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PerformancePhase 2

ACE-031

Myostatin inhibitor (activin receptor IIB-Fc fusion) that removes the natural cap on muscle growth — Phase 2 halted due to vascular side effects

Research Reality Check

Worth WatchingThere is a real signal, but it is not settled.
ClaimSome people claim ACE-031 has clear value for performance research.
RealityThere is a real research signal, but important questions remain.
Bottom LineUse the evidence score, sources, and safety notes before taking any claim seriously.
Why People Believe ThisSimple explanations and user stories can sound more certain than the research is.
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Guaranteed resultsExact protocols presented as provenAnecdotes used as proof
167Discussions
2Citations

Evidence Dossier

71Evidence

Phase 2

Evidence score reflects source depth, citations, and research maturity. It is not a medical recommendation.

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ACE-031 at a glance

A fast read for beginners, with evidence strength, route context, safety depth, and community activity surfaced before the deeper sections.

Evidence score71Phase 2 human research
Primary routeSubcutaneous InjectionRoute availability varies by context
Safety depthExperimentalReview safety notes before making assumptions
Community questions167Related discussions and experiences

ACE-031 is a fusion protein consisting of the extracellular domain of activin receptor type IIB (ActRIIB) fused to an IgG1-Fc region. By acting as a decoy receptor, it sequesters myostatin, GDF-11, activins, and other TGF-β superfamily ligands that limit muscle growth - effectively releasing the body's natural brake on skeletal muscle mass.

How It Works

In Phase 1 and Phase 2 trials for Duchenne Muscular Dystrophy and healthy postmenopausal women, ACE-031 produced significant lean mass increases of 3-5% within 1-3 months - representing some of the most dramatic muscle gains observed in a clinical setting. However, Phase 2 trials were halted due to adverse events including telangiectasias (dilated blood vessels), epistaxis (nosebleeds), and gum bleeding, attributed to the broad inhibition of multiple ActRIIB ligands beyond myostatin alone.

Bimagrumab (a monoclonal antibody targeting ActRIIB with more selectivity) subsequently advanced further in trials with a somewhat better tolerability profile, demonstrating that the mechanism remains therapeutically relevant. ACE-031 itself is no longer in active development. Its use in performance contexts carries significant unknown risk given the halted trials.

Key Benefits

Significant lean muscle mass increases
Myostatin inhibition
Potential for muscular dystrophy treatment
Strength gains