Myostatin is a protein your body makes to limit how much muscle you build. It is a brake. Animals and the rare humans born without a working version of it are conspicuously muscular, which is what made it an obvious drug target decades before anyone connected it to weight-loss medication.
The idea being tested now is simple: if a GLP-1 is going to take muscle along with fat, release the brake at the same time.
The three candidates
Trevogrumab — Regeneron. An antibody against GDF8, which is myostatin. Tested with semaglutide in the COURAGE trial. Interim results reported preserving between 50% and 80% of the lean mass that semaglutide alone would have cost. A three-drug combination adding garetosmab reached 80.9%. The trial completes late in 2026.
Regeneron’s own framing of the problem is worth quoting for its bluntness: in the semaglutide comparison, roughly 35% of the weight lost came from muscle rather than fat.
Apitegromab — Scholar Rock. Tested with tirzepatide in EMBRACE: 102 participants, 24 weeks, about 55% relative preservation of lean mass against tirzepatide plus placebo, with similar total weight loss. Smaller and shorter than the others, so weigh it accordingly.
A complication worth knowing: apitegromab was developed first for spinal muscular atrophy, and in September 2025 the FDA declined to approve it for that. That is a different indication with different requirements, and it does not settle anything here — but it is a reminder that promising Phase 2 data and an approved medicine are far apart.
Bimagrumab — a different mechanism, blocking activin type II receptors rather than myostatin directly, but aimed at the same outcome. It has the most complete published evidence, covered separately in what the BELIEVE trial found.
There is also enobosarm (Veru), which is a selective androgen receptor modulator — a third route entirely.
Reading these percentages carefully
“Preserved 55% of lean mass loss” does not mean lean mass was preserved. It means a bit over half of the loss that would otherwise have happened did not happen. The rest still did.
Similarly, “50 to 80%” is a wide range across doses and analyses, and interim results from an incomplete trial are provisional by definition. None of this is 100%, and none of it is settled.
The question underneath all of them
Every result in this field so far is a body-composition measurement. More lean tissue on a scan.
Whether that produces the outcomes people actually care about — being stronger, staying independent for longer, not becoming frail — is not yet demonstrated. Lean mass includes water, bone and organs as well as muscle, and even the muscle portion is not automatically functional muscle. A drug that adds tissue without adding capacity would look identical on these endpoints.
This is not scepticism for its own sake. It is the specific thing the trials have not yet had time or design to show, and it is what a Phase 3 programme would need to address.
What this changes for you
Not much, yet. All of it is Phase 2 or earlier, none is approved for weight management, and all of it is combination therapy on top of a medication you already inject.
The gap between now and then is measured in years. What fills that gap is unglamorous and available today: protein and resistance training. Both act on the same tissue these drugs are trying to protect, and neither is waiting on a regulator.
If you want a number for where you currently stand, the muscle check will give you one and tell you which lever is furthest out of range.