Stamulumab
Stamulumab (MYO-029), anti-myostatin monoclonal antibody
Written by Aaron CuhaReviewed Sep 2026
Also known as: MYO-029, Anti-myostatin antibody
The first anti-myostatin antibody ever given to humans, in 116 adults with muscular dystrophy in 2008. It was safe, it showed a hint of muscle growth, and it did not improve strength or function.
Overview
Every myostatin drug on this site descends from this trial. Wyeth, later Pfizer, took the first neutralising antibody against myostatin into adults with three forms of muscular dystrophy and published it in 2008. The result set the pattern the field has repeated ever since: the drug did what it was supposed to do biologically, and people did not get better.
It is worth knowing why anyone tried. Myostatin is the brake on muscle growth, and animals lacking it, including cattle, dogs and one documented human child, develop extreme muscularity. Release the brake and muscle should grow. It does. Whether that translates into strength is a separate question, and this trial was the first indication that it might not.
Mechanism of action
A neutralising monoclonal antibody against myostatin, also called GDF-8, a member of the transforming growth factor beta family secreted by skeletal muscle. Myostatin binds activin type II receptors and signals through SMAD2 and SMAD3 to suppress muscle protein synthesis and satellite cell activation. Neutralising it removes that suppression, which increases muscle fibre size. The pathway is well established; the question the trials answer is what happens downstream of a bigger fibre.
Human evidence
One randomised placebo-controlled trial in 116 adults, designed and powered for safety rather than efficacy. It is the only human data on this antibody.
- 116 adults across three muscular dystrophies, four sequential dose cohorts from 1 to 30 mg/kg against placebo.
- Safety and tolerability were good, with the exception of cutaneous hypersensitivity at the two highest doses.
- No improvement in muscle strength or function on manual muscle testing, quantitative muscle testing, timed function tests or subject-reported outcomes.
- A trend toward increased muscle size on dual-energy radiographic absorptiometry and on muscle histology, in a limited number of subjects.
- The authors' own conclusion was that systemic myostatin inhibition has an adequate safety margin and that more potent inhibitors should be evaluated. That is exactly what happened next, and the more potent ones did not improve function either.
What this does not tell you: This trial was not powered to detect efficacy and its authors say so, so the absence of a strength effect here is weak evidence on its own. It becomes strong evidence only in combination with what followed, because three better-powered antibodies later reached the same result. It also tells you nothing about healthy adults, people on GLP-1 drugs, or older adults with sarcopenia, none of whom were studied.
Reading the research record
Read the myostatin field as a set and one result repeats. Blocking myostatin reliably adds lean mass, by roughly a quarter to half a kilogram in the trials that measured it properly, and reliably fails to improve what a person can actually do. Stamulumab found no improvement in strength or function. Domagrozumab missed its primary endpoint and every secondary clinical endpoint. Landogrozumab added 0.43 kg of appendicular lean mass at p < 0.0001 and moved two of roughly seven physical performance measures. Bimagrumab, which this site covers separately, produced the largest body composition change in the class and did not deliver a matching functional gain either. The tissue appears. The capability does not follow.
The evidence, charted
Fig. 1 · evidence composition
3of 3 citations (100%) are in people
Every citation cited here is Human work; no other study type is cited on this page. This count is of our own citation list and understates any literature larger than the sources we cite.
Fig. 2 · evidence over time
Citations here span just two years, 2008 and 2009.
Too few distinct publication years on this page to plot as a timeline. The newest citation on file is from 2009, more than five years ago; the published record may have gone quiet.
Fig. 3 · legal status at a glance
US
Not approved
UK
Approved
AU
Not approved
CA
Not approved
Approved in 1 of 4, prescription route in 0, not approved in 3. A jurisdiction's classification is a regulatory fact, not a verdict on the science; see Legal status below for the full text and any notes.
Key studies & citations
- Human2008
A phase I/II trial of MYO-029 in adult subjects with muscular dystrophy
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.
Annals of Neurology - Human2009
Single muscle fiber contractile properties in adults with muscular dystrophy treated with MYO-029
A mechanistic follow-up measuring contractile properties of individual muscle fibres from trial participants. Included because it is the only look inside the muscle itself from this programme.
Muscle and Nerve - Human2008
A phase 1/2 safety and tolerability study of MYO-029 in adult muscular dystrophy
The registry record for the trial above.
ClinicalTrials.gov
Frequently asked questions
Can I get stamulumab?
No. It was never approved and development stopped after the 2008 trial. Anything sold under this name is not this antibody.
Why does this old trial matter?
Because it is where the myostatin story starts, and because its result has now been confirmed three more times by better-powered drugs. A field that repeats the same finding across four independent programmes is telling you something, and what it is telling you is that adding muscle tissue and improving function are not the same outcome.
Does that mean myostatin inhibition is useless?
It means it has not yet been shown to help anyone do anything. There are populations where the question is still genuinely open, particularly people losing lean mass rapidly on a GLP-1 drug, which is a different starting point from a person with muscular dystrophy. That trial is now running, with GYM329.