Eptifibatide
A cyclic heptapeptide antiplatelet drug modelled on rattlesnake venom, used intravenously during coronary intervention and in acute coronary syndromes.
An approved intravenous anticoagulant used during coronary intervention. Derived from leech saliva chemistry, with a very short and predictable action.
Thrombin is the enzyme that finishes the job of forming a clot. Bivalirudin is a synthetic peptide modelled on hirudin, the anticoagulant a medicinal leech uses, and it binds thrombin in two places at once — the active site and the docking site clots use. Unusually, thrombin slowly cleaves the peptide and frees itself, so the effect wears off within about half an hour. That predictability is why it is used during procedures where bleeding risk has to be managed minute by minute.
A 20-amino-acid synthetic bivalent direct thrombin inhibitor. The N-terminal D-Phe-Pro-Arg-Pro sequence occupies the catalytic site while the C-terminal dodecapeptide binds exosite 1, giving reversible bivalent inhibition of both free and clot-bound thrombin — a distinction from heparin, which cannot inhibit fibrin-bound thrombin. Thrombin slowly cleaves the Arg3-Pro4 bond, restoring its own activity, giving a plasma half-life of roughly 25 minutes with normal renal function. Predominantly renally cleared, requiring dose reduction in renal impairment. Does not require antithrombin as a cofactor and does not cause heparin-induced thrombocytopenia.
Research areas
Every protocol below is reproduced from a published study or approved labelling, with its source named. These are records of what was studied — not recommendations, and not a suggestion that any of them is appropriate for any person.
| Protocol as reported | Source |
|---|---|
| 0.75 mg/kg intravenous bolus followed by 1.75 mg/kg/hour for the duration of the procedure | Approved product labelling |
| Bivalirudin versus heparin plus a glycoprotein IIb/IIIa inhibitor in primary PCI for STEMIReduced major bleeding, with an early stent thrombosis signal that shaped subsequent practice. | HORIZONS-AMI, New England Journal of Medicine 2008 |
Multiple large completed randomised trials including HORIZONS-AMI and MATRIX.
It inhibits thrombin already bound inside a clot, which heparin cannot do; it does not need antithrombin as a cofactor; and it does not cause heparin-induced thrombocytopenia. The trade-off in trials has been a lower bleeding rate against an early stent thrombosis signal.
Medical disclaimer
This page is for informational and research purposes only. Nothing here constitutes medical advice. The compounds discussed are research chemicals. Consult a qualified clinician before starting any protocol.
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