Follistatin (FS-344): research, side effects and dosage in studies

In short

Follistatin is a protein made by the body that binds myostatin, a brake on muscle growth [1]C. In humans, only transfer of the follistatin gene into muscle has been studied, in small open-label trials [4, 5]B; the follistatin protein sold online has not been studied as a treatment and has no marketing authorisation [9]D [18]regulator.

• Two different things under one name. In trials, people received the follistatin gene in a viral vector injected straight into the thigh muscle [4, 5]B. The "follistatin 344" sold online is a protein powder, and there is no treatment study of it at all [9]D.
• In Becker muscular dystrophy, walking distance increased in four of six patients after gene transfer, with no control group [4]B. The interpretation of the inclusion body myositis trial has been strongly criticised [5]B [6]E, not peer-reviewed.
• In a doping laboratory study, only nine of 17 black-market "follistatin 344" products contained follistatin [9]D.
• Eleven bodybuilders developed a fluid build-up under the retina that impaired vision after follistatin injections (case series) [10]B.
• In Finland follistatin is in Annex 1 A of the medicines list, and the WADA Prohibited List names it in class S4.3 [22, 23]regulator.

What is follistatin?

Follistatin is a protein made by the body that binds activin and myostatin and blocks their signal [1]D [2]. Myostatin is a growth factor that holds back the growth of skeletal muscle [1]C.

Follistatin exists in several forms. FS344 is a form produced by alternative splicing of the gene, and it is modified into FS315, which circulates in the blood. It binds activin about ten times more weakly than the FS288 form, which is why it was chosen for gene therapy [2].

The name means two different things. In trials, people received the follistatin gene, packed into an AAV viral vector and injected into the thigh muscle [4, 5]B. The muscle then makes follistatin itself. The "follistatin 344" sold online is a protein powder, and there is no approved medicinal product of it [9]D. This page keeps the two apart throughout.

Basics: What are peptides? All substances: Peptides A-Z.

Evidence at a glance

Each cell gives the kind of study and its source. The letter is the evidence level, not the result.

"-" = no such study is known.

What is follistatin studied for?

Follistatin is studied in humans as gene therapy for muscle diseases, and in animals also for metabolic and kidney disease. The protein sold online is not being studied as a medicine.

• Muscle diseases: the follistatin gene has been transferred into muscle in people with Becker muscular dystrophy [4]B, inclusion body myositis [5]B and Duchenne muscular dystrophy [8]E, not peer-reviewed. In mice, gene therapy has also been tried in a model of FSHD muscular dystrophy [27]C.
• Age-related muscle loss: the ClinicalTrials.gov registry lists completed and ongoing gene therapy studies in adults, with no published results [19, 20, 21]E, not peer-reviewed.
• Metabolism and kidneys: in diabetic mice gene transfer improved blood sugar [25]C, and follistatin given as a protein eased kidney damage [26]C.
• Doping control: doping laboratories have developed tests both for the protein sold online [9]D and for a transferred follistatin gene [28]D.

How does follistatin work?

Follistatin works by binding myostatin, so that myostatin cannot reach the activin type IIB receptor. In a laboratory experiment follistatin blocked this binding [1]D.

When mice were given a gene that made their muscles produce large amounts of follistatin, muscle mass increased as much as in mice that lack the myostatin gene entirely [1]C. In macaques, the FS344 gene transferred into the thigh muscle increased muscle size and strength durably [3]C.

Follistatin also binds activin, which regulates the pituitary's release of follicle-stimulating hormone (FSH). For this reason researchers chose the FS344 form for gene therapy, as it was expected to act less outside muscle [2] [3]C.

In humans the mode of action has only been studied in muscle biopsies taken after gene transfer: in Becker muscular dystrophy there was less fibrous tissue and the muscle fibres were larger, especially at the higher vector amount [4]B.

Has follistatin been studied in humans?

