Follistatin-344

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.
• The dramatic muscle results associated with follistatin (e.g. ~15% muscle increase in primates) come almost entirely from GENE THERAPY (sustained AAV expression), not from injecting the peptide. This distinction is the most important thing to understand about it.
• As an injectable peptide it has a short half-life (~90 minutes) and very limited human data — so systemic muscle effects from daily injection are questionable, and likely far more modest than the gene-therapy headlines suggest.

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.

The crucial framing, which this profile foregrounds deliberately: almost all of the impressive evidence is from gene delivery, not from injecting follistatin peptide. It is investigational, not FDA-approved, and WADA-prohibited. Everything below is research context, not medical guidance.

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.

This is the point to internalize before reading any follistatin result. The headline outcomes — ~15% muscle-circumference increase persisting over a year in primates, and 6-minute-walk improvements in Becker muscular dystrophy patients — came from AAV gene therapy, which makes the body produce follistatin continuously. Injecting follistatin peptide is entirely different: with a ~90-minute half-life, levels spike and fall quickly, so sustained muscle effects from daily injection are doubtful. Expect injectable-peptide effects to be far more modest than the gene-therapy literature implies.

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

The short ~90-minute half-life is exactly why injectable follistatin peptide is unlikely to reproduce gene-therapy results, which rely on continuous expression.

There is no established injectable-peptide dosing. The figures below are anecdotal, included for research context only.

• Anecdotal research protocol: ~100 mcg once daily subcutaneously
• Higher anecdotal protocol: ~200 mcg/day (treated as a ceiling)
• No established timing; the short half-life means effects likely don't persist between daily doses
• Never exceed ~200 mcg/day — a vision-impairment case was reported at a 1 mg single dose (~10× this)

• Handle gently — at ~38 kDa it can denature. Add sterile or bacteriostatic water slowly down the vial wall; swirl gently, NEVER shake; discard if cloudy.
• Store lyophilized at −20°C. Reconstituted protein is fragile: refrigerate at 2–8°C, use within ~7 days, and never freeze.
• High counterfeit potential — third-party testing is essential.

Most safety data comes from gene therapy, not injectable peptide — BMD gene-therapy trials reported no serious adverse events and normal hormones. Documented or theoretical concerns include possible FSH suppression (affecting reproductive function), a minor LDL increase (~8 mg/dL) in some subjects, and — with chronic broad TGF-β inhibition — theoretical risks to bone density and organ fibrosis. A central serous chorioretinopathy (vision impairment) case occurred at ~10× the typical dose. Avoid with active cancer (growth-factor modulation); contraindicated in pregnancy.

• 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.

Note the pattern: the strong outcomes are gene therapy. There is essentially no robust human data for injectable follistatin peptide.

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.