Follistatin binds and neutralises myostatin, the TGF-beta family member that acts as a brake on muscle growth. Remove the brake and muscle mass increases — a mechanism dramatically confirmed by myostatin-null cattle, dogs and the well-documented human case of myostatin deficiency. FS-344 is the precursor isoform that is processed to FS-315. It also binds activin A, which is where the trouble starts.
Essentially all of it is preclinical or gene-therapy work in animals. Human data for administered follistatin protein are absent. Meanwhile the broader myostatin-inhibition field has a sobering track record: multiple pharmaceutical myostatin inhibitors have failed in trials, producing measurable muscle mass increases without corresponding functional benefit. Bigger muscle did not mean better outcomes.
Not FDA-approved. Gene therapy prohibited in sport, and myostatin inhibition prohibited (WADA S4.4).
No human safety data. The activin-binding activity is the serious unknown: activin signalling is involved in reproductive function, inflammation and tumour suppression, so systemic follistatin is not a clean myostatin switch. A protein of this size administered exogenously also raises real immunogenicity concerns.
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Regulatory status changes. This page reflects our reading of public sources as of July 2026 and should be independently verified before it is relied upon.