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Follistatin-344

Tier 3 · Reported use
Also known as FS-344 · Follistatin 344 · FST-344

The strongest human data come from two small open-label AAV1-FS344 gene therapy trials at Nationwide Children's Hospital (Becker muscular dystrophy n=6; sporadic inclusion body myositis n=6 vs matched controls), reported by Mendell et al. (2015/2017). These represent Tier 1 human clinical evidence but are tiny, open-label, and deliver sustained AAV-driven follistatin expression — NOT injectable recombinant peptide. No randomized, placebo-controlled trials of injectable Follistatin-344 peptide exist, and there are no published human Phase 1 or clinical pharmacokinetic data for the injectable form. Extensive supporting Tier 2 animal/in-vitro data (mice, macaques, dogs, transgenic pigs) and Tier 3 anecdotal/vendor dosing and safety reports round out the profile.

Half-life
~2 h
Routes
Subcutaneous injection · Intramuscular injection · Intravenous (research) · AAV gene therapy (intramuscular vector delivery)
Goals
Muscle growth / hypertrophy · Strength and athletic performance · Muscle-wasting/dystrophy research (Becker MD, sIBM, cachexia, sarcopenia) · Tissue repair and recovery (theorized) · Anti-fibrotic / anti-inflammatory research
Cost / mg
Not recorded

How it works

Follistatin is a natural glycoprotein that acts as a 'blocker' of muscle-limiting signals. It grabs onto and neutralizes myostatin (GDF-8) and activin A — proteins that normally put the brakes on muscle growth and promote muscle wasting. By mopping these up before they can dock onto their receptors on muscle cells, follistatin removes that brake, which in animal and gene-therapy studies allows muscles to grow larger and stronger. It also originally came to light for its ability to reduce release of follicle-stimulating hormone (FSH) from the pituitary. Importantly, the dramatic muscle-growth results reported in the research come mostly from genetic overexpression or gene therapy that keeps follistatin present continuously — not from injecting the short-lived peptide.

Overview

Overview

Follistatin-344 (FS-344, FST-344) is a research-grade form of the endogenous glycoprotein follistatin, one of the most potent natural antagonists of the TGF-beta superfamily. It was first isolated from porcine ovarian follicular fluid in 1987 as a substance that inhibits the release of follicle-stimulating hormone (FSH) from pituitary cells, and in 1990 (Nakamura et al., Science) it was identified as the endogenous high-affinity binding protein for activin.

Molecular identity

The FS gene sits on chromosome 5q11.2 and is alternatively spliced. Follistatin-344 is the 344-amino-acid precursor/isoform. After removal of a 29-amino-acid signal peptide, most sources describe it yielding the mature circulating 315-amino-acid isoform (FST-315); one source instead describes proteolytic trimming to the cell-surface-bound FS-288. These isoforms differ functionally: FS-288 has an exposed heparin-binding sequence (residues 75-86) enabling high-affinity binding to cell-surface heparan sulfate proteoglycans and paracrine action, whereas FS-315 carries an acidic C-terminal tail that masks the heparin-binding motif so it circulates more freely. FS-344 is described as having lower cell-surface binding and a more freely circulating profile, making it the isoform most studied for systemic delivery research. Reported molecular weight is ~37.8-38 kDa (36-38 kDa FST-315; 38-44 kDa glycosylated FST-344). CAS 106463-69-6; PubChem CID 378611.

How it works

Follistatin binds and neutralizes myostatin (GDF-8), activin A, activin B, and several BMPs. Myostatin normally binds activin type II receptors (ActRIIA/ActRIIB), triggering SMAD2/3 phosphorylation that negatively regulates muscle mass. By sequestering myostatin and activin extracellularly, follistatin blocks engagement of ActRIIA/B and ALK4/5 and shuts down the SMAD2/3 cascade that restricts hypertrophy and drives atrophy. Crystallography shows two follistatin molecules encircling a single activin A dimer, burying ~one-third of its surface. Binding affinities are very high — activin A ~45 pM; myostatin reported variously as ~915 pM, ~0.5-1.0 nM, and ~584 pM. Downstream, mTOR/Akt signaling and satellite-cell activation are theorized to drive hypertrophy and hyperplasia. Notably, follistatin's effect persists in a myostatin-null background and an IGF-1R dominant-negative abolishes ~63% of follistatin-induced hypertrophy, indicating the muscle-building effect is broader than myostatin inhibition alone. Follistatin is expressed across many tissues (skeletal muscle, ovary, pituitary, liver, skin, kidney, heart, endothelium, satellite cells) and is upregulated in muscle by resistance exercise and mechanical loading.

