ACE-031
A soluble activin type IIB receptor fusion protein that sequesters myostatin and other TGF-beta family members to drive skeletal muscle hypertrophy and fat loss.
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Compound Profile
ACE-031
Key Data
Research reference only
Research Focus
Preclinical data
⚠ Research & Educational Use Only. ACE-031 is a research chemical documented here for scientific education. All information references peer-reviewed literature and preclinical/clinical study data. Not for human consumption. Not medical advice. Consult a licensed researcher or healthcare professional before any laboratory use.
- Sequesters myostatin - the primary negative regulator of muscle growth - preventing it from binding ActRIIB in muscle
- Also inhibits activins and other GDF ligands that suppress muscle growth through the same receptor
- Demonstrated significant lean mass increases in clinical Phase 1 research - one of the most potent experimental muscle agents studied
- ACE-031 is not FDA-approved for human use. It is a research chemical for scientific study only.
Research At a Glance
- Sequesters myostatin - the primary negative regulator of muscle growth - preventing it from binding ActRIIB in muscle
- Also inhibits activins and other GDF ligands that suppress muscle growth through the same receptor
- Demonstrated significant lean mass increases in clinical Phase 1 research - one of the most potent experimental muscle agents studied
- Reduces fat mass simultaneously in research subjects - likely via activin pathway effects on adipose tissue
In Plain English
Simple summaryACE-031 is a fusion protein (not strictly a peptide, but categorized here as a biological compound) consisting of the extracellular domain of the activin receptor type IIB (ActRIIB) fused to human IgG1 Fc. It works as a 'ligand trap' -- it binds and neutralizes multiple TGF-beta superfamily members that limit muscle growth, including myostatin, GDF-11, activin A, and BMP-9. This makes it a broader muscle-growth promoter than follistatin or anti-myostatin antibodies that target only myostatin. In Phase 2 trials in Duchenne muscular dystrophy (DMD), ACE-031 produced statistically significant increases in lean mass, but the trial was stopped early due to adverse effects including nosebleeds, telangiectasias (dilated blood vessels), and potential vascular effects -- likely from blocking BMP-9, which maintains vascular stability.
- Sequesters myostatin - the primary negative regulator of muscle growth - preventing it from binding ActRIIB in muscle
- Also inhibits activins and other GDF ligands that suppress muscle growth through the same receptor
- Demonstrated significant lean mass increases in clinical Phase 1 research - one of the most potent experimental muscle agents studied
The full scientific detail, mechanisms, citations, and dosing data, follows below.
What is ACE-031?
Tap any underlined term for an instant definition.
ACE-031 (soluble activin receptor type IIB, or ActRIIB-IgG1-Fc) is a fusion protein consisting of the extracellular domain of the activin receptor type IIB (ActRIIB) fused to an immunoglobulin Fc region. It functions as a "ligand trap" - circulating in the bloodstream and binding to myostatin, activins, and other TGF-beta superfamily members that would otherwise suppress muscle growth.
Myostatin (GDF-8) is a secreted growth factor that acts as the primary brake on skeletal muscle mass. Animals with genetic myostatin deficiency (or mutations in the myostatin pathway) exhibit extraordinary muscular development - the "double-muscled" phenotype observed in Belgian Blue cattle, Piedmontese cattle, and rare human cases of myostatin-null mutations. Blocking myostatin therefore represents one of the most direct routes to skeletal muscle hypertrophy.
However, ACE-031's mechanism goes beyond simple myostatin inhibition. Because it presents the actual receptor binding domain, it traps any molecule that naturally binds ActRIIB - including multiple GDF (growth differentiation factor) family members and activins. This broader inhibition is a double-edged sword: it may produce more potent muscle growth than selective myostatin antibodies, but it also affects vascular biology, since ActRIIB is expressed in vascular endothelial cells.
