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Follistatin-315: quick citable summary
Follistatin-315 is listed by PeptaHub as a muscle & growth peptide with a research only legal-status classification. The page summarizes mechanism, research context, common routes, safety notes, and references for writers and AI answer engines.
PeptaHub. “Follistatin-315: Mechanism, Research Context, Safety.” peptahub.com, 2026. https://peptahub.com/peptides/follistatin-315. Licensed CC BY 4.0.
License: Creative Commons Attribution 4.0 International. Link back to https://peptahub.com/peptides/follistatin-315.
What is Follistatin-315?
Follistatin-315 is the primary circulating follistatin isoform that neutralizes myostatin and activin A. Overexpression produces 200-300% muscle mass increases in mice. Note the Becker muscular dystrophy gene-therapy trials used the FST-344 isoform, not FST-315.
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.
Reported study ranges
| Purpose | Route | Reported range | Frequency | Notes |
|---|---|---|---|---|
| myostatin inhibition research | subcutaneous | 50–200 mcg | daily (limited by ~90 min half-life) |
Reported ranges are for research context only. Consult a qualified healthcare professional before using any peptide.
Convert Follistatin-315 research-range units
Need to convert mg to mcg, dose volume, or U-100 syringe units? The Follistatin-315 dose calculator is preloaded with these ranges, or use the general dose unit converter.
Research summary
Follistatin overexpression in transgenic mice produces roughly 200–300% increases in muscle mass, and engineered follistatin improved dystrophic pathology in mdx mice. The clinical data most often cited for "follistatin" is Mendell's phase 1/2a Becker muscular dystrophy trial, but that trial delivered the FST-344 isoform by AAV gene therapy, not the FST-315 isoform this page describes and not a peptide injection; two of six patients improved on the 6-minute walk test. There is no human trial of FST-315 peptide itself. Recombinant peptide delivery is limited by a short (~90 minute) half-life, which is the usual rationale for pursuing gene therapy instead. Research in sarcopenia and metabolic disease is active but preclinical.[1][2][3][4][5]
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 is available from research suppliers. No regulatory or trial-based human dose exists; figures circulating in research communities are not from a published study.
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.
Mouse studies show dramatic 200-300% muscle mass increases with follistatin overexpression, but recombinant FST-315 peptide injection has limited utility due to its short half-life of about 90 minutes, and no human trial of the FST-315 peptide exists. The Becker muscular dystrophy gene-therapy trials that are often cited delivered the FST-344 isoform by AAV, not FST-315 and not a peptide, so they are not direct evidence for this product.
Research references
- Inhibition of myostatin with emphasis on follistatin as a therapy for muscle diseasePubMed
- Follistatin induces muscle hypertrophy through satellite cell proliferation and inhibition of both myostatin and activinPubMed
- Regulation of muscle mass by follistatin and activinsPubMed
- Myostatin and activin blockade by engineered follistatin results in hypertrophy and improves dystrophic pathology in mdx mouse more than myostatin blockade alone (mice)PubMed
- A phase 1/2a follistatin gene therapy trial for Becker muscular dystrophy (used the FST-344 isoform, not FST-315)ClinicalTrials.gov