Stamulumab dosage and evidence
Written by Aaron CuhaReviewed Sep 2026
The short answer
Stamulumab is the first myostatin-blocking antibody ever given to people. In 2008 it was tested in 116 adults with muscular dystrophy. It was safe, it showed a hint of muscle growth, and it did not improve strength or function.
Evidence grade for Stamulumab: Moderate. The rule: at least one finished study in people, and at least 100 people who took it. The sum on this page: 2 completed trials, 122 people given it. A grade counts how much has been done to people, not whether it works.
- People given it
- 122
- Human studies
- 2
- 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.
2 completed trials, 122 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.
Stamulumab was the first drug ever tested in people that blocks myostatin. Myostatin is the body's brake on muscle growth. The idea was simple: take the brake off and muscle grows. It is an antibody, a large lab-made immune protein. It was never approved, and work on it stopped after one study.
What people take it for
- Building muscle in people with muscular dystrophy.
- The hope that blocking myostatin would make weak people stronger.
What studies in people showed
There was one study, in 116 adults with three kinds of muscular dystrophy. They got one of four doses or a dummy injection. It was built to check safety, not to prove the drug works. It was safe, apart from skin reactions at the two highest doses. Strength and function did not get better. A few people showed a small gain in muscle size on scans. In a 6 person look inside the muscle, single fibres got stronger in four of the five on the drug. Their whole muscles did not.
What people report
Reports, not study results
The good
- In the study on this page, it was mostly safe and well tolerated.
The bad
- Skin reactions showed up at the two highest doses.
- No gain in strength or function.
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
More muscle on a scan is not the same as being stronger. That is the lesson this drug started. In my opinion, the tools that work are lifting and eating enough protein.
An opinion, not a finding. I am a coach, not a doctor.
What it has been measured to do
Measured in people
Goals Stamulumab 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.
- Getting stronger122 people · 2 studies · 1 found nothing
35 of the 36 indexed goals have no study of any kind behind Stamulumab
No study in people, animals or cells on this page reports a result for these. That does not prove Stamulumab does nothing for them. It does mean anything you have heard about Stamulumab and one of these did not come from a study cited here.
Show full evidence
What is Stamulumab?
Stamulumab is the first myostatin-blocking antibody ever given to people. In 2008 it was tested in 116 adults with muscular dystrophy. It was safe, it showed a hint of muscle growth, and it did not improve strength or function.
Every myostatin drug on this site traces back to this study. Wyeth, later Pfizer, gave the first antibody that blocks myostatin to adults with three kinds of muscular dystrophy. It published the results in 2008. The result set the pattern the field has repeated ever since. The drug did what it was meant to do inside the body, and people did not get better.
Why did anyone try? Myostatin is the body's brake on muscle growth. Cattle and dogs born without it grow extreme muscle. So did one documented human child. Take the brake off and muscle should grow. It does. Whether that turns into strength is a separate question. This study was the first sign that it might not.
How does Stamulumab work?
Stamulumab is an antibody, a large immune protein, that grabs and blocks myostatin (also called GDF-8). Muscle releases myostatin to hold back its own growth. It does this by slowing the building of new muscle protein and keeping muscle repair cells quiet. Blocking it lets muscle fibres grow bigger. That part is well proven. The question these studies answer is what a bigger fibre does for a person.
What have studies in people found about Stamulumab?
One study in 116 adults, built to check safety rather than prove benefit. It compared the drug with a dummy injection. It is the only human data on this antibody.
- 116 adults with three kinds of muscular dystrophy, given one of four rising doses (1 to 30 mg/kg) or a dummy injection.
- It was safe and well tolerated, except for skin reactions at the two highest doses.
- No gain in muscle strength or function. That held on hands-on strength tests, machine strength tests, timed tasks and how people said they felt.
- A trend toward bigger muscles on body scans and muscle samples, in a small number of people.
- The authors concluded that blocking myostatin looked safe enough, and that stronger blockers should be tested. That is exactly what happened next. The stronger ones did not improve function either.
