Relaxin-2 dosage and evidence
Written by Aaron CuhaReviewed Sep 2026
The short answer
Relaxin-2 is the pregnancy hormone that opens up blood flow.
Evidence grade for Relaxin-2: Strong. The rule: at least two finished studies in people, and at least 1,000 people who took it. The sum on this page: 2 completed trials, 7,706 people given it. A grade counts how much has been done to people, not whether it works.
- People given it
- 7,706
- Human studies
- 2
- 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.
2 completed trials, 7,706 people given it
5 effects reported, 4 unwanted, 1 wanted, by people using it, not a trial
Goal pages: Ageing and longevity, Injury, healing and recovery, Heart and circulation, Bone and joints
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.
This is the pregnancy hormone that opens up blood flow. The ovary and placenta make it. A lab made copy, serelaxin, was tested as a heart failure drug. It is not approved anywhere.
What people take it for
- Heart failure, which is what it was actually tested for.
- Scarring and stiff tissue, off animal work.
- Loose joints in pregnancy, a link this page does not check.
What studies in people showed
It was tested properly, twice, and it did not work. The first trial gave 1,161 people in hospital with sudden heart failure a two day drip or a dummy drip. Breathlessness improved on one scale of two. Heart deaths and return trips at 60 days did not change. Then a side count showed 42 deaths by six months on the drug against 65 on the dummy. That was not what the trial was built to test. So a bigger trial ran, with 6,545 people. Heart deaths by six months were 8.7 percent on the drug and 8.9 percent without. No difference in deaths from any cause, return trips or length of stay. Experts then went through every death and found no effect on any cause.
What people report
Reports, not study results
The good
- We have not collected user reports on this one yet.
- In the big trial, side effects on the drug matched the dummy drip.
The bad
- It failed both main goals in a trial of 6,545 people. Work on it for heart failure stopped.
- It is not approved anywhere, so there is nothing to buy.
- People still quote the smaller trial's death count without the bigger trial's result. That is misleading.
- The anti scarring work people get excited about is in animals and dishes, not in people.
Where these come from: The trial numbers and the side effect match come from the two large heart failure trials on this page. No user reports exist.
My bottom line
This is what an honest no looks like. Good idea, proper trials, no benefit. Do not let anyone quote the first one at you.
An opinion, not a finding. I am a coach, not a doctor.
What it has been measured to do
Measured in people
Goals Relaxin-2 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 strokes7,706 people · 3 studies · 2 found nothing
- Pain1,161 people · 1 study · 1 found nothing
- Living longer1,161 people · 2 studies · 1 found nothing
33 of the 36 indexed goals have no study of any kind behind Relaxin-2
No study in people, animals or cells on this page reports a result for these. That does not prove Relaxin-2 does nothing for them. It does mean anything you have heard about Relaxin-2 and one of these did not come from a study cited here.
Show full evidence
What is Relaxin-2?
Relaxin-2 is the pregnancy hormone that opens up blood flow. A drug version, serelaxin, was tested in 1,161 people with sudden heart failure, and there were 42 deaths by six months on the drug against 65 on a dummy drip. But that was a side question. The bigger follow-up in 6,545 people found heart deaths of 8.7 percent on the drug and 8.9 percent without it. Serelaxin was never approved and work on it for heart failure stopped.
Relaxin-2 is a hormone made of two linked chains, from the same family as insulin. The ovary and the placenta make it. It is why a pregnant woman's heart pumps more and her blood vessels and kidneys relax. That biology is not in question. It was a fair reason to wonder if the same hormone could help a failing heart.
Serelaxin is a lab-made copy of human relaxin-2. Its story is the clearest example on this site of why a second, bigger trial exists.
The first trial, RELAX-AHF, came out in the Lancet in 2013. It took 1,161 people in hospital with sudden heart failure. They got a 48 hour drip of serelaxin, at 30 micrograms per kilogram per day, or a dummy drip. It was built to test breathlessness, measured two ways. Breathlessness improved on one scale. On the other, 27 percent improved on the drug and 26 percent without it, so no real difference. Heart deaths and readmissions at 60 days were unchanged. Then, as a side question set out in advance, the team counted deaths at six months: 42 on serelaxin and 65 on the dummy drip. A drop in deaths in sudden heart failure is rare. That result changed what the field expected.
