F tier · safety concern
Every human datapoint attached to this name comes from AAV1-delivered FST344 complementary DNA injected into skeletal muscle in two open-label, unblinded, six-patient gene-therapy trials — not from administering a follistatin protein — so the injectable product sold as 'Follistatin-344' has effectively zero human evidence, on top of an unresolved oncology signal in the activin/follistatin axis and a molecule that cannot credibly be supplied by standard peptide synthesis.
follistatin-344
FST344 is the 344-residue precursor transcript of human follistatin, a secreted glycoprotein that binds and neutralises activin A and myostatin; after cleavage of its signal peptide it yields the mature FS-315 form. The only human data are two small open-label AAV1 gene-therapy trials in Becker muscular dystrophy and sporadic inclusion body myositis, in which the FST344 gene — not a protein product — was injected into quadriceps muscle.
// we supply this one
available as a research reagent
≥ 95% (SDS-PAGE) · lyophilised powder · batch certificate published. Grade F above is our own and is not adjusted because we stock it.
the explanation
Follistatin is a natural protein that blocks the signals telling muscle to stop growing, and a gene-therapy version has been injected into the thigh muscles of a handful of patients with muscle-wasting diseases. That is a completely different thing from the vial sold as 'Follistatin-344' — no one has ever run a human trial of injecting the protein, and a 38,000-dalton sugar-coated protein is not something a peptide lab can simply make.
regulatory status
No approved product in any jurisdiction; the only human exposure has been experimental AAV gene therapy under IND
Follistatin has never been approved as a therapeutic protein anywhere, the human trials were investigational gene-therapy studies of rAAV1.CMV.huFS344, and follistatin falls within WADA's S2.3 prohibition on 'other growth factors or growth factor modulators affecting muscle, tendon or ligament protein synthesis/degradation' — meaning the substance sold under this name is simultaneously unapproved, untested as a protein, and banned in sport.
how it works · proposed mechanism
Follistatin works by mopping up TGF-beta superfamily ligands, which is why its effects are broad, systemic and not confined to muscle.
Activin and myostatin sequestration
Follistatin is a single-chain glycosylated protein whose primary function is binding and neutralising activin family ligands, including myostatin (GDF-8). Removing the myostatin brake on the SMAD2/3 pathway permits satellite-cell activation and muscle hypertrophy.
344 is a precursor, not a product
The 344-residue sequence includes a 29-residue signal peptide that is cleaved during secretion; the biologically relevant circulating species are FS-315 and FS-288. A vial labelled 'Follistatin-344' is therefore already ambiguous about what molecule it is supposed to contain.
Gene therapy, not protein injection
All human and primate efficacy data come from an AAV1 vector carrying the FS344 complementary DNA injected directly into muscle, producing sustained local expression from transduced myofibres. Injecting a recombinant protein systemically is a fundamentally different pharmacology with different distribution, half-life and immunogenicity.
Systemic activin blockade is not muscle-specific
Activin signalling regulates reproduction, inflammation, wound healing and epithelial growth control. Follistatin is described in the oncology literature as a potential therapeutic target in prostate cancer, with proposed roles in malignant progression and bone metastasis — the same axis, read from the other direction.
what’s reported
evidence shape
6 sourcesThe composition of the cited literature by study type. This describes the shape of the evidence, not its quality — and it does not by itself set the grade.
⚠ the catch
The two human trials people cite are open-label, placebo-free, six-patient studies of a viral vector delivering the follistatin gene into quadriceps muscle — a one-time surgical-grade gene therapy administered under an IND, which has no bearing on the safety or efficacy of a lyophilised vial injected subcutaneously. Compounding that, mature follistatin is a roughly 38 kDa glycosylated protein whose activity depends on correct folding and glycosylation, which standard solid-phase peptide synthesis cannot produce, so the identity and bioactivity of grey-market 'Follistatin-344' is unverifiable in principle rather than merely unverified in practice.
key published findings
- Human phase 1/2a trial (Mendell 2015, Molecular Therapy, n=6 Becker muscular dystrophy, open-label, no placebo): bilateral intramuscular quadriceps injection of AAV1.CMV.FS344 at 3 x 10^11 vg/kg/leg (cohort 1, n=3) and 6 x 10^11 vg/kg/leg (cohort 2, n=3); six-minute walk distance improved by +58 m, +125 m, +108 m and +29 m in four patients with no change in two; follow-up 1 year (cohort 1) and 6 months (cohort 2); no adverse effects encountered.
