Abciximab (ReoPro): Drug Monograph
- 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.
- 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.
- 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
- 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
- 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.
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
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.
MESH Terms & Keywords