ANP dosage and evidence
Written by Aaron CuhaReviewed Sep 2026
The short answer
ANP is a hormone the heart releases when its chambers stretch. It is why the heart counts as a hormone-making organ. A lab-made form, carperitide, is used for sudden heart failure in Japan. A 2025 review pooled 9 studies and found more people died in hospital on carperitide.
Evidence grade for ANP: Moderate. The rule: at least one finished study in people, and at least 100 people who took it. The sum on this page: 4 completed trials, 188 people given it. A grade counts how much has been done to people, not whether it works.
- People given it
- 188
- Human studies
- 4
- Found nothing
- 2
Dose
No human dose established
Amounts that were given in studies sit in Human evidence on this page. None of them is a personal dose.
4 completed trials, 188 people given it
4 effects reported, 3 unwanted, 1 wanted, by people using it, not a trial
Goal pages: Ageing and longevity, Heart and circulation
In plain English
In plain English, from Aaron
This is how I would explain it to a friend. The evidence, with the numbers, is further down the page.
ANP is a hormone your heart makes when its chambers stretch. It tells your kidneys to dump salt and water, and it relaxes blood vessels. A lab-made form, carperitide, is given by drip for sudden heart failure in Japan. It is not approved in the US.
What people take it for
- Doctors in Japan use it for sudden heart failure.
- Some people ask about it for blood pressure or kidney health.
What studies in people showed
The results clash. In 2,435 Japanese patients, fewer died over a year on a low dose than on none. But a 2025 review of 9 studies found more deaths in hospital on carperitide, 1.38 times the odds. In 367 matched pairs of patients, deaths in hospital were about twice as likely on it. The planned trials were too small to settle it. In 109 patients, it did no better than a water tablet, and more had to stop because of problems.
What people report
Reports, not study results
The good
- In 109 patients, symptoms and a heart strain blood test got better about as much as on a water tablet.
The bad
- Blood pressure ran lower on it, and more people had to stop because heart failure got worse or blood pressure dropped.
- Potassium fell a little, and fell too low more often when a strong water tablet was added.
- More people died in hospital on it in several studies.
Where these come from: No user reports. These come from the Japanese hospital studies and the 2025 review on this page.
My bottom line
This is a hospital drug with mixed results even there. If you want to know how your heart is doing, a BNP blood test is the useful thing, not a shot.
An opinion, not a finding. I am a coach, not a doctor.
What it has been measured to do
Measured in people
Goals ANP has been tested for in people, biggest studies first. We count only what the studies on this page say, so the real numbers may be higher.
- Heart attacks and strokes2,619 people · 4 studies · 1 found nothing
- Blood pressure184 people · 2 studies
- Kidney function75 people · 1 study
- Living longer2,439 people · 3 studies · 1 found nothing
32 of the 36 indexed goals have no study of any kind behind ANP
No study in people, animals or cells on this page reports a result for these. That does not prove ANP does nothing for them. It does mean anything you have heard about ANP and one of these did not come from a study cited here.
Show full evidence
What is ANP?
ANP is a hormone the heart releases when its chambers stretch. It is why the heart counts as a hormone-making organ. A lab-made form, carperitide, is used for sudden heart failure in Japan. A 2025 review pooled 9 studies and found more people died in hospital on carperitide.
Atrial natriuretic peptide, or ANP, is a hormone 28 building blocks long. Cells in the heart's upper chambers release it when the chamber walls stretch. It makes the kidneys pass more salt and water. It relaxes blood vessels. It pushes back against the body's main blood pressure system. One detail matters for anyone reading about it. ANP is really a family of pieces cut from one parent protein. That parent also makes urodilatin, vessel dilator, kaliuretic peptide and long-acting natriuretic peptide. They are not the same molecule, and you cannot swap one for another.
Nearly all the human evidence for giving it as a drug comes from Japan. There, a lab-made form called carperitide is given by drip for sudden heart failure. The results do not match what the biology suggests. The biggest study pooled records from two Japanese patient groups, 2,435 patients in all. Over a year, fewer died in the low-dose group than in those given none. But a 2025 review pooled 9 studies and found more deaths in hospital with carperitide, 1.38 times the odds. Four of those 9 were planned trials. On their own, they were far too small to say anything. Another study paired 367 treated patients with 367 similar untreated ones. Deaths in hospital were about twice as likely on carperitide (2.13 times the odds). These results clash, and this page reports them that way.
