Follistatin
A naturally occurring protein that inhibits myostatin (the muscle growth limiter), studied for dramatic muscle growth potential.
What is Follistatin?
Follistatin is a naturally occurring glycoprotein that binds and neutralizes myostatin, activin, and other TGF-beta superfamily members. Myostatin is the body's primary brake on muscle growth. By inhibiting myostatin, follistatin allows enhanced muscle development. Gene therapy approaches using follistatin produced dramatic results in animal models and encouraging open-label signals in small human trials for muscular dystrophy between 2012 and 2017 — but those trials have long since completed, and no active registered follistatin gene therapy programme in muscular dystrophy has been identified since.
What Follistatin Is Investigated For
Follistatin is investigated for myostatin inhibition-driven muscle growth, muscular dystrophy treatment (primarily Duchenne and Becker), and body composition improvement. The strongest evidence comes from preclinical animal models, where follistatin-overexpressing animals develop dramatically increased muscle mass — a robust and reproducible finding underpinning the entire therapeutic concept. Human clinical data is largely confined to AAV-mediated FS-344 gene therapy trials in muscular dystrophy (most notably from Jerry Mendell's group at Nationwide Children's Hospital and commercially advanced by Milo Biotechnology), which produced the best available human signal — though in open-label designs with modest sample sizes and no definitive efficacy verdict. The honest caveats are substantial and often conflated: endogenous follistatin protein, recombinant full-length protein, AAV-delivered FS-344 gene therapy, and research-chemical 'follistatin peptide' fragments are four distinct products with different pharmacokinetics and risk profiles — and injectable peptide dosing with a short half-life cannot plausibly recapitulate the sustained systemic myostatin inhibition achieved in animal overexpression models. No follistatin product is FDA-approved, and follistatin is named explicitly on the WADA Prohibited List under S4.3. Two things changed in 2026 that a reader should weigh. The myostatin pathway finally produced an approved drug — apitegromab, a myostatin-neutralising antibody, was approved by the FDA in September 2026 for spinal muscular atrophy — which proves the target is druggable while saying nothing about follistatin specifically, since apitegromab is an antibody against myostatin rather than a myostatin-binding protein. And the follistatin gene therapy programme that produced the human data quoted on every vendor site has gone quiet: both registered AAV-FS344 trials completed in 2017 and nothing has replaced them.
History & Discovery
Follistatin was first isolated and characterized in 1987 by Naoto Ueno, Nicholas Ling, and colleagues at the Salk Institute as a protein from porcine ovarian follicular fluid that suppressed follicle-stimulating hormone (FSH) secretion — the source of its name. Shortly thereafter the same group and others demonstrated that follistatin's primary biochemical activity was high-affinity binding and neutralization of activin. The connection to muscle biology came later, after Se-Jin Lee's 1997 discovery of myostatin (GDF-8) as a negative regulator of skeletal muscle mass, when follistatin was shown to also bind and neutralize myostatin — positioning it as a natural double-lock on both activin and myostatin signaling. Multiple follistatin isoforms exist: Follistatin-288 (the shorter, tissue-bound isoform), Follistatin-315 (the longer, circulating isoform), and Follistatin-344 (a precursor that is processed into shorter forms). Follistatin-344 has been the dominant isoform in therapeutic gene-therapy development, most notably in work at Nationwide Children's Hospital under Jerry Mendell's group and later commercialized by Milo Biotechnology, which ran open-label AAV-mediated FS-344 gene therapy trials in Duchenne and Becker muscular dystrophy and sporadic inclusion body myositis beginning in 2010. Those trials produced the best available human data on therapeutic follistatin — though the signal was limited in size, the study designs were open-label, and the field has not converged on a definitive efficacy verdict. Critically, the 'follistatin peptide' sold on the research-chemical market is a different product from both endogenous follistatin protein and from AAV-delivered FS-344 gene therapy; conflating these three is a common and material error.
How It Works
Your body has a built-in limit on how much muscle you can build, controlled by a protein called myostatin. Follistatin acts as myostatin's natural off-switch, removing the brake and allowing greater muscle growth.
