Follistatin-344

FST-344, follistatin (precursor isoform), FS-344; related: FST-315, FST-288, ACE-083 (a follistatin-based drug candidate)

Growth hormone axis

Awaiting medical reviewEN ES DE FR PT ZH+ Follow for updates

Summary

Class: Naturally occurring glycoprotein (344 amino acids including signal peptide; mature forms are 315 or 288 residues) that binds and neutralises myostatin, activins and GDF-11. Products sold as "follistatin-344" are recombinant or synthetic versions of the full-length isoform
Mechanism: Traps myostatin and activin before they can reach their receptors, removing a brake on muscle growth and altering reproductive and metabolic signalling
Routes studied: Gene therapy (AAV vector injected into muscle) in humans and animals; recombinant protein injection in animals; subcutaneous and intramuscular (community)
Dose range reported: Human gene therapy: 6×10^11 to 2.4×10^12 vector genomes per kg, single administration. Animal protein studies: various. Community: 100 µg daily for 10–30 days, or 100 µg intramuscular 2–3 times weekly. No human protein dose has ever been studied
Half-life: Native follistatin: cleared from circulation within hours; FST-315 is the circulating form, FST-288 is tissue-bound. Injected recombinant FST-344 in humans: unknown †
Storage: Lyophilised: refrigerate or freeze. Reconstituted: refrigerate; a glycoprotein this large is more fragile than small peptides — avoid shaking and freeze–thaw
Regulatory status: Not approved for human use anywhere

Doses are as reported in studies or by the community — never recommendations.

1What it is

Follistatin is a natural protein. It was first isolated from ovarian follicular fluid in 1987 as a factor that suppressed FSH (follicle-stimulating hormone) release — hence the name — and was later found to be the body's main neutraliser of activin and, importantly, of myostatin, the protein that limits muscle size. Animals and people born without functional myostatin have roughly double normal muscle mass, which is why anything that blocks it attracts interest.

The gene produces three forms. FST-344 is the full-length transcript whose protein is cleaved to FST-315, the version that circulates in blood; FST-288 is a shorter, tissue-bound version that lingers near the ovary and testis. Gene-therapy trials used FST-344 precisely because it produces the circulating form and avoids concentrating in reproductive tissue.

What is sold as "follistatin-344" is a recombinant or synthetic copy of this protein. The important point is that nearly all the encouraging data come from gene therapy — a one-time injection of a viral vector that makes muscle cells produce follistatin continuously for years — not from injecting the protein itself, which disappears from the blood within hours. Those are very different interventions.

2How it's thought to work

Myostatin and activin trapping. follistatin binds myostatin, activin A/B and GDF-11 with high affinity, preventing them from activating the ActRIIB receptor and the SMAD2/3 signalling that limits muscle fibre growth and promotes atrophy.

Muscle. removing this brake increases protein synthesis, fibre size and satellite-cell activity; transgenic over-expression in mice produces dramatic muscle gain.

Reproductive axis. by neutralising activin it reduces FSH secretion from the pituitary — the original discovered function.

Other tissues. follistatin influences liver fat metabolism, inflammation, wound healing and bone; it is also a marker and possible mediator in several cancers, which is a central caution.

Follistatin binds myostatin and activin before they reach their receptors — a sponge rather than a blocker at the receptor itself. Myostatin limits muscle growth, so removing it lifts a brake, which is the basis of the muscle claims.Schematic — not to scale

3What the research shows

Gene therapy in muscular dystrophy

A Phase 1/2a trial injected AAV1-FST344 into the quadriceps of six adults with Becker muscular dystrophy; most showed increased 6-minute walk distance and, on biopsy, larger fibres and less fibrosis over 1–2 years, with no serious adverse events (Mendell 2015, Mol Ther). A follow-on in inclusion body myositis reported similar signals (Mendell 2017, Mol Ther). Open-label, small, no placebo group. [4][5]

Muscle growth in animals

Follistatin gene delivery produced large increases in muscle mass in mice, including myostatin-knockout mice (indicating activin blockade adds to myostatin blockade) (Lee 2007, PLoS One), and in non-human primates with strength gains and no adverse tissue findings over 15 months (Kota 2009, Sci Transl Med). [2][3]

Graded A/B (negative or stopped)

Recombinant protein or follistatin-based drugs

ACE-083, a locally acting follistatin-based fusion protein, increased muscle volume at injected sites in Phase 2 trials in facioscapulohumeral dystrophy and Charcot-Marie-Tooth disease but did not improve function, and development was discontinued in 2019–2020 (Acceleron). This is the only controlled human data on administered follistatin protein, and it shows that bigger muscle did not translate to better function in those diseases.

