Nesiritide

Natrecor, recombinant human B-type natriuretic peptide (rhBNP), Noratak (Switzerland)

Cardiovascular & circulation

Awaiting medical reviewEN ES DE FR PT ZH+ Follow for updates

Note on this profile. Nesiritide was an approved intravenous hospital medicine for acute heart failure. It is identical to a hormone the heart makes naturally, and the same molecule's blood level (BNP) is one of the most-ordered heart tests. The drug itself has been withdrawn from the US market and was never widely approved elsewhere. This page explains the natural hormone, the drug and why it faded.

Summary

Class: Recombinant human B-type natriuretic peptide: a 32-amino-acid ring peptide with one disulfide bond, identical in sequence to the hormone released by heart muscle cells; made in E. coli
Mechanism: Activates natriuretic peptide receptor-A, raising cGMP, which widens arteries and veins, lowers filling pressures, and promotes salt and water loss through the kidney
Routes studied: Intravenous bolus plus infusion (approved); subcutaneous and intranasal in small research studies
Half-life: ~18 minutes (initial phase ~2 minutes); haemodynamic effects persist longer than plasma levels suggest
Storage: Lyophilised 1.5 mg vials at room temperature or refrigerated; reconstituted and diluted solution stable 24 h
Regulatory status: FDA-approved 2001; US product discontinued (around 2018) †; never authorised in the EU or UK; approved historically in Switzerland and some other countries

Doses are as reported in studies or by the community — never recommendations.

1What it is

B-type natriuretic peptide is one of a family of hormones (with ANP and CNP) that the heart uses to tell the body it is overstretched. When the ventricles are under pressure or volume load, heart muscle cells release a precursor (proBNP) that is cut into active BNP and an inactive fragment, NT-proBNP. Both circulate and are the basis of routine blood tests for heart failure. BNP lowers blood pressure, promotes urine and sodium output, and opposes the renin–angiotensin and sympathetic systems. It is one of the more sensible endogenous molecules to have been tried as a drug.

Nesiritide is the exact recombinant copy. Scios developed it, and the FDA approved it in August 2001 for hospitalised patients with acutely decompensated heart failure who have shortness of breath at rest. It was widely used in US hospitals for a few years, then two 2005 meta-analyses raised concern about worse kidney function and higher short-term mortality. A 7,141-patient outcome trial (ASCEND-HF) then found it safe but with no meaningful benefit beyond a small improvement in breathlessness, and use dwindled to almost nothing. Johnson & Johnson (which had acquired Scios) stopped supplying it in the US around 2018. In the research community the molecule is of interest only as a marker; there is no self-directed use and no plausible reason for any.

2How it's thought to work

Binds natriuretic peptide receptor-A (NPR-A, a guanylyl cyclase) on vascular smooth muscle, endothelium and kidney cells, raising intracellular cGMP.

In vessels this relaxes smooth muscle: venous dilation lowers the pressure in the lungs and heart chambers (pulmonary capillary wedge pressure falls within 15 minutes), arterial dilation lowers afterload.

In the kidney it increases glomerular filtration and blocks sodium reabsorption, producing natriuresis and diuresis — though in trials of sick heart-failure patients the diuretic effect was weaker than hoped.

It suppresses renin, aldosterone, endothelin and sympathetic activity.

It is cleared by the natriuretic peptide clearance receptor (NPR-C) and by neprilysin; the neprilysin-inhibitor drug sacubitril works partly by raising natural BNP levels, which is the modern way the same biology is used.

Recombinant BNP given by infusion in acute heart failure. It lowers filling pressures as expected, but trials found no improvement in symptoms or survival.Schematic — not to scale

3What the research shows

Haemodynamics and breathlessness in acute heart failure

VMAC (n=489) compared nesiritide with IV nitroglycerin and placebo: nesiritide lowered pulmonary capillary wedge pressure more than nitroglycerin at 3 h and modestly improved dyspnoea versus placebo (VMAC Investigators 2002, JAMA). Earlier dose-ranging trials showed the same (Colucci 2000, NEJM). [1]

Graded A (concern then reassurance)

Mortality and kidney safety

Pooled analyses of early trials suggested worsening renal function (Sackner-Bernstein 2005, Circulation) and a trend to higher 30-day mortality (Sackner-Bernstein 2005, JAMA). ASCEND-HF (n=7,141, randomised, double-blind, placebo-controlled) found no difference in death or heart-failure readmission at 30 days (9.4% vs 10.1%), no worsening of renal function, a small and not clinically meaningful improvement in dyspnoea at 6 and 24 h, and more hypotension (26.6% vs 15.3%) (O'Connor 2011, NEJM). The drug was thus shown to be safe but largely ineffective for hard outcomes. [3][4][5]

Graded A (negative)

Low-dose nesiritide for kidney protection

ROSE-AHF (n=360) tested low-dose nesiritide (0.005 µg/kg/min without bolus) or low-dose dopamine added to diuretics in acute heart failure with renal dysfunction; neither improved urine output or kidney function (Chen 2013, JAMA). [6]

Graded A/B

Cardiac surgery

NAPA (n=272) reported better post-operative renal function and shorter stay with peri-operative nesiritide in patients with low ejection fraction having bypass surgery (Mentzer 2007, J Am Coll Cardiol); not confirmed in larger trials. [7]

Chronic outpatient infusions, subcutaneous BNP

Serial outpatient infusions (FUSION I/II) did not reduce events (Yancy 2008, Circ Heart Fail). Small studies of BNP in chronic heart failure and after myocardial infarction (Chen and Burnett group, Mayo) reported favourable haemodynamic and hormonal changes but no outcome data.