Only as gene therapy. Two small open-label follistatin gene transfer trials in humans have been published, and no randomised trial has given follistatin [4, 5]B. The follistatin protein sold online has not been given to humans in any treatment study.

Becker muscular dystrophy (2015)

Six patients received AAV1.CMV.FS344 vector injected into both thigh muscles. The trial was an open-label phase 1/2a study with no control group [4]B [6]E, not peer-reviewed.

In the six-minute walk test, the distance increased by 29-125 metres in four patients and did not change in two. According to the researchers, no adverse effects were seen [4]B.

Inclusion body myositis (2017)

Six patients received the same gene therapy in both thighs plus a supervised exercise programme [5]B. Walking distance converted to a yearly figure improved by an average of 56.0 metres in treated patients, while it declined by 25.8 metres in eight untreated comparison patients (p = 0.01) [5]B.

The comparison patients were chosen afterwards from a neuromuscular clinic's patients, and treatment was not randomised [6]E, not peer-reviewed. The problems of interpretation are gathered under Evidence against.

Duchenne muscular dystrophy (registry results)

Three boys received gene therapy into the thigh, buttock and lower leg muscles. According to the results recorded in the registry there were no dose-limiting toxicities, but the six-minute walk distance did not increase in any of the three [8]E, not peer-reviewed. The results have not been published as a peer-reviewed article.

The protein sold online: harm reports only

For the follistatin protein sold online, the only human data published is a case series: 11 bodybuilders sought eye care for impaired vision after follistatin injections [10]B. It describes a harm, not an effect.

Promising, but only in animal studies

These findings come from mice and have not been studied in humans. Results of animal studies cannot be carried straight over to humans. Evidence on muscle mass and strength is given above, because there is also data on it from gene transfer in humans.

• Type 2 diabetes no human studies

  In diabetic mice, a single intravenous follistatin gene transfer lowered blood activin B, improved blood sugar control and brought glycated haemoglobin down to the level of healthy mice. There were more insulin-producing cells in the pancreas even when treatment started in advanced diabetes [25]C.

  If it held in humans: the follistatin pathway could be a new way to protect the insulin-producing cells of the pancreas.

  Why it might not translate: this was gene transfer that makes the muscles produce follistatin continuously, not an injected protein. The study used db/db diabetic mice. In animal studies free follistatin is cleared quickly from the blood via the liver [12]C, so the effect of an injected protein could be quite different.

  Evidence now: one mouse study from Australia. We found no human study of follistatin for treating diabetes.

• Diabetic kidney damage no human studies

  In diabetic mice whose kidney damage had been accelerated with angiotensin II, follistatin protein given into the abdominal cavity reduced protein loss in the urine, kidney scarring and inflammation. In cell cultures it reduced the activation of kidney fibroblasts [26]C.

  If it held in humans: blocking activin could slow the progression of diabetic kidney disease.

  Why it might not translate: the model was an artificially accelerated mouse model, and follistatin was given only twice. According to the researchers, blocking activin may help in developing new treatments; it is not a treatment yet.

  Evidence now: one mouse study from the United States. We found no registered human study.

• FSHD muscular dystrophy no human studies

  In a mouse model of FSHD, a follistatin gene transferred with an AAV1 vector increased muscle mass and strength, even though the disease-causing DUX4 gene was still active [27]C.

  If it held in humans: blocking myostatin could ease the muscle weakness caused by FSHD, even if it did not affect the disease itself.

  Why it might not translate: the study was in mice whose disease was switched on with a drug, and the treatment did not act on the disease gene itself. A similar gene therapy did not increase walking distance in boys with Duchenne muscular dystrophy [8]E, not peer-reviewed.

  Evidence now: one mouse study. We found no human study of follistatin in FSHD.

Who studies follistatin?

The published follistatin gene therapy trials in humans are the work of one US group, at Nationwide Children's Hospital in Columbus [4, 5]B [7, 8]E, not peer-reviewed. The group's leaders and the hospital have filed a provisional patent application on gene delivery of myostatin inhibitors and follistatin use [3]C.

