Eptifibatide: a potent inhibitor of the platelet receptor integrin glycoprotein IIb/IIIa.


Journal Article (Review)

The platelet glycoprotein (GP) IIb/IIIa integrin plays a key role in mediating platelet aggregation. Blockade of the platelet GP IIb/IIIa receptor prevents arterial thrombosis in animal models much better than does aspirin. Among the most specific inhibitors in this class of drugs is eptifibatide (Integrilin(TM), Millennium Pharmaceuticals, Inc.), a cyclic heptapeptide based on a peptide recognition sequence found in snake venom. Peptide inhibitors, such as eptifibatide, bind competitively to GP IIb/IIIa and have a short half-life, allowing the effect to be rapidly reversible and providing a favourable overall safety profile. Eptifibatide has been studied in a broad range of ischaemic coronary conditions including percutaneous coronary intervention (PCI), ST-segment and non-ST-segment acute myocardial infarction (MI) and unstable angina. In PCI and non-ST-segment MI, therapy with eptifibatide has been shown to reduce acute ischaemic complications without any increased risk of life-threatening adverse events. In the recently reported Enhanced Suppression of the Platelet IIb/IIIa Receptor with Integrilin Therapy (ESPRIT) trial, two 180 microg/kg boluses of eptifibatide, 10 min apart, followed by an 18 - 24 h infusion at 2 microg/kg/min given as adjunctive therapy in non-urgent PCI reduced the 30-day composite of death, MI and need for urgent target vessel revascularisation from 10.4 to 6.8% compared with placebo. These results were achieved under conditions of typical contemporary PCI, namely the implantation of second- and third-generation stents deployed at high balloon pressures along with modern adjunctive pharmacological treatment, particularly the universal use of thienopyridines and lower-dose heparin. Few significant pharmacological effects other than inhibition of platelet aggregation and the effect on bleeding time have been reported. Future research will focus on alternative clinical applications and combinations with other therapies to further improve cardiovascular outcomes.

Full Text

Duke Authors

Cited Authors

  • O'Shea, JC; Tcheng, JE

Published Date

  • August 2002

Published In

Volume / Issue

  • 3 / 8

Start / End Page

  • 1199 - 1210

PubMed ID

  • 12150697

Pubmed Central ID

  • 12150697

International Standard Serial Number (ISSN)

  • 1465-6566

Digital Object Identifier (DOI)

  • 10.1517/14656566.3.8.1199


  • eng

Conference Location

  • England