The second trial, RELAX-AHF-2, came out in the New England Journal of Medicine in 2019. It was built to confirm the first. Same drug, same dose, same 48 hour drip, same kind of patients, 6,545 people. Heart deaths at six months: 8.7 percent on serelaxin and 8.9 percent on the dummy drip. Heart failure getting worse by day 5: 6.9 percent against 7.7 percent, no real difference. Deaths from any cause, return trips to hospital and length of stay were all the same.
Later, experts went through every death in RELAX-AHF-2. Serelaxin made no difference to any cause of death. Work on it for sudden heart failure stopped. Serelaxin is not approved anywhere.
How does Relaxin-2 work?
Relaxin-2 works through a receptor called RXFP1. It widens blood vessels across the body, makes the heart pump more, sends more blood to the kidneys and makes arteries more stretchy. It does this mostly through nitric oxide and a signal molecule called cyclic AMP. It also sends anti-scarring signals, which is what most later research has looked at. It is two chains held together by chemical bridges, built like insulin. That makes it hard and costly to make, which is why simpler one-chain versions were designed. The reason to try it in sudden heart failure made sense. Pregnancy brings more blood flow at lower resistance and keeps the kidneys well supplied. That is close to what you want in a patient who is fluid-logged, has high blood pressure and has slightly weak kidneys. The reasoning held up. The result did not.
What have studies in people found about Relaxin-2?
Two large final-stage trials in sudden heart failure, with almost 7,700 people between them. The first helped breathlessness on one of two scales and showed a surprise drop in deaths. The second, four times bigger, found no benefit on either of its main measures.
- RELAX-AHF-2, 6,545 people: heart deaths by six months were 8.7 percent on serelaxin and 8.9 percent on the dummy drip. No real difference.
- RELAX-AHF-2: heart failure got worse by day 5 in 6.9 percent against 7.7 percent, no real difference. Deaths from any cause, return trips to hospital and length of stay were the same.
- A later look at every death in RELAX-AHF-2 found serelaxin made no difference to any cause of death.
- RELAX-AHF, 1,161 people: breathlessness improved on one scale and not on the other.
- RELAX-AHF side question: 42 deaths on the drug against 65 by six months. This was not what the trial was built to test.
- Novartis or a company it owns paid for both trials. Work on the drug for sudden heart failure stopped.
What this does not tell you: We found no controlled trial of relaxin-2 in people outside sudden heart failure. And the heart failure question has been answered no, at scale. Its anti-scarring effects draw interest for scarring, kidney disease and scleroderma. That interest rests on animal and lab dish work, not on trials in people. A long-acting version has finished a mid-stage study, and we do not summarise its results here. An early kidney blood flow study of the same version was stopped early because it could not sign up enough people.
The state of the research
This page exists to stop one specific misuse of the research.
The first trial, RELAX-AHF, found fewer deaths by six months on serelaxin. That number is real, it was published in the Lancet, and people still quote it. But it was a side question in a trial built to measure breathlessness, in 1,161 people. That same trial showed no effect on heart deaths and readmissions at 60 days. A result like that is exactly what a second, bigger trial exists to check.
The second trial took 6,545 people and found nothing. Not a smaller effect. No effect: heart deaths were 8.7 percent on the drug and 8.9 percent without it. The team then went through every death, looking for any group or cause that might explain the first result. Serelaxin made no difference to any cause of death.
Anyone who quotes the 2013 death result without the 2019 result is misleading you, whether they mean to or not. The honest one-line summary of relaxin-2 in heart failure: it was tested properly, twice, and it did not work.
What is still alive is the research on scarring and blood vessels. In animals, relaxin's effects there are real, and simpler versions and long-acting versions are still being developed. Those are open questions. The sudden heart failure question is closed.
The evidence, in charts
Fig. 1a · how many people
7,706people, across 2 studies in people cited here
| Study | People | Share |
|---|---|---|
| RELAX-AHF-2, New England Journal of Medicine 2019 | 6,545 | 85% |
| RELAX-AHF, The Lancet 2013 | 1,161 | 15% |
One study holds 85% 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. 1 more study in people gives no headcount and is not counted here. Studies still signing people up are left out, and only studies cited on this page are counted.
