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Follistatin-344: The Definitive Guide

The muscle-growth protein behind the gene-therapy headlines, the vials sold online, and what the research actually shows.

Follistatin-344 at a glance.

Follistatin-344 at a glance. A natural human glycoprotein. The one-dimensional domain map spans residues 1 through 344 on one linear axis. On narrow screens, letters A through F identify the six sections in order: signal section 1–29, removed before release; N-terminal domain approximately 30–93; follistatin domain 1 approximately 94–166; follistatin domain 2 approximately 167–243; follistatin domain 3 approximately 244–318; and acidic tail approximately 319–344. These boundaries are approximate because source features overlap. Sugar attachment sites are at 124 and 288. Follistatin domain 1 binds myostatin more strongly and domain 2 is key for activin binding (Schneyer 2008). FS315 spans 30–344 and is the main form in blood. FS288 spans 30–317 and stays on cell surfaces without the acidic tail. How researchers think it works, in animal and cell studies and not proven in people: Myostatin trap binds myostatin before it reaches muscle receptors; activin block too also traps activins; growth signaling in mice needed the mTOR pathway and insulin or IGF-1 signals. Discussed for building muscle size and strength, keeping muscle during weight loss, and anti-ageing gene therapy. Most-cited protocol: 100 mcg a day, subcutaneous, for about 10 days, with no human vial dose tested. Human evidence: no trials of vials; gene therapy results for 15 patients with muscle diseases, and larger trials of ACE-083, an engineered drug; an 11-person eye-condition case series followed vial use. Not an approved medicine; prescription-only in Australia; banned in sport at all times under WADA 2026.

Follistatin-344

Follistatin, a natural human protein that blocks myostatin (a brake on muscle growth). "344" is the length of the starting chain made from the FST gene; the body trims it to the 315-amino-acid working form, FS315.

Also called FS344 · FST-344 · FS315 (mature form) · FSH-suppressing protein

Natural human glycoprotein (a full-sized protein, not a short peptide)

344 amino acids (precursor) → 315 mature C1599H2548N462O524S43 (precursor, without sugars) 38.0 kDa before sugars Natural human protein; vials are lab-made

Made by the body (mostly the liver); retail vials are lab-made protein

signal section, cut off before release

N-terminal domain
Follistatin domain 1binds myostatin more strongly
Follistatin domain 2key for activin binding
Follistatin domain 3
Acidic tail
30–344 = FS315, the main form in blood
FS288: shorter form without the acidic tail; stays on cell surfaces
  1. ASignal section (removed)
  2. BN-terminal domain
  3. CFollistatin domain 1binds myostatin more strongly
  4. DFollistatin domain 2key for activin binding
  5. EFollistatin domain 3
  6. FAcidic tail
  • Removedsignal section
  • N-terminal domain
  • Follistatin domains1–3, the parts that grip myostatin and activin
  • Acidic tail
  • Branchessugar attachment sites

Sections show order along the chain, not 3D shape.

How researchers think it works

In animal and cell studies, not proven in people

  1. Myostatin trap

    Binds myostatin before it reaches muscle receptors; engineered mice grew far larger muscles.

    Animal and cell studies

  2. Activin block too

    Also traps activins; in mice, blocking activin added to follistatin's muscle growth.

    Animal study

  3. Growth signaling

    In mice, follistatin-driven growth needed the mTOR pathway and insulin or IGF-1 signals.

    Animal study

Discussed for

Building muscle size and strength; keeping muscle during weight loss; anti-ageing gene therapy

Most-cited protocol

100 mcg a daysubcutaneous, for about 10 days (one 1 mg vial)

Most common pattern in the reviewed sources; no human dose has been tested

Human evidence

No vial trialsGene therapy results for 15 patients with muscle diseases; ACE-083, an engineered drug, in larger trials

An 11-person eye-condition case series followed vial use

Status

  • Not an approved medicine
  • Prescription-only (Schedule 4) in Australia
  • Banned in sport at all times (WADA 2026, S4.3)
Conceptual summary: the domain map shows the order of the protein's building blocks, not its 3D shape. Mechanism panels summarize animal and cell findings. The human trials used gene therapy or an engineered drug, never the vials sold online.
Published by DoserlyUpdated Next scheduled review: December 202646 min readHow this guide was made
In this guide

What is Follistatin-344?

