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ACE-031

Early human Muscle & Bone Health 2 sources

ACE-031 is an investigational protein therapeutic designed to build muscle and increase strength by inhibiting signaling through the activin receptor type IIB (ActRIIB). Research primarily focused on its potential to treat muscle-wasting diseases like Duchenne muscular dystrophy, though clinical trials were halted due to safety concerns involving bleeding.

01Dosing reference

Amount
1-3 mg/kg (in clinical trial settings)
Frequency
Once every 2-4 weeks
Cycle
Not established due to halted trials
Reference figures, not a recommendationThese values reflect amounts described in the literature and vendor documentation this database indexes. Use the reconstitution calculator to convert them into syringe units.

02Mechanism of action

01

Ligand Binding

ACE-031 acts as a decoy receptor, binding to myostatin and other TGF-beta family proteins in the bloodstream.

02

Receptor Blockade

By binding these proteins, it prevents them from interacting with the endogenous ActRIIB receptors on muscle cells.

03

Muscle Growth Disinhibition

Removing the inhibitory signal normally provided by myostatin allows for significant increases in muscle mass and strength.

03Human evidence

Increased lean body mass and thigh muscle volume in healthy postmenopausal women.

Phase 1 double-blind, placebo-controlled study evaluating single and multiple doses; showed dose-dependent increases in muscle mass.

Trends toward maintained muscle function in boys with Duchenne muscular dystrophy, but trials were halted due to adverse events.

Phase 2 dose-escalation study; stopped prematurely due to non-muscle-related side effects including epistaxis and telangiectasias.

04Preclinical evidence

Significant increases in skeletal muscle mass and improved muscle function.

Studies in mdx mice (a model for Duchenne muscular dystrophy) demonstrated enhanced muscle growth and force generation.

Dose-dependent increases in lean body mass in non-human primates.

Cynomolgus monkeys treated with ACE-031 showed substantial muscle hypertrophy without significant changes in fat mass.

05What is known vs. unknown

Reasonably established
  • ACE-031 is a recombinant fusion protein that acts as a decoy receptor for myostatin and other negative regulators of muscle mass.
  • It demonstrated a strong ability to increase lean muscle mass in both animal models and early human trials.
  • Clinical development was halted by Acceleron Pharma and Shire due to non-muscle-related adverse events.
  • It is banned by the World Anti-Doping Agency (WADA) as a performance-enhancing drug.
Unknowns & limits
  • The exact mechanism causing the vascular side effects (nosebleeds, dilated blood vessels) is not fully understood.
  • Long-term safety and viability as a therapeutic remain unknown due to the premature termination of clinical trials.

06Safety & regulatory context

Regulatory statusACE-031 is not FDA-approved for any use. Clinical trials were discontinued due to adverse events, specifically epistaxis (nosebleeds) and telangiectasias (small dilated blood vessels). It is strictly a research chemical and is banned by the World Anti-Doping Agency (WADA) as a performance-enhancing drug. Due to its vascular side effects, its safety profile is considered poor for human use outside of strictly controlled, now-halted clinical settings.

07Compared with Follistatin

ACE-031 vs. Follistatin
Key difference
ACE-031 is a recombinant fusion protein acting as a decoy receptor for ActRIIB ligands, whereas Follistatin is a naturally occurring glycoprotein that directly binds and neutralizes myostatin and activin.
When researchers discuss each
ACE-031 is often discussed in the context of pharmacological interventions for muscle wasting that failed due to off-target vascular effects, while Follistatin is explored in gene therapy contexts for localized muscle growth.

08Glossary

Myostatin
A protein produced and released by myocytes that acts on muscle cells' autocrine function to inhibit muscle cell growth and differentiation.
Decoy Receptor
A receptor that binds a ligand, preventing it from binding to its normal receptor and halting its biological signaling.
Telangiectasia
A condition characterized by dilated blood vessels near the surface of the skin or mucous membranes, often appearing as fine red lines.

09Knowledge check

Q1How does ACE-031 promote muscle growth?
Q2Why were clinical trials for ACE-031 halted?
Q3Which statement best reflects a documented limitation of the human research on ACE-031?
Q4According to the dossier, what is a key difference between ACE-031 and follistatin?
Q5Which statement correctly summarizes ACE-031's regulatory and safety status as presented in the dossier?

10Sources

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Research and educational use onlyNothing on this site is medical advice, a prescription, or a recommendation for human use. Compounds documented here are research chemicals. Consult a qualified clinician before making any health decision.