The newer registered studies are run by companies: Minicircle has registered two plasmid gene therapy studies in healthy adults [20, 21]E, not peer-reviewed, and Unlimited Biotechnology one AAV gene therapy study [19]E, not peer-reviewed. Doping analytics comes from laboratories including Seibersdorf in Austria and the German Sport University Cologne [9, 13]D.

Who wrote this page: the editorial team

This page was written by the Molecular Recovery editorial team. The draft was made with the help of AI, and the claims were checked against the sources (AI policy). The page has not been medically reviewed. How we work: About us.

How long does follistatin stay in the body?

How long injected follistatin stays in the human body is not known, because it has not been measured. In animal studies natural follistatin is cleared quickly via the liver because it binds heparin. Drug developers have therefore engineered the protein, and the engineered version gave about 20 times higher exposure in animal studies [12]C. No half-life in humans has been published.

Gene transfer is different: the muscle makes follistatin itself over a long time. In macaques the effect on muscle was durable [3]C. A doping test can tell the product sold online apart from the body's own follistatin, because the products studied carried a His tag from laboratory production [9]D.

What are the side effects of follistatin?

For injected follistatin protein, only one case series on harms in humans has been published [10]B. There is little safety data on gene transfer, because fewer than 20 people have been treated in the trials that are published or have results in the registry [4, 5]B [8]E, not peer-reviewed. A 2026 sports medicine review lists FS-344 among unapproved peptides marketed directly to patients, for which rigorous human safety data are scarce [14]. Peptide harms more generally: side effects in studies.

Fluid under the retina in bodybuilders

An eye clinic in Turkey described 11 men (mean age 36.8 years) who developed central serous chorioretinopathy, a build-up of fluid under the retina. All had injected a complete 1 mg vial of follistatin-344 under the skin of the abdomen. Eight had injected once, and in them the fluid cleared in 2.3 months on average. In the three who had injected several times, the condition came back [10]B.

A case series without a control group does not prove cause and effect, and the abstract does not say what the injected products actually contained. The authors consider follistatin injection a possible risk factor for the condition [10]B.

Harms in the gene therapy trials

In the Becker muscular dystrophy trial no adverse effects were seen [4]B. In the registry results of the Duchenne trial there were no dose-limiting toxicities; one of the three had a serious adverse event, a head injury from a fall, and all three had pain [8]E, not peer-reviewed. According to a critic, the harms data of the inclusion body myositis trial were presented misleadingly: falls occurred in a third of the patients, not in six percent [6]E, not peer-reviewed.

Reproductive organs: a warning from animal studies

In some lines of mice whose bodies made too much follistatin there were small testes, arrested sperm production, small ovaries and infertility. FSH was low only in the line in which follistatin was made widely in different tissues [11]C. According to researchers, follistatin's effect on pituitary hormones was a reason for caution in human use [2].

Product contents as a harm in itself

Of the black-market "follistatin 344" products, only some contained follistatin, and some contained other growth-promoting peptides [9]D. So users do not know what they are injecting.

Interactions and who has no data

There are no data on interactions with other medicines. In the inclusion body myositis gene therapy trial, patients received high-dose prednisone at the same time for about two months, but its effect was not assessed separately [6]E, not peer-reviewed.

There are no data on pregnancy, breastfeeding or children for the injected protein. Mouse studies suggest follistatin can affect the testes, ovaries and FSH [11]C, but there are no data on fertility in humans. The participants of the Duchenne gene therapy trial were children [8]E, not peer-reviewed.

Evidence against and what is unknown

The human evidence is small, open-label and comes from one group, and a sharp critique of how its main trial was interpreted has been published [6]E, not peer-reviewed.