Graded C/D

Metabolic and other effects

Rodent studies report improved glucose handling and reduced liver fat with follistatin over-expression; other work links follistatin to fibrosis and to tumour progression in liver, lung and other cancers in both directions, depending on the model.

Injected follistatin-344 protein in healthy people

No published human study. Community use for muscle growth rests on the gene-therapy results and anecdote, despite the pharmacokinetic gap described above.

4Reported side effects and interactions

Literature-reported

Gene therapy trials: injection-site reactions, no serious adverse events in small numbers; too few participants to detect uncommon effects. ACE-083: injection-site reactions, generally well tolerated.

Community-reported

injection-site pain and swelling, fatigue, headache; many report no measurable effect at the doses and durations used.

Theoretical. reduced FSH and possible effects on fertility and sex-hormone balance; activin is involved in wound healing and inflammation, so suppression may impair repair; follistatin is implicated in some cancers; tendon injury risk if muscle outgrows connective tissue (a concern raised in myostatin-inhibitor programmes); immune reactions to a foreign recombinant protein.

Interactions. none established. Community stacks with anabolic steroids, IGF-1 LR3 and GH have no research basis.

Markers researchers commonly monitor

Marker	Why it's watched
Myostatin and activin A (research assays)	the direct targets; not routinely available clinically.
FSH, LH, testosterone/oestradiol	follistatin suppresses FSH via activin; the most plausible measurable hormonal effect.
Creatine kinase (CK)	muscle turnover; also rises with tendon-muscle mismatch injuries.
Liver enzymes (ALT, AST)	follistatin has hepatic actions.
Fasting glucose and lipids	metabolic effects reported in animals.
Follistatin itself	baseline is measurable, but injected FST-344 cannot be distinguished from native protein on standard assays.

Free for everyone. Safety information is never behind a paywall.

5Reconstitution and handling

Typically supplied as 1 mg vials. with , add slowly down the vial wall and swirl gently; do not shake. Protein stability after reconstitution is poorer than for small peptides.

Open in calculator, pre-loaded →

6Commonly studied alongside

In research: compared with other myostatin-pathway agents (ACE-031, bimagrumab, domagrozumab, apitegromab). In the community: IGF-1 LR3, MGF, GH secretagogues.

Informational cross-links. Not stack recommendations.

7Regulatory status by region

Region	Status (checked —)
United States	Not FDA-approved; not eligible for compounding. Gene therapy remains investigational
European Union	Not authorised
United Kingdom	Not licensed
Australia	Not approved †
South Africa	Not registered
Sport (WADA)	Prohibited (S2 — myostatin inhibitors and "agents modifying myostatin function" are explicitly named; follistatin appears in the list)

8Open questions

Does injected follistatin protein survive long enough in circulation to affect muscle at all? No human pharmacokinetic data.
Does extra muscle from myostatin/activin blockade improve strength or function? ACE-083 suggests not in dystrophies.
Long-term effects on fertility, tendons and cancer risk.

9References

1Lee SJ, McPherron AC (2001). Regulation of myostatin activity and muscle growth. Proc Natl Acad Sci USA. PubMed · DOI
2Lee SJ (2007). Quadrupling muscle mass in mice by targeting TGF-β signaling pathways. PLoS One. PubMed · DOI
3Kota J et al. (2009). Follistatin gene delivery enhances muscle growth and strength in nonhuman primates. Sci Transl Med. PubMed · DOI
4Mendell JR et al. (2015). A phase 1/2a follistatin gene therapy trial for Becker muscular dystrophy. Mol Ther. PubMed · DOI
5Mendell JR et al. (2017). Follistatin gene therapy for sporadic inclusion body myositis improves functional outcomes. Mol Ther. PubMed · DOI
6Schneyer AL et al. (2004). Differential distribution of follistatin isoforms: application of a new FS315-specific immunoassay. J Clin Endocrinol Metab. PubMed · DOI
7Glasser CE et al. (2018). Locally acting ACE-083 increases muscle volume in healthy volunteers. Muscle Nerve. PubMed · DOI

† Being confirmed by our reviewers against current sources.

10Community

forum threads →

community protocols include this →

Threads and protocols are visible to members. Joining is free.

Self-reported side effects Phase 2

Not enough data yet. 0 of the 50 members needed have logged this compound for 4+ weeks. We don't show anything below 50, so no one can be identified.

11Page history

25 Oct 2026Profile published — awaiting medical review

Licensed CC BY-NC-SA 4.0. Found an error? Report it · Editorial standards — corrections are logged here.