Preclinical evidence

Animal data on genetic overexpression are striking: follistatin transgenic mice developed muscle mass increases of 194-327% (exceeding myostatin-knockout gains); muscle-specific Fst overexpression at least doubled skeletal muscle mass. Systemic follistatin in normal mice produced dose-dependent 10-40% muscle gains with improved grip strength. In mdx (Duchenne) mice, engineered follistatin increased muscle mass, grip and tetanic force, and reduced damage, inflammation, and fibrosis versus anti-myostatin antibody alone. In aged mice it improved muscle size, strength, and neuromuscular junction structure. A single AAV-delivered FS-344 dose produced sustained >20% muscle gains lasting over 2 years in normal and dystrophic mice, and AAV1-FS344 increased muscle size/strength in cynomolgus macaques with no adverse immune response and no effect on reproductive hormones. Transgenic pigs expressing human FS-344 showed increased lean meat (72.95% vs 69.18%), reduced Smad2 phosphorylation, increased Akt phosphorylation, no cardiac hypertrophy, and no reproductive abnormalities. Key papers: Whittemore et al. 2003, Lee et al. PNAS 2008, Kota et al. Sci Transl Med 2009. Muscle gains occur over weeks to months and plateau.

Human evidence

Human data come exclusively from AAV1-FS344 gene therapy (AAV1.CMV.FS344, intramuscular) in Phase 1/2a trials at Nationwide Children's Hospital: Becker muscular dystrophy (n=6) and sporadic inclusion body myositis (n=6 vs 8 matched untreated), reported by Mendell et al. (2015, 2017 Mol Ther). The Becker trial was described as the first-ever gene therapy trial to demonstrate functional improvement in any muscular dystrophy, with 6-minute walk gains of +58-125 m and improvement in 4 of 6 patients; the sIBM trial showed +56 vs -25.8 m/year versus controls. Patients showed increased muscle size/strength, reduced fibrosis, no dose-limiting toxicity, no significant organ changes, and no detectable reproductive/endocrine dysfunction over 2-year follow-up. Benefits were described as modest but durable, without serious adverse events.

Critical caveat: these are tiny, open-label gene-therapy trials producing sustained follistatin expression — fundamentally different from injecting the short-lived peptide. No large randomized, placebo-controlled human trials of injectable Follistatin-344 exist, and no injectable recombinant FS-344 peptide human trials exist. Retail/research-grade peptide is not expected to reproduce the systemic myostatin antagonism achieved by AAV delivery.

Investigated and marketed uses

Follistatin-based therapies have been investigated for sporadic inclusion body myositis, cancer cachexia, fibrosis, hair loss, metabolic inflammation, and sarcopenia. FS-344 is marketed in sports medicine for tissue repair and athletic performance as an unapproved peptide sold direct to patients. Some low-tier sources suggest wound-healing, GI-lining, and anti-inflammatory joint benefits (single source). No injectable follistatin product is FDA-approved; it remains a research compound with no approved clinical indications.

What the research shows

69 findings extracted from the 10 sources cited below, strongest evidence first within each group. Every one links to the source it came from.

What human studies found

Based on 4 animal findings.

  • animalMice genetically engineered to overexpress Fst specifically in muscle had at least twice the amount of skeletal muscle mass as controls4

  • animalTransgenic pigs expressing Fst in muscle tissue exhibited increased proportion of skeletal muscle and reduced proportion of body fat similar to myostatin-null cattle4

  • animalLean percentage of lean meat was significantly higher in F1 generation of TG pigs than in WT pigs4

  • animalUnapproved peptides like FS-344 demonstrate favorable tissue repair and metabolic outcomes in animal models9

How it works

Based on 18 animal findings, 30 in vitro findings and 1 expert opinion finding.