Follistatin-344 is the name used online for follistatin, a natural human protein that blocks myostatin, a signal that limits how large muscles grow. People discuss it for building muscle, and researchers have tested it as a gene therapy for muscle-wasting diseases.

Follistatin is made from the human FST gene, and most of it in the blood comes from the liver. The gene's instructions produce a chain of 344 amino acids (the building blocks of proteins). Before the protein leaves the cell, the first 29 are cut off, leaving the working form of 315, called FS315. A shorter version made from the same gene, FS288, stays attached to cell surfaces. So "344" names the starting instructions, not a special drug. At about 35,000 to 38,000 daltons before sugars are added, follistatin is more than 20 times longer than BPC-157, a 15-amino-acid peptide. [1], [14], [15]

Follistatin was discovered in 1987 as a protein that lowers follicle-stimulating hormone (FSH), a hormone that drives fertility. It binds several related signals: myostatin, the activins and GDF11, a closely related growth signal. [16], [17], [2]

It is investigational: anti-doping scientists noted in 2019 that no approved follistatin medicine existed, and we found none approved since. [10], [18], [167]

Gene therapy or vial: which one is “Follistatin-344”?

The name covers two very different things. In medical research, "FS344" means the follistatin gene packaged inside a harmless virus and injected once into muscle, so the muscle makes follistatin itself for months or years. Online, "Follistatin-344" usually means a vial of freeze-dried protein sold for repeated injections. Every clinical trial of FS344 used the gene therapy. No study has tested the vials in people. [6], [7], [8], [10]

Two things called Follistatin-344. What is injected: Gene therapy: The follistatin gene inside a modified virus (AAV1); Vial: Freeze-dried follistatin protein, mixed with water. Where and how often: Gene therapy: Into thigh muscles, once; Vial: Usually into the fatty layer under the skin (subcutaneous), daily for about 10 days. How the amount is counted: Gene therapy: Vector genomes per kilogram (e.g. 6 × 10¹¹ per leg); Vial: Micrograms (usually 100 mcg). How long it lasts: Gene therapy: Muscle kept making follistatin for at least 15 months in monkeys; Vial: Not measured in people; in rats, blood levels halved in about 4 minutes, then about 2 hours. Tested in people?: Gene therapy: Yes: results reported for 15 patients with muscle diseases; Vial: No clinical trial; an 11-person eye-condition case series followed vial use. Can it be stopped?: Gene therapy: No: a one-time treatment that cannot be switched off; Vial: Injections can stop; what happens afterward has not been studied. What is inside: Gene therapy: Manufactured for clinical trials; Vial: Only 9 of 17 tested black-market products contained follistatin. Gene therapy results cannot be used as evidence for vials.

Two things called Follistatin-344

What is injected
Gene therapy: The follistatin gene inside a modified virus (AAV1)
Vial: Freeze-dried follistatin protein, mixed with water
Where and how often
Gene therapy: Into thigh muscles, once
Vial: Usually into the fatty layer under the skin (subcutaneous), daily for about 10 days
How the amount is counted
Gene therapy: Vector genomes per kilogram (e.g. 6 × 10¹¹ per leg)
Vial: Micrograms (usually 100 mcg)
How long it lasts
Gene therapy: Muscle kept making follistatin for at least 15 months in monkeys
Vial: Not measured in people; in rats, blood levels halved in about 4 minutes, then about 2 hours
Tested in people?
Gene therapy: Yes: results reported for 15 patients with muscle diseases
Vial: No clinical trial; an 11-person eye-condition case series followed vial use
Can it be stopped?
Gene therapy: No: a one-time treatment that cannot be switched off
Vial: Injections can stop; what happens afterward has not been studied
What is inside
Gene therapy: Manufactured for clinical trials
Vial: Only 9 of 17 tested black-market products contained follistatin

Gene therapy results cannot be used as evidence for vials.

Two things share one name. The human studies delivered the follistatin gene once into muscle; the vials sold online contain protein injected repeatedly, and testing found that some contained no follistatin at all. Sources: Becker MD gene therapy trial · Black-market product testing · Inclusion body myositis trial · Duchenne trial results · Macaque gene therapy study · Rat IV follistatin study · PeptideWiki dosage guide (website claim) · Eye-condition case series.

