FST · Activin-binding protein · FSH-suppressing protein (FSP)
Highest evidence
Human trial
Studies recorded
4· 1 in humans
Legal status · US
Unapproved
Scientific context only. Not medical advice, not a recommendation to use.
At a glance
Follistatin is an endogenous glycosylated binding protein (~35 kDa, considerably larger than typical peptides) that binds and neutralises members of the TGF-β superfamily, including activin and myostatin (GDF-8). In animal models, raising follistatin de-represses muscle growth. Clinically it has been studied mainly via AAV gene therapy (FS344) in muscular dystrophies. Follistatin is not an approved drug; human efficacy and safety data are limited and stem mostly from early gene-therapy trials and preclinical research. A 'follistatin-344' product is sold on the grey market, the identity and purity of which cannot be verified without analytics.
Researched for
Inhibition of the myostatin/activin signalling pathway (muscle-mass regulation, preclinical)Gene therapy in Becker muscular dystrophy and inclusion body myositis (early trials)Theoretical application in muscle-wasting disorders
Official status
US: Unapproved
No FDA-approved follistatin medicine for any indication. Follistatin has been used only in clinical research (mostly as AAV gene therapy). 'Follistatin-344' products offered for sale are considered unapproved substances ('research chemicals'). Myostatin inhibitors including follistatin appear on the WADA prohibited list.
Follistatin binds with high affinity to activin and to myostatin (GDF-8), as well as related TGF-β ligands such as GDF-11 and some BMPs, preventing their binding to the activin type-II receptors. Myostatin is a negative regulator of skeletal muscle mass; by sequestering myostatin, its growth-inhibiting signalling is removed (de-repression). Because follistatin additionally neutralises activin, it acts on several muscle-inhibiting pathways at once — in animal models this produced greater muscle gain than knocking out myostatin alone. Several isoforms exist (including FST-288 and FST-315) that differ in tissue binding via heparan sulfate. The FST344 variant used in gene therapy was chosen to reduce binding to off-target structures.
02
Evidence at a glance
Reading note. The distribution shows on which evidence tier each observation sits. Strong colours mark stronger evidence — weaker tiers are deliberately visible, not hidden.
4 observations · 2 tiers
Human trial
1
Animal model
3
03
What the studies show
Animal model
Maus (transgen)
Lee S.J., McPherron A.C. 2001
Transgenic overexpression of follistatin markedly increased skeletal muscle mass in mice — beyond the level of myostatin knockout alone
What does NOT follow: Finding from genetically modified animal models with permanent overexpression — not transferable to short-term exogenous administration in humans.
Animal model
mdx-Maus
Nakatani M., Takehara Y., Sugino H., et al. 2008
Follistatin-based myostatin inhibitor increased muscle mass and ameliorated dystrophic pathology in mdx mice (animal model of muscular dystrophy)
What does NOT follow: Disease-model finding; a clinical benefit in humans cannot be inferred from it.
Human trial
Mensch (Phase 1/2a, offen, n=6)
Mendell J.R., Sahenk Z., Malik V., et al. 2015
In an early gene-therapy trial of six Becker muscular dystrophy patients, improved walking distance was reported in some participants after intramuscular AAV-FS344 transfer
What does NOT follow: Very small, uncontrolled early-phase trial without a placebo arm; results were inconsistent and do not permit an efficacy conclusion. This is gene transfer, not administration of a finished follistatin protein.
Animal model
Maus (Knockout/heterozygot)
Lee S.J., Lee Y.S., Zimmers T.A., et al. 2010
Heterozygous follistatin loss reduced muscle size and impaired regeneration after injury in mice — indicating a physiological role in muscle homeostasis
What does NOT follow: Evidence for the endogenous function of follistatin, not evidence for a benefit of exogenous administration.
04
Where studies disagree
Open question
Can the strong muscle-building effect from animal models be transferred to humans?
POSITION A
In genetic mouse models with follistatin overexpression, impressive muscle gains were observed, in part exceeding myostatin knockout.
POSITION B
The few human data come from small, uncontrolled gene-therapy trials and remained inconsistent, without robust evidence of efficacy.
CURRENT STATE · Larger controlled human trials are lacking. The gap between strong preclinical effects and weak clinical data is unresolved; transferability to humans is not established.
05
Pharmacokinetics
No robust pharmacokinetic human data available. A model curve is not invented.
06
Routes of administration in the literature
Which routes of administration the available studies describe — neutral reporting, not a usage guide.
Intramuscular
In published human research the FS344 sequence was delivered via AAV1 by direct intramuscular injection into the thigh muscles (gene transfer, not protein).
06d
Safer use & risks
Risk notes for harm reduction — descriptive, not a usage or dosing guide.
⚠ Important — please read
This platform does NOT provide usage or dosing instructions. The points below describe risks and are meant to help avoid harm — they do not replace medical advice. Anyone who uses a substance should discuss it with a doctor.
There is no approved human use for this substance. What circulates online about amounts and frequency is self-experimentation without a safety net.
