ACE-083
Muscle Building, Performance
In short
- A locally-acting follistatin-based fusion protein designed for targeted muscle growth in a specific muscle rather than systemically.
- It reached phase 2 trials in facioscapulohumeral muscular dystrophy and Charcot-Marie-Tooth disease.
- Both programmes were DISCONTINUED after the trials increased muscle volume but failed to improve function.
- That outcome is the single most informative fact about the myostatin pathway generally.
- Prohibited at all times in sport under WADA S4.4.
Structure
How it works
ACE-083 is a fusion protein combining a portion of follistatin with an antibody Fc domain, engineered by Acceleron to remain at the injection site rather than distribute systemically.
Locally it binds myostatin, activin A, and related TGF-beta ligands, removing their restraint on muscle growth in that specific muscle. The design intent — local rather than systemic action — was to avoid the off-target activin effects that complicate systemic myostatin blockade.
Mechanistically it is the most sophisticated approach in this pathway represented here.
What the research shows
Phase 2 in facioscapulohumeral muscular dystrophy: significant increases in muscle volume by MRI, with no corresponding improvement in function or strength.
Phase 2 in Charcot-Marie-Tooth disease: similar pattern — the muscle grew, the patients did not improve.
Acceleron discontinued both programmes on the basis of these results.
This is a clean, well-powered demonstration that adding muscle volume via myostatin inhibition does not necessarily add function.
Dosing in the literature
Figures below are quoted from published studies, with the species or population they were measured in. They are records of what was studied, not recommendations.
| Studied in | Amount | Route | Source |
|---|---|---|---|
| Human — phase 2 FSHD trial | 150–240 mg per muscle, every 3 weeks | intramuscular | PubMed |
| Human — phase 2 Charcot-Marie-Tooth trial | Comparable intramuscular dosing; see source | intramuscular | PubMed |
Commonly reported ranges
These are amounts people report using. They are not from any study, have not been evaluated for safety, and are reproduced here only because they circulate widely and are better seen alongside the evidence than instead of it.
No commonly reported ranges for this compound.
Trial doses are in the hundreds of milligrams per muscle, administered by clinicians into specific muscles. This is not a compound with a meaningful grey-market presence, and the trial doses bear no relationship to anything a research-chemical vendor would supply.
Handling and storage
Administered by intramuscular injection directly into the target muscle in the clinical trials, at three-week intervals.
The entire design premise is local retention, so route and site were integral to the intervention rather than incidental.
Side effects
Trial data provides genuine human safety information. Injection-site reactions were most common.
Other reported effects included myalgia and, in some participants, hypersensitivity reactions.
The local design successfully limited systemic exposure, which was the point — so the systemic activin concerns that apply to follistatin generally were less relevant here.
Combinations
Not applicable in any practical sense — this is a clinical-trial biologic administered by injection into specific muscles under supervision, not a compound people stack.
Research status
A properly conducted development programme by Acceleron with two phase 2 trials, published results, and a clear discontinuation decision.
Its value in this library is as evidence about the myostatin pathway rather than as something to use: it is the cleanest available demonstration that muscle volume and muscle function are separable.
Legal status
Not approved. Development discontinued. Not meaningfully available outside the trials.
WADA status
PROHIBITED AT ALL TIMES under WADA class S4.4 — agents modifying myostatin function, including myostatin inhibitors, are explicitly named. This is a named prohibition, not an S0 inference.
Conclusion
ACE-083 answered the question the whole myostatin field was asking, and the answer was disappointing: the muscles got bigger and worked no better.
If you are considering anything that targets myostatin — follistatin, ACE-031, or the various research-market versions — this trial is the most relevant evidence available, and it points away from the pathway.
Sources
Track your own ACE-083 protocol
Peppers logs your doses, models your levels from this half-life, tracks your vials and tells you when you will run out. Free on iPhone.
Reference and educational information only. Not medical advice. Nothing here diagnoses, treats, or prescribes, and nothing here is a recommendation to use any compound. The compounds described are research chemicals and are not approved for human consumption. Legal and anti-doping status change — the review date above is when these claims were last checked. Talk to a qualified clinician about anything you intend to take.