- Human trial (Mendell 2017, Molecular Therapy, n=6 sporadic inclusion body myositis, rAAV1.CMV.huFS344 into quadriceps, compared with 8 matched untreated controls): annualised six-minute walk change of +56.0 m/year in treated subjects versus -25.8 m/year in controls; four treated patients gained 58-153 m and two gained only 5-23 m; muscle biopsy showed decreased fibrosis and improved regeneration — but the comparison group was a non-randomised matched cohort, not a blinded placebo arm.
- Nonhuman primate (Kota 2009, Science Translational Medicine, cynomolgus macaques): AAV1-FS344 injected into quadriceps 'induced pronounced and durable increases in muscle size and strength' with no abnormal changes in the morphology or function of key organs — again, vector-delivered gene expression rather than protein administration.
- Protein identity (UniProt P19883, FST_HUMAN): the canonical 344-residue follistatin entry is 38,007 Da and is annotated as a precursor including the signal peptide; the mature secreted isoforms are FS-315 and the alternatively spliced FS-288, so 'Follistatin-344' names a precursor rather than a defined circulating therapeutic species.
- Oncology (Sepporta 2013, Targeted Oncology): follistatin, described as 'a single-chain glycosylated protein whose primary function consists in binding and neutralizing' activins, is reviewed as a potential therapeutic target in prostate cancer with proposed involvement in malignant progression and bone metastasis formation — evidence that systemic manipulation of this axis has consequences beyond skeletal muscle.
limitations of the evidence
- There is no published pharmacokinetic, bioavailability or dose-response data for administered follistatin protein in humans by any route — the field's entire human dataset is gene-therapy delivery.
- Both human trials were open-label with a total of twelve subjects and no blinded placebo control; the sIBM comparison used matched untreated patients rather than randomisation, so functional gains cannot be separated from expectancy, physiotherapy or selection effects.
- The oncology literature on the follistatin/activin axis is genuinely bidirectional — follistatin antagonism of activin A inhibits proliferation in some tumour models while follistatin is implicated in progression in others — so the net risk of chronic systemic follistatin elevation in humans is unknown rather than reassuring.
- Systemic long-term consequences of activin blockade on reproduction, inflammation and epithelial homeostasis have not been characterised in any human study.
documented safety signals
- Follistatin is implicated in prostate cancer progression and bone metastasis formation in the targeted-oncology literature, and the activin pathway it neutralises has tumour-suppressive functions in several epithelia — an unresolved bidirectional cancer signal for chronic systemic blockade.
- Activin and myostatin signalling regulate reproductive function, inflammation and wound healing; no human study has characterised the consequences of sustained systemic antagonism.
- Product identity is unverifiable by design: mature follistatin is a ~38 kDa glycosylated protein requiring eukaryotic expression and correct disulfide folding, which cannot be produced by the solid-phase synthesis used for the peptides sold alongside it.
- The only human safety data are 'no adverse effects encountered' in twelve patients receiving a single intramuscular gene-therapy dose under an IND with formal monitoring — a dataset that transfers to nothing about repeated grey-market injection.
identity
| full name | Follistatin isoform FST344 (344-residue precursor of the secreted FS-315 glycoprotein) |
| category | Growth Hormone |
| modality | protein hormone |
| molar mass | 38007 g/mol |
laboratory handling
| storage | As a recombinant glycoprotein, lyophilised material is stored at -20 °C to -80 °C, desiccated and protected from light, and reconstituted solution is kept at 2-8 °C only briefly or aliquoted and held at -80 °C; freeze-thaw cycling is avoided because large multi-domain proteins aggregate and lose activity readily. |
| solubility | Reconstituted in sterile water or phosphate-buffered saline at neutral pH, typically with a carrier protein such as bovine serum albumin added in laboratory use to prevent adsorptive loss at low concentrations. |
Handling information describes laboratory practice for a research reagent. It is not a preparation guide for use in humans.
the receipts
6 citedUniProt Knowledgebase, EMBL-EBI / SIB / PIR · 2025 · official
World Anti-Doping Agency · 2026 · official
Molecular Therapy · 2015 · peer-reviewed
Molecular Therapy · 2017 · peer-reviewed
Targeted Oncology · 2013 · review
Science Translational Medicine · 2009 · preclinical
others in Growth Hormone