Evidence against

• Critique of the inclusion body myositis trial. Harvard neurologist Steven Greenberg pointed out that the treated patients received four possibly effective things (gene therapy, high-dose prednisone, an exercise programme and the placebo effect of open-label treatment), while the comparison patients received none of them. According to him the primary outcome recorded in the registry was safety, not the walk test, and the yearly walking distance was a measure chosen afterwards [6]E, not peer-reviewed. The registry entry confirms that the primary outcome was safety [7]E, not peer-reviewed.
• Duchenne muscular dystrophy. In three boys gene therapy did not increase walking distance in any of them [8]E, not peer-reviewed.
• Blocking the myostatin pathway in the same disease. When the activin receptor antibody bimagrumab was tested in 251 patients with inclusion body myositis against placebo, walking distance at one year did not differ from placebo at any dose [15]A.
• Becker muscular dystrophy. In two of six patients walking distance did not change [4]B.

What the evidence does not support

• "Follistatin builds muscle in humans": increased muscle mass has been shown in animals [1, 3]C. In humans the effect has been measured only in patients with muscle disease after gene transfer, as walking distance and changes in muscle biopsies [4, 5]B. We found no study in healthy people.
• "The follistatin 344 sold online equals gene therapy": it does not. In gene therapy the muscle makes follistatin over a long time [3]C; the effect of the injected protein has not been studied, and in animal studies free follistatin is cleared quickly [12]C.
• "The vial contains follistatin": eight of 17 products tested did not [9]D.
• "It has been studied in healthy adults and found safe": no results have been published from the gene therapy studies in healthy people [20, 21]E, not peer-reviewed.

What is unknown

It is not known whether follistatin protein injected under the skin is absorbed and reaches muscle, how long it stays in the body, or what repeated injections lead to in the long term. The effects of stopping have not been studied either.

Follistatin dosage in studies

Follistatin has no approved dosage, and follistatin protein has not been given to humans in any treatment study. In humans only a gene therapy vector has been used, and its amount is given as vector genomes per kilogram of body weight (vg/kg). That is not a dose of follistatin and cannot be converted into an amount of protein.

What the numbers do not tell you. The vector amount says how much gene-carrying virus was injected into the muscle, not how much follistatin the muscle made. A mouse dose is not converted into a human dose by body weight. The vial size reported in the bodybuilder case series describes the amount injected, not a safe dose [10]B. Follistatin protein has not been given to humans in any published treatment study, so there is no dose page or calculator preset. Doses of other substances: Dosage.

Follistatin vs myostatin-blocking drugs: what is the difference?

Follistatin and the new antibody drugs block the same myostatin pathway, but only the antibodies have been tested in randomised trials, and one of them is an approved medicine.

• Apitegromab is an antibody that blocks the activation of myostatin. In children aged 2-12 with spinal muscular atrophy (SMA), the difference from placebo in motor function score at 12 months was 1.8 points. The difference for the higher dose alone was not statistically significant, and harms were as common as in the placebo group [16]A. The FDA approved apitegromab (Isembyld) on 11 Sep 2026 for SMA in patients who are also receiving a treatment targeting the SMN2 gene [17]regulator. In the EU its application for marketing authorisation was withdrawn [18]regulator.
• Bimagrumab is an antibody that binds the activin type IIB receptor [23]regulator. In inclusion body myositis it did not improve walking distance, and muscle spasms and diarrhoea were more common than with placebo [15]A.
• Follistatin binds myostatin and activin directly [1]C. There is no randomised human trial of it and no approved product [4]B [18]regulator.

All three are banned in sport, and class S4.3 of the WADA list names bimagrumab, apitegromab and follistatin [23]regulator.

Combinations and blends

Combinations of follistatin protein with other substances have not been studied in humans. In registered studies the follistatin gene has been combined with other genes: with the klotho gene in healthy adults [21]E, not peer-reviewed and with the gene for the blood vessel growth factor VEGF in age-related muscle loss [19]E, not peer-reviewed. No results have been published from either.