Typical Follistatin-344 Protocols

Subcutaneous injection (into the fatty layer under the skin) · protein vials sold as Follistatin-344 · Amounts in micrograms (mcg) [5]
ExampleAmount each timeFrequencyTotal per dayDuration
Low100 mcgOnce daily100 mcg10–14 days
Mid100–200 mcgOnce daily100–200 mcg10–20 days
High200–300 mcg in one injection, or that total split into twoOnce or twice daily200–300 mcg20–30 days
Longer course, followed by a longer break

The most common protocol in the reviewed sources is 100 mcg once a day by subcutaneous injection for about 10 days, which uses exactly one 1 mg vial. Most pages place it inside a wider range of about 50–200 mcg a day for 10–30 days. [3], [4], [19], [20], [21], [22]

Before relying on any row: no amount in this table has been tested for safety in people, so no safe amount is known. [3], [13] The only published harm report linked to vials describes 11 bodybuilders whose eyesight worsened because fluid collected under the retina after they injected whole 1 mg vials; all three who had injected more than once had repeat episodes. Corticosteroid medicines, such as prednisone, are a major risk factor for the same eye condition, and the report does not say whether the men were also taking them. [9], [94] Only 9 of 17 black-market products tested contained follistatin, so the label may not match the vial. [10] Work out syringe units with the reconstitution calculator rather than copying them from someone else's protocol. Follistatin changes fertility hormones in animals, and it has not been studied in pregnancy, breastfeeding or anyone under 18. It is banned in sport at all times. [16], [124], [12] Full risks ↓

Titration Changing the amount in steps
Most pages keep one fixed amount for the whole course. One presents its lowest tier, 100 mcg a day for 10–14 days, as the place to start and check tolerance. Two others start higher and then reduce: 200 mcg a day for days 1–3, then 100 mcg a day for days 4–30; or daily injections for 7 days, then twice-weekly injections for 8–12 weeks. [5], [23], [22]
Breaks and cycles
Breaks are long compared with the courses. The source of the table above describes 20–30 days off after a 10-day course, 40–60 days after a 20-day course and 60–90 days after a 30-day course, with one to three courses a year. Others describe 3–4 weeks off, a 4-week break after a 10–20-day course, or at least 4–6 weeks. [5], [22], [4], [24]

Read the units: mcg means micrograms; 1 mg equals 1,000 mcg, so a 1 mg vial holds ten 100 mcg amounts. The amounts refer to follistatin protein as labelled on the vial, and testing has shown that labels can be wrong. Gene therapy doses are counted in vector genomes, not micrograms, and cannot be converted into a vial amount. [3], [10], [6]

Each row is a complete schedule from one source, so its amount and duration belong together. Low, mid and high are alternatives, not steps to move through. These schedules come from protocol websites rather than clinical trials: no study has given people injections of follistatin protein, so no tested human dose exists. [5], [13]

Where protocols differ: per injection or per day, breaks, muscle injections and units ↓

Where these numbers come from

The complete low, mid and high rows, and the break lengths that go with them, come from PeptideWiki's follistatin dosage guide (reference [5]), which labels them conservative, standard and aggressive. Its high tier gives 200–300 mcg as the amount per day, taken once or split into two injections. [5]

The recurring 100 mcg a day for about 10 days is cross-checked by Dosage Peptide, Peptides.ID, Peptides Media, AKZOPHARMA, Peptigraph and PeptaBase. Of 23 website rows that state a single amount, the median is 100 mcg (range 50–250 mcg). Repetition is not evidence: the same 10-day, 100 mcg pattern appears in a bodybuilding forum log from 2011, and no page cites a human study behind it. [3], [4], [19], [20], [21], [22], [25]

We left out numbers that are not doses: vector-genome amounts from the gene therapy trials, the whole 1 mg vials injected by people in the eye-condition case series, and a pig-study figure converted to a human amount. Pages that give amounts per muscle for injections into several muscles are compared separately in the next chapter. [26], [24], [9]

Open the searchable source directory

What is Follistatin-344 commonly used for?

People look into follistatin because they want more muscle than training and food alone seem to give them, or because they are losing muscle they want to keep. The hope is simple: switch off the body's brake on muscle growth.

