Abciximab (ReoPro): Drug Monograph
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- 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
- 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
- Bleeding events - especially with the use of anticoagulation, e.g., from heparin, other anticoagulants, or thrombolytics.
- Allergic reactions - including anaphylaxis
- Thrombocytopenia
- Abciximab does not undergo any metabolism via CYP450 enzymes, phase 2 conjugative enzymes or movement via cell membrane transporters.
- Use caution as it is unknown if excreted in human milk or absorbed systemically after ingestion.
- 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.
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Half-Life: Initially < 10 minutes and a second phase half-life ~ 30 minutes
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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
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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
Drug Class
Indications
Dosing
Contraindications
Due to the increased risk of bleeding, contraindicated in the following clinical situations:
In patients with known hypersensitivity to any component of this product or to murine proteins.
Warnings
Drug Interactions
Breastfeeding
Mechanism of Action
Pharmacodynamics
Pharmacokinetics
MESH Terms & Keywords
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