Follistatin binds myostatin (GDF-8) and activin A/B with high affinity, preventing their interaction with ActRIIB receptors. This blocks Smad2/3 signaling that normally limits muscle growth. Follistatin-344 is the most common isoform used in research; it is processed to Follistatin-315 and Follistatin-288 with different tissue distributions. The 2026 Hok et al. crystal structure of the activin B:Fst288 complex (J Biol Chem, PMID 42607890) is the first direct structural characterization of the Fst288-ligand complex and provides computational insight into how follistatin's two isoforms achieve broad TGF-β superfamily specificity — a substantial upgrade over prior model-based understanding of the ligand-neutralization mechanism. Beyond myostatin, follistatin's inhibition of activin affects FSH secretion, inflammation, and fibrosis. Endogenous follistatin is also part of the upstream anabolic cascade activated by androgens — testosterone upregulates follistatin via androgen receptor signaling, which in turn restrains TGF-β/myostatin output and promotes myogenesis, providing a mechanistic bridge between androgen pharmacology and the myostatin axis. Plasma follistatin follows a measurable 24-hour rhythm in healthy young males (~18% relative amplitude), which has implications for biomarker timing in clinical research and complicates single-timepoint measurements. Cardiovascular follistatin biology has continued to develop: Dirakvand et al. (Cells 2026, PMID 42439678) reported that follistatin mitigates atherosclerosis through arginine-metabolism activation and adipose browning, and Gavara et al. (J Clin Med 2026, PMID 42589880) characterized follistatin as an outcome-relevant biomarker in STEMI patients at follow-up — early human evidence that partially addresses the file's cardiac-safety-and-outcomes research gap. Gene therapy (AAV-mediated follistatin) has shown promising results in Becker muscular dystrophy trials.
Evidence Snapshot
Human Clinical Evidence
Limited, and no longer growing in the direction people assume. The best human signal remains two small open-label AAV-FS344 gene therapy trials in Becker and Duchenne muscular dystrophy, both of which completed in 2017 — one enrolled 15 patients, the other only 3 against a planned 6. No successor trial has been registered. Data on injectable follistatin peptide in humans is essentially absent. What has grown since is adjacent rather than confirmatory: a 2026 crystal structure of the activin B:Fst288 complex, human circadian data showing plasma follistatin follows a 24-hour rhythm, and a cluster of 2026 cardiovascular and oncology findings that complicate rather than support the muscle-growth story.
Animal / Preclinical
Strong. Dramatic muscle growth in follistatin-overexpressing animals is well-documented.
Mechanistic Rationale
Very strong. Myostatin/activin/TGF-beta signaling is thoroughly characterized.
Research Gaps & Open Questions
What the current literature has not yet settled about Follistatin:
- 01Human pharmacokinetics of injectable follistatin peptide — circulating half-life, tissue distribution, effective exposure duration, and route-comparative bioavailability have not been rigorously characterized.
- 02Whether injectable peptide dosing can produce meaningful sustained myostatin inhibition in humans — given short half-life and continuous myostatin production, this fundamental feasibility question remains unresolved outside of gene therapy.
- 03Cardiac safety of chronic myostatin inhibition — preclinical data on cardiac remodeling under sustained myostatin suppression is mixed, and human cardiac outcome data is limited to small dystrophy cohorts.
- 04Reproductive consequences of sustained follistatin elevation in humans — effects on FSH, fertility, and reproductive hormones beyond short trial windows are not characterized.
- 05Oncologic risk, which 2026 data made more complicated rather than clearer. The long-standing concern was that activin has tumour-suppressive roles, so inhibiting it might remove a brake. Two 2026 findings point the opposite way: follistatin itself was identified as a driver of androgen-receptor-independent prostate cancer, with a follistatin-neutralising trap proposed as the therapy, and high FST expression predicted poor survival and reduced CD8+ T-cell density in head and neck squamous cell carcinoma. Whether raising systemic follistatin is oncologically risky, protective, or neither is now genuinely open in a way it was not before, and no long-term human safety data exists either way.
- 06Product identity across research-chemical suppliers — what is actually in products labeled 'follistatin peptide' varies considerably, and sequence verification is rarely performed, making even basic efficacy-vs-placebo comparisons difficult.
- 07Comparative efficacy of peptide versus gene therapy versus recombinant protein — these are three substantively different modalities with different risk-benefit profiles, and they are often conflated in lay and even clinical discussion.