Fig. 1b · evidence mix
3 of 5 sources here are studies in people. The rest are not.
- Study in people · done in people360%
- Animal study · done in animals120%
- Review of studies · sums up other studies120%
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 5 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
- The prorelaxin H2 precursor recorded in UniProt P04090 is 185 amino acids at 21,043 Da. The mature hormone is two chains, a B chain of 29 amino acids and an A chain of 24, joined by disulfide bonds.
- Half-life
- Stated in words, not a numbersee the exact wording below
- Chain length
- None on file
Half-life as stated on file: Short enough that both confirmatory trials gave it as a continuous intravenous infusion over two days rather than as injections. No single agreed circulating figure for the native hormone is asserted here; the long-acting fusion proteins now in development exist specifically to solve that problem.
No amino acid sequence is on file for Relaxin-2, so none is drawn rather than guessed from a name.
The studies we cite
- Study in people2013Serelaxin, recombinant human relaxin-2, for treatment of acute heart failure (RELAX-AHF): a randomised, placebo-controlled trial
Serelaxin eased breathlessness a little in people admitted with sudden heart failure, and changed nothing that matters more. 1,161 people got either a two day drip of the drug or a dummy drip soon after reaching hospital. Breathlessness scored better on one scale and no better on the other. Deaths from heart causes and readmissions at two months were unchanged. A death count at six months leaned the drug's way, but that was a side question, not what the trial was built to prove. Funded by a Novartis company.
1,161 patients hospitalised with acute heart failure randomised 1:1 to a 48 hour infusion of serelaxin at 30 micrograms per kilogram per day or placebo within 16 hours of presentation. Serelaxin improved the visual analogue scale dyspnoea endpoint by 448 mm times hours (95 percent CI 120 to 775, p = 0.007) but had no effect on the co-primary Likert endpoint (27 percent against 26 percent, p = 0.70). There was no effect on cardiovascular death or readmission at 60 days (hazard ratio 1.02, 0.74 to 1.41) or on days alive out of hospital. Among prespecified additional endpoints, 42 deaths occurred by day 180 on serelaxin against 65 on placebo, hazard ratio 0.63 (0.42 to 0.93, p = 0.019). Funded by Corthera, a Novartis affiliate company. Registered as NCT00520806.
- Study in people2019Effects of Serelaxin in Patients with Acute Heart Failure
The big confirming trial was run and the drug failed it. 6,545 people admitted with sudden heart failure got the same two day drip or a dummy drip. Six months later the same share had died of heart causes in each group. Worsening heart failure in the first five days was no different. Deaths of any cause, readmissions and length of hospital stay were all unchanged. Side effects matched. A trial this large would have found a real benefit if there was one. Funded by Novartis.
RELAX-AHF-2, the confirmatory trial, and it failed. 6,545 patients in the intention to treat analysis, same drug, dose, 48 hour infusion and entry criteria as RELAX-AHF. Death from cardiovascular causes at 180 days occurred in 285 of 3,274 patients (8.7 percent) on serelaxin and 290 of 3,271 (8.9 percent) on placebo, hazard ratio 0.98 (0.83 to 1.15), p = 0.77. Worsening heart failure at day 5 occurred in 6.9 percent against 7.7 percent, hazard ratio 0.89 (0.75 to 1.07), p = 0.19. No significant difference in all-cause death at 180 days, in cardiovascular death or rehospitalisation, or in length of the index hospital stay. Adverse event rates were similar. Funded by Novartis. Registered as NCT01870778.
- Study in people2020Cause of Death in Patients With Acute Heart Failure: Insights From RELAX-AHF-2
Investigators went back through every death in the failed trial to work out why the earlier trial had looked promising, and found nothing to rescue it. By six months about one patient in nine had died, and heart failure caused nearly four in ten of those deaths. The drug changed no category of death. People aged 75 and over died more often, and more often of something other than their heart. This explains the failure. It does not undo it.