That hope comes from striking animal results and a small number of gene therapy studies in people with muscle diseases. The sections below separate what people want from what has been shown. [27], [6]

Building muscle size and strength

This is the main reason follistatin appears in bodybuilding and fitness discussions. Mice bred to make extra follistatin in their muscles grew far larger muscles, with individual muscles weighing 194–327% more than normal in the most extreme mouse, and a one-time gene injection kept mouse muscles larger and stronger for more than two years. [27], [28]

In people without a muscle disease, two studies tested related products: an engineered follistatin drug, ACE-083, enlarged the injected muscle in healthy women without making it measurably stronger, and an uncontrolled company study of plasmid gene therapy reported about 2 pounds more lean mass on average. No study has tested vials. [43], [35] Public accounts from vial users mostly describe quick scale-weight gains and a "pumped" feeling, often during steroid cycles or very high-calorie eating, alongside many reports of no noticeable change. The experience section looks at these accounts in detail. [29], [30], [31]

Conceptual cross-section of an adult thigh showing skin, the fatty layer beneath it, the large quadriceps muscle at the front and the thigh bone. It shows where the gene therapy studies injected and where websites describe injecting vials; it does not show any measured effect.
The gene therapy trials injected into the quadriceps muscle at the front of the thigh. Website protocols mostly describe subcutaneous injection of vials into the fatty layer under the skin, a different place and a different treatment. This generated illustration explains anatomy; it is not microscopy or clinical evidence.

Keeping muscle during weight loss

A newer interest is protecting muscle while losing weight, especially on GLP-1 (glucagon-like peptide-1) medicines such as semaglutide and tirzepatide, which can take muscle off along with fat. Drug companies are testing antibodies that act on the same pathway for exactly this purpose. Those are different, engineered medicines. No trial has tested follistatin itself for this. [32], [33], [34]

Muscle loss with ageing and "longevity" gene therapy

Some clinics outside the United States offer follistatin gene therapy as an anti-ageing treatment, and public figures have described having it. The best-known program gave one injection of follistatin gene material (plasmid DNA, a ring of DNA that cells can read) to 43 volunteers without a comparison group, and reported its own results without peer review. It is a different product again from the vials. [35], [36], [37]

Muscle-wasting diseases

The serious medical research has been in muscular dystrophies (inherited diseases in which muscle breaks down) and inclusion body myositis (a slowly progressive muscle disease of older adults). Researchers reported results of follistatin gene therapy in 15 patients, and a related engineered drug, ACE-083, in larger trials. None of these led to an approved treatment. [6], [7], [8], [38]

Other uses you may come across

Some pages also promote follistatin for fat loss, hair growth or injury recovery. No controlled human study has tested any of these; the company plasmid study reported a small fall in body fat without a comparison group. The other fat and metabolism findings come from mice, and the direction of the effect depends on the model. [35], [39], [40]

See the human study results or explore the animal research.

Where do Follistatin-344 protocols differ?

Almost every page agrees on 100 mcg as the typical amount, but the details around it vary: how often, into which tissue, for how long and with what break. Here is what those differences mean when reading a protocol.

Is the number for one injection or the whole day?

100 mcg twice a day is 200 mcg for the day. The table above keeps the amount each time and the daily total in separate columns for that reason. [5]

Pages that describe injections into muscles add another layer. One lists 100–200 mcg "per site" every other day into both arms or both thighs, so a single injection day uses 200–400 mcg in total. Another gives 150–400 mcg for injections into a muscle without a clear frequency. Check whether a number means per injection, per muscle, per day or per week before comparing it with anything else. [24], [41]

Once a day, every other day or twice a week?

Daily injections are the most common pattern. Some pages use every other day for the same 10–30-day course, and a few use twice-weekly injections for 8–12 weeks. One page recommends 100 mcg into the target muscle twice a week without a course length. Spreading injections out changes the total amount over a course, and none of these frequencies has been compared in people. [22], [4], [42]

Should it be taken in the morning or after training?

Pages disagree without data either way. One says most protocols use morning injections; another prefers after workouts; a third limits injections to training days only. No study has tested timing. [5], [4], [41]

Do sources start low, or start high and reduce?

Most use one fixed amount. The two stepped schedules in the titration notes above both front-load. One page says a higher start "saturates" myostatin faster, then says it is debated whether this changes anything. No page ties either schedule to measured blood levels. [23], [22]

How many days, and how long is the break?

