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Bivalirudin

Also known as Angiomax, Angiox, Bivalirudin TFA

Bivalirudin is a 20-amino acid synthetic direct thrombin inhibitor (DTI) derived from hirudin, the natural anticoagulant found in medicinal leech saliva. FDA-approved under the brand name Angiomax, it is used as an anticoagulant during percutaneous coronary intervention (PCI) and in patients with or at risk for heparin-induced thrombocytopenia (HIT). Its reversible binding mechanism and short half-life allow predictable anticoagulation with rapid offset after cessation.

Last updated April 10, 2026

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Bivalirudin: quick citable summary

Bivalirudin is listed by PeptaHub as a other peptide with a prescription legal-status classification. The page summarizes mechanism, research context, common routes, safety notes, and references for writers and AI answer engines.

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License: Creative Commons Attribution 4.0 International. Link back to https://peptahub.com/peptides/bivalirudin.

SAMEAS / EXTERNAL IDS
Bivalirudin CAS: 128270-60-0
QUICK ANSWER

What is Bivalirudin?

Bivalirudin (Angiomax) is an FDA-approved 20-amino acid direct thrombin inhibitor derived from leech hirudin, used during PCI and in heparin-induced thrombocytopenia. Its reversible binding and 25-minute half-life provide predictable, controllable anticoagulation.

§ 01

Overview

Bivalirudin is a 20-amino acid synthetic direct thrombin inhibitor (DTI) derived from hirudin, the natural anticoagulant found in medicinal leech saliva. FDA-approved under the brand name Angiomax, it is used as an anticoagulant during percutaneous coronary intervention (PCI) and in patients with or at risk for heparin-induced thrombocytopenia (HIT). Its reversible binding mechanism and short half-life allow predictable anticoagulation with rapid offset after cessation.

§ 02

Mechanism of action

Bivalirudin specifically inhibits both circulating and clot-bound thrombin by bivalently binding to two distinct sites on the thrombin molecule: the catalytic active site and the anion-binding exosite 1 (fibrinogen recognition site). This dual binding differentiates bivalirudin from univalent inhibitors. Importantly, thrombin slowly cleaves bivalirudin at the Arg3-Pro4 bond, resulting in gradual recovery of thrombin activity — providing reversible inhibition proportional to drug concentration. Bivalirudin directly inhibits thrombin-catalyzed or induced reactions, including fibrin formation, coagulation factor V, VIII, and XIII activation, and platelet aggregation triggered by thrombin. The result is dose-dependent prolongation of activated clotting time (ACT), aPTT, and thrombin time.

§ 03

Reported study ranges

PurposeRouteReported rangeFrequency
Percutaneous coronary intervention (PCI)intravenous0.750.75 mg/kgIV bolus, then infusion for duration of procedure

Reported ranges are for research context only. Consult a qualified healthcare professional before using any peptide.

Convert Bivalirudin research-range units

Need to convert mg to mcg, dose volume, or U-100 syringe units? Use the peptide dose unit converter for educational calculation support.

§ 04

Research summary

REPLACE-2 (Lincoff et al., JAMA 2003, n=6,010) compared bivalirudin with provisional GP IIb/IIIa blockade against heparin with planned GP IIb/IIIa blockade during PCI. The 30-day primary composite occurred in 9.2% versus 10.0% (OR 0.92, P=.32), meeting prespecified non-inferiority criteria, while in-hospital major bleeding fell from 4.1% to 2.4% (P<.001). HORIZONS-AMI (Stone et al., NEJM 2008, n=3,602) randomized STEMI patients undergoing primary PCI and found major bleeding of 4.9% versus 8.3% (RR 0.60, P<0.001) — the 40% relative reduction commonly quoted — along with lower 30-day cardiac death (1.8% vs 2.9%, P=0.03). The same trial found more acute stent thrombosis within 24 hours on bivalirudin, without a significant excess by 30 days, which is the main counterweight to the bleeding benefit. The EUROMAX and HEAT-PPCI trials in primary PCI reached less favorable conclusions on net clinical benefit, so the balance of evidence is not uniform across settings.[1][2][3][4][5][6]

📄This section cites 6 peer-reviewed sources. View all references →
§ 04b

Evidence grading

Each claimed benefit is graded by the strength of available evidence. Grades reflect study quality, not effect size.