  • animalFollistatin is an essential regulator for muscle development4

  • animalFollistatin findings in mice are similar to results obtained in myostatin-knockout mice4

  • animalMyofiber hypertrophy was observed in the longissimus dorsi of transgenic pigs, possibly contributing to increased skeletal muscle mass4

  • animalWestern blot analysis showed significantly reduced level of Smad2 phosphorylation in skeletal muscle tissue of transgenic pigs4

  • animalWestern blot analysis showed increased level of Akt phosphorylation in skeletal muscle tissue of transgenic pigs4

  • animalFollistatin (FS), a monomeric glycoprotein which specifically binds activin, is expressed in many tissues7

  • animalFS mRNA 344 levels in the kidney showed a profound increase from the day of birth to adulthood7

  • animalFS mRNA 344 levels in the muscle peaked during the infantile period and then declined7

Show 41 more findings

  • animalBrain cortex, heart and thymus showed tissue specific expression in the steady-state mRNA level of FS during postnatal development7

  • animalNone of the tissues showed a measurable change in the ratio of the mRNA for FS 344 and FS 3177

  • animalFS mRNA 344 levels in male and female kidney were not different7

  • animalThe ontogeny of steady state FS mRNA varies in a tissue specific manner during postnatal development of the rat and may be involved in modulating the outcome of activin7

  • animalFollistatin (FS) or FSH-suppressing protein is a polypeptide which exists in multiple forms and has inhibin-like activity8

  • animalFollistatin mRNA was detected in cerebral cortex, pituitary, adrenal, thymus, pancreas, gut, kidney, heart, uterus, skeletal muscle and lung in addition to ovary and testis8

  • animalTreatment of female rats with combined Pregnant Mare Serum Gonadotropin (PMSG) and human Chorionic Gonadotropin (hCG) increased expression of FS mRNA in the ovary8

  • animalThe mRNA for the precursor of the larger known form of FS (FS 344) is much more abundant than the mRNA for the smaller molecule (less than 5%)8

  • animalStimulation of FS transcription by PMSG and hCG in the ovary does not change the relationship between FS 344 and smaller form mRNA abundance8

  • animalAlternative splicing of the rat FS gene occurs8

  • in vitroAll nine products that contained follistatin had His-tagged FS344 and a high degree of its oligomers3

  • in vitroFollistatin is the specific binding protein of activin5

  • in vitroFollistatin has broad tissue distribution and is found in serum5

  • in vitroOvary has the highest level of FS expression but ovariectomy does not cause permanent reduction in serum FS level5

  • in vitroEndothelial cells from blood vessels express FS messenger RNA and protein5

  • in vitroFS steady state levels in aortic endothelial cells decreased with time in culture5

  • in vitroFS mRNA levels in aortic endothelial cells increased approximately 20-fold within 4 hours during incubation with 100 nM phorbol 12-myristate, 13-acetate5

  • in vitro0.5 nmol/ml forskolin had no significant effect on FS mRNA levels in aortic endothelial cells5

  • in vitro0.1 microM ocadaic acid caused significant increase in FS mRNA levels5

  • in vitroFS mRNA levels in aortic endothelial cells were not significantly affected by various concentrations of porcine FSH, epidermal growth factor, or retinoic acid5

  • in vitroTreatment with 0.01-10 micrograms/ml bacterial lipopolysaccharides caused dose-dependent increase up to 10-fold in FS mRNA steady state level5

  • in vitro1-1000 nM RU 28362 synthetic glucocorticoid inhibited FS mRNA steady state levels in dose-dependent manner5

  • in vitro100 nM RU 28362 completely blocked induction of FS mRNA with 1 microgram/ml LPS5

  • in vitroStimulatory effects of LPS were visible after 4 h of treatment but not after 24 or 48 h5