We checked the US drug records on 11 September 2026. No ANP or carperitide product appears. Medical papers, including a 2025 review, say carperitide is given by drip for sudden heart failure mainly in Japan. This site did not check a Japanese regulator record directly, so we do not state its approval date or terms.
How does ANP work?
In people, ANP docks on a receptor called NPR-A. That raises a messenger called cyclic GMP inside blood vessel and kidney cells. The result is more salt and water leaving through the kidneys, and wider blood vessels. It also turns down renin and aldosterone, two hormones that hold on to salt. The body clears it through a second receptor, NPR-C, and an enzyme called neprilysin breaks it down. That is why blocking neprilysin, the sacubitril half of the heart drug sacubitril/valsartan, raises these hormones rather than adding more. How much people pee on it varies a lot. In 75 people with sudden heart failure, those who started with lower ANP and lower vasopressin passed the most urine on a carperitide drip.
What have studies in people found about ANP?
There is a lot of human dosing experience. Almost all of it is from Japan, and almost all of it comes from watching what doctors already did. The planned trials are small. The ones in the 2025 review were too few and too small to settle deaths. The one head-to-head trial against tolvaptan, a water tablet, found fewer problems on tolvaptan.
- Pooled Japanese patient groups (2022): 2,435 patients. Over a year, there were fewer deaths from heart causes and from any cause in the low-dose carperitide group than in those given none. This clashes with the in-hospital results below.
- Review of 9 studies (2025): more deaths in hospital with carperitide, 1.38 times the odds, pooling planned trials and matched records together. The planned trials alone told us nothing (odds 0.85, with a range from 0.07 to 10.49).
- Matched hospital records (2015): 367 treated patients, each paired with a similar untreated one. Deaths in hospital were 2.13 times the odds on carperitide.
- Salts in the blood: in 162 patients, potassium fell a little and sodium did not change.
- AVCMA trial (2013): 109 patients, carperitide against tolvaptan. Symptoms and a heart strain blood test improved about the same. More people on carperitide had to stop because of problems.
- Who pees more: in 75 patients, starting levels of ANP and vasopressin predicted who responded.
What this does not tell you: No planned trial has shown that carperitide or any ANP product cuts deaths. The watching studies point in opposite directions. Everything comes from sudden heart failure in hospital, mostly in Japan, mostly with short drips. Nothing here says anything about ANP for blood pressure, kidney protection or longer life in people who are not acutely ill. No product exists outside that hospital setting.
The state of the research
ANP is the reason the heart is called a hormone-making organ. That discovery has been far more useful as a blood test and as a drug target than as a drug. Measuring these heart hormones is now routine in heart failure. And the most successful modern heart failure drug works by blocking neprilysin, the enzyme that destroys them. It does not inject them.
The carperitide record shows why that difference matters. Japanese doctors took up the drip widely because the biology made sense. The results that followed came from watching what doctors did, and they clash. Matched hospital records showed more deaths in hospital. A pooled look at two patient groups showed fewer deaths at 1 year in the low-dose group. The planned trials were too small to break the tie. The 2025 review says plainly that the drug has not been shown to work. The story of nesiritide is close. That is the BNP drug that was approved in the United States and is now discontinued. Read both pages together.
One limit of this page. We report carperitide's Japanese approval only as medical papers describe it, because we did not check a regulator record directly. The research file behind this page flags that, and we do not paper over it.
The evidence, in charts
Fig. 1a · how many people
2,623people, across 4 studies in people cited here
| Study | People | Share |
|---|---|---|
| ESC Heart Failure 2022 | 2,435 | 93% |
| Journal of Clinical Pharmacology 2013 | 109 | 4% |
| ESC Heart Failure 2022 | 75 | 3% |
| BMC Cardiovascular Disorders 2025 | 4 | 0% |
One study holds 93% of these people, so the total rests more on one study than its size suggests. Counts are the number of people each study on this page says it signed up. That includes studies that only watched people and gave nobody the compound. 2 more studies in people give no headcount and are not counted here. Studies still signing people up are left out, and only studies cited on this page are counted.
Fig. 1b · evidence mix
6 of 7 sources here are studies in people. The rest is not.
- Study in people · done in people686%
- Review of studies · sums up other studies114%
Counted from the list of sources on this page. It counts only what we cite, so there may be more studies out there. A review counts once, however many studies it sums up.
