compound
Follistatin-344
A myostatin-binding protein covered claim by claim: every human trial delivered a gene rather than a protein, the developed version grew muscle without strength, and an anti-doping laboratory analysed what is actually being sold.
- Primary sources Registry records and papers are read at the source, not through summaries. Read the methodology
- Every claim graded Each claim about what a compound does carries an evidence tier and a numbered citation. How grades derive
- Sells nothing No cart, no price, and no product page anywhere on this site. Conflict disclosure
- Corrections logged Errors are fixed and recorded in a permanent public log, never edited away. Corrections log
Follistatin binds myostatin, and myostatin limits how much muscle an animal builds. That is a real and well characterised piece of biology, and it is why the idea has attracted serious money and serious trials.
The trials are where this page gets interesting, because of what they delivered. Every human study carrying the name follistatin 344 delivered the gene inside a virus or a plasmid, so that a patient's own muscle would make the protein. What is sold is the protein itself, and no registered trial has ever tested that.
Two other things are on the public record and neither appears on a page selling this. A pharmaceutical company took a follistatin-based protein into three Phase 2 trials and discontinued all three. And an anti-doping laboratory bought seventeen black-market products carrying this name and analysed them.
| Property | Value | Source |
|---|---|---|
| Category | Myostatin-binding protein, sold as an injectable for muscle growth | PMID 31758732 |
| Also known as | FS344, follistatin 344. A related splice form, follistatin 315, is also sold | PMID 31758732 |
| What the human trials delivered | A gene, not a protein. The registry types rAAV1.CMV.huFollistatin344 as a biological gene transfer and the Minicircle product as genetic | NCT01519349 |
| Registered trials of the injected protein | None. Of fifteen registry records naming follistatin or ACE-083, not one tests a follistatin protein injection of the kind sold | ClinicalTrials.gov, read 23 August 2026 |
| What is in black-market product | An anti-doping laboratory analysed seventeen products carrying this name and reported that nine contained follistatin, with other growth-promoting peptides found in some of the rest | PMID 31758732 |
| Anti-doping status | Named on the face of the WADA 2026 Prohibited List at S4.3, which covers myostatin inhibitors including myostatin-binding proteins and gives follistatin as the example | WADA 2026 Prohibited List |
Not medical advice
This page reports what has been documented about a compound. It is not medical advice, not a diagnosis, not a dosing protocol, and not a recommendation to obtain or use anything described here. Talk to a licensed clinician about anything concerning your health. Read the full disclaimer.
Reviewed against editorial standards Updated
Key takeaways
- Every human study carrying the name follistatin 344 delivered the gene rather than the protein, inside a virus or a plasmid, so that muscle would produce it. The registry states this in its own intervention-type field. What is sold is the protein, and no registered trial has tested it.
- The gene transfer trials are small. The Becker muscular dystrophy study enrolled fifteen participants and the Duchenne study enrolled three. [Human open-label] [1] [2]
- A follistatin-based protein developed by a pharmaceutical company increased muscle volume by up to 14.5 per cent in healthy volunteers, and the same report states that mean muscle strength did not significantly change. [Human RCT] [4]
- All three Phase 2 trials of that protein were terminated. The registry records the reason in the sponsor's own words: functional secondary endpoints were not achieved. [Human RCT] [5] [6] [7]
- An anti-doping laboratory obtained seventeen black-market products carrying this name and reported that nine contained follistatin. In some of the others it found different growth-promoting peptides instead, naming MGF and GHRP-2, and every positive sample carried a purification tag left over from laboratory manufacture.
- PRODUCTS TESTED, CONTAINING FOLLISTATIN
- 9 of 17
- TRIALS OF THE INJECTED PROTEIN
- 0
- NUMBERED SOURCES
- 12
- EVIDENCE GRADE
- D
Who researches Follistatin-344?
Almost everyone arrives here from the muscle claim, and the single most useful thing this page can do is separate three things that share one name.
There is a gene, delivered inside a virus, which is what every human trial used. There is a fusion protein developed as a medicine, which was tested properly and discontinued. And there is a recombinant protein sold online, which has never been in a trial and which an anti-doping laboratory has analysed.
