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Bivalirudin (Angiomax)20 residuesFPRPGGGGNGDFEEIPEEYLEach bubble = one amino acid. Size = residue mass. Color = chemical class.Also known as: Angiomax, Angiox (EU), BG-8967
Major bleeding cut nearly in half. That's the headline from HORIZONS-AMI, where bivalirudin dropped 30-day major bleeding from 8.3% to 4.9% versus heparin plus GP IIb/IIIa inhibitors in a pooled analysis of 3,602 STEMI patients from HORIZONS-AMI and EUROMAX [1]. Bivalirudin (Angiomax) is a synthetic 20-amino-acid direct thrombin inhibitor, FDA-approved since 2000 for anticoagulation during percutaneous coronary intervention. Its 25-minute half-life means the anticoagulant effect clears fast once the infusion stops. BRIGHT-4 (Lancet 2022, n=6,016) later confirmed that extending the infusion 2 to 4 hours post-PCI eliminates the stent thrombosis concern. Interventional cardiologists reach for it in STEMI, HIT cases, and high-bleeding-risk patients where heparin carries too much baggage.
Bivalirudin (brand name Angiomax, CAS 128270-60-0) is a synthetic 20-amino-acid peptide and direct thrombin inhibitor used during percutaneous coronary intervention. The HORIZONS-AMI and EUROMAX pooled analysis (n=3,602)[1] showed a 41% reduction in major bleeding and 32% drop in 30-day mortality versus heparin. It binds thrombin at two sites simultaneously: the catalytic active site and exosite-1. That dual-site engagement lets it block both circulating and clot-bound thrombin, something heparin cannot do. The FDA approved bivalirudin in 2000 for anticoagulation during percutaneous coronary intervention, including patients with heparin-induced thrombocytopenia. Because the peptide never touches platelet factor 4, there is zero HIT risk. Dosing is weight-based: a 0.75 mg/kg IV bolus followed by a continuous infusion at 1.75 mg/kg/h for the duration of the procedure. Early trials flagged a stent thrombosis signal when the infusion stopped right after PCI. BRIGHT-4 (Lancet 2022, n=6,016)[2] solved that problem. An extended post-PCI infusion at full dose for 2 to 4 hours dropped stent thrombosis to 0.37% versus 1.10% with heparin; major bleeding fell to 0.17% versus 0.80%. A 2024 JACC meta-analysis pooling 6 RCTs and 15,254 STEMI patients confirmed the benefit profile. Thrombin itself slowly chops bivalirudin apart at the Arg3-Pro4 bond. That proteolytic self-destruction accounts for about 80% of clearance. The remaining 20% goes through the kidneys. With a half-life of roughly 25 minutes, anticoagulant activity fades within 1 to 2 hours of stopping the drip. No reversal agent exists, but the short offset makes one largely unnecessary in most clinical scenarios.
Twenty amino acids, two binding sites, one target. Bivalirudin locks onto thrombin (Factor IIa) at both its catalytic active site and anion-binding exosite-1 at the same time. The N-terminal D-Phe-Pro-Arg-Pro sequence plugs into the catalytic pocket. The C-terminal hirudin-like dodecapeptide grabs exosite-1, where fibrinogen normally docks. This bivalent grip produces tighter inhibition than active-site-only blockers. It also means bivalirudin reaches clot-bound thrombin trapped in the fibrin mesh; heparin-antithrombin complexes only neutralize circulating thrombin. The interaction has a built-in off switch. Thrombin cleaves the bivalirudin peptide at the Arg3-Pro4 bond while still bound. That proteolytic cut gradually restores enzymatic function. About 80% of bivalirudin clearance happens this way; the remaining 20% is renal elimination. The result is a half-life of roughly 25 minutes with linear, predictable pharmacokinetics. By blocking thrombin, bivalirudin shuts down several downstream cascades at once. Fibrinogen stops converting to fibrin. Factor V and Factor VIII activation stalls. Factor XIII can no longer cross-link fibrin strands. Thrombin-driven platelet activation through PAR-1 and PAR-4 receptors is blocked. All of this happens within minutes of the IV bolus, and reverses within 1 to 2 hours after the infusion stops.
FDA-approved direct thrombin inhibitor with strong RCT evidence for PCI anticoagulation. Reduces major bleeding vs. heparin + GP IIb/IIIa inhibitors; eliminates HIT risk; BRIGHT-4 (2022) demonstrated extended post-PCI infusion resolves prior stent thrombosis concern. 2024 JACC meta-analysis (n=15,254 STEMI) confirmed benefit. ACC/AHA 2025 ACS Guideline: Class I for HIT, Class IIa for STEMI primary PCI (with extended infusion), Class IIb for NSTEMI PCI.