Forms & Administration
SC injection of recombinant follistatin (limited availability). Gene therapy approaches in clinical trials. Typical research dose: 100-300mcg/day SC. Rapid clearance limits efficacy of injected forms. All injectable peptides should only be administered under the guidance of a qualified healthcare provider. Never self-administer without clinician oversight.
Dosing & Protocols
The ranges below reflect protocols commonly discussed in the literature and by clinicians — not a prescription. Actual dosing for any individual should be determined by a qualified healthcare provider who knows the patient.
Typical Range
Research-chemical follistatin peptide products are commonly dosed in the 100–300 mcg/day range via subcutaneous injection, with some protocols using up to 500 mcg/day. These numbers have essentially no human dose-ranging trial basis and are extrapolated loosely from animal work with recombinant protein and from community reports. Gene therapy trials (AAV1-FS344) used viral vector doses on the order of 10^12 vector genomes, which is an entirely different modality and not comparable to injectable peptide dosing.
Frequency
Injectable protocols typically use once-daily dosing because the circulating half-life of exogenous follistatin is short (estimated at roughly 1–2 hours based on animal work), and chronic myostatin suppression would require sustained exposure. Some protocols split into twice-daily dosing. In practice, this pharmacokinetic limitation is one of the strongest arguments against injectable follistatin peptide producing meaningful sustained myostatin inhibition in humans.
Timing Considerations
No specific timing requirements: can be administered at any time of day, with or without food, and is not tied to exercise timing. Consistency matters more than the specific clock — dose at roughly the same time each day (or same day each week, for weekly protocols) to keep exposure steady.
Cycle Length
Commonly discussed cycle lengths run 10 days to 4 weeks, often tied to hypertrophy or recomposition training blocks. There is no human trial basis for any specific cycle length. Gene therapy trials use a single viral vector administration with effects measured over months to years, which is a fundamentally different time scale from peptide cycling.
Protocol Notes
The most important dosing caveat for follistatin peptide is pharmacokinetic: endogenous follistatin is a 300+ amino acid glycoprotein, and the 'follistatin peptide' products sold on the research-chemical market are often much shorter fragments or variants that cannot be assumed to recapitulate full-protein activity in vivo. Injected full-length recombinant protein is rapidly cleared. This mismatch between the pharmacokinetics required for meaningful myostatin inhibition and what injectable peptide dosing can plausibly deliver is a fundamental unresolved question. Reconstitution for injectable peptide products typically uses bacteriostatic water, with the specific concentration depending on vial size. Subcutaneous injection into the abdominal fat pad is the most common described route. Product identity, purity, and even basic sequence verification is particularly uncertain for follistatin compared to more commoditized peptides; sourcing through an accredited compounding pharmacy rather than research-chemical suppliers is a meaningful quality-control step. Users should be explicit with themselves and any clinician about which product they are actually taking: endogenous protein is not gene therapy, and neither is the same thing as a research-chemical peptide fragment.
These numbers are not a prescription. Follistatin in injectable peptide form is not FDA-approved for any condition. AAV-based follistatin gene therapy is investigational and available only through clinical trials. Any actual use of injectable follistatin peptide should be under the direct supervision of a qualified healthcare provider.
Timeline of Effects
Onset
Anecdotal reports of strength or muscle-size change from injectable follistatin peptide protocols typically describe subjective effects on the order of 1–3 weeks, but these reports are not supported by controlled human data and are frequently confounded by concurrent training, nutrition, and other peptide or anabolic use. Gene therapy trials in muscular dystrophy populations reported measurable functional and histologic changes over months, not weeks.
Peak Effect
Peak effect for injectable peptide cycles is typically described in the 3–6 week window, matching the duration of commonly discussed cycles rather than any established pharmacodynamic profile. Gene therapy effects, where they have been reported, continued to develop over 6–12 months. There is no reliable human pharmacodynamic curve for injectable follistatin peptide.
After Discontinuation
Because exogenous follistatin peptide has a short half-life and myostatin is continuously produced, myostatin suppression would be expected to reverse rapidly after dosing stops. Any gains in muscle mass would be subject to normal post-training retention dynamics. Gene therapy is a different story — a single AAV administration is intended to produce sustained follistatin expression for months to years, with effects persisting accordingly.
