Follistatin 344
Follistatin splice variant studied as a myostatin and activin antagonist for muscle-growth research
Half-life
Short (protein cleared within hours); no published PK for injectable FST-344
Typical Dose
~100mcg daily (vendor-suggested research protocol; no validated human dose)
Format
Injectable
Purity
≥98%
Overview
Follistatin 344 (FST-344) is a 344-amino-acid splice variant of follistatin, an autocrine glycoprotein that neutralizes members of the TGF-beta superfamily, including myostatin and activin [2]. It is one of the most-studied targets in muscle-growth biology: transgenic and gene-therapy models produce some of the largest muscle gains in the literature, from roughly doubling muscle mass in mice to quadrupling it when activin is blocked alongside myostatin [2,3]. Almost all of that evidence comes from genetic overexpression or viral delivery of the FS344 gene [5,6], plus one small human gene-therapy trial in Becker muscular dystrophy [7]. Injectable 'FST-344' research peptide is a separate proposition: as a bolus protein it clears quickly and has no published human efficacy or pharmacokinetic data, so its muscle effects in people remain unproven.
Mechanism
Follistatin is an activin-binding protein. It wraps around and sequesters myostatin (GDF-8), activin A and B, and GDF-11, preventing them from engaging the ActRIIB receptor and switching off the SMAD2/3 signaling that normally restrains muscle growth [1,2]. Removing that brake drives satellite cell proliferation and fiber hypertrophy [4]. Because follistatin blocks activin in addition to myostatin, it produces larger gains than myostatin-only inhibitors: myostatin-null mice roughly double muscle mass, while adding follistatin pushes toward a fourfold increase [3]. Gilson and colleagues showed follistatin overexpression raised muscle weight about 37% in normal mice, with part of the effect lost when satellite cells were disabled [4].
Researched benefits
- Sequesters myostatin (GDF-8) and activin, two brakes on muscle growth
- Largest muscle-mass gains reported in animal gene-therapy models
- Drives satellite cell proliferation and fiber hypertrophy
- Broader ligand blockade than myostatin-only inhibitors
- Studied in muscular dystrophy, sarcopenia, and cachexia models
Frequently asked
How does Follistatin 344 inhibit myostatin?
Myostatin (GDF-8) limits how large muscle fibers can get by activating ActRIIB receptors and the SMAD2/3 pathway. Follistatin binds myostatin directly and pulls it out of circulation before it reaches the receptor, so the brake on muscle growth is released. It also blocks activin and GDF-11, which is why it produces larger effects than antibodies that target myostatin alone.
Is the muscle-growth data from humans or animals?
Almost entirely animals, and almost entirely gene therapy rather than injections. Transgenic mice, AAV gene delivery in mice, and one nonhuman-primate study drive the headline numbers. The only human data come from a small phase 1/2a gene-therapy trial in Becker muscular dystrophy (Mendell 2015), where the FS344 gene was delivered into muscle by viral vector and improved walking distance with increased fiber size. Injectable FST-344 protein has no published human efficacy or safety trials.
What's the difference between FST-344 and FST-288?
They are splice variants of the same follistatin gene. FST-288 has a strong heparin-binding tail that anchors it to cell surfaces, so it acts locally. FST-344 is processed to a circulating serum form (FS315) that moves more freely and binds activin with lower affinity. Research models use the two variants to separate local from systemic follistatin effects.
What's the typical research dose?
There is no validated human protocol. Vendor-suggested research schedules commonly cite roughly 100mcg per day subcutaneously over a few weeks, but this is empirical and not backed by dose-response data. The muscle literature rests on gene therapy that produces continuous local follistatin expression, not on fixed injectable doses.
What's the half-life of Follistatin 344?
Follistatin is roughly a 38 kDa glycoprotein that clears from circulation within hours, and there is no published pharmacokinetic profile for injectable FST-344 specifically. That short residence time is exactly why the successful animal and human studies used gene therapy: a viral vector makes muscle produce follistatin continuously, rather than relying on repeated bolus injections.
How is Follistatin 344 reconstituted?
Bacteriostatic water is the standard diluent. For a 1mg vial, 1mL of BAC water gives 1mg/mL, or 100mcg per 0.1mL. Add the water slowly down the vial wall, swirl gently, never shake, and store refrigerated at 2-8°C after reconstitution.
Scientific Literature
References
- [1]
McPherron AC, Lawler AM, Lee SJ. (1997). Regulation of skeletal muscle mass in mice by a new TGF-beta superfamily member.
Nature · PubMed: 9139826
- [2]
Lee SJ, McPherron AC. (2001). Regulation of myostatin activity and muscle growth.
Proceedings of the National Academy of Sciences · PubMed: 11459935
- [3]
Lee SJ. (2007). Quadrupling muscle mass in mice by targeting TGF-beta signaling pathways.
PLoS One · PubMed: 17726519
- [4]
Gilson H, Schakman O, Kalista S, et al. (2009). Follistatin induces muscle hypertrophy through satellite cell proliferation and inhibition of both myostatin and activin.
American Journal of Physiology-Endocrinology and Metabolism · PubMed: 19435857
- [5]
Haidet AM, Rizo L, Handy C, et al. (2008). Long-term enhancement of skeletal muscle mass and strength by single gene administration of myostatin inhibitors.
Proceedings of the National Academy of Sciences · PubMed: 18334646
- [6]
Kota J, Handy CR, Haidet AM, et al. (2009). Follistatin gene delivery enhances muscle growth and strength in nonhuman primates.
Science Translational Medicine · PubMed: 20368179
- [7]
Mendell JR, Sahenk Z, Malik V, et al. (2015). A phase 1/2a follistatin gene therapy trial for Becker muscular dystrophy.
Molecular Therapy · PubMed: 25322757
Citations are provided for educational purposes. Always verify primary sources before drawing research conclusions.
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