A tested athlete has a short answer here. Follistatin is named on the face of the prohibited list as the example of a myostatin-binding protein.
What is Follistatin-344?
Plain-English version: a protein the body makes that grabs myostatin, the signal that tells muscle to stop growing, and holds it out of action.
Myostatin is a brake. Animals and people carrying inactivating mutations in it grow visibly more muscle, which is the observation the whole field rests on and which is not in dispute.
Follistatin binds myostatin and several related signalling proteins, taking them out of circulation. The body produces it in more than one length, and 344 amino acids is the splice form that gave this product its name. A shorter form, 315, is also sold [8].
The distinction that matters most on this page is not between the splice forms. It is that a protein of this size delivered by injection and a gene delivered inside a virus are different interventions with different behaviour, and the human record belongs entirely to the second.
A 344 amino acid splice form of the human follistatin protein · Approximately 38,000 Da for the unglycosylated 344 residue form
How strong is the evidence, claim by claim?
Every claim area this compound is discussed for gets a row, including the ones with the weakest support. The tier records what the row rests on, and the last column states what that work can and cannot show. Each tier links to its definition on the methodology page.
| Evidence Area | What Has Been Studied | Evidence Level | What It Can and Cannot Show |
|---|---|---|---|
| Binding myostatin | The mechanism, and the part of this page that is not in dispute. Follistatin binds myostatin and related members of the same signalling family, and myostatin restrains muscle growth. Reviews of the myostatin inhibition approach and of follistatin's own biology set this out [8] [11] | [In-vitro] | Binding a target in a laboratory is a mechanism rather than an outcome. The clearest demonstration of the gap is on this page: a follistatin-based protein built to exploit exactly this mechanism did increase muscle volume in people, and the strength measurements did not follow it |
| Muscle growth, the marketed use | The claim the product is sold for. No registered or published study has given an injected follistatin protein to a person for this or any other purpose. What exists under this name is human gene transfer, which delivers the gene inside a virus or a plasmid so that muscle produces the protein in place, and which the registry types as a biological or genetic intervention rather than a drug. Those studies are set out in the human testing table below and they are about a different intervention [1] [2] [3] [9] [10] [12] | [Anecdote] | There is nothing here to grade. The gene transfer studies do not test the product sold, and an anti-doping laboratory that analysed seventeen black-market products carrying this name reported that nine contained follistatin. A claim resting on trials of a different intervention, in a market where fewer than two thirds of tested products contained the substance on the label, is an anecdote rather than a finding |
Rolled up, that puts Follistatin-344 at evidence grade D Animals and anecdote . No completed human study of this compound for any use. The claim set is animal, in-vitro, and anecdote. A grade describes the quality of the research, not whether something works and not whether anyone should use it. The derivation is published.
How Follistatin-344 is thought to work
The mechanism is the strongest part of this compound's case and it is worth stating cleanly before the sections that complicate it.
1. Releasing a brake rather than pressing an accelerator, blocking the signal that tells muscle to stop growing (established)
Myostatin limits muscle growth, and animals and people carrying inactivating mutations in it are visibly more muscular. Follistatin binds myostatin and holds it out of action, which removes that limit.
This is why the approach attracted real investment. It is also why the results below matter more than they would for a compound with a speculative mechanism: the biology was right and the clinical outcome still did not follow. [In-vitro] [8] [11]
2. Why a gene and a protein are different interventions, making the protein inside the muscle is not the same as injecting it (established by the trial designs themselves)
A gene delivered inside a virus to a muscle turns that muscle into a factory producing the protein locally and continuously. The registry types those interventions as biological and genetic for that reason.
An injected protein arrives all at once, distributes according to its size and clearance, and is gone. Follistatin is a large protein, and nothing published describes what an injected dose of it does in a person.
A reader who takes the gene transfer results as evidence for an injected product has substituted one intervention for another. That substitution is the single most common error made about this compound. [Human open-label] [1] [2]
What we do not know
What an injected follistatin protein does in a person, at any amount. No registered trial has tested it.
What the completed 43 participant plasmid study found. It has posted no results and no publication was located.
What the published gene therapy reports say in detail. This site read the registry records and the paper titles, not the full texts.
Whether follistatin 315 behaves differently from 344 in any way that matters to a reader. Both are sold and this site did not establish a difference.
