/DISCLAIMER · RESEARCH_COMPOUND

This page is reference information only. Most compounds described here are research chemicals, not FDA-approved medications. MyTRT does not sell, recommend, or endorse the use of these substances. Always consult a qualified physician.

/ACE_031_ACTRIIB_FC
Protein Therapeutic / Myostatin–Activin Pathway

ACE-031

Soluble Activin Type IIB Receptor–Fc Fusion (Myostatin/Activin Ligand Trap)

/HALF_LIFE
Approximately 10–15 days (human PK, single-dose SC)
/DELIVERY
Subcutaneous injection; historical clinical protocols dosed every 2–4 weeks.

/WHAT_IT_IS

ACE-031 (ActRIIB-Fc Ligand Trap) is a recombinant fusion protein consisting of the extracellular domain of activin receptor type IIB (ActRIIB) linked to an IgG1 Fc fragment. It serves as a decoy receptor that binds myostatin (GDF8) and related ligands (e.g., activins), thereby reducing SMAD2/3 signaling to promote muscle and bone anabolism in research settings.

/USAGE

Used to study muscle-wasting disorders, sarcopenia/cachexia models, bone mass regulation, and downstream metabolic/functional outcomes (lean mass, strength, BMD).

/MECHANISM_OF_ACTION

Ligand trap that sequesters myostatin and select activins from ActRIIA/B receptors, attenuating TGF-β/SMAD2/3 signaling; results include increased muscle protein synthesis/hypertrophy and bone accrual.

Reported Benefits

  • +Increases lean body mass and muscle volume in human and animal studies
  • +May improve functional measures (e.g., 6-minute walk trends in DMD studies)
  • +Associated increases in bone mineral density in some models

Reported Side Effects

  • Epistaxis (nosebleeds) and telangiectasias reported in clinical studies
  • Injection-site reactions (pain, pruritus, hematoma)
  • Potential vascular effects linked to broader ligand binding (e.g., BMP9/10 cross-reactivity in class)

/STACKED_WITH

Physical therapy/exercise paradigms for functional endpointsNutritional/protein standardization in metabolic studiesComparators in the pathway: anti-ActRII antibodies, follistatin constructs, or next-gen ligand traps (for mechanistic contrasts)

/RESEARCH_NOTES

Clinical development in DMD was halted/terminated after non-muscle AEs (epistaxis, telangiectasias) despite PD signals for lean mass/BMD; contemporary designs aim to narrow ligand specificity to mitigate vascular findings. Not approved for therapeutic use.

/REFERENCE

https://pubmed.ncbi.nlm.nih.gov/23169607/
/TRACK_THIS

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Last reviewed: 2026-06-04 · Reference only. Not medical advice. Consult a qualified physician.