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Follistatin-344

Also known as FST-344, FS-344, follistatin 344 isoform, FST344

A 344-residue follistatin precursor protein that binds myostatin and activin; sold as an injectable with no human data.

early-clinical Recovery & tissue research chemical

At a glance

Category
Recovery & tissue
Status
research chemical
Made from
recombinant A recombinant glycoprotein expressed in cultured cells; it is not a chemically synthesised peptide.
Route
In trials: intramuscular gene transfer. Grey-market use is subcutaneous or intramuscular injection of protein.
Half-life
Circulating follistatin is cleared rapidly, on the order of minutes to a few hours depending on isoform and glycosylation. There is no published pharmacokinetic study of injected recombinant FST-344 in humans.
Onset
In the Becker muscular dystrophy gene therapy trial, functional outcomes were assessed over 6-12 months of follow-up - one year for the first cohort and six months for the second 3
Molecular weight
approximately 38 kDa for the unglycosylated 344-residue chain; the glycosylated protein is heavier and heterogeneous
Sequence
344-amino-acid glycoprotein - a precursor isoform, not a synthetic peptide. It is post-translationally processed to the 315-residue circulating form (FST315). The alternative precursor of 317 residues yields the heparin-binding, cell-surface-associated FST288.

Not approved for human use anywhere. Follistatin has been administered to humans only as a gene therapy (AAV1.CMV.FS344) delivered by intramuscular injection in small open-label academic trials 12, never as an injected protein. The material sold online is a recombinant protein of unverified identity and purity.

Doping status: Prohibited. Myostatin-binding proteins including follistatin are named under WADA S4.3 (agents preventing activin receptor IIB activation).

Checked against the WADA 2026 Prohibited List. For a specific product and country, Global DRO is the lookup athletes are expected to use — the List names substances, not brand names.

Correct folding and glycosylation are the hard part of making it, and neither can be judged from a vial label, so grey-market material is of unverifiable identity even when the mass is right.

Mechanism of action

Follistatin is an endogenous secreted glycoprotein that acts as a high-affinity trap for several TGF-beta superfamily ligands. It binds activin A and activin B, myostatin (GDF-8) and GDF-11, physically preventing them from engaging activin receptor type IIB. Because myostatin is the principal negative regulator of skeletal muscle mass, removing it from circulation permits muscle hypertrophy - this is the same node in the pathway that ACE-031 targets, approached from the ligand side rather than the receptor side.

The isoform matters more than the marketing suggests. FST344 is a precursor: it is processed to FST315, the soluble form that circulates bound to alpha-2-macroglobulin. FST288, derived from the shorter precursor, carries a heparin-binding site that anchors it to cell surface proteoglycans, and it is that anchoring that produces localised muscle growth after intramuscular delivery. In a direct test, an FST288 variant lacking the heparin-binding site produced markedly less muscle hypertrophy. Selling 'follistatin-344' for systemic injection therefore chooses the isoform least suited to local muscle action.

The consequence of systemic activin blockade is the safety problem. Activin signalling is not confined to muscle: it participates in reproductive endocrinology (activin regulates FSH secretion), erythropoiesis, inflammation and bone metabolism. Follistatin also has established roles in ovarian function and in the pituitary. A systemic follistatin load is not a muscle-selective intervention, and the endocrine consequences of sustained elevation in humans have not been characterised.

There is a further oncological consideration. Follistatin is overexpressed in a number of solid tumours and has been discussed as a prognostic marker; activin A is growth-inhibitory in several epithelial tissues, so neutralising it is not obviously benign.

What the research shows

The human evidence for follistatin is real but concerns gene therapy, not an injectable protein. Two small open-label academic trials from Nationwide Children's Hospital delivered the FS344 gene by AAV1 vector into quadriceps muscle and reported functional improvement on the six-minute walk test. There is no published human study of injected recombinant follistatin protein, and no randomised controlled trial of follistatin in any form.

Research in humans

A phase 1/2a trial delivered AAV1.CMV.FS344 by bilateral intramuscular quadriceps injection to six patients with Becker muscular dystrophy 1. Two patients improved by 58 m and 125 m on the six-minute walk test; in the higher-dose cohort two improved by 108 m and 29 m 1. Muscle biopsies showed reduced fibrosis and larger fibre size. A companion trial in six patients with sporadic inclusion body myositis reported a median annualised change of +56.0 m/year in treated subjects against -25.8 m/year in eight matched untreated subjects (p = 0.01) 2. No serious treatment-related adverse events were reported in either. Both were open-label, uncontrolled or historically controlled, and very small.

Animal and lab research

Extensive. Follistatin overexpression, transgenic or AAV-delivered, produces large increases in muscle mass in mice - in some reports substantially exceeding what myostatin knockout alone achieves, which implies that ligands beyond myostatin contribute. Local intramuscular delivery of FST288-based constructs produces hypertrophy confined to the injected muscle.

Caveats. The gap between the evidence and the product is the whole problem. Gene therapy delivers sustained local expression from within muscle fibres; injecting a recombinant protein subcutaneously delivers a transient systemic bolus of a rapidly cleared glycoprotein. Nothing in the trial data supports the latter. Beyond that: the trials were open-label with n=6, an exercise regimen was part of the protocol and the inclusion body myositis paper itself notes a striking difference between exercising and non-exercising participants, and follow-up was short. For the injectable products there is also no verifiable identity or purity: correctly folded, correctly glycosylated 38 kDa recombinant protein is not trivially manufactured, and there is no way for a buyer to confirm what is in the vial.

