Follistatin 344
Myostatin-pathway inhibitor
A 344-amino-acid isoform of follistatin referenced in myostatin-pathway and muscle-research literature.
Also referenced as: FST-344
Overview
Follistatin 344 (FST-344) is one of the naturally occurring isoforms of follistatin, an endogenous glycoprotein that binds and neutralizes members of the TGF-beta superfamily. It is studied as a research protein in the myostatin/activin pathway.
At a glance
What Follistatin 344 does
Follistatin-344 is a 344-amino-acid isoform of follistatin, a naturally secreted protein whose defining action is to bind and neutralize members of the TGF-beta superfamily - most importantly activin and the muscle-growth suppressor myostatin (GDF-8). Where ACE-031 mimics a receptor, follistatin works differently: it wraps around the ligand itself with very high affinity, forming a near-irreversible complex that hides the growth factor from all of its receptors. FST-344 in particular contains an N-terminal heparin-binding sequence that lets it stick to cell-surface heparan-sulfate proteoglycans, concentrating its activity at tissues; it is often processed to the shorter FST-315/FST-288-type forms in circulation.
Functionally, by sequestering myostatin, follistatin removes the dominant negative regulator of skeletal-muscle growth, and by binding activin it also modulates reproductive, inflammatory, and fibrotic signaling. In muscle, the downstream effect is a marked increase in muscle fiber size and total mass - in gene-transfer experiments where follistatin is expressed locally in muscle, animals develop pronounced, durable hypertrophy exceeding what myostatin knockout alone produces, because activin is neutralized too.
The muscle-hypertrophy evidence is robust but overwhelmingly preclinical and largely from AAV/gene-delivery studies in mice and non-human primates; some early gene-therapy trials in muscular dystrophy patients have used follistatin transgenes. As an injected recombinant protein, follistatin has a short half-life and limited systemic exposure, so most of the dramatic muscle data comes from sustained local expression rather than from a peptide injection. It should be understood as a potent research tool for myostatin/activin blockade, not an established therapeutic.
Effects reported in research
- Binds myostatin (GDF-8) with high affinity and neutralizes it, removing the principal brake on skeletal-muscle growth (established mechanism).
- Also binds and neutralizes activin, broadening its effect beyond myostatin alone and contributing to larger hypertrophy than myostatin blockade by itself (established mechanism).
- Drove pronounced, durable increases in muscle fiber size and mass when expressed locally via AAV gene transfer in mice and non-human primates (animal only).
- The FST-344 isoform's N-terminal heparin-binding domain anchors it to cell-surface heparan-sulfate proteoglycans, concentrating activity at tissue (biochemical property).
- Modulates activin-driven reproductive, inflammatory, and fibrotic signaling as part of its broader ligand-trapping role (established physiology).
- Used as a follistatin transgene in early gene-therapy trials for muscular dystrophy (limited human data).
- As an injected protein it has a short half-life and limited systemic exposure, so most striking muscle effects come from sustained local expression, not bolus dosing (pharmacokinetic caveat).
Effects listed reflect findings reported in the research literature — many in animal or in-vitro models. Listing an effect is not a claim of efficacy or a therapeutic indication in humans.
Mechanism of action
Follistatin is a secreted protein that binds with high affinity to activin and to myostatin (GDF-8), neutralizing these ligands and preventing them from activating activin type II receptors. By sequestering myostatin, follistatin removes a negative regulator of skeletal muscle growth, which in animal studies is associated with increased muscle mass. The 344 isoform includes an N-terminal signal/acidic region and is processed to shorter forms such as FST-315 and FST-288 with differing tissue-binding properties.
Mechanistic description reflects published research-literature understanding. Much peptide research is preclinical (in-vitro or animal-model); mechanism in humans may differ and is not established for many compounds.
What it's studied for
Research contexts in which Follistatin 344 appears in the literature. Listing a research area is not a claim of efficacy or a therapeutic indication.
Key characteristics
- A natural follistatin isoform (344-residue precursor form).
- Endogenous high-affinity binder of activin and myostatin.
- Neutralizes myostatin to relieve inhibition of muscle growth.
- Related to shorter isoforms FST-315 and FST-288.
- Research/investigational; not an approved therapeutic.
Reported research dosing reference only
Educational reference, not dosing guidance. The figures below summarize amounts reported in published research and research-community protocols, provided for educational and research context only. They are not medical advice, not a recommendation, and not instructions for human use. Follistatin 344 is a research compound.
Follistatin-344 dosing in the literature is drawn from animal studies and is expressed per kilogram of body weight; no validated human research protocol exists.
