ACE-031

ACE-031 is a soluble ActRIIB-Fc fusion protein designed to bind myostatin-pathway ligands and thereby increase skeletal-muscle mass. It generated strong mechanistic interest as an anabolic biologic, especially in Duchenne muscular dystrophy and other muscle-wasting settings, but development was halted after safety issues emerged in human studies.

ACE-031 is commonly described as a soluble activin type IIB receptor fused to an Fc domain. It is a biologic rather than a short peptide, but it fits this repository because it targets a highly relevant muscle-growth pathway frequently discussed alongside peptide therapeutics.

ACE-031 functions as a ligand trap. By sequestering myostatin and related activin-family ligands upstream of ActRIIB signaling, it reduces inhibitory signaling on skeletal-muscle growth and tends to increase lean mass. The same broad pathway coverage likely contributed both to anabolic activity and to off-target vascular effects.

Primary development focus was Duchenne muscular dystrophy and other muscle-wasting indications. In a research context it is also relevant as an archetype for myostatin-pathway inhibition and for explaining the safety tradeoffs between broad ligand traps and more selective anti-myostatin agents.

Clinical studies used intermittent subcutaneous administration every 2 to 4 weeks. As a fusion protein, ACE-031 behaves unlike a simple peptide: exposure, tissue distribution, and persistence are shaped by protein size and Fc-linked disposition rather than by rapid peptide degradation alone.

Human trials showed pharmacodynamic evidence consistent with anabolic activity, including trends toward increased lean body mass. The efficacy package, however, never matured into a successful late-stage program or approval pathway, so the overall evidence is mechanistically strong but clinically incomplete.

Safety was the limiting issue. Published accounts describe epistaxis and telangiectasia-like vascular findings, and later discussion in the literature links the bleeding phenotype to broader BMP9-related pathway interference rather than selective muscle-only signaling.

Human studies reported subcutaneous administration every 2 to 4 weeks in dose-escalation style protocols. Because development stopped, there is no approved dosing regimen.

The following dosing information has been compiled from community forums, researcher discussions, and gray-market sources. This information has NOT been verified through peer-reviewed scientific studies or clinical trials. It does NOT constitute medical advice, a prescription, or a recommendation for human use.

This data is presented solely for informational and educational purposes to document what is commonly discussed in research communities. Dosing protocols may be inaccurate, dangerous, or based on anecdotal reports with no scientific validation. Individual responses vary significantly, and unregulated compounds carry inherent risks including contamination, mislabeling, and unknown side effects.

Always consult qualified medical professionals before making any health-related decisions. The repository maintainers assume no liability for the use or misuse of this information.

Researcher-Reported Dosing Protocols

Common Dose Range: 1-3 mg/kg per injection

Administration Route: Subcutaneous injection

Frequency: Once every 2 to 4 weeks

Timing: Not specified in the researched sources.

Schedule / Protocol: Intermittent dosing, not a continuous cycle.

Dose Escalation: No specific dose escalation protocols are commonly discussed. Clinical trials utilized a single ascending dose design to find a tolerable dose.

Additional Notes: Development of ACE-031 was halted due to safety concerns, including reports of bleeding. The high cost and the prevalence of counterfeit or low-quality products on the black market are also significant issues. Consequently, it is not a commonly used peptide in research communities.

This researcher-reported dosing information was compiled from unverified community sources and does not represent validated scientific or medical guidance.

A randomized placebo-controlled trial in ambulatory boys with Duchenne muscular dystrophy evaluated safety, PK, and PD. The program was terminated early after safety concerns, making ACE-031 an important cautionary case study in this target class.

Investigational only; not approved. Public literature and trial reporting indicate discontinued development.

As a recombinant fusion protein, manufacture would require biologics-style expression, purification, and characterization rather than straightforward synthetic peptide production. Public CMC detail in open sources is limited.

Closest repository comparators include follistatin-based approaches, anti-myostatin antibodies, GDF-8-targeting programs, and other muscle-anabolic agents. ACE-031 is broader than selective myostatin blockade, which may explain both stronger pathway reach and worse vascular tolerability.

Version 0.1 starter entry created March 14, 2026. Evidence basis for this draft: peer-reviewed DMD trial report, ClinicalTrials.gov study record, and review literature on ActRIIB ligand traps.