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Explore  /  Follistatin (FST-344)
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Follistatin (FST-344)

D
best evidence
Protein (not a peptide)⚠ WADA-banned
also called — Follistatin · FST · FST-344 / FS344 (the "research-peptide" isoform) · FST-315 (the circulating form) · FST-288 (the tissue-bound form). INCI: none
muscle / myostatin inhibition(studied:) muscular-dystrophy gene therapy — research context

Reference entry — not sold here. The muscle world's holy grail — myostatin inhibition — and the honest reality behind the hype. Two things to know up front: it's a large protein, not a peptide, and the jaw-dropping numbers you've seen come from transgenic animals and gene therapy, not from an inject

In brief

Follistatin is a natural myostatin inhibitor whose biology is spectacular — releasing the body's brake on muscle produces the "double-muscling" seen across species. But "follistatin, the injectable muscle drug" does not exist in any proven form: the dramatic gains are from transgenic animals and gene therapy, the human gene-therapy trials were modest and unapproved, the pharma myostatin-inhibitor programs mostly failed on function or safety, and the online "FST-344" is a large protein of dubious authenticity. Fascinating science; unproven and risky as a product. Banned in sport.

Legal standing, by region
International
See note

- Everywhere — not approved for any human indication. Sold only as a "research" chemical — and because it's a large protein, gray-market "Follistatin-344" is frequently underdosed, mislabelled or contaminated. - ⚠ Sport: WADA-prohibited — myostatin-inhibiting agents are explicitly banned (Section S4.4, Hormone and Metabolic Modulators). Do not touch it in tested sport.

⚠ WADA-prohibited in sportSport: WADA-prohibited — myostatin-inhibiting agents are explicitly banned (Section S4.4, Hormone and Metabolic Modulators). Do not touch it in tested sport.
Evidence, by outcome

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

OutcomeEvidence base · effectGrade
Muscle hypertrophy via myostatin inhibition (the biology)
This is the biology in transgenic / gene-therapy models — not injected protein in humans
Transgenic + gene-therapy animals (20–40%, more in overexpression); Lee 2007 · Dramatic muscle growth
Injected follistatin protein → muscle in healthy humans (the marketed use)
No human clinical evidence; the animal gains were transgenic / gene-therapy
None · Not demonstrated
F
Gene therapy for muscular dystrophy / IBM
Well tolerated locally, but modest; never became an approved therapy
Phase 1/2 (Mendell) · Modest
D
Broader myostatin-inhibitor drug class
Antibodies: modest/no functional benefit; ACE-031 terminated on vascular safety
Antibodies (MYO-029 etc.) + ACE-031 · Largely failed
Safety
Suppresses FSH/LH (reproductive); vascular risk (class); may lower bone density (GDF-11 block); muscle may outpace tendon; theoretical oncogenic concern; effects may not "cycle off"; gray-market product often mislabelled/contaminated; WADA-banned
Preclinical + gene-therapy + mechanism · Real concerns
The honest part

the myostatin story is real and thrilling — but the gap between "myostatin knockout doubles muscle in mice" and "inject this vial and grow" is enormous and unbridged. The compounds that tried to bridge it with rigorous trials mostly failed (function or safety), and what's sold online is a large, fragile protein you can't verify. Respect the biology; don't trust the product.

Identity Follistatin is a naturally occurring glycoprotein produced in the gonads, pituitary and liver. At ~300+ amino acids it is a protein, well above the "peptide" range — which matters, because a large protein is far harder to synthesise, verify and keep stable than a short peptide. FST-344 (the 344-residue isoform sold online) is converted in the body to FST-315, the systemic circulating form. ## Mechanism (as proposed) follistatin binds and sequesters myostatin (GDF-8) plus activin A, GDF-11 and several BMPs, removing multiple TGF-β "brakes" on muscle → increased protein synthesis and reduced degradation → hypertrophy. Its breadth ("biological shotgun") is why it out-performs myostatin-only antibodies in animals — and also why its off-target effects (reproductive, vascular, bone) are a genuine concern. FST-344 converts in vivo to the systemic FST-315.

Sources — 4 cited
01Lee SJ. (Follistatin overexpression roughly doubles muscle mass; effect on a myostatin-null background.) PNAS, 2007.
02Mendell JR, et al. (AAV-follistatin gene therapy trials in muscular dystrophy / inclusion-body myositis.) Phase 1/2.
03Kota J, Sumner CJ, et al. Inhibition of myostatin, with emphasis on follistatin as a therapy for muscle disease. (Review; PMC2717722.)
04ACE-031 clinical-termination reports; myostatin-antibody trial reviews (MYO-029 and successors).
Review status
Not yet reviewed

A credentialed reviewer (PharmD / PhD / MD) will be named before this entry is finalised. Until then, treat it as a working draft. Last updated July 2026.

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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Protein (not a peptide)
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Follistatin (FST-344) — myostatin inhibition, what the evidence really shows & status · Vallydia