Follistatin-344 research

The Follistatin-344 evidence base cited here is 7 sources — 1 clinical, 6 preclinical. Its strongest evidence is human — a clinical study, most recently 2015 ("A phase 1/2a follistatin gene therapy trial for Becker muscular dystroph…"). Regulatory status: Not FDA-approved.

• Follistatin-344 is a large (~38 kDa) glycoprotein — NOT a small peptide — that inhibits both myostatin and activin A, the TGF-β-family signals that normally suppress muscle growth.

Follistatin-344 (FS-344) is a naturally occurring glycoprotein studied for muscle growth and as a therapy for muscular dystrophy. It works by neutralizing the body's brakes on muscle — myostatin and activin A — and in gene-therapy form has produced large, durable muscle gains in animals and meaningful function gains in human muscular-dystrophy trials.

Follistatin-344 is the name of a 344-amino-acid precursor that is cleaved to the circulating FS-315 isoform (~37,800 Da). That makes it a large glycoprotein — orders of magnitude bigger than the small peptides usually discussed in this space (compare BPC-157 at ~1,400 Da). The FS-315 form carries a C-terminal acidic tail that reduces its binding to cell surfaces, keeping more of it circulating.

Its size and fragility matter practically: as a glycoprotein it denatures more easily than a small peptide and behaves differently on handling and clearance.

Follistatin binds and neutralizes myostatin and activin A, preventing them from engaging the ActRIIB receptor on muscle cells. Myostatin and activin A normally activate TGF-β signaling that suppresses muscle growth; by blocking both, follistatin removes that suppression and allows hypertrophy. Inhibiting activin A in addition to myostatin is what makes it potentially more powerful than myostatin-only inhibitors — but also raises broader TGF-β-pathway concerns.

• Time to peak: ~9 minutes
• Half-life: ~1.5 hours (~90 minutes)
• Largely cleared within ~7.5 hours (Datta-Mannan et al., 2013)

• Follistatin gene delivery in nonhuman primates (2009): AAV1-FS344 produced a ~15% muscle-circumference increase by 8 weeks, persisting 15+ months, with no adverse organ effects.
• Phase 1/2a gene therapy for Becker MD (2015): AAV1.CMV.FS344 in 6 patients produced 6-minute-walk improvements up to +125 m, increased fiber diameter, and 35–43% fibrosis reduction, with no serious adverse events.
• Long-term myostatin-inhibitor study (2008, mice): transgenic and AAV approaches produced large muscle-mass increases; FS-344 produced the greatest effect, persisting 2+ years.

Follistatin is not FDA-approved as a peptide therapeutic and is sold for laboratory research only, not intended for human consumption. It has been on the WADA Prohibited List since 2019 — banned for athletes in and out of competition.

All citations link to the original source (PubMed, journal site, or regulatory filing). Independent research database — no vendor influence on what's cited.