ACE-031

What it is

A recombinant fusion protein (~101 kDa) consisting of the extracellular domain of human activin receptor type IIB (ActRIIB) fused to the Fc portion of human IgG1. Not a traditional peptide — it is approximately 10× larger than IGF-1 LR3 and requires mammalian cell expression systems for proper folding and glycosylation. Developed by Acceleron Pharma (acquired by Merck in 2021). ACE-031 functions as a soluble decoy receptor (ligand trap), binding myostatin, activin A/B, GDF-11, and other TGF-β superfamily ligands before they engage endogenous ActRIIB receptors. Phase 1 trials in healthy postmenopausal women demonstrated a 3.3% increase in lean mass from a single injection. A Phase 2 trial in ambulatory boys with Duchenne muscular dystrophy showed a 5.2% lean mass increase, but trials were permanently halted in 2013 due to vascular safety signals (epistaxis, telangiectasias, gum bleeding) caused by off-target inhibition of BMP9/BMP10 in the ALK1 endothelial signaling pathway. Research chemical suppliers listing 'ACE-031' typically sell truncated peptide fragment analogs that are structurally distinct from the clinical-grade fusion protein.

Community-reported ranges

Clinical trial dosing from published Phase 1/2 data. Community protocols for research chemical analogs mirror trial doses but use structurally distinct products. Dose units are mcg/kg body weight (clinical trials used mg/kg). Not dosing guidance.

Frequently discussed alongside

Based on community forum discussions. Not a recommendation to combine compounds.

Published research

ACE-031 is the only compound in this batch with controlled human clinical trial data. Attie et al. (2013) reported dose-dependent lean mass increases up to 3.3% from a single subcutaneous injection in 48 healthy postmenopausal women. Campbell et al. (2017) published results from the Phase 2 DMD trial showing 5.2% lean mass increase (P=0.015) and a trend toward improved 6-minute walk test (+12 m vs. -30 m placebo, P=0.06) in 24 steroid-treated boys. Preclinical data showed 26-46% increases in individual muscle weights in mice after 28 days (Cadena et al., 2010). Trials were permanently halted due to BMP9/10-mediated vascular adverse events. Successor compounds ACE-2494 and ACE-083 also failed in clinical development. The ActRIIB decoy receptor approach remains stalled as of March 2026.

Reported side effects

From community self-reports. Not from controlled studies.

Clinical trial data (the most complete safety dataset among these four compounds): injection site erythema (50% of subjects), epistaxis/nosebleeds (25%), telangiectasias/dilated blood vessels (21%), vomiting (21%), gum bleeding. Also 43% decrease in serum FSH at 3 mg/kg in healthy women (from activin A/B blockade). The vascular effects were caused by off-target inhibition of BMP9/BMP10 in the ALK1 endothelial pathway, pharmacologically mimicking hereditary hemorrhagic telangiectasia (HHT). All vascular adverse events resolved upon treatment discontinuation. No serious adverse events or individual subject discontinuations occurred.

Regulatory status