Community / self-directed use

None documented.

4Reported side effects and interactions

Literature-reported

Hypotension is the main adverse effect (about 1 in 4 patients in ASCEND-HF), often symptomatic and sometimes prolonged because the haemodynamic effect outlasts plasma levels; headache, nausea, bradycardia, dizziness, back pain. Worsening renal function was suggested by meta-analyses but not confirmed in ASCEND-HF. Not for patients with cardiogenic shock or systolic blood pressure below 90 mmHg, significant valvular stenosis or restrictive cardiomyopathy.

Community-reported

none; no community use.

Theoretical. antibody formation to a native-sequence peptide was not observed; natriuretic peptides are involved in lipolysis and bone growth (CNP) but no such effects were reported at infusion doses.

Interactions. additive hypotension with ACE inhibitors, ARBs, nitrates, other vasodilators and diuretics; the label advised caution with concurrent IV vasodilators. No CYP interactions. Physically incompatible in the same line with heparin, insulin, bumetanide, enalaprilat, hydralazine and furosemide.

Markers researchers commonly monitor

These follow heart-failure practice; nesiritide infusion has one laboratory quirk worth knowing:

Marker	Why it's watched
Blood pressure (continuous or every 15 minutes initially)	hypotension is the dominant adverse effect.
Urine output and body weight	the intended diuretic/natriuretic effect.
Serum creatinine and eGFR	the 2005 renal-safety concern; checked daily during and after infusion.
Serum sodium and potassium	shifts with diuresis and vasodilator therapy.
BNP assay	nesiritide is BNP and cross-reacts with BNP immunoassays, so BNP measured during or soon after infusion is uninterpretable; NT-proBNP is unaffected and is the marker to use.
Heart rate and rhythm	bradycardia and ventricular arrhythmia were monitored in trials.

Free for everyone. Safety information is never behind a paywall.

5Reconstitution and handling

Hospital use only. The 1.5 mg vial is with 5 mL of drawn from a 250 mL bag of 5% dextrose, 0.9% saline or mixed solution, gently rocked (not shaken), then returned to the bag to give 6 µg/mL for bolus and infusion. Heparin-coated catheters bind the peptide, so a non-heparin line is used. No longer commercially available in the US. The site calculator is not applicable.

6Commonly studied alongside

Loop diuretics (furosemide, bumetanide) as standard background; IV nitroglycerin and dobutamine as comparators; low-dose dopamine (ROSE-AHF). In the modern era, sacubitril/valsartan raises endogenous BNP rather than giving it. Related endogenous natriuretic peptides covered elsewhere on the site, if present, include ANP and CNP analogues (vosoritide, earlier profile) †.

Informational cross-links. Not stack recommendations.

7Regulatory status by region

Region	Status (checked —)
United States	FDA-approved (Natrecor, August 2001); Janssen/Scios discontinued the product (last supplies around 2018) †; no generic exists
European Union	Never authorised; the EU application was withdrawn in the early 2000s †
United Kingdom	Not licensed
Australia	Not registered with the TGA †
South Africa	Not registered with SAHPRA
Switzerland and others	Approved as Noratak in Switzerland and several Latin American and Asian markets historically; current availability †
Sport	Not prohibited by WADA

8Open questions

Whether any subgroup (e.g. hypertensive acute heart failure) benefits meaningfully; ASCEND-HF subgroup analyses were inconclusive.
Whether designed natriuretic peptides (e.g. cenderitide, a CNP/DNP chimera; or M-ANP) will succeed where the native hormone did not.
Why the renal protection seen in cardiac-surgery and small studies did not translate to larger trials.

9References

1Colucci WS et al. (2000). Intravenous nesiritide, a natriuretic peptide, in the treatment of decompensated congestive heart failure. NEJM. PubMed · DOI
2Publication Committee for the VMAC Investigators (2002). Intravenous nesiritide vs nitroglycerin for treatment of decompensated congestive heart failure: a randomized controlled trial. JAMA. PubMed
3Sackner-Bernstein JD et al. (2005). Short-term risk of death after treatment with nesiritide for decompensated heart failure: a pooled analysis of randomized controlled trials. JAMA. PubMed · DOI
4Sackner-Bernstein JD et al. (2005). Risk of worsening renal function with nesiritide in patients with acutely decompensated heart failure. Circulation. PubMed · DOI
5O'Connor CM et al. (2011). Effect of nesiritide in patients with acute decompensated heart failure (ASCEND-HF). NEJM. PubMed · DOI
6Chen HH et al. (2013). Low-dose dopamine or low-dose nesiritide in acute heart failure with renal dysfunction: the ROSE acute heart failure randomized trial. JAMA. PubMed · DOI
7Mentzer RM et al. (2007). Effects of perioperative nesiritide in patients with left ventricular dysfunction undergoing cardiac surgery: the NAPA trial. J Am Coll Cardiol. PubMed · DOI
8Natrecor (nesiritide) US prescribing information (last version). PubMed

References are being resolved to PubMed/DOI identifiers; links search PubMed for the citation until then.

† Being confirmed by our reviewers against current sources.

10Community

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Self-reported side effects Phase 2

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11Page history

30 Oct 2026Profile published — awaiting medical review

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