Atrial natriuretic peptide (ANP) is a 28-amino-acid hormone (MW ~3080 g/mol) secreted primarily by atrial cardiomyocytes in response to atrial stretch from volume overload. It is a key regulator of blood volume, sodium balance, and blood pressure. A recombinant form, carperitide (hANP), is approved in Japan for acute heart failure but is not approved in Western markets.
Category: Cardiovascular / Natriuretic. Evidence rating: B (meaningful human data).
Clinical status: Carperitide (recombinant hANP) approved in Japan (1995) for acute heart failure. Not approved in the US, EU, or other Western markets.
ANP binds to natriuretic peptide receptor A (NPR-A), a transmembrane guanylyl cyclase receptor, stimulating intracellular cGMP production. cGMP activates protein kinase G (PKG), which relaxes vascular smooth muscle (vasodilation), increases glomerular filtration rate, inhibits sodium reabsorption…
Safety considerations: Hypotension is the primary adverse effect and is dose-dependent; Japanese post-marketing surveillance reported increased in-hospital mortality in the higher-dose groups (ATTEND registry analysis, Mebazaa et al., Eur J Heart Fail 2015, PMID: 25684603); Bradycardia may occur due to vagal stimulation.
Reviewed by the PeptideAtlas Editorial Team.
| Molecular weight | ~3080 g/mol |
|---|---|
| CAS number | 85637-73-6 |
| Half-life | ~2-5 minutes |
| Production method | synthetic |
| Anti-doping status | not-listed |
| US regulatory status | Not approved. ANP is used as a research reagent. NT-proANP/MR-proANP used as diagnostic biomarker. |
Related peptides: Nesiritide, B-type Natriuretic Peptide.
Carperitide was developed and approved in Japan in 1995 based on Japanese clinical trials. Western regulatory bodies (FDA, EMA) have not approved it, partly because no sponsor pursued Western clinical trials and because similar agents like nesiritide (recombinant BNP) were developed for Western markets.
ANP (28 AA) is released primarily from atrial cardiomyocytes in response to atrial stretch, while BNP (32 AA) is released mainly from ventricular cardiomyocytes in response to ventricular wall stress. Both signal through NPR-A and have similar effects (vasodilation, natriuresis), but BNP has a slightly longer half-life. BNP/NT-proBNP is more widely used as a clinical biomarker for heart failure.
Yes. The mid-regional fragment of pro-atrial natriuretic peptide (MR-proANP) is an established heart failure biomarker, validated in the BACH trial. It is particularly useful when BNP may be unreliable (e.g., patients on sacubitril-valsartan, which elevates BNP but not MR-proANP).