Fig. 2 · evidence over time
The studies cover 6 different years, 2013 to 2025, counted from the list of sources on this page.
Fig. 3 · legal status at a glance
US
Not approved
UK
Not approved
AU
Not approved
CA
Not approved
Not approved in any of the four countries shown. This is what the law says, not a verdict on the science. See Legal status below for the full text and any notes.
Fig. 4 · how much does what
Nobody has tested different amounts in people
This chart would show how the effect changes as the amount goes up. For this compound, nobody has measured that in people. So we leave it empty. We will not borrow an animal chart and pretend it works the same in people.
Fig. 5 · what the molecule is
- Kind of compound
- Peptide
- Molecule weight
- Not on file
- Half-life
- None on file
- Chain length
- 28 amino acidscounted from the chain below
SLRRSSCFGGRMDRIGAQSGLGCNSFRY
- Water-shy 12
- Water-loving 10
- Acidic 1
- Basic 5
One square per amino acid, left to right from the start of the chain, coloured by type. The type is a fact about the amino acid, not a finding about this compound.
The studies we cite
- Study in people2025Effect of carperitide on clinical outcomes among patients with acute heart failure: a meta-analysis of randomized and propensity-matched studies
Pooled across every study they could find, people given this drug were more likely to die in hospital. The researchers gathered 9 studies. 4 were planned trials and 5 compared matched patients from hospital records. The studies disagree with each other a lot, which weakens the pooled answer. The 4 planned trials alone were far too small to say anything either way. Long-term deaths, return trips to hospital, low blood pressure and length of stay were all similar. This is a warning sign, not a settled harm.
9 studies, 4 randomised and 5 propensity score-matched. Pooled in-hospital mortality was higher with carperitide, odds ratio 1.38, 95 percent confidence interval 1.07 to 1.78, with high heterogeneity (I squared 77 percent). The 4 randomised trials alone gave odds ratio 0.85 with a 95 percent confidence interval of 0.07 to 10.49, which is uninformative. No significant difference in long-term mortality, rehospitalisation, hypotension or length of stay.
- Study in people2015Carperitide Is Associated With Increased In-Hospital Mortality in Acute Heart Failure: A Propensity Score-Matched Analysis
In Japanese hospital records, patients given this drug died more often than closely matched patients who were not. Researchers looked back at 402 treated patients and paired 367 of them with similar untreated ones. Death in hospital was about twice as likely in the treated group, and the gap was wider in older patients. Doctors chose who got this drug, and sicker patients are more likely to be chosen. So treatment and how sick people were cannot be pulled apart here.
Retrospective multicentre cohort, 402 of the patients treated with carperitide, 367 matched pairs analysed. Carperitide was associated with in-hospital mortality, odds ratio 2.13, 95 percent confidence interval 1.17 to 3.85, with a larger association in older patients (odds ratio 2.93, 1.54 to 5.91). Observational, so treatment choice and severity cannot be separated.
- Study in people2022Effect of carperitide on the 1 year prognosis of patients with acute decompensated heart failure
This one points the other way, and the page keeps both. Two Japanese groups of patients were pooled, 2,435 in all, and sorted by how much carperitide they had been given. Over the following year, deaths from heart causes and from any cause were lower in the low-dose group than in those given none or almost none. This is watching what doctors already did. It cannot tell you what the drug caused.
Pooled analysis of two Japanese cohorts, 2,435 patients with acute decompensated heart failure split by carperitide dose. Cardiovascular and all-cause mortality within 1 year were lower in the low-dose group (at or above 0.02 micrograms per kilogram per minute) than in the no-carperitide and very-low-dose groups. This observational result points in the opposite direction to the propensity-matched in-hospital analyses and is reported here alongside them, not instead of them.
- Study in people2013Acute heart failure volume control multicenter randomized (AVCMA) trial: comparison of tolvaptan and carperitide
Head to head against a water tablet called tolvaptan, this drug came off slightly worse. 109 people in hospital with heart failure got either tolvaptan or carperitide. Symptoms and a blood test for heart strain improved about equally on both. Blood pressure ran lower on carperitide. More people on carperitide had to stop because their heart failure got worse or their blood pressure dropped. Just over a hundred people is a small study for a comparison like this.
109 hospitalised patients randomised to tolvaptan or carperitide. Symptoms and plasma BNP improved similarly in both groups. Blood pressure was lower after carperitide, and fewer adverse events such as worsening heart failure and hypotension requiring discontinuation occurred with tolvaptan (p = 0.027).