Courses of 10–30 days are short compared with most peptides, and breaks are often longer than the course itself. [5], [22], [24] Pages explain the long breaks by cost, missing long-term safety data and possible effects on fertility hormones. Those are reasons for caution, not evidence that a particular break length works. [5]

Into the belly or into the muscle you want to grow?

Most schedules use subcutaneous injections into the belly, thigh or upper arm. A separate group of pages describes intramuscular injections (into a muscle) on both sides of the body, into the biceps, thighs or calves, on the idea that follistatin acts where it is injected. [5], [24], [20]

An engineered follistatin drug did grow only the muscles it was injected into, but no study has tested this with vials. The route chapter explains why. [43]

FS344 or FS315 vials?

Some sellers offer "Follistatin 315" as a separate product with nearly the same protocols (often 100 mcg a day for 10 days, or 100–300 mcg a day for 4–8 weeks). Because FS344 is the precursor of FS315, a product labelled 344 would, if accurate, still carry the 29-building-block front section that the body normally removes. Tested black-market "344" products that did contain follistatin were a lab-tagged form, not the body's own version. [44], [45], [1], [10]

One 2026 dosing page says injected FS344 splits into both FS315 and FS288. That is not how FS288 is made: it comes from a differently spliced copy of the gene's message, not from cutting up FS344. [169], [1]

Why do some pages list vector genomes or "1 mg"?

Some pages print the gene therapy amounts (for example, 6 × 10¹¹ vector genomes per kilogram per leg) next to microgram protocols, or list "1,000 mcg" because the people in the eye-condition case series injected whole 1 mg vials. The first is a count of virus particles, not a protein amount; the second is a harm report, not a dose. Neither is a protocol. [46], [26], [9]

What do community education groups describe?

Two courses in the community education groups we reviewed print an amount: 100 mcg once daily in the morning, or 100–300 mcg once daily around training. Neither gives a course length, and one listed it as an optional add-on that its own full schedule never includes. The educators themselves mostly rank follistatin as a low-evidence, last-resort option. The experience section explains more.

How do micrograms convert to syringe units?

Many people meet "units" on an insulin syringe. A U-100 syringe has 100 units per millilitre, so units measure volume, not an amount of follistatin. How much follistatin each unit holds depends on how much liquid was added to the vial.

For example, a 1 mg (1,000 mcg) vial mixed with 2 mL gives 500 mcg per mL, or 5 mcg per unit, so 100 mcg would be 20 units. Mixed with 1 mL instead, the same 100 mcg is 10 units. That is why a number of units copied from someone else's protocol can be wrong. Doserly's reconstitution calculator works this out for any vial and shows each step. [3], [5]

Source-by-source comparison and registered study plans

What does each page actually say?

Unit key: 1 milligram (mg) = 1,000 micrograms (mcg).

  • PeptideWiki: conservative 100 mcg once daily for 10–14 days; standard 100–200 mcg once daily for 10–20 days; aggressive 200–300 mcg a day, once or twice daily, for 20–30 days. Cycling table: 10 days on and 20–30 off, 20 on and 40–60 off, or 30 on and 60–90 off. Storage after mixing: 2–8 °C, not frozen, used within 14–21 days. [5]
  • Dosage Peptide: about 50, 100 or up to 200 mcg once daily in 10–30-day blocks, with a 1 mg vial mixed into 2 mL so that 100 mcg is 20 units. It states that none of these figures comes from human dose-finding data. [3]
  • PeptaBase: 100–200 mcg per injection daily or every other day for 10–30 days, or twice weekly for 8–12 weeks; some protocols use 7 daily injections, then twice weekly. 3–4 weeks off between cycles. [22]
  • Peptides.ID: 100 mcg daily for 10 days, or 100 mcg every other day; 10–20 days per cycle, then a 4-week break; after-workout timing preferred. Its separate FS315 page uses a similar layout with longer courses (10–30 days) and breaks (4–8 weeks). [4], [44]
  • Nova Pharma: 100 mcg once daily in the morning for 10–30 days, with an optional front-loaded 200 mcg a day for days 1–3. [23]
  • Peptides.NYC: three alternatives, each every other day for 10–14 days: 100 mcg at one site, 100–200 mcg per site into both arms or thighs, or 200–300 mcg per site on both sides; at least 4–6 weeks off and no more than 2–4 short cycles a year. [24]
  • Peptides Insider: the same three tiers (100, 100–200 and 200–300 mcg once daily), each for 10–30 days, starting at 100 mcg a day for the first week. [169]
  • Other cross-checks: AKZOPHARMA 50–100 mcg daily for 10–30 days; Peptigraph 50–200 µg a day; Peptides Media about 100 mcg a day for 10–20 days; PeptideDojo 100 mcg twice a week into the target muscle. [20], [21], [19], [42]

Is that a genuine consensus?