strong
Non-inferior to heparin plus planned GP IIb/IIIa blockade for PCI ischemic endpointsREPLACE-2 (Lincoff et al. JAMA 2003, PMID 12588269): randomized double-blind trial, n=6,010; 30-day primary composite 9.2% vs 10.0% (OR 0.92, P=.32), prespecified non-inferiority met, in-hospital major bleeding 2.4% vs 4.1% (P<.001)
strong
40% relative reduction in 30-day major bleeding in primary PCI for STEMIHORIZONS-AMI (Stone et al. NEJM 2008, PMID 18499566): n=3,602 STEMI patients; major bleeding 4.9% vs 8.3% (RR 0.60, P<0.001), 30-day cardiac death 1.8% vs 2.9% (P=0.03). Acute stent thrombosis within 24 hours was increased on bivalirudin, with no significant excess by 30 days
strong
Reversible dual-site thrombin inhibitionMechanism established via biochemical and pharmacokinetic studies; FDA-approved since 2000
moderate
Use in patients with heparin-induced thrombocytopenia undergoing PCIWithin the FDA-labeled indication, which explicitly covers PCI patients with HIT and HITTS. Supporting efficacy data in this subgroup are case series and registries rather than dedicated RCTs
strong
25-minute half-life for predictable offsetLabeled PK: 25 minutes with normal renal function, ~57 minutes in severe renal impairment, and ~3.5 hours in dialysis-dependent patients

Strong = multiple RCTs · Moderate = limited trials or observational · Preliminary = animal or in vitro only · Insufficient = anecdotal or no published data

§ 05

Side effects

Bleeding (major and minor)
Thrombocytopenia
Back pain
Nausea
Hypotension
Headache
Injection/infusion site reactions
Acute stent thrombosis (rare, vs. heparin + GP IIb/IIIa inhibitors)

Side effects vary by individual. This is not an exhaustive list. Report unusual symptoms to a healthcare professional.

§ 06

Common stacks

Peptides commonly paired with Bivalirudin for synergistic effects.

§ 08

Sourcing & access

Prescription required

Bivalirudin is an FDA-approved prescription medication available through licensed healthcare providers, pharmacies, and label-appropriate access programs; compounded access depends on current FDA shortage status and compounding rules.

§ 09

Frequently asked questions

Bivalirudin (Angiomax) is used as an anticoagulant during percutaneous coronary intervention (PCI) and for patients with or at risk of heparin-induced thrombocytopenia (HIT). It is administered intravenously in catheterization laboratory settings.

Bivalirudin directly inhibits both circulating and clot-bound thrombin by binding to two distinct sites: the catalytic active site and the anion-binding exosite 1. Thrombin slowly cleaves bivalirudin, providing reversible inhibition that wears off predictably when the infusion stops.

In HORIZONS-AMI, bivalirudin alone reduced 30-day major bleeding from 8.3 percent to 4.9 percent versus heparin plus a GP IIb/IIIa inhibitor — a 40 percent relative reduction — with lower 30-day cardiac mortality. The trade-off is that acute stent thrombosis within the first 24 hours was more common on bivalirudin, though the excess was no longer significant at 30 days. Its short half-life and predictable offset are advantages in procedural settings.

Bivalirudin has a half-life of approximately 25 minutes with normal renal function, about 57 minutes in severe renal impairment, and roughly 3.5 hours in dialysis-dependent patients. The labeled infusion rate is reduced to 1 mg/kg/h when creatinine clearance is below 30 mL/min and to 0.25 mg/kg/h in hemodialysis patients; the bolus dose is unchanged.

US labeling contraindicates bivalirudin in patients with active major bleeding and in those with known hypersensitivity, including anaphylaxis, to bivalirudin or its components. It is given only under medical supervision in a catheterization laboratory setting, and dosing must be adjusted for renal impairment.

§ 10

Research references

  1. Bivalirudin and provisional glycoprotein IIb/IIIa blockade compared with heparin and planned glycoprotein IIb/IIIa blockade during percutaneous coronary intervention: REPLACE-2 randomized trialLincoff AM, Bittl JA, Harrington RA, Feit F, Kleiman NS, Jackman JD, et al.JAMA, 2003PubMed
  2. Bivalirudin during primary PCI in acute myocardial infarction (HORIZONS-AMI)Stone GW, Witzenbichler B, Guagliumi G, Peruga JZ, Brodie BR, Dudek D, et al.New England Journal of Medicine, 2008PubMed
  3. Bivalirudin: a direct thrombin inhibitorGladwell TDClinical Therapeutics, 2002PubMed
  4. Bivalirudin: pharmacology and clinical applicationsShammas NWCardiovascular Drug Reviews, 2005PubMed
  5. Safety and efficacy of bivalirudin with and without glycoprotein IIb/IIIa inhibitors in patients with acute coronary syndromes undergoing percutaneous coronary intervention: 1-year results from the ACUITY trialWhite HD, Ohman EM, Lincoff AM, Bertrand ME, Colombo A, McLaurin BT, et al.Journal of the American College of Cardiology, 2008PubMed
  6. Bivalirudin reduces platelet and monocyte activation after elective percutaneous coronary interventionBusch G, Steppich B, Sibbing D, Braun SL, Stein A, Groha P, et al.Thrombosis and Haemostasis, 2009PubMed
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