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What is ACE-031?

7 min read · Updated October 2026 · MY PEPTIDES Research Team

Key facts

ACE-031, also known as ramatercept, is a fusion protein: the ligand-binding extracellular part of activin receptor type IIB joined to the Fc region of human IgG1. It is a large dimeric protein, not a peptide, even though many online sellers list it as one. It acts as a decoy, binding myostatin and related signalling proteins before they reach their receptors on muscle cells. Acceleron Pharma developed it, later in partnership with Shire, and tested it in healthy postmenopausal women and in boys with Duchenne muscular dystrophy. The Duchenne study was terminated in 2011, recorded on ClinicalTrials.gov as based on preliminary safety data, after nosebleeds and small dilated blood vessels were reported, and in 2013 the companies said they would not restart development. A 2025 doping-control study found that black-market products sold as ACE-031 did not contain the fusion protein. It is not an approved medicine and MY PEPTIDES does not stock it. General information only, not medical advice.

The short answer

ACE-031 is not a peptide. It is a fusion protein: the part of activin receptor type IIB that sits outside the cell and binds signalling molecules, joined to the Fc portion of a human IgG1 antibody. Two of these chains pair up into one large molecule. It was designed to act as a decoy receptor, soaking up myostatin and related proteins that normally hold muscle growth in check.

It was taken into human trials, and it is one of the few compounds discussed in this market whose clinical story has a clear ending. Its development was stopped.

A receptor fragment with an antibody tail

Receptor-Fc fusions are an established class of biologic. The receptor fragment provides the binding, and the antibody Fc region gives the molecule size, stability and a longer persistence in the body than the fragment would have alone. ACE-031, given the non-proprietary name ramatercept, belongs to this class.

That has practical consequences. Molecules of this kind are produced by recombinant expression in cultured cells, not by the solid-phase chemical synthesis used for short peptides, and their identity cannot be confirmed by a single mass and an HPLC purity percentage. Our guide on IGF-1 LR3 explains why even an 83-residue protein behaves differently from a short peptide; ACE-031 is several times larger again.

Why a decoy receptor affects muscle

Myostatin restrains muscle growth by signalling through activin type II receptors. A soluble version of the receptor competes for myostatin before it reaches muscle cells.

In 2005, Lee and colleagues reported that a soluble form of activin receptor type IIB produced dramatic increases in muscle mass in wild-type mice. The effect was weaker, but still present, in mice genetically lacking myostatin, which pointed to other ligands acting through the same receptors. That is the key mechanistic point: ACE-031 does not block myostatin alone, it traps a family of related signals.

Acceleron's own preclinical work followed. Cadena and colleagues reported in 2010 that ACE-031 increased muscle mass in mice across both major fibre types. A study in common marmosets, carried out by former Acceleron scientists and academic collaborators and published in 2026, reported increases in lean body mass, fibre cross-sectional area and muscle force. Each is an animal result.

What happened in the clinic

ACE-031 reached people, which most compounds in this market never do. An early placebo-controlled safety study in 48 healthy postmenopausal women measured safety, how the body handled the molecule and markers of body composition, and its authors described it as generally well tolerated.

The next step was a Phase 2 study in ambulatory boys with Duchenne muscular dystrophy, registered as NCT01099761, which began in April 2010 with safety as its primary objective. It did not finish. Participants experienced nosebleeds, gum bleeding and small dilated blood vessels in the skin, known as telangiectasias. These were not in themselves considered dangerous, but after review with regulators the study was terminated and a follow-on extension study was stopped too. ClinicalTrials.gov records both as terminated based on preliminary safety data, and the companies later said the trials had been on hold since February 2011.

The published report of the Duchenne study, by Campbell and colleagues in 2017, describes trends, rather than statistically significant effects, in some secondary measures, and states that non-muscle adverse events contributed to the decision to discontinue. In May 2013 Acceleron and Shire announced that they had concluded their collaboration on ACE-031 and would not restart development, saying additional non-clinical and toxicology studies did not support it.

What black-market vials contained

ACE-031 is listed by name on the World Anti-Doping Agency prohibited list, so anti-doping laboratories have reason to know what circulates under its name. In 2025, Reichel and colleagues analysed 14 products sold as ACE-031. Two contained no protein that reacted as activin receptor IIB at all. The other twelve contained the full-length human activin receptor IIB rather than ACE-031, with no Fc fusion present, alongside many other proteins.

For anyone comparing listings, that is the most important finding on this page. A vial sold as ACE-031 was, in every product tested, not ACE-031.

Why a peptide certificate cannot identify it

A short synthetic peptide can be characterised convincingly with HPLC and mass spectrometry: one main peak, one exact mass. A dimeric fusion protein needs a different toolkit, such as gel electrophoresis, immunoblotting, enzymatic tests for the Fc region and mass spectrometry, which is broadly the approach the 2025 study took. A certificate offering only a purity percentage for a product labelled ACE-031 is not evidence of identity. Our guide to certificates of analysis covers what a certificate can reasonably establish.

Where MY PEPTIDES stands

We do not stock ACE-031, there is no certificate for it in our library, and this page is not an offer to supply it. What we do sell is listed in the catalogue with batch documentation, and our guide on what research peptides are explains the category ACE-031 is often wrongly placed in.

The bottom line

ACE-031, or ramatercept, is an activin receptor type IIB-Fc fusion protein designed as a decoy for myostatin and related signals. It increased muscle mass in animal models, reached Phase 2 in Duchenne muscular dystrophy, and was stopped over non-muscle adverse events, with development formally ended in 2013. Products sold under its name and tested in 2025 did not contain it. It is not a peptide, not an approved medicine, and not something we supply.

All compounds referenced on this site are discussed strictly in the context of in-vitro laboratory research. Nothing here is a medicine, a supplement or a therapeutic product, nothing here describes administration to humans or animals, and this guide is general information rather than medical, legal or research advice.

Frequently asked questions

Is ACE-031 a peptide?
No. ACE-031 is a recombinant fusion protein made of two identical chains, each joining the extracellular domain of activin receptor type IIB to the Fc region of a human antibody. Each chain runs to hundreds of amino acids. Calling it a peptide is a marketing convenience, and it matters, because a molecule of this kind is made and verified in completely different ways from a short synthetic peptide.
What is ramatercept?
Ramatercept is the generic, non-proprietary name for ACE-031. The "-cept" ending is used for receptor fusion proteins, which is a useful reminder of what the molecule is. Both names refer to the same activin receptor type IIB-Fc construct developed by Acceleron Pharma.
What does ACE-031 do in research models?
It works as a ligand trap. Because it carries the binding domain of activin receptor type IIB, it captures myostatin and related proteins that normally restrain muscle growth. In mice, soluble forms of this receptor produced marked increases in muscle mass, and a study in marmosets published in 2026 reported increases in lean mass and muscle fibre size. Those are animal findings.
Why was ACE-031 discontinued?
The Phase 2 study in boys with Duchenne muscular dystrophy was stopped after reports of nosebleeds, gum bleeding and small dilated blood vessels in the skin. ClinicalTrials.gov records the termination as based on preliminary safety data. The companies later said further non-clinical and toxicology studies did not support restarting, and in May 2013 they ended the programme.
Is ACE-031 an approved medicine?
No. ACE-031 never completed clinical development and holds no marketing authorisation from any regulator. It is also listed by name on the World Anti-Doping Agency prohibited list, among agents preventing activin receptor IIB activation.
Do you sell ACE-031?
No. We do not stock ACE-031, and there is no Certificate of Analysis for it in our library. As this guide explains, a peptide-style certificate could not establish its identity in any case.