Also known as: FST-344 · FS-344 · Follistatin 344
Follistatin-344 is a naturally occurring glycoprotein that inhibits myostatin and activin signalling, promoting skeletal muscle hypertrophy and reducing fibrosis. It is one of the most potent anabolic proteins identified in preclinical research.
Follistatin-344 (FST-344) is the predominant isoform of follistatin found in muscle tissue. It functions as a binding protein that sequesters myostatin (GDF-8) and activin A, two powerful inhibitors of muscle growth. By neutralising these signals, FST-344 allows unchecked activation of the Akt/mTOR pathway, leading to pronounced skeletal muscle hypertrophy in animal models.
Research in mice with FST-344 overexpression shows muscle mass increases of 200–300% over controls, with no observed cardiac hypertrophy. Human and primate studies remain in early phases, with gene therapy vectors currently in clinical trials for Duchenne muscular dystrophy and spinal muscular atrophy.
FST-344 binds myostatin and activin A with high affinity, preventing their interaction with activin type II receptors (ActRIIA/B). This disinhibits Smad2/3 phosphorylation suppression, allowing full Akt/mTOR/p70S6K anabolic signalling. FST-344 also upregulates satellite cell proliferation, accelerating muscle repair and regeneration.
Follistatin-344 is a research-only compound with no approved human therapeutic form. Recombinant protein administration is studied in preclinical models; most human research uses AAV gene delivery vectors currently in muscular dystrophy trials. Quality and purity vary widely between research suppliers — critical given the complex glycoprotein structure.
Limited human cycling data available. Animal studies suggest sustained effects beyond the active administration period due to satellite cell population changes. Extended off-cycles are recommended given the unknown long-term effects of sustained myostatin suppression.
Research-only. No approved human use. Mechanism could theoretically affect cardiac muscle. Myostatin also plays roles in tendon/ligament strength — unchecked muscle hypertrophy without connective tissue adaptation may increase injury risk.
Research-only compound. No approved human therapeutic form exists. Most studies use recombinant protein or AAV-delivered FST-344 gene constructs. Exogenous peptide administration has very short circulatory half-life due to rapid receptor binding and clearance.
Ask anything about Follistatin-344 — mechanisms, dosing protocols, interactions, or research comparisons.
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