Black-market "follistatin 344" products sometimes contained other growth-promoting peptides instead of follistatin [9]D, so a product can be an unintended blend. Blends in general: Peptide blends: what is in the vial and why the seller's declaration is not enough.

Another substance sold online and linked to muscle growth is MGF (mechano growth factor).

Is follistatin legal in Finland?

Follistatin has no marketing authorisation and may not be sold or marketed as a medicine. It is in Annex 1 A of Fimea's medicines list, so in Finland it is controlled as a medicine and always treated like a prescription-only medicine [22]regulator.

• Medicines list. Annex 1 A of Fimea's decision 230/2025 names "Follistatiini" (follistatin). Substances in Annex 1 A are always treated, by their effect, like medicines supplied only on prescription [22]regulator.
• Marketing authorisation. On 14 Oct 2026 the EMA medicine data contained no medicine with follistatin [18]regulator. According to doping researchers there is no approved follistatin product, but the substance is available on the black market [9]D.
• Fimea's warning. Fimea has specifically warned against using injectable peptides bought online [24]regulator.
• The label "research use only" says what the product is meant for. It is not a permit for human use.

Overview of the law: Peptides and the law in Finland. Bringing them back from travel: Travelling with peptides.

This is not legal advice. Disclaimer.

Is follistatin doping?

Yes. Class S4.3 of the WADA 2026 Prohibited List (agents preventing activin receptor IIB activation) names myostatin-binding proteins such as follistatin. The class is prohibited at all times, in and out of competition [23]regulator.

Gene transfer is also prohibited: class M3 bans the use of nucleic acids that may alter gene expression, including gene transfer technologies, when they have the potential to enhance performance [23]regulator.

Tests exist. An Austrian doping laboratory developed a method that finds FS344 sold online in urine and serum and tells it apart from the body's own follistatin [9]D. In Cologne a test was developed for myostatin-blocking peptides derived from follistatin [13]D, and researchers at Australia's National Measurement Institute developed a blood test that detects a transferred follistatin gene [28]D.

Competitive athletes should check the current status with their national anti-doping agency, because the list is updated every year.

Product quality: how to assess a follistatin product

For follistatin, product contents are a documented problem. A doping laboratory tested 17 black-market products, most labelled "follistatin 344" and a few "follistatin 315". Only nine contained follistatin, and some of the others contained other growth-promoting peptides such as MGF and GHRP-2 [9]D.

All nine products that contained follistatin had His-tagged FS344, as used in laboratory production, and a lot of its clumps (oligomers) [9]D. The His tag shows that it is a laboratory-made protein, and it is what lets the test tell the product apart from the body's own follistatin [9]D. The effect of the clumps in humans is not known.

On a certificate of analysis (COA), look at the method used to identify the protein. Follistatin is a protein, not a short peptide, so an HPLC purity figure alone does not show whether the vial contains the right substance or whether it has clumped. In the study, identification was done with antibodies and electrophoresis [9]D. A guide: How to read a COA.

The future: what comes next?

The next results will probably come from gene therapies, not from the protein sold online. A phase 1/2 study that started in June 2026 is recruiting an estimated 12 participants with age-related muscle loss. They receive AAV9 follistatin gene therapy and a VEGF plasmid into muscle, and the primary outcome is harms. Estimated completion is June 2028 [19]E, not peer-reviewed.

Two plasmid gene therapy studies in healthy adults are completed according to the registry, but no results have been recorded there, and no peer-reviewed publication of them is known as of October 2026 [20, 21]E, not peer-reviewed.

Of the myostatin pathway drugs, apitegromab is already approved in the United States for SMA [17]regulator. There is no registered human study of follistatin protein.

FAQ

Read the research yourself: sources

Every source opens the original publication or the regulator's page. The level shows what the source itself reports.

