Chemical structures and mode of action of intravenous glycoprotein IIb/IIIa receptor blockers: A review

Abstract

Glycoprotein (GP) IIb/IIIa receptor antagonists compose a subcategory of antiplatelet medications that reduce thrombus formation through the blockade of key binding sites needed to stabilize the forming platelet aggregate. The GP IIb/IIIa receptors have been identified as a therapeutic target in reducing the occurrence of platelet-dependent thrombus formation. One advantage of GP IIb/IIIa receptor antagonists is that because GP IIb/IIIa is platelet-specific, inhibition of this receptor does not affect platelet adhesion. This may contribute to hemostasis without leading to ischemic damage. The platelet-specific pharmacological activity of GP IIb/IIIa receptor antagonists has allowed for its broad use in clinical settings. Based on clinical trials, GP IIb/IIIa receptor antagonists have been extensively studied and used in patients with acute coronary syndrome or during percutaneous coronary interventions. The goal of the present article is to provide a detailed review of the chemical structures and mode of action of currently used Food and Drug Administration-approved GP IIb/IIIa receptor antagonists in the United States.

Keywords: Acute coronary syndrome; Antagonist; Antiplatelet; Antithrombotic; Glycoprotein IIb/IIIa receptor; Stenting.