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ACE-031 (Ramatercept)

F

lead outcome

Duchenne muscular dystrophy (the lead…

grades vary by outcome ↓

Protein (not a peptide)⚠ WADA-banned

also called — ACE-031 · Ramatercept · ACVR2B-Fc · soluble activin receptor type IIB fusion protein. INCI: none

muscle / myostatin-activin blockade(terminated:) Duchenne muscular dystrophy — research context

Reference entry — not sold here. Two things up front: it is a large fusion protein, not a short peptide, and its lead clinical program was terminated on safety. The muscle biology is real; the product is discontinued and WADA-banned. No dosing published here.

In brief

ACE-031 (ramatercept) is a soluble activin-receptor-IIB fusion protein — a decoy that mops up myostatin, activin A and GDF-11 to release the brakes on muscle. The biology is the same thrilling myostatin story as follistatin, and an early Phase 1 in postmenopausal women did raise lean-mass and bone markers. But the lead program — Phase 2 in Duchenne muscular dystrophy — was terminated early after bleeding events (nosebleeds, gum bleeding, telangiectasia) traced to the activin axis acting on blood vessels, not just muscle. It is approved nowhere, is a large hard-to-verify protein on the gray market, and is banned in sport. A program that was stopped, not one that is promising.

Legal standing, by region

European Union

Not approved

Not approved for any indication; no EMA authorisation. Development discontinued. Sold only as a research chemical.

United States

Not FDA-approved (development terminated)

Not FDA-approved. The DMD program was terminated at Phase 2 on vascular safety signals; no successor approval.

International

Approved nowhere

Approved nowhere. Gray-market "ACE-031" is a large fusion protein — hard to synthesise, verify or keep stable.

⚠ WADA-prohibited in sportSport: myostatin-inhibiting / activin-receptor agents are explicitly banned (WADA S4.4, Hormone and Metabolic Modulators). Do not touch it in tested sport.

Evidence, by outcome

How we grade →

An honest grade per outcome — drawn from the evidence, not any catalogue. Hype and undemonstrated marketing claims grade low.

OutcomeEvidence base · effectGrade

Duchenne muscular dystrophy (the lead indication)

Stopped over safety, not efficacy readout — the program did not deliver an approved therapy.

Phase 2 in DMD boys (Acceleron/Shire) — TERMINATED early · Development halted

F

Myostatin/activin blockade → muscle (the biology)

This is the class biology (same axis as follistatin) — not a demonstrated human benefit from this molecule.

Decoy receptor soaks up myostatin, activin A and GDF-11; robust muscle-mass increase in animal models · Real, dramatic in animals

—

Muscle mass / bone in humans (early trial signal)

Short, small, biomarker-level. Never progressed to a functional-outcome approval.

Phase 1 in healthy postmenopausal women showed increased lean mass and bone-formation markers · Measurable biomarker changes

D

Safety

Trial halted after nosebleeds and gum bleeding (telangiectasia / vascular effects) — the activin-receptor class hits blood-vessel biology, not just muscle. This is the defining fact of ACE-031.

Phase 2 termination · Serious concerns

—

Disclosure

Vallydia sells its own cosmetic serums, and some ingredients graded here belong to the same categories as those products. Grades are drawn from the published evidence by the method we publish, and applied to our own ingredients on the same terms — our copper-peptide serum is graded no more kindly than the peptides it competes with. We disclose the interest so you can weigh it.

Trade names shown here (for example Matrixyl, Argireline, Syn-Ake) are the property of their respective owners and are used only to identify the ingredient under discussion. Their appearance implies no affiliation with, or endorsement by, the proprietor.

Evidence changes

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The honest part

The single most important fact about ACE-031 is why it stopped: the activin receptor it blocks governs blood-vessel as well as muscle biology, and the Duchenne trial was halted over bleeding events. "Muscle drug that was discontinued on vascular safety" is the honest one-line summary — not "promising myostatin peptide."

Identity

ACE-031, or ramatercept, is a soluble fusion protein: the extracellular domain of the activin receptor type IIB (ActRIIB) fused to an antibody Fc region. It is not a short peptide but a large engineered protein, which matters for the same reason it does with follistatin — a big protein is far harder to synthesise, verify and keep stable than a short peptide, and gray-market material is easy to mislabel.

Mechanism (as proposed)

ActRIIB is the receptor that myostatin (GDF-8), activin A and GDF-11 all signal through to restrain muscle growth. ACE-031 acts as a decoy: a free-floating copy of the receptor that binds those ligands before they reach real receptors, lifting multiple TGF-β "brakes" on muscle at once. Because it blocks the whole cluster rather than myostatin alone, it drives muscle gain strongly in animals — and, by the same breadth, reaches biology well beyond muscle.

Why it stopped

The defining event of ACE-031's history is not an efficacy result — it is a safety termination. The Phase 2 trial in boys with Duchenne muscular dystrophy was halted early after participants developed nosebleeds, gum bleeding and dilated small blood vessels (telangiectasia). The activin-receptor axis ACE-031 blocks is active in vascular biology, not just skeletal muscle, and that off-target reach produced bleeding-related adverse events serious enough to end the program. The molecule didn't fail to grow muscle — it grew concern about where else it acts. That is the honest frame for anyone encountering "ACE-031" as a research product today.

Sources — 3 cited

01Attie KM, et al. (A single ascending-dose study of ACE-031 in healthy postmenopausal women — lean mass and bone markers.) Muscle Nerve, 2013.

02Campbell C, et al. (Phase 2 ACE-031 in Duchenne muscular dystrophy — terminated; vascular safety signals.)

03Reviews of the myostatin/activin-inhibitor drug class (follistatin, MYO-029, ACE-031, bimagrumab) and their mixed efficacy/safety record.

Updated 2026-08-07 (Development discontinued years ago — grade reflects a program that failed on safety, not one still pending.)

Grades reflect the published evidence, not our interest. No dosing, reconstitution, or administration is published for research compounds — that restraint is deliberate.

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