# ACE-031

> Evidence tier A — Controlled human trials · GH & Growth · reviewed 2026-11-08
> Source page: https://peptidemeta.com/p/ace-031/

Also known as: Ramatercept, ActRIIB-Fc

## Quick answers

**What is ACE-031?**

A soluble activin receptor type IIB-Fc fusion protein that traps myostatin and related ligands. Fusion protein of the activin receptor IIB extracellular domain and an IgG1 Fc region, not a short peptide.

**How strong is the evidence for ACE-031?**

Tier A (controlled human trials) on the peptidemeta evidence scale. Randomized, placebo-controlled trials were run in healthy volunteers and boys with Duchenne muscular dystrophy; the DMD study was halted over safety signals.

**Is ACE-031 FDA-approved?**

No. ACE-031 is not approved by the FDA for any use.

**Is ACE-031 banned in sport?**

Yes. ACE-031 is prohibited in sport by the World Anti-Doping Agency under S4 (hormone and metabolic modulators).

**How does ACE-031 work?**

ACE-031 is a soluble ActRIIB-Fc fusion protein that acts as a ligand trap, binding and neutralizing myostatin, activin A, GDF-11, and other TGF-beta superfamily members before they can signal through cell-surface receptors. This broad ligand sequestration promotes robust muscle hypertrophy and reduces fat mass but also explains the off-target vascular effects.

**What is known about the safety of ACE-031?**

Phase II trials in Duchenne muscular dystrophy were halted due to epistaxis and telangiectasias (likely from BMP9/10 trapping affecting vascular biology). Lean mass gains were confirmed in humans.

## Key facts

- **Evidence tier:** A (Controlled human trials)
- **FDA:** not approved
- **WADA:** prohibited (S4)
- **Peptide:** yes
- **Routes studied:** Subcutaneous, Intravenous

## Overview

A soluble activin receptor type IIB-Fc fusion protein that traps myostatin and related ligands. It was developed for muscle wasting but clinical trials were halted due to off-target effects.

## Mechanism

ACE-031 is a soluble ActRIIB-Fc fusion protein that acts as a ligand trap, binding and neutralizing myostatin, activin A, GDF-11, and other TGF-beta superfamily members before they can signal through cell-surface receptors. This broad ligand sequestration promotes robust muscle hypertrophy and reduces fat mass but also explains the off-target vascular effects.

## Effects reported in research

_Reported outcomes, not promises; see the evidence tier._

- Robust myostatin pathway inhibition
- Significant lean mass gains in trials
- Reduced fat mass
- Potential bone mineral density improvement

## Safety & unknowns

Phase II trials in Duchenne muscular dystrophy were halted due to epistaxis and telangiectasias (likely from BMP9/10 trapping affecting vascular biology). Lean mass gains were confirmed in humans. Demonstrates the risk of broad ligand-trap approaches. Not FDA-approved; development discontinued.

## Status sources

- [Attie et al. 2013, Muscle Nerve (phase 1 RCT)](https://pubmed.ncbi.nlm.nih.gov/23169607/)
- [Campbell et al. 2017, Muscle Nerve (DMD trial)](https://pubmed.ncbi.nlm.nih.gov/27462804/)
- [WADA 2026 Prohibited List](https://www.wada-ama.org/en/prohibited-list)

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Educational reference only — not medical advice. No dosing information is published. Tiers rate the strength of published evidence, not effectiveness or safety.