ACE-031
also known as Ramatercept, ActRIIB-Fc
Dimeric fusion protein combining soluble activin receptor IIB fragment with Fc domain of human IgG1. Acts as decoy receptor for myostatin, GDF11, and other TGF-β superfamily ligands, preventing binding to endogenous ActRIIB and disinhibiting skeletal muscle growth. Phase 2 trial in Duchenne muscular dystrophy discontinued in 2011 due to safety signals including epistaxis, telangiectasia, and vascular abnormalities. Not pharmaceutically approved; circulates on black market as research chemical.
At a glance
SQ · Weekly dosing investigated
Primary target — Myostatin, GDF11, activin A — TGF-β superfamily ligands.
Pathway — Soluble decoy receptor binds circulating myostatin/TGF-β ligands → prevents ActRIIB activation → SMAD2/3 pathway inhibition.
Downstream effect — Disinhibition of myogenic signaling, increased skeletal muscle mass and strength.
Origin — Recombinant fusion protein: human ActRIIB extracellular domain + IgG1-Fc fragment [reichel-2025].
| Parameter | Value |
|---|---|
| Clinical dosing | Weekly or biweekly SQ injections (exact doses undisclosed pre-halt)Phase 2 DMD trial protocol not fully published. |
| Black market products | Variable purity; 12/14 tested products contained target protein plus contaminants [reichel-2025]SDS-PAGE revealed multiple protein bands; quality control absent. [reichel-2025] |
| Evidence basis | Phase 2 trial discontinued — incomplete dataset |
| Half-life | Days to weeks (Fc-fusion typical kinetics)IgG1-Fc domain confers extended circulation time. |
| Duration investigated | 12–24 weeks (trial cut short) |
Reconstitution
A pure mass-to-volume utility. Enter what you have in the vial; the atlas computes the volume per dose. No prescription information.
- — History of vascular disorders (epistaxis, telangiectasia, HHT)
- — Pregnancy (TGF-β pathway critical for fetal development)
- — Active malignancy (myostatin inhibition may affect tumour growth)
- — Use of non-pharmaceutical grade ACE-031 (contamination risk) [reichel-2025]
- — Coagulation disorders or anticoagulant use (epistaxis risk)
- — Hereditary hemorrhagic telangiectasia (HHT) family history
- — Cardiovascular disease (vascular remodeling effects unknown)
- 01Pharmaceutical status
ACE-031 is not FDA-approved or commercially available. Phase 2 development was discontinued in 2011 due to safety concerns. Any ACE-031 on the black market is unregulated research chemical.
- 02Black market quality
12 of 14 tested black market ACE-031 products contained the target protein but also carried multiple unidentified protein contaminants detectable by SDS-PAGE. Two products contained no ACVR2B-immunoreactive material. [reichel-2025]
- 03Detection in sport
ACE-031 is prohibited under WADA S4.3 (Myostatin Inhibitors). Gel electrophoresis and Western blotting using ACVR2B-specific antibodies can detect the ~58.4 kDa protein in biological samples. [reichel-2025]
- 04Clinical trial route
Phase 2 protocol used subcutaneous injections at weekly or biweekly intervals. Exact dosing protocols remain unpublished.
Sources
of 44 rendered claims carry a resolvable citation.
- [reichel-2025]Reichel 2025 — Gel Electrophoretic Detection of Black Market ACE-031.
journal, 2025