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PeptidesInjectable

Follistatin 344

Muscle Building, Performance

Half-life
1 h
Sources
4
Reviewed
2026-08-11

In short

  • A myostatin and activin binding protein — it neutralises myostatin, the principal negative regulator of muscle mass.
  • The gene-therapy version has reached human trials for muscular dystrophy, with encouraging early results.
  • The injectable research-market protein is a completely different proposition from gene therapy and has no human data.
  • Follistatin binds activin as well as myostatin, and activin has roles in reproduction, inflammation, and wound healing — so the effects are not muscle-specific.
  • Explicitly prohibited in sport under WADA S4.4 as a myostatin-function modifier.

Structure

A 344-amino-acid glycoprotein. PubChem has no entry under this research-market name, and peptides and proteins of this size are represented by sequence rather than a small-molecule structure diagram.

How it works

Myostatin (GDF-8) restrains muscle growth; animals and rare humans with loss-of-function mutations show dramatic muscle hypertrophy. Follistatin binds myostatin with high affinity and prevents it signalling through the activin type II receptor.

Follistatin 344 is an isoform. It also binds activin A and other TGF-beta superfamily members, which is the source of the off-target concern — activin signalling is involved in reproductive function, inflammation, and fibrosis, not just muscle.

As a 344-amino-acid glycoprotein it is a substantial protein rather than a peptide, with correspondingly poor stability and no oral route.

What the research shows

Gene therapy delivering follistatin has been trialled in Becker muscular dystrophy and inclusion body myositis, with reported improvements in walking distance in small open-label studies. That work is legitimate and ongoing.

Animal studies with follistatin overexpression show substantial muscle hypertrophy.

No trial of injected recombinant follistatin protein exists in humans. The gene-therapy results do not transfer — sustained local expression from a viral vector is a different intervention from intermittent injection of a protein with a short half-life.

Dosing in the literature

Figures below are quoted from published studies, with the species or population they were measured in. They are records of what was studied, not recommendations.

Studied inAmountRouteSource
Human — follistatin gene therapy trials (AAV-delivered, not injected protein)Vector doses; not comparable to protein administration—PubMed
Animal — recombinant follistatin studiesVaries widely by model; see source—PubMed

Commonly reported ranges

These are amounts people report using. They are not from any study, have not been evaluated for safety, and are reproduced here only because they circulate widely and are better seen alongside the evidence than instead of it.

Reported byAmountRoute
Commonly reported, in short cycles100 µg daily for 10–30 dayssubcutaneous

No published human pharmacokinetic study establishes a dose, interval, or duration for this compound. Community figures below have no trial behind them and are reports of practice, not evidence. The human evidence is for GENE THERAPY, which produces sustained local expression from a viral vector. Injecting a recombinant protein intermittently is a fundamentally different intervention, and no data supports translating one to the other. Protein of this size also has poor bioavailability by subcutaneous injection.

Handling and storage

Supplied as a lyophilised powder requiring reconstitution with bacteriostatic water. The powder is comparatively stable; once reconstituted it is refrigerated and used within weeks. Track the date you reconstitute each vial — the Inventory section does this, and it is the difference between knowing a vial is three weeks old and guessing.

Subcutaneous injection in short cycles is the community pattern. As a large glycoprotein it is fragile — handling, temperature, and reconstitution technique matter more than for small peptides, and degraded protein is inactive rather than merely weaker.

Side effects

No human safety data for injected follistatin protein exists.

The mechanistic concerns follow from what else follistatin binds. Activin signalling is involved in reproductive endocrinology, inflammation, and tissue repair, so systemic myostatin/activin blockade is not a muscle-only intervention.

The broader myostatin-inhibitor field is instructive: multiple pharmaceutical programmes (bimagrumab, landogrozumab, others) produced muscle mass increases without corresponding functional or clinical benefit, and several were discontinued. Muscle mass and muscle function came apart.

Combinations

No interaction data. Combining with other anabolic agents compounds an unstudied intervention.

The myostatin-inhibitor programme results suggest that added mass without added function is the realistic ceiling for this pathway, which is worth weighing before stacking anything onto it.

Research status

Myostatin and follistatin biology is genuine, important, and well published.

The therapeutic translation has been repeatedly disappointing: the pharmaceutical myostatin-inhibitor class has largely failed to convert mass gains into functional benefit. Gene therapy remains the more promising route and is where the real human work is happening.

Legal status

Not approved in any jurisdiction. Sold for research use only.

WADA status

PROHIBITED AT ALL TIMES under WADA class S4.4 — agents modifying myostatin function, including myostatin inhibitors, are explicitly named. This is a named prohibition, not an S0 inference.

Conclusion

Follistatin is important biology with a striking animal phenotype and a discouraging clinical track record — the myostatin-inhibitor class has repeatedly produced bigger muscles that did not work better.

The human results that get cited for it come from gene therapy, which is not what is in the vial.

Sources

  1. [1]Follistatin gene therapy in muscular dystrophy — clinical trialsPubMed
  2. [2]Follistatin and myostatin/activin bindingPubMed
  3. [3]Myostatin inhibitors — mass versus function in clinical trialsPubMed
  4. [4]WADA Prohibited List (current)WADA

Track your own Follistatin 344 protocol

Peppers logs your doses, models your levels from this half-life, tracks your vials and tells you when you will run out. Free on iPhone.

Reference and educational information only. Not medical advice. Nothing here diagnoses, treats, or prescribes, and nothing here is a recommendation to use any compound. The compounds described are research chemicals and are not approved for human consumption. Legal and anti-doping status change — the review date above is when these claims were last checked. Talk to a qualified clinician about anything you intend to take.