Quick summary
Follistatin-315 is the primary circulating follistatin isoform that neutralizes myostatin and activin A. Overexpression produces 200-300% muscle mass increases in animals; AAV gene therapy is in early clinical trials.
Overview
Follistatin-315 is the primary circulating isoform of follistatin, a glycoprotein that binds and neutralizes members of the TGF-β superfamily, most notably myostatin (GDF-8) and activin A. FST-315 is produced by alternative splicing and accounts for approximately 95% of circulating follistatin. Unlike the tissue-bound FST-288 isoform, FST-315 has lower heparin affinity and acts systemically, making it the dominant endocrine regulator of muscle mass.
Mechanism of action
Follistatin-315 binds myostatin and activin A with nanomolar affinity (Kd ~5–10 nM), forming high-affinity complexes that prevent ligand binding to the ActRIIB/ALK4/5 receptor complex on muscle satellite cells. By blocking myostatin signaling, FST-315 disinhibits Smad2/3-mediated suppression of muscle protein synthesis, promoting myofiber hypertrophy and satellite cell proliferation. It also inhibits activin A signaling in bone, gonads, and brain, producing broader endocrine effects beyond skeletal muscle.
Dosing protocols
| Purpose | Route | Dosage | Frequency | Notes |
|---|---|---|---|---|
| myostatin inhibition research | subcutaneous | 50–200 mcg | daily (limited by ~90 min half-life) |
Dosing information is for educational purposes only. Consult a qualified healthcare professional before using any peptide.
Research summary
Follistatin overexpression in mice produces 200–300% increases in muscle mass without apparent toxicity in early studies. Intramuscular gene therapy with follistatin AAV vectors has been evaluated in Becker muscular dystrophy Phase 1/2 trials (Mendell et al.). Recombinant FST-315 peptide injection studies show shorter-acting effects (~90-minute half-life) vs. gene therapy, limiting practical utility. Research in sarcopenia and metabolic disease is active.[1][2][3][4]
Evidence grading
Each claimed benefit is graded by the strength of available evidence. Grades reflect study quality, not effect size.
Strong = multiple RCTs · Moderate = limited trials or observational · Preliminary = animal or in vitro only · Insufficient = anecdotal or no published data
Side effects
Side effects vary by individual. This is not an exhaustive list. Report unusual symptoms to a healthcare professional.
Common stacks
Peptides commonly paired with Follistatin-315 for synergistic effects.
Legal status
Follistatin-315 is a research peptide, not approved for human use. Gene therapy applications are investigational (IND-stage). Peptide form available from research suppliers; recommended limit ≤200 mcg/day in research protocols.
Sourcing & access
Research compound
Follistatin-315 is classified as a research compound. Regulatory status varies by jurisdiction. Always verify current legal status and source from vendors providing third-party certificates of analysis (COA).
Frequently asked questions
Follistatin-315 is a glycoprotein produced by alternative splicing that accounts for approximately 95% of circulating follistatin. It binds and neutralizes myostatin and activin A, making it the dominant endocrine regulator of muscle mass.
Follistatin-315 binds myostatin and activin A with nanomolar affinity, preventing them from activating the ActRIIB/ALK4/5 receptor complex on muscle satellite cells. By blocking myostatin signaling, it disinhibits Smad2/3-mediated suppression of muscle protein synthesis, promoting myofiber hypertrophy and satellite cell proliferation.
Follistatin-315 is a research peptide with potential side effects including reproductive effects from activin A inhibition, possible joint hypermobility, and injection site reactions. No approved human therapeutic applications exist; gene therapy approaches are in early clinical trials.
While mouse studies show dramatic 200-300% muscle mass increases with follistatin overexpression, recombinant FST-315 peptide injection has limited utility due to its short half-life of approximately 90 minutes. AAV gene therapy vectors delivering follistatin have been evaluated in Phase 1/2 Becker muscular dystrophy trials.
Research references
- Follistatin-315 inhibits activin signaling and promotes muscle hypertrophyPubMed
- Follistatin and myostatin in muscle growth: antagonism and therapeutic potentialPubMed
- Follistatin gene delivery as a therapeutic for muscular dystrophyPubMed
- Follistatin isoform 315 suppresses activin A and enhances skeletal muscle massPubMed