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Pick up to three peptides to see how their mechanisms, studied uses and evidence levels differ. Rows where the entries disagree are marked with a blue edge.
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Comparison
Nesiritide
Cardiovascular & blood
Evidence level
Moderate evidence
Approval status
Approved drug
Mechanism of action
- 1.Binds natriuretic peptide receptor A on vascular smooth muscle and the kidney.
- 2.Raises intracellular cGMP, relaxing veins and arteries and lowering filling pressures.
- 3.Increases sodium and water excretion through the kidney.
- 4.Suppresses renin, aldosterone and sympathetic tone.
- 5.Its short half-life of about 18 minutes makes it titratable by infusion.
Studied for
- Acute decompensated heart failure
- Haemodynamic effects on pulmonary capillary wedge pressure
- Comparisons against nitroglycerin and dobutamine
- Renal function during acute heart failure (ROSE)
Reported effects
- Rapid fall in pulmonary capillary wedge pressure and improvement in dyspnoea in early studies
- No significant improvement in dyspnoea or 30-day outcomes in ASCEND-HF
- Hypotension is the most frequent adverse effect
- Possible worsening renal function in some analyses
Side effects
- Hypotension
- Headache
- Nausea
- Ventricular arrhythmia in early reports
- Raised creatinine
- Injection-site reactions
Research protocol
Research context only - a hospital infusion. The labelled regimen is a 2 microgram per kilogram intravenous bolus optionally followed by an infusion of 0.01 micrograms per kilogram per minute, avoiding a bolus in hypotensive patients; ASCEND-HF randomised over 7,000 patients and measured dyspnoea at 6 and 24 hours plus 30-day death and rehospitalisation.
Research context only
Evidence justification
Small haemodynamic trials show clear pressure effects, but the large ASCEND-HF trial found no meaningful symptom or outcome benefit, leaving approval resting on surrogate endpoints.