  • in vitroFS proteins were secreted into culture medium upon stimulation with LPS5

  • in vitroTreatments did not have obvious effect on ratio of two different forms of FS mRNA (FS 344:FS 317)5

  • in vitroFS mRNA is expressed in uncultured plexus choroideus epithel and meninges5

  • in vitroFS protein is found in human cerebrospinal fluid5

  • in vitroEndothelial cells produce and secrete FS protein and are a likely source of FS in serum5

  • in vitroTreatment of cultured rat renal mesangial cells with epidermal growth factor (10 nM) caused an 8- to 9-fold increase in follistatin mRNA level after 4 h6

  • in vitroBasic fibroblast growth factor (0.28 or 0.56 nM) showed no consistent change in follistatin mRNA levels after treatment for between 4 and 48 h6

  • in vitroSomatostatin (3.7-73 nM) showed no consistent change in follistatin mRNA levels after treatment for between 4 and 48 h6

  • in vitroFollistatin itself (0.29 nM) showed no consistent change in follistatin mRNA levels after treatment for between 4 and 48 h6

  • in vitroRetinoic acid significantly increased follistatin steady state mRNA level at 3 nM, and at 1000 nM stimulated follistatin mRNA up to 5-fold within 4 h6

  • in vitroProstaglandin E2 (30 microM) for 4 h caused a 10-fold increase in follistatin mRNA level6

  • in vitroPhorbol 12-myristate, 13-acetate (100 nM) increased follistatin mRNA level 3-fold within 4 h6

  • in vitroForskolin (25 microM) increased follistatin mRNA level 4-fold within 4 h6

  • in vitroRU 28362 synthetic glucocorticoid (100 nM) caused a 5- to 6-fold increase in follistatin mRNA level6

  • in vitroProgesterone (1000 nM) increased follistatin mRNA level up to 3.5-fold above control6

  • in vitroNone of the tested hormones had an obvious effect on the ratio of the two different forms of follistatin mRNA (FS 344:FS 317)6

  • expert opinionFollistatin is a myostatin-inhibiting protein3

Dosing

Based on 1 human study finding.

  • human studyAll patients injected complete 1 mg vials of follistatin-344 subcutaneously in the abdomen1

Safety and side effects

Based on 3 human study findings, 2 animal findings, 2 in vitro findings, 2 expert opinion findings and 1 theoretical finding.

  • human studyFollistatin-344 injection can be considered as a risk factor for central serous chorioretinopathy (CSCR)1

  • human studyIn patients with a history of only one follistatin-344 injection, subretinal fluid completely disappeared after an average of 2.3 ± 0.7 months and symptoms regressed1

  • human studyRecurrent CSCR developed in patients with a history of multiple follistatin-344 injections1

  • animalNo cardiac muscle hypertrophy was observed in transgenic pigs expressing muscle-specific Fst4

  • animalNo reproductive abnormality was observed in transgenic pigs expressing muscle-specific Fst4

  • in vitroOnly 9 of 17 tested black market follistatin 344 products actually contained follistatin3

  • in vitroSome black market products labeled as follistatin contained other growth promoting peptides (e.g. MGF, GHRP-2) instead3

  • expert opinionRigorous human safety data for unapproved peptides including FS-344 are scarce9

Show 2 more findings

  • expert opinionThere is potential for serious harm to patients from unapproved peptides like FS-3449

  • theoreticalFollistatin is prohibited according to chapter S4 of the WADA 2019 List of Prohibited Substances and Methods3

What people use it for

Based on 1 human study finding and 3 expert opinion findings.

  • human studyHigh-dose subcutaneous follistatin-344 injections are used by bodybuilding athletes as a performance and image enhancing drug to increase muscle mass1

  • expert opinionNo approved pharmaceutical formulations of follistatin are currently available3

  • expert opinionFS-344 (follistatin-344) is an unapproved peptide marketed direct to patients9

  • expert opinionFS-344 is utilized in sports medicine for tissue repair and athletic performance9

Other findings

Based on 1 in vitro finding.