What this evidence can and cannot show
These results come from Human gene transfer trials, non-human primates, and cell work for the binding itself. in Becker and Duchenne muscular dystrophy; healthy volunteers for the developed protein., not from people. An animal model is a deliberate simplification: the injury is created on purpose, the animal is young and healthy, the dose is scaled to body weight in a way that does not translate directly, and the outcome is measured at a fixed point rather than lived with. Cell and tissue work is a further step removed, because the concentrations that produce an effect in a dish are often far above anything a body reaches. Mechanism is a reason to run a trial. It is not a substitute for one, and compounds that looked mechanistically convincing have failed in people many times.
Has Follistatin-344 been tested in humans?
Fifteen registry records name follistatin or the follistatin-based drug ACE-083 as an intervention, pulled from the ClinicalTrials.gov v2 API on 23 August 2026 and filtered to records whose interventions actually name one of them.
They divide into two programmes that share a mechanism and share nothing else. Neither tested a follistatin protein injection.
| Study | People | What was done | Result | Evidence level |
|---|---|---|---|---|
| NCT01519349 | 15 | Gene transfer of rAAV1.CMV.huFollistatin344 to muscle, in Becker muscular dystrophy | Completed. No posted results | [Human open-label] |
| NCT02354781 | 3 | The same gene transfer, in Duchenne muscular dystrophy | Completed. Results posted | [Human open-label] |
| NCT06411366 and NCT07285629 | 43 and 30 | An injectable follistatin plasmid in frailty and ageing, and follistatin with klotho in healthy adults | One completed with no posted results, one recruiting | [Human open-label] |
| NCT02257489 | 58 | Phase 1 of ACE-083, a follistatin-based fusion protein, given locally in healthy postmenopausal women | Completed. Muscle volume rose by up to 14.5 per cent; mean strength did not significantly change | [Human RCT] |
| NCT02927080 | 95 | Phase 2 of ACE-083 in facioscapulohumeral muscular dystrophy | Terminated. The registry states it did not achieve functional secondary endpoints | [Human RCT] |
| NCT03124459 | 63 | Phase 2 of ACE-083 in Charcot-Marie-Tooth disease | Terminated for the same stated reason | [Human RCT] |
| NCT03943290 | 62 | Long-term extension of both Phase 2 programmes | Terminated because the parent trials did not achieve their functional secondary endpoints | [Human RCT] |
Why we are not calling this proof
Not one of these tested the product that is sold. The first three rows delivered a gene or a plasmid. The last four tested a fusion protein that is a different molecule, acting in one named muscle rather than circulating.
The ACE-083 rows are the most informative on the page even though they are about a different molecule, because they are the only place where the follistatin premise was tested to a standard capable of settling something. The muscle grew and the function did not follow.
Benefits: what the research shows
The claims table holds what is claimed and what sits behind each claim. This section is the shape of the record as a whole.
The honest bottom line on benefits
The mechanism is sound, the human evidence belongs to a different intervention, and the one properly conducted test of the idea separated the two things a buyer assumes go together. Muscle volume rose measurably. Strength and function did not follow, and three Phase 2 trials were discontinued on exactly that point.
For a reader deciding whether to buy the protein, the analytical finding matters as much as any of it: of seventeen products carrying this name that a doping laboratory tested, nine contained follistatin.
How long Follistatin-344 stays in the body
The gene transfer studies do not produce pharmacokinetic data of the usual kind, because nothing is administered that then clears. A gene delivered into muscle produces protein locally for as long as the transduced cells keep expressing it, which is a different question from a half-life.
The ACE-083 programme did produce human data, and it is data about a different molecule engineered to act locally where it is placed rather than to circulate.
For the protein that is sold, there is nothing. No human half-life, no exposure figure, no route comparison, because no study has been run. Follistatin is also a large protein, which is generally an obstacle to absorption by any route other than injection, and nothing published addresses how much of an injected dose reaches muscle.
No pharmacokinetic data exists for an injected follistatin protein in a person. [Human open-label] [1] [4]
What is documented about dosing
Nothing here is a dosing recommendation. Statements about dosing reflect community and research reports only.