ACE-031 was developed by Acceleron Pharma and advanced to Phase 2 clinical trials for Duchenne muscular dystrophy. The Phase 1 results were remarkable - even single doses produced significant increases in thigh muscle volume and reductions in fat mass. However, Phase 2 was halted when an unacceptable rate of bleeding events (nosebleeds, gum bleeding) and telangiectasia were observed, attributed to ActRIIB's role in vascular endothelial cell biology.
This safety finding distinguishes ACE-031 from more selective myostatin approaches and explains why the clinical program was discontinued. Research continues into whether selective myostatin blockade (without broader ActRIIB inhibition) can achieve similar muscle benefits without vascular effects.
By the Numbers
Key Research Benefits
Documented effects observed in preclinical and clinical studies on ACE-031. See all Muscle & Performance peptides for comparison.
Common Stacks
ACE-031 is frequently combined with the following peptides for synergistic effects. Click any peptide to compare profiles before deciding.
CJC-1295 drives endogenous IGF-1 production via GH; combining with exogenous IGF-1 LR3 amplifies the anabolic signal significantly.
Ipamorelin + CJC-1295 as a GH stack pairs with IGF-1 LR3 for a comprehensive GH-axis and direct IGF-1 receptor anabolic protocol.
IGF-1 LR3 provides systemic long-acting IGF-1 exposure while IGF-1 DES can be used for localised site-specific anabolism.
Side Effects & Risks
Adverse effects reported in the research literature. All data sourced from preclinical and clinical study reports. View all peptides' side effects →
Dosing Data from the Literature
Doses referenced below are sourced from published preclinical and clinical studies. Use the peptide dose calculator to convert these values to injection volume.
ACE-031's Phase 1 clinical research used single doses of 1-3 mg/kg subcutaneously. Given its 10-15 day half-life, dosing frequency is very low.
Clinical trial doses (reference only): 0.03-3 mg/kg single dose SC Half-life: 10-15 days - monthly or bi-monthly dosing in sustained protocols NOTE: The Phase 2 clinical program was suspended due to vascular adverse events (bleeding, telangiectasia). Research use should carefully monitor for these effects.
Administration in Research Settings
Standard reconstitution and administration methodology for laboratory research use.
ACE-031 is a large protein (IgG1-Fc fusion) requiring subcutaneous injection. Reconstitute with sterile water for injection. Administer once monthly or less frequently given the extended half-life.
What the research doesn't show
The vascular safety issue stopped ACE-031's development and is a cautionary tale about broad ligand trap approaches. BMP-9 is important for vascular endothelium health -- blocking it alongside myostatin and GDF-11 caused off-target vascular effects. More selective approaches (anti-myostatin antibodies, selective ActRIIB ligand traps) are now preferred in clinical development for muscle wasting diseases.
Medical Expert Videos
Physicians, researchers, and pharmacologists explain ACE-031, covering mechanisms of action, clinical context, and study findings.
Videos sourced from YouTube search. KnowYourPeptide does not endorse any individual creator. For research education only.
The Bottom Line
ACE-031 has a growing body of preclinical evidence and a well-characterised safety profile in research settings. The most-studied application is: sequesters myostatin - the primary negative regulator of muscle growth - preventing it from binding actriib in muscle.
The most commonly reported side effect in research subjects is epistaxis (nosebleeds) and gum bleeding - likely related to actriib expression in vascular endothelium; caused phase 2 trial discontinuation. It is a research chemical, not approved for human use.
Frequently Asked Questions
Explore Further
Quick Reference
How It Compares
Follistatin-344 is an endogenous ligand of ActRIIB that works similarly -- both neutralize myostatin and related ligands. Anti-myostatin antibodies (apitegromab, SRK-015) are more selective, targeting only myostatin -- which may avoid the vascular side effects seen with broad ActRIIB blockade. Luspatercept is an approved ActRIIB-Fc fusion for anemia in myelodysplastic syndrome, showing the therapeutic concept works but has different safety from the muscle-focused ACE-031.
Compare ACE-031 side-by-sideResearch Use Only
This information is for educational research purposes only. This is not medical advice. Consult a qualified healthcare professional.