  • in vitroDetection method based on immunomagnetic purification followed by SDS-PAGE and Western blotting can differentiate FS344 from endogenous follistatin due to His-tags3

Points of contention

Where the evidence is unsettled, thin, or says less than the popular claim — worth knowing before you draw conclusions.

Limited evidence

Human efficacy evidence is limited to tiny gene-therapy trials, not injectable peptide

The strongest human data come from two small open-label AAV1-FS344 gene therapy trials (Becker muscular dystrophy n=6; sporadic inclusion body myositis n=6), totaling fewer than 50 human subjects. No randomized, placebo-controlled trials of injectable Follistatin-344 peptide exist, and there are no published human Phase 1 or clinical pharmacokinetic data for the injectable peptide. Gene therapy produces sustained expression, unlike the short half-life of injected peptide.

Contested

Sources disagree substantially on injectable follistatin half-life

Reported plasma half-life estimates for injectable follistatin peptide range widely: native follistatin ~4 min initial/~130 min terminal (Follistatin: 38 Studies Reviewed (2026) | PepCodex); minutes to ~1 hour for FS-315 (Follistatin-344 Peptide Guide 2026: Myostatin Inhibitor); roughly 90 minutes (Follistatin 344 — Independent peptide research & reviews); 2-3 hours (Follistatin 344 Dosage for Bodybuilding: Protocols and); and 3-4 hours (Follistatin 344 Dosage Guide: How Much Should You Take? (2026)). Several sources describe half-life only vaguely as 'minutes to hours.'

Contested

Sources disagree on whether the FS-344 precursor matures into FS-315 or into FS-288.

Several sources state that the 344-residue precursor, after removal of the 29-amino-acid signal peptide, yields the mature 315-amino-acid circulating isoform FS-315, with FS-288 arising instead from a separate (FS-317) transcript (Follistatin-344 (FST-344): Research Evidence & Safety Profile | PeptideInsight; Follistatin-344: Myostatin Inhibitor Research Guide). One source reverses this, stating that the FS-344 transcript, after signal-peptide cleavage and C-terminal proteolytic trimming, gives rise to the FS-288 mature protein, while FS-315 derives from the FS-317 transcript (Follistatin-344 Peptide Guide 2026: Myostatin Inhibitor). Sources also vary on which isoform circulates more freely versus binds cell surfaces: some describe FS-315 as the freely circulating form and FS-288 as cell-surface bound (PeptideInsight), while others describe FS-344 itself as the freely circulating, low-cell-surface-binding form (Follistatin 344: Myostatin Pathway Research and the Gene Therapy Evidence · Peptides:Enhanced; Follistatin 344 — Independent peptide research & reviews), and one describes the 344 isoform as tissue-retained with FS-288 circulating more freely (Follistatin-344: Myostatin Regulation & Muscle Signaling).

Contested

Reported myostatin binding affinity (Kd) varies by more than an order of magnitude

Myostatin binding affinity is reported as Kd = 915 pM (Follistatin 344 Dosage for Bodybuilding: Protocols and), Kd ≈ 0.5-1.0 nM (Follistatin 344 Dosage Guide: How Much Should You Take? (2026)), and Kd ~5.84 x 10^-10 M i.e. ~584 pM (Follistatin-344: Remove the Brake on Muscle (2026)). Activin A binding is separately reported at Kd ~45 pM (Follistatin: 38 Studies Reviewed (2026) | PepCodex).

Limited evidence

Dosing protocols are anecdotal or vendor-derived, not clinically validated

All specific injectable dosing guidance (e.g., 50-200 mcg, 100 mcg/day, 200-300 mcg 3x weekly, bioavailability percentages, injection specifics) comes from community protocols, vendor suggestions, or expert-opinion blog content, explicitly noted as not supported by published clinical trials. The degree of myostatin inhibition achieved through brief subcutaneous exposure is unknown.

Limited evidence

Ocular harm evidence is from a single case series of high doses

The central serous chorioretinopathy (CSCR) safety signal derives from a single 2020 case series of 11 male bodybuilders using high doses (typically full 1 mg vials, or 500-1000+ mcg 3-4x weekly), far above community-suggested doses. This is observational and cannot establish incidence rates.