Common Questions
Can follistatin really block myostatin?
Yes. Follistatin is one of the body's natural myostatin inhibitors. Animals with follistatin overexpression develop dramatically increased muscle mass. The challenge is delivering enough follistatin to achieve meaningful myostatin inhibition in humans.
Is injectable follistatin peptide the same as the gene therapy used in muscular dystrophy trials?
No, and conflating them is the single most common error in follistatin discussion. AAV-FS344 gene therapy delivers the follistatin coding sequence via a viral vector for sustained in-vivo expression over months to years from a single administration. Research-chemical 'follistatin peptide' is typically a much shorter fragment or synthetic variant with a circulating half-life on the order of 1–2 hours. The two modalities differ fundamentally in pharmacokinetics, exposure duration, and what they can plausibly do in humans.
Is follistatin banned in sports?
Yes, and by name. The WADA 2027 Prohibited List names follistatin in S4.3, the subsection covering agents that prevent activin receptor IIB activation, under "Myostatin-binding proteins (e.g. follistatin, myostatin propeptide)". That is a specific listing, not an inference from a catch-all clause, and it applies at all times rather than only in competition. Every form is covered: recombinant protein, research-chemical peptide, and gene therapy — the last also falling under M3.1, which prohibits gene transfer. What is worth separating from the rule itself is enforcement. There is no validated routine test for exogenous follistatin in doping control, and no publicised sanction naming follistatin has been identified, so an absence of positive cases should not be read as evidence that nobody is using it.
Does follistatin affect fertility?
Mechanistically, yes — and this is one of its most under-discussed risks. Follistatin was originally named for its ability to suppress follicle-stimulating hormone (FSH) by binding activin. Sustained follistatin elevation would be expected to disrupt FSH signaling and therefore ovulation in women and spermatogenesis in men. Human data on reproductive consequences of exogenous follistatin is essentially absent, which is why it's contraindicated in pregnancy, breastfeeding, and anyone trying to conceive.
A myostatin drug just got approved — does that validate follistatin?
It validates the pathway, not the molecule, and the distinction matters commercially as much as scientifically. Apitegromab was approved by the FDA on 11 September 2026 as ISEMBYLD, for spinal muscular atrophy in patients aged two and over who are already on an SMN2-targeted therapy. It is the first approval of any myostatin-pathway drug. But apitegromab is a monoclonal antibody that neutralises pro- and latent myostatin specifically; follistatin is a broad-spectrum binding protein that also sequesters activins, which is exactly why it carries reproductive and oncologic questions that a selective antibody does not. The pathway's other recent results cut both ways: taldefgrobep alfa drove myostatin below detection for 48 weeks and still missed its phase 3 primary endpoint in SMA, and bimagrumab's most interesting phase 2b result is as a lean-mass-sparing partner to semaglutide rather than as a standalone muscle-builder. Target engagement has repeatedly proved easier than functional benefit.
Who Follistatin Is NOT For
- •Pregnancy — no human pregnancy safety data; activin signaling (which follistatin inhibits) is critical to reproductive biology, placentation, and FSH regulation, and disrupting this axis during pregnancy is contraindicated on mechanistic grounds alone.
- •Breastfeeding — no data on transfer into breast milk, and effects on the activin-FSH axis during lactation are not studied.
- •Active or recent-history cancer — activin and myostatin signaling play tumor-suppressive roles in several cancer types, and inhibiting them carries a theoretical risk of accelerating tumor progression. This concern is underexplored in the clinical literature and is reason for caution.
- •Reproductive disorders or individuals actively trying to conceive — follistatin's documented effect on FSH secretion raises direct concerns about ovulation and spermatogenesis; both male and female reproductive effects are under-characterized in humans.
- •Pediatric use (under 18) — use outside of approved gene therapy trials for specific dystrophies is contraindicated; developmental effects of systemic myostatin/activin inhibition are unknown.
- •Cardiomyopathy or significant cardiac disease — myostatin inhibition's effects on cardiac muscle in humans are unsettled, and preclinical data on cardiac remodeling under chronic myostatin suppression is mixed.
- •Known hypersensitivity to peptide or protein therapeutics, or to excipients in compounded preparations.
