Evidence Grade D — Primarily preclinical. 14 published studies, mostly animal models. 0 registered clinical trials.
Medically reviewed by a licensed medical professional
Follistatin 315 is the mature circulating form of follistatin — a natural protein that intercepts signals limiting muscle growth. It is the protein actually produced by the gene therapy approach being tested in clinical trials for muscular dystrophy. As a standalone injectable, it is rapidly cleared from the body, making direct injection impractical. It has no pharmaceutical approval.
Follistatin 315 is also known by these brand and alternate names:
14 published studies: 9 human, 4 animal, 1 in-vitro, 2 reviews
Follistatin 315 has no marketing authorisation. All clinical evidence comes from gene therapy trials described under Follistatin 344 (#141), where FS-315 is the secreted product. Pharmacokinetic studies have confirmed that native FS-315 protein is rapidly cleared from circulation, making direct injection impractical.
This entry should be read in conjunction with Follistatin 344 (#141). The practical limitations of direct protein injection apply even more strongly to this isoform. Products from unregulated sources lack pharmaceutical quality assurance.
Follistatin 315 operates through the same myostatin/activin-trapping mechanism as described for Follistatin 344 (#141). The key distinction is pharmacokinetic: FS-315's C-terminal domain prevents it from binding to cell surfaces when unbound to a ligand, keeping it in systemic circulation as a surveillance molecule for myostatin and activin.
Research suggests follistatin 315 is well-characterised structurally, and its role as the circulating myostatin-trapping isoform is firmly established. However, clinical evidence comes only from gene therapy trials (described under the Follistatin 344 entry), not from direct protein injection. The rapid clearance of the injectable protein is a fundamental pharmacokinetic limitation. As a complex glycoprotein, counterfeit or degraded product risk from unregulated sources is very high. No randomised controlled trials exist for injectable follistatin 315. Products from unregulated channels lack pharmaceutical quality assurance.
PeptideTrace tracks 0 registered clinical trials for Follistatin 315 sourced from ClinicalTrials.gov.
No trials registered on ClinicalTrials.gov for this compound.
Follistatin 315 (FS-315) is the 315-amino acid mature circulating isoform produced from FS-344 after signal peptide cleavage. Its molecular weight is approximately 35 kDa (CAS 80449-31-6, shared with FST gene products). FS-315 is the actual therapeutic protein produced by AAV-FS344 gene therapy. The C-terminal acidic tail (44% acidic amino acids) masks the heparin-binding site in the unbound state, making FS-315 the dominant circulating isoform rather than tissue-bound. When FS-315 binds myostatin, heparin affinity increases, facilitating local clearance via a 'seek and destroy' mechanism. Native FS-315 has rapid clearance (approximately 2-hour half-life in mice), rendering parenteral use impractical.
Research suggests FS-315 operates via the same ligand-trapping mechanism as described for FS-344, since FS-315 is the processed product of FS-344. The critical distinction is pharmacokinetic: FS-315's C-terminal acidic domain prevents cell-surface binding in the unbound state, maintaining it in circulation. By contrast, FS-288 (the tissue-bound isoform lacking this tail) binds cell surfaces with high affinity and has approximately 10-fold higher FSH-suppressing activity. FS-315 blocks the same ActRIIA/ActRIIB to ALK4/ALK5 to Smad2/3 phosphorylation pathway. Engineered variants (FS-EEE-Fc) achieved approximately 100-fold improvement in terminal half-life and 1,600-fold improvement in exposure.
All AAV-FS344 gene therapy clinical data (BMD and sIBM trials under compound 141) produce FS-315 as the secreted therapeutic protein. Pharmacokinetic characterization (Datta-Mannan et al. 2013) confirmed native FS-315 is poorly suited for parenteral administration due to rapid clearance. Nanoparticle mRNA delivery (2018) created hepatic protein reservoirs producing 2.4-fold increased serum follistatin at 8 hours, with approximately 10% higher lean mass after 8 weeks in mice. Acceleron developed ACE-083 (follistatin 291-Fc fusion) for localized intramuscular action, tested in Phase 2 for FSHD and CMT with dose-dependent hypertrophy.
The information on this page is provided for educational and research reference purposes only. This is not medical advice. Always consult a qualified healthcare professional before making any health-related decisions.
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This content is for informational purposes only and does not constitute medical advice. Always consult a qualified healthcare professional before making decisions about your health.