Limited evidence

Extreme muscle-growth figures come from transgenic/gene-therapy animal models, not peptide injection

Dramatic muscle mass increases (194-327% in transgenic mice, 2-3x doubling, >20% with single AAV dose lasting 2 years, transgenic pig gains) were produced by genetic overexpression or AAV gene therapy — sustained expression models — not by exogenous injectable peptide administration, which sources note has very different pharmacokinetics.

Single source

Some pharmacokinetic and mechanism details rest on a single low-tier source

Specific bioavailability figures (85-90% SC, 75-80% IM, <5% oral) appear only in Follistatin 344 Dosage Guide: How Much Should You Take? (2026), and theoretical anti-inflammatory/wound-healing/GI use cases appear only in Follistatin 344 (FST344 / Myostatin Inhibitor) — Dosing, Side Effects, FDA Status & Research | PeptIQ | PeptIQ. Both are tier-3 web sources labeled expert_opinion or theoretical.

Using it with other compounds

Check a stack
  • MOTS-cSame downstream effect

    Worth caution

    MOTS-c is reported to regulate myostatin through a CK2-PTEN-mTORC2-AKT-FOXO1 axis, converging on the same muscle-limiting signal that Follistatin neutralizes directly. Both also add metabolic/anti-inflammatory benefits, so they may reinforce each other on body composition, though this convergence is only weakly characterized.

    Tier 4Theoretical — not established
    What the research doesn't establish
    Follistatin-344 acts directly on myostatin/GDF-8, sequestering the ligand and blocking SMAD2/3 signaling; MOTS-c has no comparable direct action, and its influence on myostatin—if any—would be indirect via a CK2-PTEN-mTORC2-AKT-FOXO1 route that is not established as a primary mechanism. Their anti-inflammatory effects also arise through different pathways (TGF-beta antagonism versus Keap1-Nrf2 and AMPK), so a shared muscle-limiting target is not demonstrated.

    Shares anti inflammatory

  • SermorelinComplementary

    May be complementary

    Sermorelin boosts the body's own GH/IGF-1 output to support lean mass, whereas Follistatin drives hypertrophy by neutralizing myostatin. Different upstream mechanisms converge on the same goal of building muscle, so they complement rather than duplicate each other.

    Tier 4Theoretical — not established

    Shares protein synthesis · IGF1 signaling

  • TesamorelinComplementary

    May be complementary

    Tesamorelin raises GH/IGF-1 and preferentially strips visceral fat, while Follistatin adds muscle mass and reduces adiposity by blocking myostatin. Their combined effect leans toward improved body composition (more lean mass, less fat) through distinct pathways.

    Tier 4Theoretical — not established

    Shares IGF1 signaling

  • MK-677Complementary

    May be complementary

    MK-677 elevates GH/IGF-1 and improves nitrogen balance, supporting protein synthesis from the anabolic-hormone side, while Follistatin releases the myostatin brake. The two attack muscle growth from separate angles, making them additive rather than redundant.

    Tier 4Theoretical — not established

    Shares protein synthesis · IGF1 signaling

  • HexarelinComplementary

    May be complementary

    Hexarelin raises IGF-1 and, notably, suppresses TGF-beta driven fibrosis — overlapping with Follistatin's own anti-fibrotic, muscle-sparing action. One works through GH/IGF-1, the other through myostatin/activin blockade, so they converge on healthier, larger muscle through different routes.

    Tier 4Theoretical — not established

    Shares IGF1 signaling · mTOR PI3K · anti inflammatory

  • KlothoSame downstream effect

    No documented conflict

    Klotho suppresses TGF-beta/SMAD2/3 signaling to curb fibrosis, and Follistatin also acts as a TGF-beta superfamily antagonist that inhibits the SMAD2/3 cascade and reduces muscle fibrosis. They arrive at the same anti-fibrotic downstream endpoint from different upstream targets.