Commonly cited protocols (extrapolated, not validated)
Nothing here is a dosing recommendation. Statements about dosing reflect community and research reports only.
| Study | What was given | Frequency | Duration | Notes |
|---|---|---|---|---|
| Gene transfer trials | A quantity of viral vector, not a quantity of protein | Single administration to muscle | One-off, with the muscle then expressing the protein | Becker and Duchenne studies, 15 and 3 participants. Not comparable to a protein injection |
| ACE-083 Phase 2 | 240 mg per muscle in the published reports | Injected bilaterally as described in each protocol | Six months to the primary endpoint | A different molecule, designed to act in one named muscle rather than to circulate. Both trials terminated |
| Injected follistatin protein | Nothing documented | Nothing documented | Nothing documented | No registered or published study exists of the product that is sold |
Commonly cited protocols (extrapolated, not validated) circulate for this compound in microgram amounts by injection. They did not come from a study, because no study of an injected follistatin protein in a person exists.
Neither trial figure converts. A quantity of viral vector is not a quantity of protein and the two are not related by any published conversion. The ACE-083 figure belongs to a different molecule designed to stay where it is placed, which is the opposite of what a systemic product is meant to do.
Nothing here is a dosing recommendation. Statements about dosing reflect community and research reports only.
Main routes people compare, and what each source class actually reported, are set out on the documented protocols page.
Reported effects and what has been measured
What the trials recorded
The Phase 1 study of the follistatin-based protein in 58 healthy postmenopausal women reported no serious adverse events, no dose-limiting toxicities and no discontinuations resulting from adverse events. That is a real observation and it belongs to a different molecule, acting in a single muscle, over a short period.
The gene transfer studies are small, at fifteen and three participants, and this site read their registry records rather than their published reports, so no safety findings from them are stated here. [Human RCT] [4]
What the product itself introduces
The analytical finding on this page is a safety-relevant fact of a kind that rarely exists for these compounds. Of seventeen black-market products carrying this name that an anti-doping laboratory tested, nine contained follistatin, and in some of the others the laboratory found different growth-promoting peptides, naming MGF and GHRP-2.
Every one of the nine positive samples carried a His-tag, a handle attached to a protein to purify it in a laboratory, and a high degree of oligomerisation. A protein carrying its purification tag is a research reagent rather than a preparation made for administration.
Long-term exposure to an injected follistatin protein has not been characterised in any published study, because no such study exists. [In-vitro] [12]
What has been measured about Follistatin-344, and what has never been studied
Talk to a licensed clinician about anything concerning your health.
Sourcing and quality
What a credible product should show
There is no approved follistatin product of any kind, so there is no reference standard and no pharmacopoeial monograph for a laboratory to check a batch against.
This is one of the few compounds in this catalogue where independent analysis of the market has been published. An anti-doping laboratory tested seventeen products and reported what it found, which is a far better basis for judgement than any vendor document [12].
Red flags
Gene therapy trials cited as evidence for an injected protein. Those studies delivered a gene inside a virus and the registry types them as biological gene transfer.
ACE-083 results cited as this compound's. That is a different molecule acting in one named muscle, and all three of its Phase 2 trials were terminated.
Muscle volume presented as strength. The one place both were measured in people, volume rose and mean strength did not significantly change.
A certificate of analysis offered as proof of identity. In the published analysis, eight of seventeen products contained no follistatin at all.
Will it show on a drug test?
Named on the face of the WADA 2026 Prohibited List at section S4.3, which covers myostatin inhibitors including myostatin-binding proteins and gives follistatin as the example. The same section names decoy activin receptors, giving ACE-031.
The 2019 analytical paper states the same class placement for its own year, which corroborates the position across two editions of the list.
Section S4 substances are prohibited at all times. This site has not established the Specified status of the S4 class and does not state one.
Storage
No storage guidance is given here. Storage belongs to a characterised formulation, and the published analysis of market products found purification tags and oligomerisation rather than a characterised preparation.
