Follistatin-344
FST344 is the 344-amino-acid precursor encoded by one follistatin transcript; after signal-peptide processing it yields circulating FST315. The only human intervention used AAV gene transfer in six men, not injected purified protein.
follistatin precursor or expression-cassette designation
- FST344 precursor yields mature FST315
- FST317 precursor yields mature FST288
- Human trials used AAV-mediated gene transfer
- No direct injected-protein human trial in the cited records
Is Follistatin-344 a mature 344-amino-acid protein?
Usually no. FST344 denotes the precursor encoded by the transcript; removal of its signal peptide yields mature FST315. FST317 similarly yields FST288. A retail label must identify the actual mature sequence, termini, glycosylation, fold, aggregation state, and bioactivity.
| Name | What it denotes | Typical behavior |
|---|---|---|
| FST344 | Precursor coding sequence | Processed to FST315 |
| FST315 | Mature circulating isoform | Lower cell-surface retention |
| FST317 | Alternative precursor | Processed to FST288 |
| FST288 | Mature shorter isoform | Stronger heparan-sulfate and tissue binding |
FST structure · 344-amino-acid precursor
Molecular biology study
Shimasaki S et al. Proceedings of the National Academy of Sciences, 1988.
The cDNA work identified the 344-amino-acid follistatin precursor. Signal-peptide processing produces the mature 315-amino-acid form. The number 344 therefore does not describe the mature circulating protein in a vial.
- Participants / model
- Human cDNA and molecular systems
- Treatment
- Follistatin gene cloning and sequence analysis
- Study design
- Molecular structure study
Isoforms · mature proteins compared
Protein biochemistry study
Inouye S et al. Endocrinology, 1991.
Researchers expressed and compared mature human FST315 and FST288. The forms differed in heparin-binding and biological behavior, supporting the need to distinguish precursor transcript names from mature proteins.
- Participants / model
- Recombinant protein and cell systems
- Treatment
- FST315 and FST288
- Study design
- Protein chemistry and bioactivity comparison
FST315 versus FST288 · circulation and tissue binding
Protein physiology study
Sidis Y et al. Endocrinology, 2005.
The study supports FST315 as the principal circulating form and FST288 as more strongly associated with cell surfaces and tissues. Isoform distribution affects exposure and cannot be treated as cosmetic nomenclature.
- Participants / model
- Experimental protein and tissue systems
- Treatment
- Follistatin isoforms
- Study design
- Isoform-distribution and binding study
Has injected Follistatin-344 protein built muscle in people?
The cited records contain no human trial of purified injected Follistatin-344 protein. The human program used AAV vectors carrying an FS344 gene cassette in muscular dystrophy. Its six-person uncontrolled result does not test retail protein or bodybuilding use.
Why can’t gene-therapy results transfer to a vial?
AAV gene transfer creates sustained local protein expression inside treated muscle and adds vector-specific immune and distribution effects. A purified protein injection has different identity, exposure, duration, and risks.
Six-person gene trial · not protein injection
Phase 1/2a gene-therapy trial
Mendell JR et al. Molecular Therapy, 2015.
Six men received bilateral intramuscular injections of an AAV vector carrying an FS344 expression cassette. Four improved and two did not on six-minute walk distance, with no untreated control group. The intervention causes muscle cells to express follistatin and is not an injection of purified FST344 protein.
- Participants / model
- Six men with Becker muscular dystrophy
- Treatment
- Bilateral quadriceps AAV1.CMV.FS344 gene transfer
- Follow-up
- Six or 12 months of follow-up
- Study design
- Open-label Phase 1/2a gene-therapy study
AAV vector exposure and sustained local expression are fundamentally different from a peptide vial.
Read the original sourceSix-person gene trial · not protein injection
Phase 1/2a gene-therapy trial
Mendell JR et al. Molecular Therapy, 2015.