1. Lee SJ, McPherron AC. Regulation of myostatin activity and muscle growth. Proc Natl Acad Sci U S A. 2001;98(16):9306-9311. PMID 11459935 C
2. Al-Zaidy SA, Sahenk Z, Rodino-Klapac LR, Kaspar B, Mendell JR. Follistatin Gene Therapy Improves Ambulation in Becker Muscular Dystrophy. J Neuromuscul Dis. 2015;2(3):185-192. PMID 27858738 (review)
3. Kota J, Handy CR, Haidet AM, et al. Follistatin gene delivery enhances muscle growth and strength in nonhuman primates. Sci Transl Med. 2009;1(6):6ra15. Erratum: Sci Transl Med. 2026;18(861):eaek4223. PMID 20368179 C
4. Mendell JR, Sahenk Z, Malik V, et al. A phase 1/2a follistatin gene therapy trial for becker muscular dystrophy. Mol Ther. 2015;23(1):192-201. PMID 25322757 B
5. Mendell JR, Sahenk Z, Al-Zaidy S, et al. Follistatin Gene Therapy for Sporadic Inclusion Body Myositis Improves Functional Outcomes. Mol Ther. 2017;25(4):870-879. PMID 28279643 B
6. Greenberg SA. Unfounded Claims of Improved Functional Outcomes Attributed to Follistatin Gene Therapy in Inclusion Body Myositis. Mol Ther. 2017;25(10):2235-2237. Letter to the editor. PMID 28927986 E, not peer-reviewed
7. ClinicalTrials.gov. NCT01519349: Follistatin Gene Transfer to Patients With Becker Muscular Dystrophy and Sporadic Inclusion Body Myositis (phase 1, Nationwide Children's Hospital, completed 2017, 15 participants, registered primary outcome: safety). Registry record, read 15 Oct 2026. ClinicalTrials.gov E, not peer-reviewed
8. ClinicalTrials.gov. NCT02354781: Clinical Intramuscular Gene Transfer of rAAV1.CMV.huFollistatin344 Trial to Patients With Duchenne Muscular Dystrophy (phase 1/2, completed 2017, 3 participants, results posted in the registry). Registry record, read 15 Oct 2026. ClinicalTrials.gov E, not peer-reviewed
9. Reichel C, Gmeiner G, Thevis M. Detection of black market follistatin 344. Drug Test Anal. 2019;11(11-12):1675-1697. Erratum: Drug Test Anal. 2020;12(10):1522-1533. PMID 31758732 D
10. Dağ U, Çağlayan M, Öncül H, Alakuş MF. Central serous chorioretinopathy associated with high-dose follistatin-344: a retrospective case series. Int Ophthalmol. 2020;40(11):3155-3161. PMID 32671599 B
11. Guo Q, Kumar TR, Woodruff T, et al. Overexpression of mouse follistatin causes reproductive defects in transgenic mice. Mol Endocrinol. 1998;12(1):96-106. PMID 9440814 C
12. Shen C, Iskenderian A, Lundberg D, et al. Protein Engineering on Human Recombinant Follistatin: Enhancing Pharmacokinetic Characteristics for Therapeutic Application. J Pharmacol Exp Ther. 2018;366(2):291-302. PMID 29752426 C
13. Walpurgis K, Agricola J, Thomas A, Thevis M. Myostatin inhibitory peptides in sports drug testing. Drug Test Anal. 2023;15(11-12):1477-1487. PMID 36946003 D
14. Mendias CL, Awan TM. Safety and Efficacy of Approved and Unapproved Peptide Therapies for Musculoskeletal Injuries and Athletic Performance. Sports Med. 2026;56(8):1921-1935. PMID 41966639 (review)
15. Hanna MG, Badrising UA, Benveniste O, et al. Safety and efficacy of intravenous bimagrumab in inclusion body myositis (RESILIENT): a randomised, double-blind, placebo-controlled phase 2b trial. Lancet Neurol. 2019;18(9):834-844. PMID 31397289 A
16. Crawford TO, Servais L, Mercuri E, et al. Safety and efficacy of apitegromab in nonambulatory type 2 or type 3 spinal muscular atrophy (SAPPHIRE): a phase 3, double-blind, randomised, placebo-controlled trial. Lancet Neurol. 2025;24(9):727-739. PMID 40818473 A