Online numbers are not a benchmark
Amounts from TikTok, YouTube and forums are mostly imitation rather than data — and are often wrongly derived from animal studies (µg/kg). Not a reliable benchmark for humans.
Sterility & infection risk
Injection solutions prepared or stored non-sterile carry an infection and abscess risk. Contamination is common with grey-market product.
Unknown product quality
Research-/grey-market product is not quality-tested: identity, purity and actual content are often unknown, and counterfeits occur.
Mind interactions
Combinations with medications or pre-existing conditions can carry risks (see the Interactions section). Clarify with a doctor beforehand.
Warning signs — seek medical help
With persistent pain, redness/swelling at the injection site, fever, shortness of breath, racing heart, chest pain or allergic reactions, seek medical help immediately.
A doctor, not a forum
Concrete questions about use and amount belong in a conversation with a doctor — not in a comment thread.
07
Known adverse events from studies
Factual reporting of what studies observed. Not a safety statement for individual use.
Theoretical
Pharmacovigilance for an exogenous follistatin product in humans practically non-existent
In the early gene-therapy trials, local intramuscular AAV transfer was described as broadly tolerable, but in very small groups and without long-term safety data. For an injected follistatin protein from the grey market, no established safety profile exists; broad inhibition of the TGF-β family carries theoretical risks.
07b
Interactions & combinations
Documented interactions and contraindications from studies, prescribing information and guidelines. Where no data exists, this is stated.
Reporting of risks, NOT a combination guide. The absence of an entry does not mean „safe to combine“ but „not sufficiently studied“.
No documented interactions recorded
We have not yet found robustly documented interactions for this peptide. This does NOT mean none exist — the data is limited.
08
Risks & hygiene aspects in the literature
What regulatory and scientific literature reports on risks, sterility and identity in non-pharmaceutical sources — descriptive, not a hygiene guide.
Identity and purity problem of grey-market 'follistatin-344'
Follistatin is a large, glycosylated protein whose correct folding and modification are demanding to produce. What is sold on the grey market as 'follistatin-344' is not analytically standardised; identity, purity and biological activity cannot be verified without laboratory testing. Published analytics exist for detecting black-market follistatin-344.
10
Anecdotal observations
Weakest evidence tier — not supported by studies
Reading note. This section gathers popular claims from communities and forums. They are explicitly marked as weakest-tier evidence. Unblinded self-reports are particularly prone to placebo, recall and confirmation biases.
Why no amounts or protocols are listed here. We deliberately show only WHAT communities report — not in what amount or how it is used. Anecdotal "doses" or "biohacker protocols" are neither verified nor standardised nor safe; publishing them would be a usage guide, which we do not provide on principle. Specific amounts belong in a conversation with a doctor, not in a forum.
In bodybuilding circles, 'follistatin-344' is described as a means of inhibiting myostatin and thereby increasing muscle mass.
common in the grey market, often citing the animal-study results
Not supported by studies: The spectacular muscle gains come from genetic animal models with permanent overexpression or from AAV gene transfer — not from injecting a finished protein. Controlled human trials of an injected follistatin protein for muscle building do not exist; the pharmacological plausibility of such use is unresolved.
Follistatin is promoted in bodybuilding and longevity circles as a myostatin inhibitor for exceptional muscle growth — partly as an injected peptide, partly as gene therapy (FST gene).
strong interest in muscle/anti-aging communities
Not supported by studies: The dramatic muscle effects come from genetic animal models (myostatin knockout); injected follistatin peptides have a very short half-life and no demonstrated systemic muscle effect in humans. Gene-therapy approaches are purely experimental with unknown risks.
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Legal status by country
Country
Status
Note
Checked
United States
Unapproved
No FDA-approved follistatin medicine for any indication. Follistatin has been used only in clinical research (mostly as AAV gene therapy). 'Follistatin-344' products offered for sale are considered unapproved substances ('research chemicals'). Myostatin inhibitors including follistatin appear on the WADA prohibited list.
2026-06-07
Germany
Unapproved
No EMA approval for a follistatin product. Sale as a 'research chemical' is not covered by medicines law. As a myostatin inhibitor, follistatin is WADA-prohibited in competitive sport; gene doping with follistatin vectors is separately banned.
2026-06-07
12
Reconstitution calculator
Pure mg/mL maths — works like a calculator. Not a usage recommendation.
Peptides ship as a dry powder. Once dissolved in a liquid (reconstitution), this calculator answers a single question: how much substance is in one millilitre of solution afterwards?
1Enter the vial's substance amount (printed on the label).
2Enter how much solvent you add.
3Result = concentration in mg per mL.
Printed on the label
/
Liquid you add
=
2.50
mg / mL
5 mg in 2 mL gives 2.50 mg/mL — each millilitre contains 2.50 mg of substance.
Nakatani M., Takehara Y., Sugino H., et al. · 2008
Transgenic expression of a myostatin inhibitor derived from follistatin increases skeletal muscle mass and ameliorates dystrophic pathology in mdx mice