Six men received bilateral intramuscular injections of an AAV vector carrying an FS344 expression cassette. Four improved and two did not on six-minute walk distance, with no untreated control group. The intervention causes muscle cells to express follistatin and is not an injection of purified FST344 protein.
- Participants / model
- Six men with Becker muscular dystrophy
- Treatment
- Bilateral quadriceps AAV1.CMV.FS344 gene transfer
- Follow-up
- Six or 12 months of follow-up
- Study design
- Open-label Phase 1/2a gene-therapy study
AAV vector exposure and sustained local expression are fundamentally different from a peptide vial.
Read the original sourceClinicalTrials.gov · gene transfer only
Registry record set
ClinicalTrials.gov records.
FST344-relevant ClinicalTrials.gov records used AAV gene transfer or plasmid approaches. They contain no credible human trial injecting purified recombinant Follistatin-344 protein.
- Study design
- Exact-name, isoform, protein, and gene-therapy coverage with intervention classification
Does follistatin only block myostatin?
No. Follistatin binds multiple TGF-beta-family ligands, including activins as well as myostatin. Tissue distribution and isoform strongly affect that biology, so “selective myostatin blocker” is an oversimplification.
Broad ligand binding can affect reproductive, endocrine, inflammatory, vascular, and tissue-remodeling pathways. No product-specific human data quantify cancer or fertility risk.
Isoforms · mature proteins compared
Protein biochemistry study
Inouye S et al. Endocrinology, 1991.
Researchers expressed and compared mature human FST315 and FST288. The forms differed in heparin-binding and biological behavior, supporting the need to distinguish precursor transcript names from mature proteins.
- Participants / model
- Recombinant protein and cell systems
- Treatment
- FST315 and FST288
- Study design
- Protein chemistry and bioactivity comparison
FST315 versus FST288 · circulation and tissue binding
Protein physiology study
Sidis Y et al. Endocrinology, 2005.
The study supports FST315 as the principal circulating form and FST288 as more strongly associated with cell surfaces and tissues. Isoform distribution affects exposure and cannot be treated as cosmetic nomenclature.
- Participants / model
- Experimental protein and tissue systems
- Treatment
- Follistatin isoforms
- Study design
- Isoform-distribution and binding study
What are the material safety unknowns?
Purified-product pharmacokinetics, systemic ligand suppression, immune reactions, fertility, vascular effects, tumor biology, tendon-muscle balance, pregnancy, and repeated-use safety are not established for retail “Follistatin-344.”
The six-person AAV study reported no adverse effects, but it was far too small for uncommon harms and tested a different modality in a severe disease population.
ClinicalTrials.gov · gene transfer only
Registry record set
ClinicalTrials.gov records.
FST344-relevant ClinicalTrials.gov records used AAV gene transfer or plasmid approaches. They contain no credible human trial injecting purified recombinant Follistatin-344 protein.
- Study design
- Exact-name, isoform, protein, and gene-therapy coverage with intervention classification
Six-person gene trial · not protein injection
Phase 1/2a gene-therapy trial
Mendell JR et al. Molecular Therapy, 2015.
Six men received bilateral intramuscular injections of an AAV vector carrying an FS344 expression cassette. Four improved and two did not on six-minute walk distance, with no untreated control group. The intervention causes muscle cells to express follistatin and is not an injection of purified FST344 protein.
- Participants / model
- Six men with Becker muscular dystrophy
- Treatment
- Bilateral quadriceps AAV1.CMV.FS344 gene transfer
- Follow-up
- Six or 12 months of follow-up
- Study design
- Open-label Phase 1/2a gene-therapy study
AAV vector exposure and sustained local expression are fundamentally different from a peptide vial.
Read the original sourceFST315 versus FST288 · circulation and tissue binding
Protein physiology study
Sidis Y et al. Endocrinology, 2005.
The study supports FST315 as the principal circulating form and FST288 as more strongly associated with cell surfaces and tissues. Isoform distribution affects exposure and cannot be treated as cosmetic nomenclature.