No. The numbers repeat across pages and go back to an old forum pattern, not to anyone measuring what 100 mcg does in a person. Several pages say so themselves: they describe their amounts as community practice with no human dose-finding data behind them. [3], [22], [5]

What are the registered studies planning?

These are gene therapy studies, not vial protocols. Registry dates describe the records, not new results.

Gene therapy into muscle · Phase 1/2a

AAV9-follistatin for age-related muscle loss

Two vector doses (5 × 10¹⁰ and 1 × 10¹¹ vector genomes per kilogram) into muscle, with or without a blood-vessel growth gene, alongside rapamycin, at a clinic in Honduras.

Recruiting. Last registry update: July 2026. No results posted.

[47]
Plasmid gene therapy · early study

Klotho plus follistatin gene therapy

Adults aged 50–80 at sites in Texas and Honduras. The record lists 14 participants.

Completed April 2026. No results posted.

[48]
Plasmid gene therapy · registered after it ended

Single follistatin plasmid injection in 43 volunteers

The company's own study ran from August 2022 to August 2023 and was first submitted to the registry in May 2024.

No results posted on the registry; the company published its own report.

[36]

What happens when you stop Follistatin-344?

This has not been studied for vials. No human study has looked for withdrawal effects or a rebound after stopping injected follistatin, because no human study has given it. That is an absence of data, not proof that nothing happens. [13], [5]

  • The closest human evidence is short. In healthy women given ACE-083 into one muscle, muscle volume was still higher 8 weeks after the last dose at the highest amounts, but the difference was no longer statistically significant. In the dose groups tested, the drug was detectable in the blood only during the first day after dosing. ACE-083 is an engineered drug, so this does not show what happens after stopping a vial. [43]
  • Gene therapy cannot be stopped. It is a one-time treatment. In monkeys, the injected muscles kept making follistatin for at least 15 months, and in mice the effect lasted more than two years. There is no way to switch it off if a problem appears. [49], [28]
  • Animal protein studies are thin. In mice given follistatin genetic instructions (mRNA) in tiny particles, blood follistatin stayed raised for about three days after each injection and then fell back. In rats, researchers speculated, without testing it, that stopping local follistatin might speed muscle breakdown. [50], [51]
  • Websites contradict each other. One vendor publishes one page saying gains reverse within 4–6 weeks of stopping and another saying there is no rebound. Neither cites human data. [52], [53]
  • Community accounts point both ways. Some forum users said they kept their gains, though one partly credited the steroids he was taking at the same time and another had also taken ACE-031. Others said the early gain was mostly water, or that they kept nothing. [54], [129], [30], [55]

The long breaks protocols describe are a source convention based on cost and caution, not a response to known withdrawal effects. [5]

Do injected follistatin, gene therapy and ACE-083 behave the same way?

No. They start in different places and last for very different lengths of time, which is why results from one cannot be carried over to another.

  • Subcutaneous injection of a protein vial puts follistatin into the fatty layer, from where it has to reach the blood. This is what most websites describe. [5]
  • Intramuscular injection (into a muscle) of a protein vial is described by a minority of pages that want a local effect. [24]
  • Gene therapy injects the follistatin gene, carried by a modified adeno-associated virus (AAV), into muscle once. The muscle cells then make follistatin themselves. [6]
  • Plasmid gene therapy injects a ring of DNA carrying the gene into belly fat once; the company that ran it says the tissue then makes follistatin for a period. [35]
  • Intravenous (IV) injection (into a vein) has been used only in animal studies of follistatin protein. [13]
How long each form lasts. Log scale from 1 minute to 3 years, ticks at 1 min, 1 hour, 1 day, 1 week, 1 month, 1 year. Native follistatin injected into a vein (rats): half-life about 4 minutes, then about 131 minutes (Animal study). ACE-083, engineered follistatin, injected into muscle (people): detectable in blood only on the first day after a dose (Human trial). ACE-031, a different drug in the same pathway (people): half-life 10–15 days (Human trial). Apitegromab, approved antibody in the same pathway (people): half-life about 31 days (label) (Label). Follistatin gene therapy into muscle (monkeys): still making follistatin at 15 months (Animal study). Follistatin gene therapy (mice): larger, stronger muscles for more than 2 years (Animal study). Half-life of a follistatin vial has never been measured in people. Values come from different species and molecules and are not interchangeable.