What this does not tell you: This study was not big enough to prove the drug works, and its authors say so. So on its own, the missing strength effect is weak evidence. It becomes strong only next to what came after. Three better-designed antibodies later got the same result. It tells you nothing about healthy adults, people on GLP-1 drugs, or older adults losing muscle with age. None of them were studied.
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
122people, across 2 studies in people cited here
| Study | People | Share |
|---|---|---|
| Annals of Neurology 2008 | 116 | 95% |
| Muscle and Nerve 2009 | 6 | 5% |
One study holds 95% 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
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, 2008 and 2009.
Too few different years on this page to draw a timeline. The newest source on file is from 2009, 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
- 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. No half-life figure was resolved for this antibody in the sources loaded. Antibodies of this class generally clear over weeks.
No amino acid sequence is on file for Stamulumab, so none is drawn rather than guessed from a name.
The studies we cite
- Study in people2008A phase I/II trial of MYO-029 in adult subjects with muscular dystrophy
The first myostatin blocker tested in people was safe enough but did nothing for strength. 116 adults with three kinds of muscular dystrophy were split by chance across four dose levels or a dummy, and nobody involved knew which. Skin reactions appeared at the two highest doses. The authors state plainly that no improvement was seen in muscle strength or function. Muscle size crept up slightly on scans in a few people. The study was never built to prove the drug works, only to check it was tolerable.
116 adults with Becker, facioscapulohumeral or limb-girdle muscular dystrophy, randomised, double-blind, placebo-controlled, across four dose cohorts from 1 to 30 mg/kg. Safety and tolerability were good apart from cutaneous hypersensitivity at 10 and 30 mg/kg. Verbatim: there were no improvements noted in exploratory end points of muscle strength or function, though the study was not powered for efficacy. Bioactivity was supported by a trend toward increased muscle size on DXA and histology in a limited number of subjects.
- Study in people2009Single muscle fiber contractile properties in adults with muscular dystrophy treated with MYO-029
Inside the muscle, individual fibres did look better, in a handful of people. Researchers took muscle fibre samples from trial participants before and after six months. Five of them had been given the myostatin blocker and one had the dummy. Four of those five showed improved force and speed in single fibres. The one on the dummy showed none. Six people is not a result, it is a hint. Whole-muscle strength in these same patients did not improve, so whatever happened at the cellular level did not reach them.
6 patients from the MYO-029 trial, 5 on drug and 1 on placebo, with single muscle fibres examined directly. Four of the five on drug showed improved single fibre force and speed and the placebo patient showed none. Whole muscle strength did not improve in those same patients, which is the result that matters to a person. The only look inside the muscle itself from this programme.
- Study in people2008A phase 1/2 safety and tolerability study of MYO-029 in adult muscular dystrophy
This is the registry entry for the trial described above. It confirms the trial ran and finished. The registry itself carries no posted results, so the published paper above is the only place the outcome appears. That paper is where the strength finding comes from, and the finding there was nothing.
The registry record for the trial above.
Common questions
Has Stamulumab been tested in people?
Yes. 122 people given it across 2 completed trials cited here, 1 of which found nothing. Stamulumab is the first myostatin-blocking antibody ever given to people. In 2008 it was tested in 116 adults with muscular dystrophy. It was safe, it showed a hint of muscle growth, and it did not improve strength or function.
What is the Stamulumab 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, 122 people given it
Is Stamulumab FDA-approved?
Never approved. Development did not continue past this trial.
Can I get stamulumab?
No. It was never approved, and work on it stopped after the 2008 study. Anything sold under this name is not this antibody.
Why does this old trial matter?
It is where the myostatin story starts. And its result has now been repeated three more times, by stronger drugs in better-designed studies. When four separate drug programmes find the same thing, that tells you something. Adding muscle tissue and improving what a person can do are not the same result.
Does that mean myostatin inhibition is useless?
It means it has not yet been shown to help anyone do anything. For some groups, the question is still truly open. The main one is people losing lean mass fast on a GLP-1 drug, which is a different starting point from muscular dystrophy. That study is now running, with GYM329.