    Tier 4Theoretical — not established

    Shares anti inflammatory · IGF1 signaling

  • TB-500Complementary

    No documented conflict

    TB-500 promotes tissue repair, angiogenesis and matrix remodeling, while Follistatin reduces muscle fibrosis and inflammatory infiltration and drives hypertrophy. Different mechanisms both favoring healthier muscle/soft-tissue recovery, so they can be viewed as complementary repair agents.

    Tier 4Theoretical — not established

    Shares anti inflammatory · mTOR PI3K

  • CJC-1295Complementary

    Worth caution

    Follistatin-344 builds muscle by blocking myostatin/activin (disinhibiting mTOR/Akt), an entirely different mechanism from CJC-1295's GH/IGF-1 elevation. Both converge on protein synthesis and lean mass, so they can be complementary for body-composition goals via independent pathways.

    Tier 4Theoretical — not established

    Shares protein synthesis · IGF1 signaling

Safety and side effects

Safety and side effects

Regulatory and evidence status. No injectable follistatin product is FDA-approved, and there are no approved pharmaceutical formulations. Injectable peptide forms remain understudied in humans: no published human Phase 1, no published clinical pharmacokinetics, extremely limited human safety data, and no long-term (>2 year) safety data outside the gene-therapy trials. Rigorous safety data for unapproved peptides including FS-344 are scarce, with potential for serious harm.

Documented ocular risk

The most concrete human safety signal is ocular: retinal detachment and central serous chorioretinopathy (CSCR). A 2020 case series documented 11 male bodybuilders (mean age 36.8) who developed CSCR after subcutaneous FS-344 injections of complete 1 mg vials into the abdomen (10 unilateral, 1 bilateral). Doses involved exceeded 500 mcg (500-1000+ mcg), given 3-4 times weekly over 8-12 weeks. In patients with only a single injection, subretinal fluid resolved after an average of 2.3 ± 0.7 months (typical recovery 3-6 months) and symptoms regressed; recurrent CSCR developed in those with multiple injections. Caveat: this is a single observational case series at high doses (far above community-suggested amounts) and cannot establish incidence rates.

Gene-therapy trial safety

In the AAV1-FS344 trials, there was no dose-limiting toxicity, no significant organ changes, no serious adverse events, and no clinically detectable reproductive or endocrine dysfunction over 2-year follow-up. Because follistatin can suppress activin-driven FSH secretion, reproductive endocrine consequences remain a theoretical concern, though the 344 isoform is reported to have less impact on FSH.

Anecdotal side effects

In research settings FS-344 is reported as generally well-tolerated, with anecdotal effects including mild nausea at higher doses, injection-site redness or discomfort, rare dizziness/lightheadedness, and potential effects on blood pressure (single low-tier source).

Product quality and contamination

Grey/black-market products have serious quality-control problems: WADA testing found only 9 of 17 products actually contained follistatin; some were instead other growth-promoting peptides (e.g., MGF, GHRP-2) or contaminated with growth-promoting substances. All nine that did contain follistatin had His-tagged FS344 with a high degree of oligomers. A detection method (immunomagnetic purification + SDS-PAGE + Western blot) can distinguish His-tagged FS344 from endogenous follistatin (detection limits ~0.1 ng/mL in urine, 5 ng/mL in serum).

Anti-doping status

Follistatin-344 is prohibited by WADA at all times under Section S4 (Hormone and Metabolic Modulators), with follistatin-related substances banned in 2019.

Reconstitution and handling

Reconstitution and preparation

No dose has been established for this compound. No regulatory label exists for it, so the figures below are what sources report — not guidance.

Important: No clinically validated or FDA-approved injectable dose exists for Follistatin-344, and there is no data on optimal dosing for recreational or fitness use. All specifics below are drawn from community protocols, vendor suggestions, and expert-opinion/blog content — they are not supported by published clinical trials. The degree of myostatin inhibition achievable through brief subcutaneous peptide exposure is unknown.

Reconstitution

Guidance from low-tier sources recommends reconstituting with bacteriostatic water (avoiding saline, which may cause precipitation), to a concentration of roughly 1-5 mg/mL. Subcutaneous injection is described using 29-31 gauge insulin syringes at 4-6 mm depth and a 45-90° angle. Reconstituted product is stored refrigerated at 2-8°C, with reported stability of 14-28 days after reconstitution.

