From the Guidelines
Abciximab works by occupying the glycoprotein IIb/IIIa receptors on the surface of platelets, preventing fibrinogen from binding and thereby preventing platelet aggregation, which is the final and obligatory pathway for platelet aggregation 1. The mechanism of action of Abciximab is based on its ability to bind to the glycoprotein IIb/IIIa receptors, which are abundant on the platelet surface. When platelets are activated, this receptor undergoes a change in conformation that increases its affinity for binding to fibrinogen and other ligands, resulting in platelet aggregation. By occupying these receptors, Abciximab prevents fibrinogen from binding, thereby preventing platelet aggregation.
- The binding of Abciximab to the glycoprotein IIb/IIIa receptors is independent of the stimulus for platelet aggregation and represents the final common pathway for platelet aggregation.
- Experimental and clinical studies have suggested that occupancy of at least 80% of the receptor population and inhibition of platelet aggregation to ADP by at least 80% results in potent antithrombotic effects 1.
- Abciximab is a Fab fragment of a humanized murine antibody that has a short plasma half-life but strong affinity for the receptor, which results in some receptor occupancy that persists in part for weeks 1. The clinical relevance of Abciximab's mechanism of action is supported by studies that have shown its effectiveness in reducing the risk of ischemic complications in patients with acute coronary syndromes and during percutaneous coronary interventions (PCI) 1.
From the Research
Mechanism of Action of Abciximab
The mechanism of action of Abciximab, a Glycoprotein IIb/IIIa receptor antagonist, involves:
- Inhibiting platelet aggregation by blocking the binding of fibrinogen to the Glycoprotein IIb/IIIa receptor on the surface of activated platelets, thereby decreasing crosslinking of platelets and platelet aggregation 2
- Having anticoagulant activity and other beneficial effects, such as inhibiting migration and promoting apoptosis of smooth muscle cells 3
- Preventing platelet aggregation by blocking platelet glycoprotein (GP) IIb/IIIa receptor 4
Key Findings
- Abciximab has been shown to improve patient outcome after percutaneous coronary revascularisation by reducing the incidence of ischemic complications 3
- The drug provides particular benefit in patients with unstable angina or myocardial infarction who are undergoing percutaneous coronary revascularisation 3
- Abciximab can be administered intravenously or intracoronary, but the optimal route of administration is still being debated 5
Comparison with Other Glycoprotein IIb/IIIa Receptor Antagonists
- Abciximab has been compared to other Glycoprotein IIb/IIIa receptor antagonists, such as tirofiban and eptifibatide, in terms of its anti-aggregatory effects during percutaneous coronary intervention 6
- The relative efficacy and safety of these drugs may vary depending on the patient population and clinical setting 2, 4