- Study in people2021Moderate potassium lowering effect of exogenous atrial natriuretic peptide in patients with acute heart failure
This measured what the drug does to salts in the blood rather than whether it helps anyone. 162 people in hospital with heart failure were given carperitide through a drip. Sodium did not move over two days. Potassium drifted down slightly. Potassium falling too low was rare unless a strong water tablet was added on top, and then it was about four times more common. This is a look back at data already collected, so treat it as something to watch for rather than proof.
Post-hoc analysis of a multicentre prospective cohort, 162 patients with acute heart failure given intravenous carperitide. Serum sodium was unchanged over 48 hours; serum potassium fell from 4.32 to 4.08 mEq/L with carperitide alone (p = 0.004). Hypokalaemia at 24 hours was uncommon unless 20 mg or more of furosemide was added (12.5 versus 2.8 percent, p = 0.039).
- Study in people2022Neuroendocrine hormone status and diuretic response to atrial natriuretic peptide in patients with acute heart failure
This looked for who passes more water on the drug, and found two blood tests that predict it. 75 people in hospital with heart failure got a low dose of carperitide through a drip for six hours. Those who started with lower levels of their own natriuretic hormone, and lower vasopressin, produced the most urine. Blood pressure, kidney function and previous water tablets predicted nothing. Everyone here got the drug, so there is no comparison group and no way to know what would have happened anyway.
75 patients with acute heart failure given 0.0125 micrograms per kilogram per minute of carperitide for 6 hours. Lower baseline plasma ANP (r = -0.35, p = 0.002) and lower vasopressin (r = -0.54, p < 0.001) predicted a larger diuretic response; baseline blood pressure, renal function and prior loop diuretic use did not.
- Review of studies2019Atrial Natriuretic Peptide, Heart Failure and the Heart as an Endocrine Organ
A review of how ANP was discovered, the family of pieces cut from its parent protein, how it signals through NPR-A, and how NPR-C and neprilysin clear it. NIH money supported it.
Physiology review covering the discovery of ANP, the precursor-derived family of fragments, NPR-A signalling and clearance by NPR-C and neprilysin. NIH supported.
Where to buy ANP
No seller we track lists ANP yet. We read sellers’ public product lists every week, and this section fills in as soon as one does. Every seller, graded
Common questions
Has ANP been tested in people?
Yes. 188 people given it across 4 completed trials cited here, 2 of which found nothing. ANP is a hormone the heart releases when its chambers stretch. It is why the heart counts as a hormone-making organ. A lab-made form, carperitide, is used for sudden heart failure in Japan. A 2025 review pooled 9 studies and found more people died in hospital on carperitide.
What is the ANP dosage?
No human dose established. Amounts that were given in studies sit in Human evidence on this page. None of them is a personal dose. 4 completed trials, 188 people given it
Is ANP FDA-approved?
Not FDA approved. No ANP or carperitide product showed up when we checked the FDA drug database (Drugs@FDA) on 11 September 2026. Medical papers describe carperitide as in use in Japan for heart failure that comes on or gets worse suddenly. We did not confirm that approval with Japan's regulator, so we do not give its date or terms.
Is ANP available as a drug?
Not in the United States. No ANP or carperitide product showed up in the FDA records on 11 September 2026. Medical papers say a lab-made form, carperitide, is used for sudden heart failure in Japan. This site did not confirm that with the Japanese regulator.
Does carperitide help people with acute heart failure?
The evidence does not show that it does. A 2025 review of 9 studies found more deaths in hospital with carperitide, 1.38 times the odds. The planned trials on their own were too small to say anything. A separate pooled look at 2,435 Japanese patients found fewer deaths at 1 year in the low-dose group. Those results clash, and none of them is a large planned trial that counted deaths.
Is ANP the same as BNP or NT-proBNP?
No. ANP comes from the heart's upper chambers, and its parent protein also makes urodilatin and several other pieces. BNP comes from a different gene. Its inactive piece, NT-proBNP, is the blood test used in heart failure. They work on the same receptor, NPR-A, but they are different molecules with different medical uses.
Can ANP be taken for blood pressure or kidney health?
No. There is no pill, no approved product outside Japanese hospitals, and no human study of ANP in people who are not acutely ill. Everything published is short drips in sudden heart failure.