Drug & Supplement Interactions
Documented human drug interactions for follistatin peptide are absent. What follows is theoretical and derived from mechanism. Concurrent use with anabolic agents (androgens, selective androgen receptor modulators, growth hormone, IGF-1 analogs) is common in performance contexts and would be expected to produce additive effects on muscle hypertrophy — but the safety consequences of combining multiple growth-promoting pathways are not characterized, and cumulative oncologic and cardiac risks could compound. Concurrent use with other myostatin-pathway inhibitors (bimagrumab, trevogrumab, ramatercept, or related agents in development) is not advised because it would compound the same mechanism. Follistatin's suppression of FSH raises theoretical interactions with fertility medications (clomiphene, letrozole, gonadotropins) where the intended effect depends on FSH signaling; suppressing FSH via follistatin would blunt those therapies. Similarly, hormonal contraceptive interactions are not studied. Patients on any regular medication — particularly cardiac medications, anticoagulants, or oncology therapies — should disclose follistatin use to their prescribing clinician. Absence of documented interactions reflects absence of study, not absence of risk.
Safety Profile
Common Side Effects
Cautions
- • Not FDA-approved
- • May affect reproductive hormones
- • Protein is rapidly cleared, limiting practical use of injected forms
- • Gene therapy approaches carry their own risks
What We Don't Know
Long-term effects of chronic myostatin inhibition in humans are unknown. Reproductive and cardiac effects need more study.
Legal Status
United States
Recombinant follistatin protein and follistatin peptide fragments are not FDA-approved for any indication. AAV-mediated follistatin gene therapy is investigational and available only through clinical trials. Follistatin peptide sold through research-chemical channels is not intended or authorized for human use, and product identity and purity is often not verified. The FDA's 2023 peptide compounding review did not produce a carve-out for follistatin.
International
No major regulator (EMA, MHRA, TGA, Health Canada) has authorized follistatin as a medicine in either protein or peptide form. Gene therapy programs have proceeded under investigational frameworks in the US and select international jurisdictions. Importation of research-chemical follistatin is restricted or prohibited in several jurisdictions.
Sports & Competition
Prohibited, and named explicitly rather than captured by a general clause. The WADA 2027 Prohibited List covers follistatin under S4.3, "Agents preventing activin receptor IIB activation", in the entry for myostatin inhibitors: "Myostatin-binding proteins (e.g. follistatin, myostatin propeptide)". The same subsection separately names decoy activin receptors such as ACE-031, anti-activin receptor IIB antibodies such as bimagrumab, and myostatin-neutralising antibodies such as apitegromab. The prohibition applies at all times, in and out of competition, and there is no form of the molecule that escapes it — recombinant protein, research-chemical peptide and gene therapy are all within scope, and M3.1 separately prohibits gene transfer. One practical caveat worth stating honestly: prohibition and detection are different things. No validated routine assay for exogenous follistatin is in use in doping control and no publicised sanction naming follistatin has been identified, which means the absence of positive tests says nothing about whether the rule is being broken.
Regulatory status changes over time. Verify current local rules with a qualified professional.
Myths & Misconceptions
Myth
Injectable follistatin peptide produces the dramatic muscle growth seen in follistatin-overexpressing animals.
Reality
Animal hypertrophy models use genetic or gene-therapy-level sustained overexpression of follistatin, producing chronic, systemic myostatin inhibition. Injectable peptide dosing with a short half-life cannot plausibly recapitulate that exposure. Extrapolating myostatin-knockout-like muscle phenotypes to research-chemical peptide cycles is a category error.
Myth
Follistatin, recombinant follistatin protein, and AAV-FS344 gene therapy are the same product.
Reality
They are three distinct things. Endogenous follistatin is a 300+ amino acid glycoprotein produced by the body. Recombinant follistatin protein is a manufactured version of that full protein. AAV-FS344 gene therapy delivers the FS-344 isoform's coding sequence via viral vector for sustained in-vivo expression. Research-chemical 'follistatin peptide' is typically a shorter fragment or synthetic variant whose identity and activity vs. the full protein is not verified. These distinctions matter for both expected efficacy and safety.
Myth
Follistatin is FDA-approved or near approval.