- Participants / model
- Experimental protein and tissue systems
- Treatment
- Follistatin isoforms
- Study design
- Isoform-distribution and binding study
Is Follistatin-344 approved?
FDA approval records contain no Follistatin-344 protein product or prescribing label. Investigational AAV trials do not approve a protein vial, and WADA prohibits myostatin-function modifiers for covered athletes.
ClinicalTrials.gov · gene transfer only
Registry record set
ClinicalTrials.gov records.
FST344-relevant ClinicalTrials.gov records used AAV gene transfer or plasmid approaches. They contain no credible human trial injecting purified recombinant Follistatin-344 protein.
- Study design
- Exact-name, isoform, protein, and gene-therapy coverage with intervention classification
WADA 2026 · myostatin inhibitors
Sports rule
World Anti-Doping Agency, effective 1 January 2026.
Myostatin-function modifiers and related agents are prohibited under S4.3 for athletes covered by the Code.
- Study design
- Binding sport rule for covered athletes
Studies and sources
FST structure · 344-amino-acid precursor
Molecular biology study
Shimasaki S et al. Proceedings of the National Academy of Sciences, 1988.
The cDNA work identified the 344-amino-acid follistatin precursor. Signal-peptide processing produces the mature 315-amino-acid form. The number 344 therefore does not describe the mature circulating protein in a vial.
- Participants / model
- Human cDNA and molecular systems
- Treatment
- Follistatin gene cloning and sequence analysis
- Study design
- Molecular structure study
Isoforms · mature proteins compared
Protein biochemistry study
Inouye S et al. Endocrinology, 1991.
Researchers expressed and compared mature human FST315 and FST288. The forms differed in heparin-binding and biological behavior, supporting the need to distinguish precursor transcript names from mature proteins.
- Participants / model
- Recombinant protein and cell systems
- Treatment
- FST315 and FST288
- Study design
- Protein chemistry and bioactivity comparison
FST315 versus FST288 · circulation and tissue binding
Protein physiology study
Sidis Y et al. Endocrinology, 2005.
The study supports FST315 as the principal circulating form and FST288 as more strongly associated with cell surfaces and tissues. Isoform distribution affects exposure and cannot be treated as cosmetic nomenclature.
- Participants / model
- Experimental protein and tissue systems
- Treatment
- Follistatin isoforms
- Study design
- Isoform-distribution and binding study
Six-person gene trial · not protein injection
Phase 1/2a gene-therapy trial
Mendell JR et al. Molecular Therapy, 2015.
Six men received bilateral intramuscular injections of an AAV vector carrying an FS344 expression cassette. Four improved and two did not on six-minute walk distance, with no untreated control group. The intervention causes muscle cells to express follistatin and is not an injection of purified FST344 protein.
- Participants / model
- Six men with Becker muscular dystrophy
- Treatment
- Bilateral quadriceps AAV1.CMV.FS344 gene transfer
- Follow-up
- Six or 12 months of follow-up
- Study design
- Open-label Phase 1/2a gene-therapy study
AAV vector exposure and sustained local expression are fundamentally different from a peptide vial.
Read the original sourceClinicalTrials.gov · gene transfer only
Registry record set
ClinicalTrials.gov records.
FST344-relevant ClinicalTrials.gov records used AAV gene transfer or plasmid approaches. They contain no credible human trial injecting purified recombinant Follistatin-344 protein.
- Study design
- Exact-name, isoform, protein, and gene-therapy coverage with intervention classification
WADA 2026 · myostatin inhibitors
Sports rule
World Anti-Doping Agency, effective 1 January 2026.
Myostatin-function modifiers and related agents are prohibited under S4.3 for athletes covered by the Code.
- Study design
- Binding sport rule for covered athletes
Why is Follistatin-344 in F tier?
F reflects the absence of a human trial for injected purified protein. The only human intervention used AAV gene transfer in six men, which is a different treatment.