How long each form lasts

Log scale · 1 min · 1 hour · 1 day · 1 week · 1 month · 1 year

Native follistatin protein

  1. Native follistatin injected into a vein (rats)Animal study

    half-life about 4 minutes, then about 131 minutes

Engineered drugs in the same pathway

  1. ACE-083, engineered follistatin, injected into muscle (people)Human trial

    detectable in blood only on the first day after a dose

  2. ACE-031, a different drug in the same pathway (people)Human trial

    half-life 10–15 days

  3. Apitegromab, approved antibody in the same pathway (people)Label

    half-life about 31 days (label)

Gene therapy

  1. Follistatin gene therapy into muscle (monkeys)Animal study

    still making follistatin at 15 months

  2. Follistatin gene therapy (mice)Animal study

    larger, stronger muscles for more than 2 years

Half-life of a follistatin vial has never been measured in people. Values come from different species and molecules and are not interchangeable.

How long each form lasts depends on what is injected. Native follistatin protein cleared within hours in rats, an engineered injected drug was detectable in people for about a day, and gene therapy kept muscle making follistatin for more than a year in monkeys. Sources: Rat IV follistatin study · ACE-083 in healthy volunteers · Macaque gene therapy study · Mouse gene therapy durability · ACE-031 in healthy volunteers · Apitegromab prescribing information.

Native follistatin is cleared quickly in animals. In rats, follistatin injected into a vein collected in the liver more than in any other organ measured. Researchers who later redesigned the protein wrote that native follistatin is "poorly suited" to work as an injected drug throughout the body, and that fast clearance through the liver, helped by its tendency to stick to cell surfaces, "limits its therapeutic potential". Their fix was to engineer new versions that last longer; those versions have not been tested in people and are not what vials contain. [13], [56], [57]

Bioavailability, the share of a dose that reaches the blood in a usable form, has never been measured for a follistatin vial in people. The only direct data on raising blood levels with injected follistatin protein come from mice. Daily injections of FS288 for 13 weeks significantly raised blood follistatin and lean mass only at the highest of three amounts tested: 100 micrograms a day. The two lower amounts did not raise blood levels significantly and reduced fat only by the end of the study. That highest amount is the same number websites give a full-grown adult, who weighs thousands of times more than a mouse. This is not a human dose; it shows how little the online amounts are anchored to evidence. [58]

How long does follistatin last in the body?

Half-life is the time it takes for the level in the blood to fall by half. It is not how long an effect lasts.

No one has measured it in people. In the one published study of follistatin injected into a vein, in rats, blood levels fell by half in about 4 minutes during a fast first phase and in about 131 minutes (a little over 2 hours) during a slower second phase. Websites quote half-lives from about 1 hour to 8–12 hours, and one describes the body's own follistatin as lasting 10–15 hours; none of them cites a human measurement. [13], [59], [60], [46]

Engineered relatives last much longer by design. ACE-031, a different drug that blocks the same pathway, had a half-life of 10–15 days in healthy volunteers, and apitegromab, an approved antibody in the same pathway, has a label half-life of about 31 days. Those numbers belong to those drugs, not to follistatin. [61], [62]

A short half-life does not by itself prove that a daily 100 mcg injection does nothing. It does mean that the long-lasting effects seen with gene therapy, which keeps muscle making follistatin day and night, cannot simply be carried over to protein injections. [49], [13]

Does injecting into one muscle make that muscle grow?

With engineered drugs, yes; with vials, nobody knows. ACE-083, a version of follistatin fused to part of an antibody so that it stays near the injection site, enlarged only the muscles it was injected into, and a similar engineered form did the same in mice. Native follistatin from a vial is a different molecule, and no study has tested whether a small vial injection grows the muscle it goes into. [43], [63]

Is there a follistatin pill or nasal spray?

