Evidence Grade E — Very limited evidence. 5 published studies. 0 registered clinical trials.
Medically reviewed by a licensed medical professional
Follistatin 344 is a natural protein that neutralises the signals limiting muscle growth, including myostatin. Clinical investigation has used gene therapy (viral delivery of the follistatin gene into muscle cells) rather than direct protein injection, because injected follistatin protein is cleared from the body within hours. Small gene therapy trials in muscular dystrophy have shown encouraging results.
Follistatin 344 is also known by these brand and alternate names:
5 published studies: 3 human, 0 animal, 0 in-vitro, 1 reviews
Follistatin 344 has no marketing authorisation as a direct pharmaceutical product. Phase I/II gene therapy trials (AAV1-FS344) in Becker muscular dystrophy (6 patients) and sporadic inclusion body myositis (6 patients) have been conducted, delivering the gene for follistatin via intramuscular viral vector injection. Results showed improvements in walking distance and muscle fibre size.
Direct injection of follistatin protein is pharmacologically challenging due to rapid clearance. The gene therapy approach circumvents this by having muscle cells produce follistatin continuously. Products sold as injectable follistatin through unregulated channels face fundamental pharmacokinetic problems that gene therapy is designed to solve. Products from unregulated sources lack pharmaceutical quality assurance.
Research has established that follistatin works by physically wrapping around and neutralising myostatin (the primary brake on muscle growth) and activin (involved in muscle wasting and inflammation). Two follistatin molecules encircle one myostatin or activin dimer, preventing it from activating its receptors. This ligand-trapping mechanism is well characterised structurally.
Research suggests Phase I/II gene therapy trials (6 patients each in Becker muscular dystrophy and inclusion body myositis) showed improvements in walking distance and muscle fibre size. These are small, open-label studies without randomised controls, and a detailed methodological critique has been published. Direct protein injection faces a fundamental pharmacokinetic problem — approximately 2-hour half-life — that gene therapy is designed to solve. Products sold as injectable follistatin through unregulated channels face this same problem. Research suggests chronic follistatin overexpression may weaken bone. Products from unregulated sources lack pharmaceutical quality assurance.
PeptideTrace tracks 0 registered clinical trials for Follistatin 344 sourced from ClinicalTrials.gov.
No trials registered on ClinicalTrials.gov for this compound.
Follistatin 344 (FS-344) is a 344-amino acid preprotein (315 amino acids mature form after signal peptide cleavage) encoded by the FST gene on chromosome 5q11.2. It is a glycoprotein with a molecular weight of approximately 38 kDa (CAS 80449-31-6, UniProt P19883). The mature protein contains three follistatin domains (FSD1-3), an N-terminal domain, and a C-terminal acidic tail. FS-344 produces the circulating FS-315 isoform, which constitutes approximately 95% of serum follistatin. The half-life of recombinant protein is approximately 2 hours IV, but AAV gene therapy delivery provides months to years of sustained expression. Research suggests follistatin functions as an extracellular ligand trap for TGF-beta superfamily members including activin A, myostatin (GDF-8), and GDF-11.
Research suggests two follistatin molecules encircle one dimeric ligand (activin or myostatin), burying approximately one-third of ligand residues and blocking both type I (ALK4/ALK5) and type II (ActRIIA/ActRIIB) receptor binding sites. Binding affinities include activin A (Kd ~50-680 pM), myostatin (Kd 0.5-12.3 nM), and GDF-11 (similar to myostatin). By preventing Smad2/3 phosphorylation and nuclear translocation, follistatin removes negative regulators of muscle growth, activating the Smad3/AKT/mTOR/S6K signaling axis. The C-terminal acidic tail masks the heparin-binding site in the unbound state, making FS-315 the major circulating isoform. FS-344 was selected for gene therapy due to its approximately 10-fold lower FSH-suppressing potency versus FS-288 (ED50 115.2 pM versus 9.6 pM).
A Phase 1/2a AAV1.CMV.FS344 trial in Becker muscular dystrophy (Mendell et al. 2015, N=6) showed 6-Minute Walk Test improvements of 9-125 meters at 1 year and muscle fiber diameter increase from 40.14 to 59.33 microM (p<0.0001). In sporadic inclusion body myositis (Mendell et al. 2017, N=6 treated vs. N=8 controls), annualized 6MWT change was +56.0 m/year (treated) versus -25.8 m/year (untreated, p=0.01). In transgenic mice, follistatin overexpression produced 194-327% increases in muscle mass, exceeding myostatin knockout alone. No treatment-related adverse events or hormone abnormalities were reported in any human trial (total N=12).
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This content is for informational purposes only and does not constitute medical advice. Always consult a qualified healthcare professional before making decisions about your health.