Regulatory status, as of 23 August 2026
| Body | Position | Date | Document |
|---|---|---|---|
| No agency | No approved follistatin product exists in any indication, anywhere | Read 23 August 2026 | ClinicalTrials.gov and the absence of any approval |
| ClinicalTrials.gov | Fifteen records name follistatin or ACE-083 as an intervention. None tests an injected follistatin protein of the kind sold | Swept 23 August 2026 | ClinicalTrials.gov v2 API |
| Acceleron Pharma | Three Phase 2 trials of the follistatin-based protein ACE-083 terminated, with the registry recording that functional secondary endpoints were not achieved | Records read 23 August 2026 | NCT02927080, NCT03124459, NCT03943290 |
| WADA | Named at S4.3 as the example of a myostatin-binding protein. Prohibited at all times. Specified status not established by this site | 2026 list, read 23 August 2026 | WADA 2026 Prohibited List |
There is no approval to report for follistatin in any form. The regulatory record for this compound is its trial registrations and the discontinuation of the one programme that got as far as Phase 2.
The three termination entries are quoted rather than summarised because a registry field recording why a trial stopped is a primary source, and the sponsor's own wording is more precise than any paraphrase of it.
This section is dated and re-checked on review. It records actions and their documents, not evidence about an effect, and carries no evidence tier.
Follistatin-344 compared with other performance peptides
| Compound | Evidence grade | What the human record covers | Read more |
|---|---|---|---|
| Follistatin gene therapy | Covered on the comparison page | The intervention every human trial carrying this name actually used: a gene delivered inside a virus so muscle produces the protein in place | /peptides/difference/follistatin-344-vs-gene-therapy/ |
| ACE-083 | Not covered as a compound on this site | A follistatin-based fusion protein developed as a medicine. Grew muscle volume without a significant strength change, and all three Phase 2 trials were terminated | Described in the human testing table above |
| ACE-031 and the myostatin inhibitors | Graded on the performance group page | Other approaches to the same brake, with separate evidence bases. WADA names ACE-031 in the same S4.3 entry | /peptides/groups/performance/ |
The comparison that decides this page is with gene therapy, because that is what the human evidence actually is. The comparison page covers it in full and this hub points there rather than repeating it.
The ACE-083 row is the one a reader is least likely to have seen. A company built a protein to exploit this mechanism, measured muscle growth in people, and stopped when function did not follow.
What Follistatin-344 typically costs
Frequently asked questions
Has injected follistatin been tested in humans?
No. Fifteen registry records name follistatin or the follistatin-based drug ACE-083, and none tests an injection of the follistatin protein of the kind that is sold.
What did the human trials actually deliver?
A gene. The muscular dystrophy studies delivered rAAV1.CMV.huFollistatin344, a gene inside a virus, which the registry types as a biological gene transfer. Two other studies delivered a plasmid. In each case the muscle then produces the protein in place.
Why does the difference between a gene and a protein matter?
They are different interventions. A gene delivered into muscle produces protein locally and continuously; an injected protein arrives at once, distributes by size and clearance, and is gone. Nothing published describes the second for this compound.
What was ACE-083?
A follistatin-based fusion protein developed by a pharmaceutical company, designed to act in one named muscle rather than to circulate. It is the closest thing to a proper test of the follistatin premise.
What happened to it?
Its Phase 1 increased muscle volume by up to 14.5 per cent in healthy volunteers, and the same report states mean muscle strength did not significantly change. All three of its Phase 2 trials were terminated, with the registry recording that functional secondary endpoints were not achieved.
Does more muscle volume mean more strength?
In the one programme where both were measured in people, it did not. That is the most useful single fact on this page.
What is actually in black-market follistatin?
An anti-doping laboratory tested seventeen products carrying this name and reported that nine contained follistatin. In some of the others it found different growth-promoting peptides, naming MGF and GHRP-2. All nine positive samples carried a His-tag and a high degree of oligomerisation.
What is a His-tag and why does it matter?
It is a handle attached to a protein so a laboratory can purify it. Finding it in every positive sample indicates material made as a research reagent rather than as a preparation intended for administration.
Is follistatin 315 different from 344?
They are different splice forms of the same protein and both are sold. This site did not establish whether the difference matters for a reader's purposes, and it is recorded as an open question rather than answered.
Is it banned in sport?
Yes, by name. The WADA 2026 Prohibited List names follistatin at S4.3 as the example of a myostatin-binding protein. Section S4 substances are prohibited at all times.
