Domagrozumab dosage and evidence
Written by Aaron CuhaReviewed Sep 2026
The short answer
A well-built study in 120 boys with Duchenne muscular dystrophy. On its main test, stair climbing, the drug and the dummy injection came out the same. No other health measure differed either, and both studies were stopped early.
Evidence grade for Domagrozumab: Limited. The rule: people have taken it in a published study, but fewer than 100 of them. The sum on this page: 1 completed trial, none stating how many people. A grade counts how much has been done to people, not whether it works.
- People given it
- 0
- Human studies
- 1
- Found nothing
- 1
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.
1 completed trial, 0 people given it
No first-hand reports gathered yet. That is a gap in what we have collected, not a finding that nothing has been reported.
Goal pages: Muscle and strength
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.
Domagrozumab is a lab-made antibody that blocks myostatin, the body's brake on muscle growth. Pfizer tested it in boys with Duchenne muscular dystrophy. It was given at higher doses than earlier drugs like it. Both studies were stopped. It was never approved.
What people take it for
- Slowing muscle loss in boys with Duchenne muscular dystrophy.
- Helping boys keep walking and climbing stairs longer.
What studies in people showed
The main study had 120 boys with Duchenne who could still walk. 80 got the drug and 40 got a dummy shot, for nearly two years. The main test was how fast they could climb four stairs. At week 49, the gap between the groups was 0.27 seconds. That is no difference at all. No other health measure was different either. Muscle size rose a little, but not enough to call. Pfizer stopped both studies.
What people report
Reports, not study results
The good
- It was mostly safe and well tolerated, with mostly mild side effects.
The bad
- It did not help boys climb stairs any faster.
- No other health measure got better.
Where these come from: These come from the study on this page. We have not collected user reports on this one yet.
My bottom line
This was a fair test, and it failed. In my opinion, if anyone pitches a myostatin blocker to you as a muscle fix, show them this page.
An opinion, not a finding. I am a coach, not a doctor.
What it has been measured to do
Measured in people
Goals Domagrozumab 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.
- Keeping or building muscleno headcount stated · 1 study · 1 found nothing
35 of the 36 indexed goals have no study of any kind behind Domagrozumab
No study in people, animals or cells on this page reports a result for these. That does not prove Domagrozumab does nothing for them. It does mean anything you have heard about Domagrozumab and one of these did not come from a study cited here.
Show full evidence
What is Domagrozumab?
A well-built study in 120 boys with Duchenne muscular dystrophy. On its main test, stair climbing, the drug and the dummy injection came out the same. No other health measure differed either, and both studies were stopped early.
This is the clearest negative result among the myostatin blockers. It is clear because the study was well built. 120 boys with Duchenne muscular dystrophy who could still walk took part. 80 got rising doses up to 40 mg/kg and 40 got a dummy injection. It ran for two 48-week periods, and its main test was a real-world task: climbing four stairs. Afterwards, boys could keep taking the drug in a follow-on study.
The answer was about as close to nothing as a study gets. At week 49, the gap in four-stair climb time was 0.27 seconds. The likely range ran from 7.4 seconds worse to 7.9 seconds better. No other health measure differed between the groups. Muscle volume rose a little, but not enough to call.
Pfizer stopped both studies. The honest way to present this drug class is to show this result next to the good muscle results from other antibodies.
How does Domagrozumab work?
Domagrozumab is an antibody that blocks myostatin, the same target as stamulumab and landogrozumab. Here it was given into a vein at 5, 20 and 40 mg/kg. Those are higher doses than the earlier antibodies used. The thinking was that the earlier ones failed because they were not strong enough.
What have studies in people found about Domagrozumab?
A well-built study with a real-world main test that found nothing. It was run in Duchenne, the disease where blocking myostatin has the strongest case on paper.
- 120 boys with Duchenne muscular dystrophy. Two got the drug for every one on a dummy injection, for 48 weeks per period, plus a follow-on study.
- Main test, four-stair climb at week 49: the gap was 0.27 seconds. The likely range spans 15 seconds, so this is not a near miss. There is simply no signal.
- No other health measure differed between the groups.
- Muscle volume rose a little, but not enough to call. That fits the rest of this drug class: tissue without ability.
- It was mostly safe and well tolerated. Most side effects were mild and not caused by the drug.
- The drug company stopped both studies.
What this does not tell you: This result is about Duchenne. In Duchenne, muscle is being destroyed because a key structural protein is missing. So taking the brake off growth may just be the wrong lever. It does not prove that blocking myostatin cannot help someone losing muscle for another reason, such as not moving, ageing or fast weight loss. What it does show: a strong antibody at a high dose, given for a year, in a disease with clear muscle loss, changed nothing a boy could do.