Reported (anecdotal/vendor) dosing protocols

  • Subcutaneous: 50-200 mcg daily for 10-30 days then cycle off; or 100 mcg/day for 10-30 day cycles (common vendor suggestion 100 mcg/day).
  • Pulse/pre-workout: intramuscular 50-100 mcg on training days only, injected ~30 minutes pre-workout into the target muscle group.
  • One source: research SC dosing starting at 100 mcg once daily, standard 250 mcg once daily.
  • Another source: SC 200 mcg three times weekly (Mon/Wed/Fri) as most commonly reported, 100 mcg starting dose for tolerance, 300 mcg upper range where adverse effects become more prevalent; IM 150-400 mcg; typical hypertrophy research 200-300 mcg SC 3x weekly for 6-8 week cycles.
  • Timing: one source suggests administration 2-3 hours post-exercise to potentially enhance the anabolic window.

Subcutaneous 85-90%, intramuscular 75-80%, intravenous 100%, oral <5% (due to first-pass metabolism and GI proteolytic degradation), with peak concentrations 1-2 hours post-injection.

Context vs. gene therapy

All of the above concerns injectable peptide, which has a very short serum half-life (estimates range from minutes to a few hours across sources). This differs fundamentally from AAV gene therapy, which produces sustained follistatin expression over weeks to months and is responsible for the dramatic muscle-growth figures seen in animal and the small human trials. A transgenic pig study demonstrating large muscle gains modeled an equivalent human dose of ~250 mcg every other day — but achieved via tissue-specific overexpression, not exogenous injection. Ocular (CSCR) risk in the human case series was associated with high doses (full 1 mg vials, 500-1000+ mcg, 3-4x weekly).

Sources

Ordered by evidence quality — the strongest first.

  1. Central serous chorioretinopathy associated with high-dose follistatin-344: a retrospective case series.(opens in a new tab)
    Tier 1PubMed · pubmed.ncbi.nlm.nih.gov · 2020
  2. Long-term enhancement of skeletal muscle mass and strength by single gene administration of myostatin inhibitors(opens in a new tab)
    Tier 2Web · pmc.ncbi.nlm.nih.gov
  3. Detection of black market follistatin 344.(opens in a new tab)
    Tier 2PubMed · pubmed.ncbi.nlm.nih.gov · 2020
  4. The transgenic expression of human follistatin-344 increases skeletal muscle mass in pigs.(opens in a new tab)
    Tier 2PubMed · pubmed.ncbi.nlm.nih.gov · 2017
  5. Production of follistatin in porcine endothelial cells: differential regulation by bacterial compounds and the synthetic glucocorticoid RU 28362.(opens in a new tab)
    Tier 2PubMed · pubmed.ncbi.nlm.nih.gov · 1996
  6. Follistatin steady state messenger ribonucleic acid levels in confluent cultures of a rat renal mesangial cell line are regulated by multiple factors.(opens in a new tab)
    Tier 2PubMed · pubmed.ncbi.nlm.nih.gov · 1992
  7. Rat follistatin: ontogeny of steady-state mRNA levels in different tissues predicts organ-specific functions.(opens in a new tab)
    Tier 2PubMed · pubmed.ncbi.nlm.nih.gov · 1991
  8. Rat follistatin: gonadal and extragonadal expression and evidence for alternative splicing.(opens in a new tab)
    Tier 2PubMed · pubmed.ncbi.nlm.nih.gov · 1990
  9. Safety and Efficacy of Approved and Unapproved Peptide Therapies for Musculoskeletal Injuries and Athletic Performance.(opens in a new tab)
    Tier 3PubMed · pubmed.ncbi.nlm.nih.gov · 2026
  10. Sub-200  fs, 344  MHz mode-locked Tm-doped fiber laser.(opens in a new tab)
    Tier 4PubMed · pubmed.ncbi.nlm.nih.gov · 2020

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