CLOTINAB
ISU ABXIS
Identification
- Active ingredient (INN)
- ABCIXIMAB
- Internal code
- 06 C 317
- Country of Origin
- South Korea
- Pharmaceutical form
- Injection
- Prescription List
- Highly Regulated (List I)
- Packaging
- b/01 flacon de 5 ml
DAWA Clinical Workbench v2.0
Information may not be accurate. Always consult a physician, pharmacist, or specialist before acting on any data shown here.
Description
Abciximab is a
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 by preventing the binding of fibrinogen, von Willebrand factor, and other adhesive molecules.
It also binds to vitronectin (αvβ3) receptor found on platelets and vessel wall endothelial and smooth muscle cells.
Indications
Abciximab is indicated as an adjunct to percutaneous coronary intervention for the prevention of cardiac ischemic complications in patients undergoing percutaneous coronary intervention and in patients with unstable angina not responding to conventional medical therapy when percutaneous coronary intervention is planned within 24 hours.
Abciximab is intended for use with aspirin and heparin and has been studied only in that setting.
Pharmacodynamics
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.
A single intravenous bolus dose from 0.15 mg/kg to 0.30 mg/kg produced rapid dose-dependent inhibition of platelet function.
After two hours post-injection with a dose of 0.25-0.30 mg/kg, 80% of the GPIIb/IIIa receptors were blocked and platelet aggregation was prevented.
GPIIb/IIIa is the major surface receptor involved in the final pathway of platelet aggregation.
Bleeding time increases to over 30 minutes at the aforementioned doses.
To compare, baseline values were five minutes.
Metabolism
Most likely removed by opsonization via the reticuloendothelial system when bound to platelets, or by human antimurine antibody production.
Excreted renally.
Half-life
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.
Adverse Effects
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