Follistatin-344
FST-344
Growth Hormone
CAS
100053-10-9
Molecular Weight
37000
Da
Animal / In Vitro
A 344-amino acid glycoprotein that acts as a natural antagonist of myostatin, the body's primary brake on muscle growth. By binding and neutralizing myostatin and activin, Follistatin-344 removes the inhibitory signal on muscle fiber development. Compelling animal data. Early human gene therapy trials for muscular dystrophy. Not approved for general use.
Injectable
Intranasal Suitable
No
Research Compound
Community Signal
Community signal is very thin and dominated by skepticism, Follistatin-344 is heavily marketed in the muscle-building space but lacks the anecdotal depth to match those claims. r/Peptides and r/PEDs threads frequently challenge the bioavailability of injectable Follistatin-344 and question whether sourced product actually contains what it claims. Positive reports exist but are difficult to evaluate given the confounding factor of concurrent anabolic use. The community is more skeptical of this compound than most in the Growth Hormone category. Those who do report positive outcomes are usually in the context of multi-compound stacks where isolation is impossible.
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What It Is
Follistatin-344 is a naturally occurring glycoprotein and one of two main isoforms of follistatin produced through alternative splicing of the FST gene. The 344 designation refers to the 344-amino-acid precursor sequence, which after cleavage of its signal peptide yields the active FS315 isoform. Follistatin was first isolated from ovarian follicular fluid and is known to suppress follicle-stimulating hormone (FSH), but its most researched function in the performance and longevity space is its role as a potent antagonist of myostatin, the primary negative regulator of skeletal muscle growth. Animals and humans with naturally elevated follistatin or loss-of-function myostatin mutations display dramatic muscle hypertrophy, most famously the "double-muscled" phenotype seen in Belgian Blue cattle and a documented case in a human infant. Follistatin also antagonizes activin, another TGF-β superfamily member involved in muscle catabolism and inflammation.
Mechanism of Action
Follistatin functions as a molecular trap rather than a receptor agonist. It binds myostatin (GDF-8) and activin directly in the extracellular space with high affinity, preventing them from reaching their receptor ActRIIB on muscle cells. Without myostatin signaling, the Smad2/3 pathway is not activated, and transcriptional repression of muscle growth genes is lifted. The result is increased muscle protein synthesis, fiber hypertrophy, and potentially hyperplasia (new fiber formation). Satellite cell proliferation, the muscle stem cells responsible for repair and growth, is also enhanced. Follistatin overexpression in animal models increases muscle weight by 20–37% depending on model and delivery method.
Use Cases
In animals, follistatin gene delivery via adeno-associated virus (AAV-FS344) has produced significant and sustained increases in muscle mass and grip strength across mice, aged mdx mice (a muscular dystrophy model), and non-human primates. A landmark review in Muscle & Nerve (2009) documented that AAV1-FS344 increased hindlimb grip strength significantly in aged mdx mice and showed no organ pathology or reproductive effects using the alternatively spliced FS344 construct. The first human clinical trial using AAV-delivered follistatin gene therapy in muscular dystrophy patients has been conducted, representing the most direct human evidence. Bodybuilding and performance communities discuss follistatin peptide injections, but direct injection of the protein is poorly characterized pharmacologically and distinct from gene therapy delivery.
Known Risks
The full-length follistatin protein binds to heparan sulfate proteoglycans on cell surfaces, raising concerns about off-target binding in reproductive tissue and effects on the hypothalamic-pituitary-gonadal axis. The alternatively spliced FS344 construct used in gene therapy was specifically designed to avoid cell-surface binding and circulate freely, reducing off-target effects. Direct protein injection as practiced in some research communities lacks the pharmacokinetic characterization of the gene therapy approach. FSH suppression is a known effect of follistatin. Long-term safety of exogenous follistatin administration in humans has not been established.
Available Forms
Available from research chemical suppliers as lyophilized powder for reconstitution. No approved pharmaceutical formulation exists. Gene therapy delivery via AAV vector is a separate and investigational clinical modality distinct from peptide supplementation.
Regulatory Status
Not FDA approved for human use as a supplement or therapeutic compound. AAV-FS344 gene therapy has been investigated in clinical trials for muscular dystrophy under IND, representing the only regulated human use pathway. Exogenous follistatin protein is not on the 503A bulk drug substances list and has no approved compounding pathway.
Sources
https://pubmed.ncbi.nlm.nih.gov/15136138/
https://pmc.ncbi.nlm.nih.gov/articles/PMC5240576/
https://pubmed.ncbi.nlm.nih.gov/19208403/
Similar Compounds
Ipamorelin, Hexarelin, TB-500
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