BRIGHT-4 (Lancet 2022, PMID 36351459) + 2024 JACC meta-analysis 6 RCTs n=15,254 STEMI; HORIZONS-AMI (PMID 25572507)
Bleeding advantage diminished at high-volume radial-access centers; no reversal agent; cost 20–50× UFH even with generics; IV-only hospital administration: no outpatient use
Hospital-only IV drug: no self-administration community exists. Clinical community (interventional cardiologists, cath lab nursing, pharmacists) sentiment is positive for STEMI/HIT indications since BRIGHT-4. Cost and no-reversal-agent concerns remain common objections. Radial-access operators question incremental benefit for elective PCI.
Hospital-administered IV anticoagulant with no self-administration community. All dosing data from clinical trials and FDA label. No lay-community protocols or self-experimentation data exist.
| Level | Dose / Injection | Frequency |
|---|---|---|
| Beginner | 0.75mg | Single dose |
| Moderate | 0.75mg | Single dose |
| Aggressive | 0.75mg | Single dose |
This is a hospital-only IV drug. You won't be reconstituting this at home; cath lab pharmacists and nurses handle preparation under physician supervision. Reconstitution math for the record: each 250 mg vial gets 5 mL of Sterile Water for Injection (SWFI), giving a 50 mg/mL concentrate. That concentrate then gets diluted into 50 mL of D5W or 0.9% NaCl for a final working concentration of 5 mg/mL. For an 80 kg patient, the bolus is 60 mg (0.75 mg/kg x 80 kg), which works out to 12 mL from the 5 mg/mL solution. The procedural infusion runs at 140 mg/h (1.75 mg/kg/h x 80 kg), so 28 mL/h from the same bag. The non-obvious thing most clinicians miss early on: a subtherapeutic ACT at the 5-minute check almost always traces back to a weight calculation error. Recheck actual body weight before giving the supplemental 0.3 mg/kg bolus. Estimated weights in emergency STEMI settings cause real dosing errors.
Bivalirudin is used acutely during percutaneous coronary intervention and is not cycled. It is administered as a single-session IV bolus plus continuous infusion lasting the duration of the procedure (typically 30-90 minutes) with optional post-PCI infusion extension of up to 4 hours for STEMI patients.
Bivalirudin is a single-session acute procedural anticoagulant administered IV during PCI. There is no cycling protocol: the drug is administered once per procedure and cleared within 1–2 hours of stopping infusion due to its ~25-min half-life and proteolytic self-inactivation. The concept of on/off cycles does not apply.
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Expected: ACT >225 sec throughout PCI; reduced major bleeding vs. heparin + GP IIb/IIIa; effective anticoagulation without HIT risk
Monitor: ACT at 5 min post-bolus; supplemental bolus if subtherapeutic; renal function confirmed pre-procedure
All dosing is weight-based. A miscalculated weight is the leading cause of subtherapeutic ACT.
Reconstitute one 250 mg vial with 5 mL Sterile Water for Injection. Gently swirl until dissolved (50 mg/mL concentrate).
Withdraw the required volume and dilute in 50 mL of D5W or 0.9% sodium chloride to achieve a 5 mg/mL working solution.
Administer the IV bolus: 0.75 mg/kg injected over 3 to 5 seconds. For an 80 kg patient, that's 60 mg, or 12 mL from the 5 mg/mL solution.
For 80 kg: 140 mg/h, which is 28 mL/h at 5 mg/mL concentration.
At 5 minutes post-bolus, check the activated clotting time (ACT). Target is above 225 seconds. If below 225 seconds, give a supplemental 0.3 mg/kg bolus (24 mg for an 80 kg patient, or 4.8 mL).
Continue the infusion for the duration of the PCI procedure (typically 30 to 90 minutes).
For STEMI patients: extend the infusion at the full 1.75 mg/kg/h rate for 2 to 4 hours after the procedure ends (BRIGHT-4 protocol).
Renal dose adjustments: reduce infusion to 1.0 mg/kg/h for CrCl below 30 mL/min; reduce to 0.25 mg/kg/h for dialysis patients. The bolus dose stays at 0.75 mg/kg regardless of renal function.
Sheath removal: wait until ACT falls below 175 seconds after stopping the infusion.
Store reconstituted solution at 2 to 8 degrees Celsius; stable for 24 hours. Diluted solution is stable at room temperature for 24 hours. Do not freeze.
DAPT is standard of care alongside bivalirudin for all PCI. Aspirin cyclooxygenase inhibition complements direct thrombin inhibition. Not a peptide but mandatory co-administration.
81–325 mg loading dose pre-PCI; 81 mg/day indefinite maintenance
Preferred P2Y12 inhibitor with bivalirudin in STEMI per BRIGHT-4 protocol and PLATO evidence. Reversible binding and faster onset/offset preferred in acute settings vs. clopidogrel.
