Bivalirudin
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| Clinical data | |
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| Trade names | Angiomax |
| AHFS/Drugs.com | Monograph |
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| Routes of administration |
Intravenous injection/infusion only |
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| Pharmacokinetic data | |
| Bioavailability | N/A (IV application only) |
| Metabolism | Angiomax is cleared from plasma by a combination of renal mechanisms and proteolytic cleavage |
| Biological half-life | ~25 minutes in patients with normal renal function |
| Identifiers | |
| Synonyms | d-Phenylalanyl-l-prolyl-l-arginyl -l-prolylglycylglycylglycylglycyl-l-asparaginylglycyl -l-alpha-aspartyl-l-phenylalanyl -l-alpha-glutamyl-l-alpha-glutamyl-l-isoleucyl -l-prolyl-l-alpha-glutamyl-l-alpha-glutamyl -l-tyrosyl-l-leucine |
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| Chemical and physical data | |
| Formula | C98H138N24O33 |
| Molar mass | 2180.29 g/mol |
| 3D model (Jmol) | |
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  (what is this?)
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Bivalirudin (Angiomax or Angiox, manufactured by The Medicines Company) is a specific and reversible direct thrombin inhibitor (DTI).
Chemically, it is a synthetic congener of the naturally occurring drug hirudin (found in the saliva of the medicinal leech Hirudo medicinalis).
Bivalirudin is a DTI that overcomes many limitations seen with indirect thrombin inhibitors, such as heparin. Bivalirudin is a short, synthetic peptide that is potent, highly specific, and a reversible inhibitor of thrombin. It inhibits both circulating and clot-bound thrombin, while also inhibiting thrombin-mediated platelet activation and aggregation. Bivalirudin has a quick onset of action and a short half-life. It does not bind to plasma proteins (other than thrombin) or to red blood cells. Therefore, it has a predictable antithrombotic response. There is no risk for Heparin Induced Thrombocytopenia/Heparin Induced Thrombosis-Thrombocytopenia Syndrome (HIT/HITTS). It does not require a binding cofactor such as antithrombin and does not activate platelets. These characteristics make bivalirudin an ideal alternative to heparin.
Bivalirudin clinical studies demonstrated consistent positive outcomes in patients with stable angina, unstable angina (UA), non-ST segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI) undergoing PCI in 7 major randomized trials. Patients receiving bivalirudin had fewer adverse events compared to patients that received heparin.
US (United States) Indications:
EU (European) indications:
Mechanism of action
Bivalirudin directly inhibits thrombin by specifically binding both to the catalytic site and to the anion-binding exosite of circulating and clot-bound thrombin. Thrombin is a serine proteinase that plays a central role in the thrombotic process. It cleaves fibrinogen into fibrin monomers, activates Factor V, VIII, and XIII, allowing fibrin to develop a covalently cross-linked framework that stabilizes the thrombus. Thrombin also promotes further thrombin generation, and activates platelets, stimulating aggregation and granule release. The binding of bivalirudin to thrombin is reversible as thrombin slowly cleaves the bivalirudin-Arg3-Pro4 bond, resulting in recovery of thrombin active site functions.
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