Follistatin-344

Identity: what FST344 actually means

Follistatin-344 (FST344) is not the name of a standardised short peptide drug. It is the 344-amino-acid precursor encoded by the longer human FST transcript variant (RefSeq NM_013409.3; protein NP_037541.1). UniProt identifies residues 1–29 as a signal peptide. After that signal peptide is removed, residues 30–344 form the 315-amino-acid mature chain, commonly called FS315.

The second major splice form is a 317-amino-acid precursor that yields FS288 after signal-peptide removal. FST344/FS315 and FST317/FS288 are therefore related isoforms, not interchangeable names for one fixed vial product.

Biological role and proposed mechanism

Follistatin is an endogenous extracellular regulatory glycoprotein. It binds several ligands in the transforming-growth-factor-beta superfamily, including activins, myostatin (GDF-8), GDF11 and some BMPs, and can block their access to type-II receptors.

This makes “myostatin inhibitor” directionally useful but incomplete. Follistatin is not myostatin-specific. Its broader ligand binding is relevant both to the experimental rationale and to uncertainty about off-target biological effects. Cell and animal findings showing reduced myostatin signalling or increased muscle mass do not by themselves establish safe or clinically useful muscle growth in humans.

What has been studied in humans

The strongest published human evidence concerns local FST344 gene transfer in neuromuscular disease:

• In a proof-of-principle Becker muscular dystrophy study, six participants received bilateral intramuscular AAV1.CMV.FS344 gene transfer. Four increased their six-minute walk distance and two did not. The study was small, open-label and lacked a randomised control group, so disease variability, training and expectation effects cannot be separated reliably from treatment.
• In sporadic inclusion-body myositis, six treated participants were compared with eight matched untreated participants. The treated group also followed an exercise programme. The reported annualised six-minute-walk difference was encouraging, but the comparison was not randomised or placebo-controlled and is highly vulnerable to selection, exercise and small-sample effects.
• NCT02354781 enrolled only three participants with Duchenne muscular dystrophy. The registry reports no dose-limiting toxicity events, but such a sample cannot establish uncommon or long-term safety. Planned muscle biopsies were cancelled, and the trial cannot establish efficacy.

These studies investigated specific gene-transfer constructs in serious diseases. They are not trials of repeated injections of purified Follistatin-344 protein in healthy people.

What the studies do not establish

The current evidence does not establish:

• reliable hypertrophy, strength or “anti-ageing” benefit in healthy people;
• a dose-response relationship for purified or recombinant Follistatin-344 protein;
• that a commercially sold vial contains human FST344, mature FS315 or a correctly folded and glycosylated bioactive product;
• local-only action after intramuscular administration;
• a 24-hour circulating half-life;
• safe cycling, combination use or laboratory-monitoring rules;
• long-term safety for muscle, tendon, heart, reproductive, endocrine, immune or tumour-related outcomes.

The published patient studies used vector genomes per kilogram or per limb. Those quantities cannot be translated into the source site's 100–200 microgram injection schedules.

Safety and pharmacokinetic limits

The early AAV studies were designed primarily to explore feasibility and safety in small groups. Their reassuring observations are limited by open-label designs, narrow populations and very low participant counts. Gene transfer also creates a different exposure pattern from injected protein: transduced cells may express follistatin over time, while an injected protein would have separate manufacturing, distribution, degradation and immune-response characteristics.

No regulator-approved injectable Follistatin-344 protein label, validated product-specific pharmacokinetic study or generally established clinical half-life was identified. PeptideGuide's “approximately 24 hours” value should therefore not be presented as a human pharmacokinetic fact.

Newer registry entries include a completed 43-participant follistatin-plasmid study without posted results, a recruiting nonviral follistatin-plus-klotho plasmid study, and a recruiting AAV9-follistatin study. These registrations show continuing experimentation; they are not evidence of approval or efficacy, and they remain distinct products with no posted confirmatory results.

Regulatory and anti-doping status

No Follistatin-344 product appears on the FDA's current list of approved cellular and gene-therapy products, and no approved clinical protein regimen was identified. ClinicalTrials.gov registration is not marketing authorisation.

For sport, the distinction is clearer: the 2026 WADA Prohibited List explicitly names follistatin as a myostatin-binding protein under S4.3, Agents preventing activin receptor IIB activation. It is prohibited at all times, in and out of competition. Anti-doping status is separate from medicine approval and from country-specific law.

PeptideGuide claims under review

Bottom line

Follistatin-344 is best understood as a human follistatin precursor and gene-transfer payload, not as a validated short peptide injection. Small early studies provide a human research signal for specific AAV constructs in neuromuscular disease, but they do not validate retail protein identity, bodybuilding effects, microgram dosing, a 24-hour half-life or long-term safety. Any human-use product remains investigational, and use in sport is prohibited under WADA S4.3.