An adjudicated analysis of every death in RELAX-AHF-2, run specifically to understand why the two trials disagreed. By 180 days 11.5 percent of patients had died, 38 percent of those deaths from heart failure. Unlike in RELAX-AHF, there was no apparent effect of serelaxin on any category of cause of death. Patients aged 75 or over died more often (14.2 percent against 8.8 percent) and more often from non-cardiovascular causes. Patients with preserved ejection fraction had less heart failure mortality (30 percent against 40 percent) and more non-cardiovascular mortality (36 percent against 20 percent).
- Review of studies2016Serelaxin and acute heart failure
A review written between the two big trials, which is exactly why it is worth reading. It shows what experts believed about serelaxin after the first trial. That was before the second trial came in and wiped it out.
A review written in the window between the two phase 3 trials, which is exactly why it is worth reading. It records what the field believed about serelaxin on the strength of RELAX-AHF, before the confirmatory result arrived and removed it.
- Animal study2025A novel long-acting relaxin-2 fusion, AZD3427, improves cardiac performance in non-human primates with cardiac dysfunction
In non-human primates, the animals closest to us, a long-acting relaxin-2 drug helped weak hearts pump better. This is still an animal result. In people, the drug, AZD3427, has since finished a mid-stage study in 260 people with heart failure and high blood pressure in the lungs. A separate early kidney study was stopped because too few people signed up.
The current direction of the field, and it is preclinical. A long-acting relaxin-2 fusion protein improved cardiac performance in non-human primates with induced cardiac dysfunction. Non-human primates are the closest animal model available and this is still an animal result. AZD3427 has since completed a phase 2 study of 260 participants with heart failure and pulmonary hypertension (NCT05737940, AstraZeneca, completed August 2025); a separate phase 1 renal perfusion study was terminated early after recruitment difficulties (NCT06611423).
Where to buy Relaxin-2
No seller we track lists Relaxin-2 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 Relaxin-2 been tested in people?
Yes. 7,706 people given it across 2 completed trials cited here, 2 of which found nothing. Relaxin-2 is the pregnancy hormone that opens up blood flow.
What is the Relaxin-2 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. 2 completed trials, 7,706 people given it
Is Relaxin-2 FDA-approved?
Relaxin-2 is a hormone the body makes. Serelaxin, a lab-made copy of it, is not approved by the FDA or any other regulator. It drew attention after the RELAX-AHF result. But the larger follow-up study, RELAX-AHF-2, missed both of its main goals, and work on it for sudden heart failure was stopped.
Does relaxin help heart failure?
No, on the evidence we have. Serelaxin, a lab-made copy of human relaxin-2, was tested in 6,545 people with sudden heart failure in RELAX-AHF-2. It missed both main goals. Heart deaths by six months were 8.7 percent on the drug and 8.9 percent on a dummy drip. Work on it stopped, and it is not approved anywhere.
But I read that it reduced deaths. Was that wrong?
It was a real result in the earlier, much smaller RELAX-AHF trial: 42 deaths against 65 by six months. But it was a side question in a trial built to measure breathlessness. The bigger follow-up trial did not repeat it. A check of every death in that trial found no effect on any cause of death. An honest account includes both facts.
Is serelaxin approved anywhere?
No. It is not approved by the US, UK, Australian or Canadian regulators. Work on it for sudden heart failure ended after the second, confirming trial.
What about relaxin for fibrosis or scarring?
That is where the live science is, and it is still in animals. Relaxin really does fight scarring in animal studies. That is why simpler one-chain versions such as B7-33 exist. None of that has been shown to help a person in a controlled trial.
Is anything still in development?
Yes. Long-acting versions of relaxin-2 are being developed, most visibly AZD3427. In non-human primates, the animals closest to us, it helped weak hearts pump better. In people, it has finished a 260 person mid-stage study in heart failure with high blood pressure in the lungs. A separate early kidney blood flow study of the same drug was stopped early because it could not sign up enough people. Nothing is approved.
Is relaxin what makes joints loose in pregnancy?
That link is widely repeated, and this page does not check it. What the trials here show is relaxin's effect on the heart, blood vessels and kidneys. That is what made it a heart failure hope. They also show what happened when it was given as a drug.