Follistatin-315
The full-length follistatin found in human blood: it keeps an acidic tail that weakens its grip on cell surfaces, so it circulates while the shorter FS288 stays tissue-bound.
The 315-residue form of follistatin that circulates in human serum. Its acidic 26-residue C-terminal tail, absent from the shorter FS288, lowers its binding to cell-surface proteoglycans (FS288 > FS303 > FS315), which is why FS315 is the soluble form; it is what the FS344 precursor becomes once its signal peptide is removed.
Mechanism of action
Binds and neutralises activin and related TGF-beta family ligands, including myostatin. In laboratory comparisons it bound activin A less tightly than FS288 (Kd about 432 against 46.5 pM) and inhibited activin signalling less potently; structural work shows both isoforms bind activin in a similar way.
Primary uses
- Muscle biology research
- Activin and reproductive biology research
- Sold online, usually as FS344, which becomes FS315 once processed
Typical dosing
No validated human dosing. Community sourcing typically does not verify which isoform is actually supplied.
Regulatory status
Not approved anywhere. Products sold online as follistatin are usually labelled FS344; a 2019 analysis found only 9 of 17 contained follistatin at all. Follistatin is prohibited in sport under WADA S4.
Status as of this entry's last review, October 4, 2026. Approvals, compounding rules and sport rules change; the regulatory tracker is checked more often.
What we checked
No product called follistatin-315 has been tested in people, but the isoform itself is well described in the laboratory. This section records what can be checked: what FS315 is, how it differs from the other forms, its status on the date below, and every search we ran.
Identity, computed
| Type | Protein, not a peptide: the 315-residue full-length follistatin isoform, a glycoprotein of about 35 kDa |
| Precursor | FS344, which includes a 29-residue signal peptide removed before secretion |
| Other forms | FS288 (alternative splicing, no C-terminal tail) and FS303 (tail partly cut) |
The isoform names count amino acids. FS315 keeps an acidic 26-residue tail at its C-terminus; FS288 lacks it; FS303 is presumably made by cutting the tail (Schneyer et al., 2004). An earlier version of this entry had this backwards, describing FS315 as the shorter, more tissue-bound form; it was corrected on October 4, 2026.
Regulatory status, read October 5, 2026
Drugs@FDA: 0 records for “follistatin”. EMA medicines list: 0 records for “follistatin”. Run for semaglutide, the same queries return 6 and 5 records (and the registry search 84 trials), so a zero here is an absence, not a broken search. WADA 2026: section S4.3; WADA 2027: section S4.3.
What the maker or sellers claim
Claim, from research-chemical sellers: follistatin builds muscle by blocking myostatin and is sold as 315 or 344. A 2019 analysis of 17 products labelled follistatin 344 found follistatin in only nine, all carrying an artificial His tag, and other growth-promoting peptides in some of the rest (Reichel et al., 2019).
How FS315 differs from FS288
The tail changes where the protein goes. Binding to cell-surface proteoglycans ranks FS288 > FS303 > FS315, so FS288 sticks to tissue and FS315 circulates; an FS315-specific immunoassay confirmed it as the main form in human serum (Schneyer et al., 2004). In laboratory tests FS315 bound activin A about nine times less tightly than FS288 and inhibited activin signalling less potently (Hashimoto et al., 2000), although the crystal structure of the FS315-activin A complex shows both bind activin in a similar way (Lerch et al., 2007).
The only human data involve the gene, not the protein. In a gene-therapy trial in men with Becker muscular dystrophy, the FS344 gene was injected into leg muscles so the body would make FS315; it was chosen partly because FS315 binds activin less strongly than FS288 and so should disturb the pituitary hormone FSH less (Al-Zaidy et al., 2015). That is gene transfer under specialist care, not an injection of follistatin protein.
What we looked for and did not find
No trial giving follistatin protein, of either isoform, to people; no pharmacokinetic data; no regulator record. The registered human trials deliver the follistatin gene, mostly FS344, or measure natural follistatin in blood. Follistatin is prohibited in sport under WADA section S4.
| Source | Query | Results, October 5, 2026 | What it was |
|---|---|---|---|
| PubMed | FS315 follistatin | 15 | isoform biochemistry and the gene-therapy review |
| PubMed | follistatin 344 | 21 | |
| PubMed | follistatin black market | 3 | the 2019 product analysis |
| ClinicalTrials.gov | follistatin | 13 | 5 gene-therapy trials (AAV or plasmid FS344, some with klotho or VEGF); the rest measure follistatin levels |
| Drugs@FDA (openFDA) | follistatin | 0 | |
| EMA medicines list | follistatin | 0 |
References
- [pubmed] Sugino K, et al. "Molecular heterogeneity of follistatin, an activin-binding protein: higher affinity of the carboxyl-terminal truncated forms for heparan sulfate proteoglycans on the ovarian granulosa cell." J Biol Chem, 1993;268:15579-15587. PMID: 8340384.
- [pubmed] Schneyer A, et al. "Differential distribution of follistatin isoforms: application of a new FS315-specific immunoassay." J Clin Endocrinol Metab, 2004;89:5067-5075. PMID: 15472207.
- [pubmed] Hashimoto O, et al. "Difference between follistatin isoforms in the inhibition of activin signalling: activin neutralizing activity of follistatin isoforms is dependent on their affinity for activin." Cell Signal, 2000;12(8):565-71. PMID: 11027950.
- [pubmed] Lerch TF, et al. "Structural and biophysical coupling of heparin and activin binding to follistatin isoform functions." J Biol Chem, 2007;282(21):15930-9. PMID: 17409095.
- [pubmed] Reichel C, et al. "Detection of black market follistatin 344." Drug Test Anal, 2019;11(11-12):1675-1697. PMID: 31758732.
- [pubmed] Al-Zaidy SA, et al. "Follistatin Gene Therapy Improves Ambulation in Becker Muscular Dystrophy." J Neuromuscul Dis, 2015;2(3):185-192. PMID: 27858738.
Related peptides
Guides & tools
This entry is for educational purposes only and does not constitute medical advice. Dosing information reflects published regulatory or research data and is not a recommendation. Many compounds described here are not approved for human use in the United States. Consult a licensed medical professional before considering any peptide therapy.