- Small-animal studies: on the order of ~1-2 mg/kg has been referenced around the range where high-affinity target binding approaches saturation
- Administration commonly reported as daily or every-other-day in animal protocols rather than continuous infusion
These are reference figures for research context only, not dosing guidance for humans. Because target affinity is picomolar, reported effects scale with dose until receptor occupancy saturates.
How it compares
Follistatin-344 is a natural ligand-binding antagonist of myostatin/activin, distinct from ACE-031, which is an engineered ActRIIB-Fc decoy receptor acting at the receptor.
Commonly studied alongside
Compounds frequently researched together with Follistatin 344 in the literature. Cross-referenced for research context — not a usage or combination recommendation.
Compare and calculate
Side-by-side pages for the pairings the literature already documents for Follistatin 344, plus the unit-conversion reference for a reconstituted vial. Factual comparisons of documented characteristics — not a recommendation to combine or use any compound.
Follistatin 344 reconstitution calculator → Concentration, volume per measured amount and syringe units for a stated vial mass and diluent volume. A unit-conversion reference, not a dosing recommendation.
Handling & Stability
Lyophilized peptides are stored cold, protected from light, and reconstituted only at the time of intended in-vitro work.
- Avoid repeated freeze-thaw cycles
- Verify supplier lot and Certificate of Analysis
- Follow institutional lab-safety protocols
Analytical & COA Concepts
Reputable research suppliers publish a third-party Certificate of Analysis per batch. Key analytical concepts referenced in COAs include:
Category Context
Follistatin 344 sits in the Specialty & Research area of the PeptiDex library.
- Entry type: Research compound reference
- Specialty & Research category hub →
- Browse the full library →
- Glossary of terms →
Where researchers source Follistatin 344
For researchers studying Follistatin 344, third-party suppliers such as Practically Natty Peptides offer research-grade material, third-party tests every batch and provides Certificates of Analysis on request, and ship from the US.
PeptiDex does not maintain a direct supplier listing for this compound. The link above goes to a third-party research-supplier directory.
Frequently asked questions
What is follistatin-344 (FST-344)?
Follistatin-344 is the 344-amino-acid isoform of follistatin, a naturally occurring secreted glycoprotein. It carries a heparin-binding N-terminal domain followed by three cysteine-rich follistatin domains that form its ligand-binding surface. It is studied as a high-affinity inhibitor of myostatin and activin A.
What is follistatin-344 studied for?
In research it is examined for its ability to bind and neutralize myostatin and activin A - TGF-beta superfamily members that restrain muscle growth - and thereby its effects on lean muscle mass in preclinical models. Human data are very limited and no injectable follistatin protocol has been validated in controlled clinical trials. It is a research-only compound.
How does follistatin-344 differ from FST-315 and FST-303?
FST-344 is the full-length precursor isoform. After removal of a 29-amino-acid signal peptide it yields the mature 315-residue circulating isoform (FST-315), a portion of which is further cleaved at the C-terminus to the 303-residue gonadal isoform (FST-303). The isoforms differ mainly in tissue distribution and heparin/cell-surface binding behavior.
How does follistatin-344 differ from ACE-031?
Follistatin-344 is a natural glycoprotein that directly binds and neutralizes myostatin and activin with picomolar affinity, whereas ACE-031 is an engineered ActRIIB-Fc decoy receptor that traps the same ligands in circulation. Both are common reference points in myostatin-inhibition research but represent different molecular strategies.
How is follistatin-344 supplied and stored?
It is typically supplied as a lyophilized glycoprotein that is reconstituted before research use. As a protein it requires cold storage - frozen when lyophilized, refrigerated once reconstituted - and protection from repeated freeze-thaw. A COA with purity and identity data is standard to expect.
Answers are educational summaries of research-literature context and do not constitute medical advice. See the Research Library, COA guide, and Storage & Handling guide for more.
References
Primary literature indexed in PubMed for Follistatin 344. Listing a study records that it exists and is indexed — it is not a claim of efficacy, a therapeutic indication, or an endorsement of its conclusions. Much of this literature is preclinical (in-vitro or animal-model).
- Follistatin gene delivery enhances muscle growth and strength in nonhuman primates
- Follistatin Gene Therapy Improves Ambulation in Becker Muscular Dystrophy
Each reference was checked against its PubMed record on 2026-07-28: the PMID resolves and the title, journal and year match. Where no indexed literature exists for a compound, PeptiDex says so rather than substituting a citation about a different molecule. See the editorial policy.