Reality
No follistatin product — injectable peptide, recombinant protein, or gene therapy — is FDA-approved. Gene therapy programs have produced interesting but limited open-label data in muscular dystrophy populations and have not converged on a regulatory approval path.
Myth
Follistatin isn't on the WADA list by name, so it sits in a grey area.
Reality
The premise is factually wrong. Follistatin appears on the WADA 2027 Prohibited List by name, in S4.3, in the phrase "Myostatin-binding proteins (e.g. follistatin, myostatin propeptide)". There is no grey area to occupy. The genuine ambiguity lies somewhere else entirely, and it is about testing rather than rules: no validated routine assay for exogenous follistatin is in use in doping control, and no publicised sanction naming follistatin has been identified. An athlete reasoning from the absence of positive tests to the absence of a rule has confused a detection gap with permission.
Myth
Because follistatin is a naturally occurring protein, exogenous administration carries minimal risk.
Reality
Endogenous presence is not an argument for supraphysiologic exogenous dosing being safe. Chronic myostatin and activin inhibition disrupts fertility signaling, has unsettled cardiac implications, and theoretical oncologic risk given activin's tumor-suppressive roles. Long-term human safety at any dosing scale is not characterized.
Myth
Follistatin gene therapy is in clinical trials you could potentially join.
Reality
Not in muscular dystrophy, and not under a regulator anyone would recognise. The two registered AAV-FS344 trials — one in Becker muscular dystrophy and inclusion body myositis, one in Duchenne — both completed in 2017, the Duchenne study enrolling three patients against a planned six. No successor has been registered and no sponsor announcement has followed. What is currently recruiting under the follistatin gene therapy banner is a small intramuscular AAV9-follistatin study for age-related muscle loss run at a clinic in Honduras, outside the regulatory frameworks that govern drug development in the US or EU. Quoting the 2014–2017 dystrophy data as though it describes an ongoing programme is the most common way this page's subject is oversold.
Myth
More muscle from follistatin means more strength.
Reality
Not reliably, and this is a recognised problem for the whole myostatin-inhibitor class rather than a quibble. Bimagrumab, taldefgrobep and the ACE-031 programme all produced measurable changes in lean mass without the functional gains that would justify them, and a 2026 analysis argues that follistatin's anabolic effect depends on intact neuromuscular junction integrity — so denervated or ageing muscle can gain bulk without proportional force. A 2026 review of emerging myostatin modulators put it plainly: myostatin inhibition increases lean body mass but has shown inconsistent functional benefits.
Published Research
28 studiesGene, microbiome, and anti-aging doping in sport: molecular mechanisms, detection strategies, and implications for sports rehabilitation medicine
Follistatin-Mediated Browning of Adipose Tissue Improves Cardiometabolic Health
Minimalist d-Tripeptide Prodrug Mimetics of the Myostatin Prodomain as Selective Inhibitors of Skeletal Muscle Atrophy Signaling
Shim and colleagues, ACS Medicinal Chemistry Letters, October 2026. Relevant here because it is what an actual myostatin-inhibiting peptide looks like: minimalist D-tripeptide prodrugs modelled on the myostatin prodomain, inhibiting myotube atrophy at sub-micromolar potency and increasing soleus mass and grip strength in mice. The contrast with the 300-plus-amino-acid glycoprotein sold as "follistatin peptide" is the point.
Circulating Anti-Mullerian Hormone, Activins, Inhibins, and Follistatin in Women with Polycystic Ovary Syndrome and Idiopathic Hirsutism: A Case-Control Study
Follistatin drives AR-independent prostate cancer through BMP signaling inactivation and microenvironmental remodeling
PNAS, September 2026. Identifies follistatin itself as a driver of androgen-receptor-independent prostate cancer and treatment resistance, and reports an FST-Trap that neutralises it, resensitises resistant tumours to AR-targeted therapy and improves immunotherapy response. This inverts the usual oncology framing on this page: the concern is not only that inhibiting activin could remove a tumour suppressor, but that follistatin is itself oncogenic in some contexts — to the point that neutralising it is the therapeutic strategy.
