Follistatin 344
Also known as: FST-344, Follistatin isoform 344, FST
Follistatin 344 is a research compound not approved for human use. For informational purposes only.
Overview
Follistatin 344 is a 344-amino acid isoform of follistatin — an endogenous glycoprotein that functions primarily as a myostatin and activin inhibitor. Myostatin (GDF-8) is the body's primary muscle growth suppressor; follistatin binds and neutralizes it with high affinity, removing this brake on muscle protein synthesis. Research and animal data show dramatic increases in muscle fiber size and strength when follistatin is elevated or myostatin is inhibited.
Research Summary
Follistatin's muscle effects were dramatically illustrated when mice and cattle with follistatin overexpression or myostatin knockouts developed 2–3x normal muscle mass. Human follistatin gene therapy trials (AAV-mediated) are ongoing for Becker Muscular Dystrophy, showing sustained myostatin inhibition and improved muscle function over years from a single injection. Follistatin also inhibits activin A and B (involved in muscle wasting during illness), FSH secretion (reproductive effects), and inflammatory cytokines. The 344 isoform has an extended heparin-binding domain that increases tissue retention compared to the shorter FST-288 isoform.
Dosing Range
low
50mcg
moderate
100mcg
high
200mcg
Units: mcg · Frequency: Once daily or every other day for 10–30 day cycles
Dosing ranges are aggregated from preclinical research and community protocols. Not medical dosing guidance.
Administration Routes
Reconstitution Notes
Reconstitute with bacteriostatic water to 1mg/mL. Highly sensitive to heat and agitation — reconstitute gently (do not vortex), store at 4°C, use within 14 days. Some protocols use intramuscular injection into the target muscle to exploit local myostatin inhibition, though systemic effects occur regardless of route.Step-by-step reconstitution guide →
Supplies you'll need
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Reported Side Effects
- Potential FSH suppression (reproductive effects in females — may affect menstrual cycle)
- Accelerated hair follicle cycling (Wnt pathway involvement — theoretical hair loss concern at high doses)
- Joint discomfort with rapid muscle tissue growth
- Limited long-term human safety data
- Unknown interaction with cancer biology (activin inhibition has mixed effects on tumor biology)
Research Papers
3 peer-reviewed sourcesCommunity Experiences
Aggregated from public forums. Anecdotal — not clinical evidence.
Community experience with follistatin-344 — dosing protocols, cycle lengths, and muscle hypertrophy observations.
View original threadBodybuilding community discussions on myostatin inhibitors including follistatin 344.
View original threadOverview
Myostatin — a TGF-β family member — exists for one reason: to limit muscle growth. It's an evolutionary brake that prevents muscle from consuming excessive energy resources. Follistatin removes this brake by binding myostatin with high affinity, preventing it from signaling. The result in animal models is muscle hypertrophy that defies normal physiological limits.
The Myostatin System
Myostatin (GDF-8) is produced primarily by skeletal muscle and acts in an autocrine/paracrine feedback loop:
- Muscle grows → produces more myostatin
- Myostatin activates ActRIIB receptor on muscle stem cells (satellite cells)
- Signaling suppresses satellite cell activation and protein synthesis
- Muscle growth is limited
Follistatin breaks this loop by binding myostatin before it reaches ActRIIB.
The Myostatin Knockout Effect
The clearest evidence for myostatin inhibition's muscle effects comes from genetic models:
- Myostatin knockout mice: 2–3x normal muscle mass, dramatically reduced fat
- Whippet dogs with myostatin mutation: Visibly "double-muscled" phenotype
- Human child with myostatin mutation: Developed extraordinary muscle mass by age 4 with no adverse effects
- Belgian Blue cattle: Breed with natural myostatin mutation — 100% more muscle than standard cattle
Follistatin overexpression produces similar results to myostatin knockout.
FST-344 vs FST-288
Two main isoforms exist:
- FST-344: Extended C-terminal domain with heparin-binding sequence → stays bound to extracellular matrix, more localized/sustained effect
- FST-288: Shorter, more systemic distribution
FST-344 is preferred for muscle applications due to tissue retention; FST-288 is preferred in reproductive biology research (less FSH suppression).
Practical Considerations
Short cycles (10–30 days) are typically used because:
- The effect is potent enough that extended cycles aren't needed
- Allows the activin/FSH axis to recover
- Long-term myostatin suppression effects on tendon/joint adaptation are unknown
Intramuscular injection into a target muscle is used by some researchers to exploit the local tissue-retention property of FST-344 — the heparin-binding domain keeps it concentrated near the injection site.
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