The state of the research
Look at all the myostatin blockers together and one result repeats. Blocking myostatin reliably adds lean mass, by roughly a quarter to half a kilogram in the studies that measured it well. And it reliably fails to improve what a person can actually do. Stamulumab found no gain in strength or function. Domagrozumab missed its main goal and every other clinical measure it checked. Landogrozumab added 0.43 kg of arm and leg lean mass, a very clear result, and moved two of about seven movement tests. Bimagrumab, which this site covers on its own page, made the biggest change in body makeup in the group, and it did not bring a matching gain in function either. The muscle shows up. The ability does not follow.
The evidence, in charts
Fig. 1a · how many people
3studies in people cited, but none says how many people took part
number of people not stated
We do not draw a total, because none of the studies in people on this page gives one. Read the sources below for what each study measured.
We read the number of people from the source lines on this page. Where a line gives no number, we count nothing for it. We do not guess.
Fig. 1b · evidence mix
All 3 sources here are studies in people.
- Study in people · done in people3100%
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
Sources here come from just two years, 2019 and 2020.
Too few different years on this page to draw a timeline. The newest source on file is from 2020, more than five years ago. Research on it may have gone quiet.
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
- Biologic
- Molecule weight
- Humanised monoclonal antibody, roughly 150 kDa. Not a peptide.
- Half-life
- Stated in words, not a numbersee the exact wording below
- Chain length
- None on file
Half-life as stated on file: Not asserted. Serum concentrations rose with dose within each dose level; no half-life figure was resolved in the sources loaded.
No amino acid sequence is on file for Domagrozumab, so none is drawn rather than guessed from a name.
The studies we cite
- Study in people2020Randomized phase 2 trial and open-label extension of domagrozumab in Duchenne muscular dystrophy
A second myostatin blocker was tested properly in boys with Duchenne and it failed. 120 boys aged six to fifteen were split by chance across three doses or a dummy injection, for nearly two years. The thing the trial was built to measure was how fast they climbed four stairs. The two groups came out the same. No other clinical measure separated either. Muscle volume rose a bit, but not enough to call. An error notice was published afterwards correcting part of the paper.
120 ambulatory boys aged 6 to under 16 with Duchenne muscular dystrophy, 80 on domagrozumab at 5, 20 and 40 mg/kg and 40 on placebo, two 48-week periods. Primary endpoints were safety and change in four-stair climb time at week 49. The difference in mean change was 0.27 seconds (95% CI minus 7.4 to 7.9), p = 0.94. There were no significant between-group differences in any secondary clinical endpoint. Non-significant increases in muscle volume were observed. An erratum was published in 2021.
- Study in people2020A study of domagrozumab in boys with Duchenne muscular dystrophy
The registry entry for the Duchenne trial above shows it was stopped early. The word on the record is terminated. The published paper is where the outcome lives, and the outcome was that the drug did not help the boys climb stairs any faster.
Registry status TERMINATED. The trial reported above.
- Study in people2019An extension study of domagrozumab in Duchenne muscular dystrophy
This was the follow-on study that let boys from the main trial keep taking the drug. It too was stopped early, and the registry marks it terminated. Nothing was published from it. When the main trial failed, the extension had nothing left to extend.
Registry status TERMINATED. The open-label extension.
Common questions
Has Domagrozumab been tested in people?
Yes. 0 people given it across 1 completed trial cited here, 1 of which found nothing. A well-built study in 120 boys with Duchenne muscular dystrophy. On its main test, stair climbing, the drug and the dummy injection came out the same. No other health measure differed either, and both studies were stopped early.
What is the Domagrozumab 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. 1 completed trial, 0 people given it
Is Domagrozumab FDA-approved?
Never approved. Both mid-stage studies are marked TERMINATED (stopped early) on ClinicalTrials.gov.
Was this trial too small to find an effect?
No. That criticism fits the 2008 stamulumab study, which was openly too small. Here the gap was 0.27 seconds, with a likely range from 7.4 seconds worse to 7.9 seconds better. That is what no effect looks like, not what too few people looks like.
Why did Pfizer stop it?
The public record shows both studies were stopped early (listed as terminated), and a published result with no effect on any health measure. The company's internal reasons are not on the record, and this page does not guess at them.
Does this kill the idea of blocking myostatin?
For Duchenne, on this evidence, it is very hard to defend. For muscle loss from other causes the question is still open, because the groups differ in ways that could matter. This site's position: four drug programmes have now added tissue without adding function. Anyone claiming this class protects what you can do is ahead of the evidence.