What it is used for

  • Becker muscular dystrophy 1 and sporadic inclusion body myositis 2, as intramuscular gene therapy in small open-label academic trials
  • Sold for muscle hypertrophy in bodybuilding, on the strength of the animal overexpression data
  • Occasionally marketed for body composition and fat loss, which the human trial data do not address

Dosing

Dose
Trials: AAV1.CMV.FS344 at 6 x 10^11 vg/kg by intramuscular injection - a gene therapy dose, not translatable to protein. Grey-market protein protocols quote 100 mcg per day.
Frequency
protein protocols quote daily administration
Route
intramuscular gene transfer in trials; subcutaneous protein injection in grey-market use
Duration
protein protocols quote 10-30 day cycles
  • The 100 mcg/day figure has no published origin. No dose-finding study of injected follistatin protein has been conducted in humans or, as far as can be established, in any species.
  • The gene therapy dose cannot be converted into a protein dose. The trial delivered AAV1.CMV.FS344 by ultrasound-guided bilateral injection into three quadriceps muscle groups, at 3 x 10^11 vg/kg per leg in the first cohort and 6 x 10^11 vg/kg per leg in the second 3. These are different interventions with different kinetics, different distribution and different durations.
  • Products labelled 'follistatin-344' are recombinant proteins of unverified glycosylation and folding. Bioactivity of such material is not assured by mass alone.

These figures describe what the literature and published protocols report. They are not advice and not a dosing instruction.

Protocols

Phase 1/2a gene therapy trial in Becker muscular dystrophy

published trial

Source: Molecular Therapy, 2015

Single administrationAAV1.CMV.FS344 at 6 x 10^11 vg/kg, by intramuscular injection

This is a one-off gene transfer, not a peptide course. It is listed because it is the only published human follistatin schedule, and because it cannot be converted into a milligram dose of injected protein: the intervention, the kinetics and the duration of exposure are all different.

Grey-market follistatin protein course

user protocol — not validated

Source: Vendor pages for recombinant 'follistatin-344'

This is not a validated schedule. It is a pattern that circulates among users and sellers, reproduced because it is what people actually follow — not because it has been tested. No trial established these doses, this interval or this duration, and nobody is checking what is in the vial. Treat every number below as an assertion, not a finding.

Days 1-10 to 30100 mcg per day subcutaneously
After the coursea break; cycles of 10-30 days are what circulate

The 100 mcg figure has no published origin — no dose-finding study of injected follistatin protein has been conducted in humans or, as far as can be established, in any species. It borrows its credibility from the gene therapy trial above, which was a different intervention entirely.

Schedules are reproduced as their source states them. Units, IU and milligrams explains why the figures are not interchangeable between products.

Reconstitution

Vial sizes
1 mg
Solvent
bacteriostatic water (0.9% benzyl alcohol)
Storage
Reconstituted at 2-8 °C. A 38 kDa glycoprotein is considerably less robust than a short synthetic peptide; no stability data have been published for these products. Lyophilised powder frozen, protected from light.

Worked example

1 mg vial + 2 ml bacteriostatic water = 500 mcg/ml. 100 mcg = 0.2 ml, i.e. 20 units on a U100 insulin syringe.

Do not shake - protein aggregation on agitation is a genuine concern at this size, not a formality. Let the diluent run down the vial wall and swirl very gently. Do not use if the solution is cloudy or contains visible particulates.

Work it out for Follistatin-344

Safety

Side effects

  • The gene therapy trials reported no serious treatment-related adverse events, in six patients each, over limited follow-up - the Becker trial states there were no significant adverse events related to gene transfer 3 - this is reassurance of a very limited kind
  • Theoretical endocrine effects from systemic activin blockade: disturbance of FSH regulation and reproductive hormone balance. Worth noting as a partial counterweight: the Becker trial monitored FSH, LH, oestrogen and testosterone and found no change after localised intramuscular gene transfer 3. That says nothing about a systemic protein load
  • Potential effects on erythropoiesis, given activin's role there
  • Tendon and connective tissue are not strengthened in proportion to rapid muscle hypertrophy; this is a recognised concern with myostatin-pathway agents and has been observed in myostatin-deficient animals
  • No trial of injected recombinant follistatin protein in humans appears in PubMed or ClinicalTrials.gov as of July 2026 - a registry search returns only gene-transfer studies 6 - and the only published human data are the two gene therapy trials 12

Do not use if

  • Active or previous malignancy - follistatin is overexpressed in several solid tumours, including hepatocellular, gastric, prostate, ovarian and lung cancer, and higher expression has been associated with poorer overall survival in gastric, ovarian and lung cancer 4. Neutralising activin A removes a growth-inhibitory signal in epithelial tissue
  • Pregnancy and breastfeeding - follistatin has established roles in reproductive endocrinology and placental biology; absolute contraindication on mechanistic grounds
  • Children and adolescents outside a trial setting
  • Known or suspected disorders of the hypothalamic-pituitary-gonadal axis
  • Competitive athletes under the WADA code: prohibited at all times under S4.3, "Agents preventing activin receptor IIB activation", which names myostatin-binding proteins including follistatin and classes them as non-Specified substances 5

Interactions

Not systematically studied. Mechanistically, follistatin acts on the same pathway as ACE-031, bimagrumab and other activin receptor IIB-directed agents, and combining them would be expected to compound both effect and risk. Effects on gonadotropin regulation could in principle interact with fertility treatments or hormonal therapy. None of this has been studied in humans.

Sources