17. U.S. Food and Drug Administration. Drugs@FDA: BLA 761463, Isembyld (apitegromab-mstn), original approval 11 Sep 2026; label (revised 9/2026), section 1 Indications and usage. Read 15 Oct 2026. FDA regulator
18. European Medicines Agency. Medicine data (data set of 14 Oct 2026): no product with follistatin; Isembyld (apitegromab): application withdrawn. EMA regulator
19. ClinicalTrials.gov. NCT07443826: CALM-AF-AI: Counteracting Age-related Loss of Muscle With AAV-Follistatin Combined With Angiogenesis-Inducing VEGF Plasmid Gene Therapy (phase 1/2, Unlimited Biotechnology LLC, recruiting, estimated 12 participants). Registry record, read 15 Oct 2026. ClinicalTrials.gov E, not peer-reviewed
20. ClinicalTrials.gov. NCT06411366: Phase I: Safety and Efficacy of an Injectable Follistatin Plasmid Gene Therapy in Humans (Minicircle, completed 2023, 43 healthy participants, no results posted). Registry record, read 15 Oct 2026. ClinicalTrials.gov E, not peer-reviewed
21. ClinicalTrials.gov. NCT07285629: Safety and Efficacy of Klotho and Follistatin Gene Therapy (Minicircle, early phase 1, completed 2026, 14 healthy adults, no results posted). Registry record, read 15 Oct 2026. ClinicalTrials.gov E, not peer-reviewed
22. Finland. Lääkeluettelo (Fimea medicines list), 230/2025, section 2 and annex 1 A ("Follistatiini"). Finlex regulator
23. World Anti-Doping Agency. 2026 Prohibited List, section S4.3 ("Myostatin-binding proteins (e.g. follistatin, myostatin propeptide)") and section M3 Gene and cell doping. WADA regulator
24. Fimea. Fimea warns: do not use injectable peptides purchased online (29 Jun 2026). Fimea regulator
25. Davey JR, Estevez E, Thomson RE, et al. Intravascular Follistatin gene delivery improves glycemic control in a mouse model of type 2 diabetes. FASEB J. 2020;34(4):5697-5714. PMID 32141144 C
26. Bian X, Snow ZK, Zinn CJ, et al. Activin A Antagonism with Follistatin Reduces Kidney Fibrosis, Injury, and Cellular Senescence-Associated Inflammation in Murine Diabetic Kidney Disease. Kidney360. 2025;6(8):1278-1291. PMID 40152935 C
27. Giesige CR, Wallace LM, Heller KN, et al. AAV-mediated follistatin gene therapy improves functional outcomes in the TIC-DUX4 mouse model of FSHD. JCI Insight. 2018;3(22):e123538. PMID 30429376 C
28. Baoutina A, Bhat S, Li DK, Emslie KR. Towards a robust test to detect gene doping for anabolic enhancement in human athletes. Drug Test Anal. 2023;15(3):314-323. PMID 36445200 D

Sources read on 15 Oct 2026: PubMed abstracts (the Greenberg letter in full), the ClinicalTrials.gov registry, Fimea decision 230/2025, the EMA medicine data and Drugs@FDA. The WADA 2026 Prohibited List was read from the PDF published by WADA.

Evidence levels: A = randomised human trial or meta-analysis · B = observational human study or case series · C = animal study · D = cell or laboratory study · E = not peer-reviewed · regulator = a regulator's assessment or decision, not research evidence. The marker official means official product information (summary of product characteristics or label); it is not research evidence. For a review, the level shows what kind of research the statement rests on. No level: statements that something has not been studied, reviews' interpretations, named hypotheses and the general rules in our certificate-of-analysis guide.

Content is general information about research, not medical advice. If you have symptoms, contact a healthcare professional.