180 mg loading dose pre-PCI; 90 mg twice daily maintenance
Alternative P2Y12 inhibitor when ticagrelor or prasugrel are contraindicated (prior hemorrhagic stroke, high cost, drug interactions, age >75 in STEMI).
300–600 mg loading dose; 75 mg/day maintenance
Concurrent administration markedly increases major bleeding risk. Do not give UFH with bivalirudin. Note: prior UFH administered en route for STEMI (pre-hospital) is NOT a contraindication to initiating bivalirudin upon cath lab arrival: sequential use per EUROMAX is acceptable.
Do not combineMarkedly increased hemorrhagic risk and confirmed IV incompatibility. Do not mix in same IV line. Pharmacoinvasive STEMI strategies (thrombolytic → transfer for PCI) typically require a bivalirudin hold period.
Do not combinePlanned concurrent use negates bivalirudin's bleeding benefit and is not supported by trial data. Bail-out use is acceptable clinically (BRIGHT-4 allowed it) but the bail-out subgroup showed equivalent, not superior, outcomes vs. heparin. Avoid planned combination.
Concurrent anticoagulant use increases bleeding risk without therapeutic benefit. If transitioning from pre-hospital LMWH (NSTEMI), bivalirudin bolus timing must account for timing and dose of last LMWH administration.
Pricing updated 2026-04-09
Bleeding is the primary safety concern. Major bleeding events occur in 1.4% to 3.8% of patients across clinical trial populations, including retroperitoneal hemorrhage, intracranial hemorrhage, pulmonary hemorrhage, and cardiac tamponade. Post-marketing surveillance has identified rare fatal hemorrhages and anaphylaxis cases. No approved reversal agent exists. If a patient starts bleeding during the infusion, the only option is stopping the drug and waiting; coagulation normalizes within 1 to 2 hours in patients with normal renal function. For dialysis patients (half-life 3.5 hours), hemodialysis can actively remove it. Acute stent thrombosis was a legitimate concern in early trials. When the infusion stopped immediately after PCI, stent thrombosis rates within 24 hours exceeded heparin. BRIGHT-4 resolved this by showing that a 2 to 4 hour extended full-dose infusion (1.75 mg/kg/h) eliminated the excess risk. Omitting that extended infusion in STEMI patients is the most preventable adverse outcome with this drug. Back pain affects up to 42% of patients in clinical trials. That number sounds alarming until you learn the cause: catheterization table positioning during prolonged procedures, not a pharmacologic effect of the drug itself. Nausea occurs in roughly 14% of patients. Headache and vomiting are also reported. Hypotension can occur, particularly in the acute STEMI population where hemodynamic instability is common regardless of anticoagulant choice. Cardiac tamponade and cardiogenic shock have been reported as serious adverse events, though these are procedural complications rather than drug-specific effects. Thrombocytopenia has been reported rarely. INR elevation can occur when transitioning to warfarin, not because of a true coagulation change, but because bivalirudin interferes with the PT assay reagent. Ecarin clotting time or dilute thrombin time should be used if accurate DTI monitoring is needed. Anaphylaxis is rare but documented in post-marketing reports. Any patient with prior hypersensitivity to bivalirudin or hirudin-derived compounds should not receive it. Contraindications include active major bleeding, severe uncontrolled hypertension, subacute bacterial endocarditis, and severe hepatic impairment with coagulopathy. Bivalirudin is FDA Pregnancy Category B; animal studies showed no harm, but human data is limited. Whether the drug enters breast milk is unknown.
Verify Bivalirudin (Angiomax) dosing and safety with a second opinion
FDA-approved pharmaceutical-grade product administered exclusively in hospital settings under physician supervision. Multiple generics (Sandoz, Hospira/Pfizer, Mylan/Viatris, Meitheal) with full FDA CMC oversight. No compounding, grey-market supply, or self-administration quality risk.
| Test | When | Target |
|---|---|---|
| Activated Clotting Time (ACT) | 5 minutes after initial IV bolus; periodically during prolonged procedures (>60 min) | >225 sec during PCI; <175 sec before sheath removal |
| Serum Creatinine / eGFR (CrCl) | Pre-procedure (routine pre-cath laboratory evaluation) | Baseline; guides dose calculation: no target, only dose adjustment thresholds |
| Complete Blood Count (CBC) | Pre-procedure baseline; post-procedure if clinically significant bleeding suspected | Baseline: watch for Hgb drop >2 g/dL or platelet fall post-procedure |
| Ecarin Clotting Time (ECT) or Dilute Thrombin Time (dTT) | If direct thrombin inhibitor plasma level monitoring specifically required (unusual circumstance) | Context-dependent; correlates linearly with bivalirudin plasma concentration |
Confirms therapeutic anticoagulation; determines need for supplemental bolus; guides sheath removal timing
Required for infusion rate dose adjustment: CrCl <30 → 1.0 mg/kg/h; dialysis → 0.25 mg/kg/h
Baseline hemoglobin and platelet count; identifies bleeding-related anemia; rule out thrombocytopenia
INR and aPTT are unreliable for bivalirudin therapeutic monitoring; ECT and dTT are DTI-specific assays
Immediate anticoagulant effect upon IV bolus injection. ACT should be checked at 5 minutes to confirm therapeutic anticoagulation (target ACT >225 seconds).
