Follistatin vs ACE-031

Both block myostatin signalling but in different ways. Follistatin is an endogenous glycoprotein that binds myostatin and activins; ACE-031 is an engineered soluble activin receptor (ActRIIB-Fc) that soaks up several ligands — its Duchenne trial was stopped over nosebleeds and small dilated blood vessels (telangiectasias).

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Follistatin

A secreted glycoprotein that binds and neutralises myostatin and activin — studied as a route to muscle growth in muscle-disease research.

BEST STUDIED FOR

GH secretagogues

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ACE-031

A fusion protein of the activin type IIB receptor and an antibody Fc fragment that traps myostatin and related ligands.

BEST STUDIED FOR

GH secretagogues

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SIDE BY SIDE

	Follistatin	ACE-031
The key difference	Binding protein that neutralises myostatin and activins	Decoy activin receptor type IIB fusion protein
Class	GH secretagogues	GH secretagogues
Mechanism	Follistatin binds TGF-β-superfamily ligands, most notably myostatin (a negative regulator of muscle growth) and activin A, preventing them from signalling.	By acting as a decoy receptor, ACE-031 binds myostatin, activin A and other ActRIIB ligands, removing a brake on muscle growth.
Status	Investigated mainly through gene-therapy approaches in muscle-disease research; no approved follistatin medicine.	Trialled in healthy volunteers and boys with Duchenne muscular dystrophy; the Duchenne trial was stopped early. Detected in black-market products; WADA-prohibited.
Reported safety signals	Because it also neutralises activins, effects extend beyond muscle (including reproductive hormones). Human data are limited to small gene-therapy studies.	The Duchenne trial was stopped after its second dosing regimen because of potential safety concerns — nosebleeds (epistaxis) and telangiectasias (small dilated blood vessels).
A key study	Reviews myostatin-pathway inhibition, with emphasis on follistatin, as a strategy in genetic muscle disorders. (Muscle Nerve 2009, PMID 19208403)	In 48 healthy postmenopausal women, a single dose was generally well tolerated and the top dose increased lean mass and thigh muscle volume at day 29. (Muscle Nerve 2013, PMID 23169607)

WHEN TO RESEARCH WHICH

Follistatin suits gene-therapy and physiology research; ACE-031’s halted programme is mainly a cautionary dataset on broad ActRIIB ligand traps. Both are discussed here strictly as research compounds; nothing on this page is medical advice or a dosing guide.

REFERENCES (PUBMED)

[Follistatin] Inhibition of myostatin with emphasis on follistatin as a therapy for muscle disease — Muscle Nerve 2009. PMID 19208403
[Follistatin] Follistatin — Int J Biochem Cell Biol 1998. PMID 9785474
[Follistatin] Discovery of a follistatin-derived myostatin inhibitory peptide — Bioorg Med Chem Lett 2020. PMID 31874826
[ACE-031] A single ascending-dose study of muscle regulator ACE-031 in healthy volunteers — Muscle Nerve 2013. PMID 23169607
[ACE-031] Myostatin inhibitor ACE-031 treatment of ambulatory boys with Duchenne muscular dystrophy: Results of a randomized, placebo-controlled clinical trial — Muscle Nerve 2017. PMID 27462804
[ACE-031] Gel Electrophoretic Detection of Black Market ACE-031 — Drug Test Anal 2025. PMID 40312924

FREQUENTLY ASKED

What is the difference between Follistatin and ACE-031?

What is the regulatory status of Follistatin and ACE-031?

Follistatin: Investigated mainly through gene-therapy approaches in muscle-disease research; no approved follistatin medicine. ACE-031: Trialled in healthy volunteers and boys with Duchenne muscular dystrophy; the Duchenne trial was stopped early. Detected in black-market products; WADA-prohibited.

What safety signals have been reported?

Follistatin: Because it also neutralises activins, effects extend beyond muscle (including reproductive hormones). Human data are limited to small gene-therapy studies. ACE-031: The Duchenne trial was stopped after its second dosing regimen because of potential safety concerns — nosebleeds (epistaxis) and telangiectasias (small dilated blood vessels).

Which studies is this comparison based on?

For Follistatin: “Inhibition of myostatin with emphasis on follistatin as a therapy for muscle disease” (PMID 19208403); “Follistatin” (PMID 9785474); “Discovery of a follistatin-derived myostatin inhibitory peptide” (PMID 31874826). For ACE-031: “A single ascending-dose study of muscle regulator ACE-031 in healthy volunteers” (PMID 23169607); “Myostatin inhibitor ACE-031 treatment of ambulatory boys with Duchenne muscular dystrophy: Results of a randomized, placebo-controlled clinical trial” (PMID 27462804); “Gel Electrophoretic Detection of Black Market ACE-031” (PMID 40312924).