Is there a dose?
No amount has been established for an injected follistatin protein in a person, and neither the gene transfer figures nor the ACE-083 figure converts into one.
References
- Nationwide Children's Hospital. Follistatin Gene Transfer to Patients With Becker Muscular Dystrophy. Phase 1, 15 participants, completed, no posted results. Intervention rAAV1.CMV.huFollistatin344, typed BIOLOGICAL in the registry record. Read through the v2 API on 23 August 2026. ClinicalTrials.gov. 2012. NCT01519349
- Mendell JR. Clinical Intramuscular Gene Transfer of rAAV1.CMV.huFollistatin344. Phase 1/2, 3 participants, completed, results posted. Duchenne muscular dystrophy. ClinicalTrials.gov. 2015. NCT02354781
- Mendell JR, Sahenk Z, Malik V, Gomez AM, Flanigan KM, Lowes LP, Alfano LN, Berry K, Meadows E, Lewis S, Braun L, Shontz K, Rouhana M, Clark KR, Rosales XQ, Al-Zaidy S, Govoni A, Rodino-Klapac LR, Hogan MJ, Kaspar BK. A phase 1/2a follistatin gene therapy trial for becker muscular dystrophy. Mol Ther. 2015. PMID 25322757 Identified from PubMed metadata; the full text was not read for this page.
- Glasser CE, Gartner MR, Wilson D, Miller B, Sherman ML, Attie KM. Locally acting ACE-083 increases muscle volume in healthy volunteers. Muscle Nerve. 2018. PMID 29486514 DOI 10.1002/mus.26113 Phase 1 in 58 healthy postmenopausal women, 42 on drug and 16 on placebo. Maximum mean muscle volume increases of 14.5 per cent and 8.9 per cent, with no significant changes in mean muscle strength, and no serious adverse events or dose-limiting toxicities. Read as an abstract.
- Acceleron Pharma, Inc. Study of ACE-083 in Patients With Facioscapulohumeral Muscular Dystrophy. Phase 2, 95 participants, terminated, results posted. The registry's whyStopped field reads: Study was discontinued as it did not achieve functional secondary endpoints. ClinicalTrials.gov. 2016. NCT02927080
- Acceleron Pharma, Inc. Study of ACE-083 in Patients With Charcot-Marie-Tooth Disease. Phase 2, 63 participants, terminated, results posted. The registry's whyStopped field records that investigation was discontinued as it did not achieve functional secondary endpoints in the parent trial. ClinicalTrials.gov. 2017. NCT03124459
- Acceleron Pharma, Inc. Extension Study to Evaluate the Long-Term Effects of ACE-083. Phase 2, 62 participants, terminated, results posted. The registry records that investigation was discontinued because functional secondary endpoints were not achieved in the parent trials. ClinicalTrials.gov. 2019. NCT03943290
- Patel K. Follistatin. Int J Biochem Cell Biol. 1998. PMID 9785474 A review of the protein and its splice forms, including the 344 and 315 residue variants.
- Minicircle. Phase I: Safety and Efficacy of an Injectable Follistatin Plasmid. 43 participants, completed, no posted results. Intervention typed GENETIC in the registry record. This site states what the registry records and nothing about the organisation. ClinicalTrials.gov. 2024. NCT06411366
- Minicircle. Follistatin and klotho gene therapy in healthy adults. Early Phase 1, 30 participants, recruiting as of 23 August 2026. ClinicalTrials.gov. 2026. NCT07285629
- Rodino-Klapac LR, Haidet AM, Kota J, Handy C, Kaspar BK, Mendell JR. Inhibition of myostatin with emphasis on follistatin as a therapy for muscle disease. Muscle Nerve. 2009. PMID 19208403 Identified from PubMed metadata; the full text was not read for this page.
- Reichel C, Gmeiner G, Thevis M. Detection of black market follistatin 344. Drug Test Anal. 2019. PMID 31758732 DOI 10.1002/dta.2741 Seventeen black-market products were analysed. Nine contained follistatin; in some of the others growth-promoting peptides including MGF and GHRP-2 were found. All nine positive samples contained His-tagged FS344 and a high degree of its oligomers. Read as an abstract, which states these figures explicitly.