Prognostic Value of FST and Relevance to Immune Infiltration in Head and Neck Squamous Cell Carcinoma
Genetic and Pharmacologic Inhibition of Myostatin Restores Muscle Mass in a Dynamin 2-Related Centronuclear Myopathy Mouse Model
Grip strength as a systems biomarker of aging: neuromuscular junction constraints and biomarker decoupling in gene therapy
Sewell and colleagues, Frontiers in Aging, August 2026. Argues that follistatin's anabolic effect depends on intact neuromuscular junction integrity, so denervated fibres gain mass without proportional function — a therapeutic paradox directly relevant to anyone expecting muscle size to translate into strength. Read with the disclosure in mind: both authors hold interests in a company developing AAV-FST344 follistatin gene therapy.
Strengthening muscle for healthy ageing: innovative treatments for sarcopenia
Emerging Myostatin and Metabolic Hormone Pathway Modulators in Cardiometabolic Disease
Follistatin Alleviates Vascular Dysfunction by Reducing Oxidative Stress and Promoting Browning in Perivascular Adipose Tissue
Kuganathan and colleagues, Hypertension November 2026. One of the few studies using follistatin as the intervention rather than measuring it as a biomarker: spontaneously hypertensive rats treated for eight weeks with follistatin or hydralazine as active comparator. Follistatin restored perivascular-adipose-mediated vascular relaxation through reduced reactive oxygen species, activin neutralisation and AMPK-dependent browning.
The crystal structure of the activin B:Fst288 complex and computational insights into the broad antagonistic activity and specificity of follistatin
Hok and colleagues, Journal of Biological Chemistry 2026. First crystal structure of the activin B:Fst288 complex with computational analysis of follistatin's broad TGF-β-family binding specificity. Direct structural-biology anchor for the FST-288/315/344 isoform discussion and the mechanistic breadth of follistatin's ligand-neutralization activity — meaningful upgrade over prior model-based understanding.
Follistatin and Systolic Function at Follow-Up in STEMI Patients: A Cardiac Magnetic Resonance Study
Follistatin Mitigates Atherosclerosis Through Activation of Arginine Metabolism and Adipose Browning
Safety and Efficacy of Approved and Unapproved Peptide Therapies for Musculoskeletal Injuries and Athletic Performance
2026 Sports Medicine narrative review (Mendias and colleagues) covering FS-344 follistatin among approved and unapproved peptide therapies for musculoskeletal injury and athletic performance — the most current expert synthesis distinguishing AAV-FS344 gene therapy from research-chemical follistatin peptide products and articulating the WADA-prohibited status.
Circulating plasma follistatin follows a 24-hour rhythm in healthy young males
Effects of liraglutide treatment for 35-days on total and regional fat free, lean, and bone mass, and on the Myostatin-Activin-Follistatin-IGF-1 axes: a secondary analysis of a randomized placebo-controlled crossover study
Mechanisms of Testosterone's Anabolic Effects on Muscle and Function: Controversies and New Insights
The Effect of Exercise on Spexin and Follistatin in Elderly Individuals
Effectiveness of resistance training on body composition, muscle strength, and biomarker in sarcopenic older adults: A meta-analysis of randomized controlled trials
The effects of resistance training on myostatin and follistatin in adults: A systematic review and meta-analysis
Circulating follistatin concentrations in adolescent PCOS: Divergent effects of randomized treatments
Circulating resistin and follistatin levels in obese and non-obese women with polycystic ovary syndrome: A systematic review and meta-analysis
Effects of Oral Contraception and Lifestyle Modification on Incretins and TGF-ß Superfamily Hormones in PCOS
The effects of concurrent training order on body composition and serum concentrations of follistatin, myostatin and GDF11 in sarcopenic elderly men
Effects of upper-body, lower-body, or combined resistance training on the ratio of follistatin and myostatin in middle-aged men
Follistatin induces muscle hypertrophy through satellite cell proliferation and inhibition of both myostatin and activin
Myostatin inhibition by a follistatin-derived peptide ameliorates the pathophysiology of muscular dystrophy model mice
Quick Facts
- Class
- Activin-Binding Protein
- Tier
- C
- Evidence
- Emerging
- Safety
- Limited Data
- Updated
- Oct 2026
- Citations
- 28PubMed
Also known as
Tags
Related Goals
Conditions Discussed
Evidence Score
Clinical Trials
View Clinical TrialsLinks to ClinicalTrials.gov for reference. Listing does not imply endorsement.