Stable steady-state anticoagulation maintained by continuous infusion at 1.75 mg/kg/h during the PCI procedure. Therapeutic ACT levels sustained throughout.
Extended infusion period for STEMI patients to prevent acute stent thrombosis. Continued anticoagulation monitoring. Sheath removal can be considered once ACT falls below 175 seconds.
Rapid offset of anticoagulant effect due to short half-life (~25 min). Coagulation parameters return to baseline within 1-2 hours of stopping infusion in patients with normal renal function.
0 to 5 minutes (bolus phase): Anticoagulant effect begins immediately at end of the IV bolus. Therapeutic plasma concentration lands within 2 minutes. The 5-minute ACT check should read above 225 seconds in most patients. Roughly 15 to 25% of cases need a supplemental 0.3 mg/kg bolus per institutional experience data. Transient hypotension can occur. No patient self-reports exist for this drug. 5 to 90 minutes (procedural infusion): Stable anticoagulation at therapeutic ACT levels, maintained by the continuous 1.75 mg/kg/h drip. Clinical trial data confirms procedural success rates equivalent to heparin. Back pain affects up to 42% of patients during this window; it's a positioning issue, not a drug effect. Nausea occurs in about 14%. 1 to 4 hours post-PCI (STEMI extended infusion): This is the window that matters for stent thrombosis prevention. BRIGHT-4 tracked the numbers: stent thrombosis 0.37% with bivalirudin versus 1.10% with heparin; major bleeding 0.17% versus 0.80%. Sheath removal is held until ACT drops below 175 seconds. Access site hematoma monitoring is standard during this phase, especially with femoral access. 25 to 120 minutes post-cessation: The 25-minute half-life means anticoagulant effect fades quickly once the infusion stops. Coagulation parameters return to baseline within 1 to 2 hours for patients with normal kidneys. That rapid offset is why bivalirudin allows earlier ambulation compared to heparin. No drug-specific adverse effects during this offset period; the only pharmacologic concern is transient rebound thrombin activity, which the BRIGHT-4 extended infusion protocol covers.
Immediate anticoagulation onset at end of IV bolus; ACT should reach >225 sec at 5-min check in most patients. Therapeutic plasma concentration achieved within 2 minutes.
Cath lab experience: 5-min ACT check is standard workflow; supplemental bolus needed in ~15–25% of cases per institutional data. No self-report data exists.
Stable therapeutic ACT (>225 sec) maintained by continuous 1.75 mg/kg/h infusion. Clinical trial data confirms procedural success rates equivalent to heparin.
Clinical: back pain reported in up to 42% of patients: primarily catheterization positioning, not a pharmacologic drug effect.
Extended 1.75 mg/kg/h infusion covers peak acute stent thrombosis risk window. BRIGHT-4: stent thrombosis 0.37% (bivalirudin) vs 1.10% (heparin); major bleeding 0.17% vs 0.80%.
CCU/nursing: sheath removal held until ACT <175 sec; access site hematoma monitoring standard during this window.
Anticoagulant effect decays with ~25-min half-life; coagulation parameters normalize within 1–2h in normal renal function. No reversal agent required in most cases.
Clinical: enables earlier ambulation and sheath removal vs. heparin; particularly valued in radial-access center protocols where bleeding risk is already low.
Source: FDA-approved Angiomax prescribing information; 25 minutes in PCI patients with normal renal function
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Bivalirudin is FDA-approved (NDA 020873, original approval 2000, most recent label revision 2019). The branded product Angiomax has been largely displaced by generic versions from Sandoz, Hospira/Pfizer, Mylan/Viatris, and Meitheal. All generics carry the same FDA-approved indications: anticoagulation during PCI, including patients with or at risk of HIT/HITTS. This is a prescription pharmaceutical product administered exclusively in hospital catheterization laboratories and ICU settings. It is not available through compounding pharmacies, research chemical suppliers, or for self-administration. All administration occurs under direct physician supervision. Bivalirudin is not a WADA-prohibited substance, though the question is largely academic given its IV-only hospital route. The information on this page is for educational purposes. It does not replace medical advice from a qualified interventional cardiologist. Dosing decisions require clinical judgment, patient-specific factors, and real-time monitoring. Peptide Schedule is a research platform, not a prescriber.
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