ACE-031

ACE-031 is ramatercept, an experimental ActRIIB-Fc fusion protein - not a peptide - that increased muscle measurements in a small human trial but was abandoned after boys with Duchenne developed nosebleeds, gum bleeding, and skin telangiectasias. The same broad ligand trap that releases muscle’s growth brake also disrupts signals that help maintain blood vessels.

Key facts

• What it is: a 77.49 kDa dimeric decoy receptor protein
• Evidence: human randomized trials; muscle-size signal, unproven functional benefit, harmful vascular signal
• U.S. status (July 2026): development discontinued; no approved use; sold research-use-only
• Study dosing: 0.02-3 mg/kg once in Phase 1; 0.5-1 mg/kg every two to four weeks in the stopped Duchenne trial
• Main risks: nosebleeds, gum bleeding, telangiectasias, and unknown long-term vascular effects
• Sport: prohibited at all times under WADA S4.3

What is ACE-031?

ACE-031 is the development code for ramatercept, a lab-made protein built from the outside portion of activin receptor type IIB (ActRIIB) and the Fc portion of an antibody. At roughly 77,490 daltons, this is not a peptide in the usual short-chain sense, regardless of which online menu files it under “peptides.”

The NIH NCATS record identifies ramatercept as investigational and confirms ACE-031, DrugBank DB15116, and UNII 42HQC6QLEK as the same substance. The original goal was treatment of muscle-wasting disease, especially Duchenne muscular dystrophy, not bodybuilding.

How does the ACE-031 myostatin inhibitor work?

The ACE-031 myostatin inhibitor works like a floating fake receptor: myostatin docks with the decoy instead of reaching muscle cells. Myostatin normally acts as a brake on muscle growth. Catching it releases part of that brake, but ACE-031 also traps activins, GDF-11, and bone morphogenetic proteins BMP-9 and BMP-10.

That lack of selectivity is the whole story. BMP-9 and BMP-10 help regulate the lining and stability of blood vessels. A wide ActRIIB-Fc net can therefore catch muscle-limiting signals and vessel-maintenance signals at the same time. The mechanism behind ACE-031 muscle growth is also the mechanism behind the bleeding problem; those are not two unrelated footnotes.

What does the human research show?

ACE-031 produced a real human body-composition signal, but not proof of better strength or athletic performance. In a randomized Phase 1 study of 48 healthy postmenopausal women, one subcutaneous dose from 0.02 to 3 mg/kg was compared with placebo. At 3 mg/kg, total lean mass rose 3.3% and thigh muscle volume rose 5.1% by day 29 (Attie et al., 2013).

The Phase 2 Duchenne study tells the harder half. Twenty-four ambulatory boys were randomized; 18 received ACE-031 and six received placebo. Researchers saw trends toward more lean mass and bone density and maintenance of six-minute walking distance, but the walking result was not statistically significant. The Campbell et al. trial stopped after the second dosing regimen because of vascular safety concerns. Human RCT is the right evidence tier. “Proven muscle-building drug” is not the right conclusion.

Why did ACE-031 stop, and what are the side effects?

ACE-031 stopped because nosebleeds and telangiectasias - small widened vessels visible near the skin - appeared in the Duchenne program; gum bleeding was also reported. The published trial recorded no serious or severe adverse events, but the pattern mattered enough to halt dosing. An extension study was likewise terminated on preliminary safety data.

Later work tied that pattern to broad ligand trapping, particularly BMP-9 inhibition. Loss of BMP-9/10 vascular signaling resembles the biology behind hereditary hemorrhagic telangiectasia, a disorder marked by fragile abnormal vessels and bleeding. No longer trial established a safe long-term exposure. ACE-031 side effects are therefore not a generic list copied from another muscle drug; vascular fragility sits inside this molecule’s design.

What ACE-031 dosage was used in studies?

ACE-031 dosage in human research was weight-based and experimental, not a usable bodybuilding protocol. The single-dose Phase 1 trial tested 0.02-3 mg/kg subcutaneously. The Duchenne trial used 0.5 mg/kg every four weeks or 1 mg/kg every two weeks for 12 weeks, then stopped early on safety data (ClinicalTrials.gov).

Those numbers describe what investigators tested under monitoring. They do not define a safe dose, and no approved label supplies one. Vendor schedules that convert trial doses in children with muscular dystrophy or older women into self-use instructions skip the exact reason development ended.

Is ACE-031 FDA-approved, legal, or banned in sport in 2026?

ACE-031 is not FDA-approved, has no approved medical indication, and remains prohibited in sport. Acceleron reported to the SEC that it and Shire ended development in 2013 and had no plan to continue. As of July 2026, online material is sold research-use-only, not as a legitimate prescription product. See the site’s dated regulatory-status guide for what that label does and does not mean.

The supply problem is worse than a missing approval. A 2025 laboratory analysis tested 14 black-market products advertised as ACE-031 and found that none contained genuine ACE-031; 12 held full-length ActRIIB instead of the Fc fusion, while the others contained follistatin or ipamorelin (Reichel et al., 2025). WADA’s 2026 list is in force, and S4.3 names decoy activin receptors such as ACE-031 as prohibited at all times.

How does ACE-031 compare with follistatin, bimagrumab, and GDF-11?

ACE-031, follistatin, bimagrumab, and GDF-11 belong in the same muscle-signaling conversation, not the same chemical bucket. Follistatin is a natural binding protein that traps several TGF-beta-family signals. Bimagrumab and other ActRIIB-directed approaches use a different strategy; bimagrumab is an antibody that blocks ActRIIB itself. GDF-11 is one of the ligands ACE-031 can catch, not a substitute version of the drug.

The useful comparison is selectivity. ACE-031 casts a broad decoy-receptor net and gained muscle size while disturbing vascular signaling. Bimagrumab approaches the receptor with an antibody, while newer myostatin programs try to narrow the target and leave BMP signaling alone. The growth-hormone and muscle-growth hub maps those approaches without pretending every item sold beside a peptide is one.