Abciximab

Abciximab is a chimeric monoclonal antibody fragment that targets the glycoprotein IIb/IIIa receptor on platelets. It is derived from a mouse antibody (7E3) and produced as a Fab fragment. By binding with high affinity to the GPIIb/IIIa receptor, abciximab prevents fibrinogen and von Willebrand factor from cross-linking platelets, thereby inhibiting platelet aggregation and thrombus formation.

Abciximab is used mainly in unstable angina or non–ST-segment elevation myocardial infarction and during percutaneous coronary intervention (PCI) to reduce ischemic complications. It is administered intravenously as an initial bolus followed by a continuous infusion, typically for up to 12–24 hours, with concurrent antithrombotic therapy such as heparin and aspirin. The goal is rapid platelet inhibition during the high-risk intervention or acute event, with recovery of platelet function after discontinuation.

Pharmacodynamics and pharmacokinetics involve rapid receptor blockade with substantial inhibition of platelet aggregation. Platelet function generally begins to recover within 24–48 hours after stopping the infusion. Abciximab is cleared primarily by the reticuloendothelial system, and its effects on platelets persist beyond its circulating half-life, due to receptor occupancy and removal of immune complexes. It is not primarily renally excreted.

Adverse effects are dominated by bleeding, including major and minor hemorrhage. Thrombocytopenia is a serious but relatively uncommon risk and may require discontinuation of therapy. Hypersensitivity and rare anaphylactic reactions can occur. Bleeding risk is compounded when combined with other anticoagulants or antiplatelet agents. Contraindications include active major bleeding, history of hemorrhagic stroke or intracranial hemorrhage, known hypersensitivity to the drug, and significant platelet dysfunction or thrombocytopenia.