Follistatin
Follistatin 344 (FS-344)
Block myostatin, unlock muscle growth potential
Follistatin is a naturally occurring glycoprotein that binds and neutralises myostatin, the primary negative regulator of muscle growth. It has attracted significant interest for muscle wasting conditions and athletic performance.

Admin routes
Subcutaneous
Popularity
Medium
Side effects
Generally mild
AU vendors
0 rated
✓Key benefits
📈What to expect
Improved muscle fullness and recovery between sessions
Noticeable increase in training capacity and pumps
Measurable lean mass gains when combined with resistance training
Peak body recomposition effects; begin off-cycle period
Based on community reports and published research. Individual results vary significantly.
💊Dosing protocols
Lean mass support
100 mcg
Once daily
30 days on, 30 days off
Body recomposition
100–200 mcg
Once daily
4–6 week cycles
Dosing information is sourced from published research and community protocols. This is not a recommendation. Consult a healthcare professional.
Research status|Preclinical - extensive animal data, gene therapy trials in muscular dystrophy
Overview
Follistatin is a single-chain glycoprotein produced in nearly all tissues, with the highest concentrations in ovarian follicular fluid where it was first identified. Its primary role is binding and inhibiting activin and myostatin - two members of the TGF-beta superfamily that limit muscle growth. Follistatin 344 (FS-344) is the most commonly referenced isoform in the peptide community. Animal studies, particularly the famous 'mighty mouse' experiments, demonstrated that follistatin overexpression can double muscle mass without exercise. While the human picture is more nuanced, follistatin remains one of the most discussed peptides for body composition.
⚙️How it works
Follistatin binds directly to myostatin (GDF-8) and activin A, preventing them from signalling through their receptors. Myostatin normally acts as a brake on muscle growth by inhibiting satellite cell proliferation and protein synthesis. By neutralising this brake, follistatin shifts the balance toward muscle hypertrophy and hyperplasia. It also influences follicle-stimulating hormone (FSH) regulation, fat metabolism, and has shown anti-fibrotic properties in preclinical models.
⚡Side effects
📅Research history
Follistatin first isolated from ovarian follicular fluid
Myostatin discovered - follistatin identified as its natural inhibitor
Review establishes follistatin as lead candidate for muscle disease therapy
Clinical gene therapy trial for Becker muscular dystrophy published
Growing adoption in biohacking community for body recomposition
The myostatin connection
Myostatin was discovered in 1997 when Se-Jin Lee at Johns Hopkins showed that mice lacking the myostatin gene developed roughly twice the normal muscle mass. Since then, naturally occurring myostatin mutations have been documented in cattle (Belgian Blue breed), dogs (whippets), and at least one human child. Follistatin became a target because it is the body's natural myostatin inhibitor. The challenge with synthetic follistatin peptide is that injectable forms have a short half-life, and the dramatic results seen in gene therapy and knockout models have not been replicated with peptide administration at practical doses.
Gene therapy vs peptide form
Most of the dramatic follistatin results come from gene therapy studies, where AAV vectors deliver the follistatin gene directly into muscle tissue for sustained expression. Nationwide Children's Hospital has conducted clinical trials using follistatin gene therapy for Becker muscular dystrophy with measurable improvements in the 6-minute walk test. The injectable peptide form, while popular in the biohacking community, produces more modest effects due to its short circulating half-life. Users should set expectations accordingly.
References
- [1]Rodino-Klapac LR, et al. 'Inhibition of myostatin with emphasis on follistatin as a therapy for muscle disease.' Muscle & Nerve, 2009.
- [2]Mendell JR, et al. 'Follistatin gene therapy for Becker muscular dystrophy.' Molecular Therapy, 2015.
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Disclaimer: This guide is for educational and informational purposes only. It is not medical advice. The dosing protocols listed are sourced from published research and community reports and do not constitute a recommendation. Always consult a qualified healthcare professional before using any peptide. Australian regulations classify many peptides as Schedule 4 (prescription-only) substances. Check current TGA guidelines before purchasing.