa receptor blockade prevented acute thrombosis and yielded lower rates of thrombosis compared with aspirin and/or heparin.
    • Degree of Platelet Inhibition:  IV administration of a single bolus doses of Abciximab from 0.15 mg/kg to 0.30 mg/kg produced rapid dose-dependent inhibition of platelet function as measured by ex vivo platelet aggregation in response to adenosine diphosphate (ADP) or by prolongation of bleeding time.
    • The median bleeding time increased to over 30 minutes at both doses compared in human studies with a baseline value of approximately 5 minutes.
    • Low levels of GPIIb/IIIa receptor blockade are present for more than 10 days following cessation of the infusion. After discontinuation of Abciximab infusion, platelet function returns gradually to normal. Bleeding time returned to ≤ 12 minutes within 12 hours following the end of infusion 75% patients, and within 24 hours of 90% of patients.
    • Half-Life: Initially < 10 minutes and a second phase half-life ~ 30 minutes
      • Platelet function generally recovers over the course of 48 hours, although abciximab remains in the circulation for 15 days or more in a platelet-bound state
      • At the termination of the infusion period, free plasma concentrations fall rapidly for approximately six hours then decline at a slower rate.
    • Volume of Distribution: 0.07 L/kg
    • Metabolism:  Primarily by proteolytic cleavage.  Abciximab does not undergo any metabolism via CYP450 enzymes, phase 2 conjugative enzymes or movement via cell membrane transporters
    • Elimination:  Unknown
    • Possibly from a single nucleotide polymorphism of on the allele for GPIIIa or ITGB3 where there is a change from Leu or Pro in the codon 33 in exon 2 which is located on chromosome 17q21.32

    Abciximab (ReoPro).  Product Insert.  Eli Lilly and Company.  Indianapolis, IN.  2013.

MESH Terms & Keywords

  • Abciximab (ReoPro), Glycoprotein IIbIIIa Receptor Blocker, Antiplatelet Agents