No product has been tested. Follistatin is a large protein, and one page selling a related form says itself that absorption by mouth is poor. Supplements such as epicatechin are sometimes marketed as raising follistatin; the questions section covers them. [45]

How should Follistatin-344 be stored, and how long does it last?

We found no published stability study of the vials sold as Follistatin-344, so storage advice comes from sellers and protocol pages, not from a tested medicine label.

  • Powder, before mixing. Pages disagree. Most say to keep the freeze-dried powder frozen at −20 °C (one adds "away from light"), while another says the powder is stable at room temperature. [3], [24], [64], [23]
  • After mixing. Once the powder is mixed with liquid (reconstituted), pages give very different limits at 2–8 °C (fridge temperature): "days to a couple of weeks", "1–2 weeks at most", 7–14 days, up to 2 weeks, 14–21 days, or 28 days. The shorter limits come from pages that point out follistatin is a large, fragile protein rather than a small peptide. [3], [24], [169], [42], [5], [64]
  • Freezing and light. Most pages say never to freeze the mixed solution; another suggests freezing single-use portions for longer storage. [3], [5], [24], [64], [42] Several pages advise keeping the vial away from light before and after mixing. [3], [24], [42], [169]

None of these limits has been tested on a retail vial; they are seller and website claims, not expiry dates.

Tested black-market vials also contained a large share of clumped protein (aggregation); product quality covers what that means. This guide does not cover mixing or injection technique; the Academy note below covers practical handling. [10]

What do we actually know about Follistatin-344 in people?

The human evidence comes in three groups, and none of them tested the vials sold online: gene therapy in people with muscle diseases, an engineered follistatin drug called ACE-083, and company-run gene therapy offered as an anti-ageing treatment. A fourth kind of evidence, a case series of eye problems in bodybuilders, is covered in the risks section.

Conceptual comparison of cells in a laboratory dish, an animal study notebook, and human study records. Each answers a different research question. A lab finding cannot by itself establish patient benefit.
Cell studies explore biological activity. Animal studies explore effects in another species. Human studies must test patient outcomes with an appropriate design. These are different kinds of evidence, not interchangeable steps to a proven treatment.
Who has received a follistatin-based treatment in a study. Gene therapy (AAV1-FS344), Becker muscular dystrophy: 6, No comparison group. Gene therapy (AAV1-FS344), Inclusion body myositis: 6, Historical comparison, a further 3 in a low-dose group were never reported. Gene therapy (AAV1-FS344), Duchenne muscular dystrophy: 3, No comparison group. Engineered drug (ACE-083), Healthy women: 42 + 16 placebo, Placebo-controlled. Engineered drug (ACE-083), Facioscapulohumeral muscular dystrophy: 95 enrolled, Placebo-controlled, then open-label. Engineered drug (ACE-083), Charcot-Marie-Tooth disease: 63 enrolled, Placebo-controlled, then open-label. Plasmid gene therapy (company), Volunteers aged 23–88: 43, Company-run, not peer reviewed. Harm report after vial use, Eye condition (CSCR) in bodybuilders: 11, Case series. Protein vials, Follistatin-344 vials in any study: 0 people, No study. Numbers are people who received the treatment (trial totals where marked 'enrolled'). No row is a test of the vials sold online.

Who has received a follistatin-based treatment in a study

Gene therapy (AAV1-FS344)

Becker muscular dystrophy
6No comparison group
Inclusion body myositis
6Historical comparisona further 3 in a low-dose group were never reported
Duchenne muscular dystrophy
3No comparison group

Engineered drug (ACE-083)

Healthy women
42Placebo-controlled+ 16 placebo
Facioscapulohumeral muscular dystrophy
95 enrolledPlacebo-controlled, then open-label
Charcot-Marie-Tooth disease
63 enrolledPlacebo-controlled, then open-label

Plasmid gene therapy (company)

Volunteers aged 23–88
43Company-run, not peer reviewed

Harm report after vial use

Eye condition (CSCR) in bodybuilders
11Case series

Protein vials

Follistatin-344 vials in any study
0 peopleNo study

Numbers are people who received the treatment (trial totals where marked 'enrolled'). No row is a test of the vials sold online.

Who has actually received a follistatin-based treatment in a study. Every treatment group used gene therapy or the engineered drug ACE-083. The only people linked to vials are 11 bodybuilders in an eye-condition case series, and no study has given anyone a follistatin vial. Sources: Becker MD trial · Inclusion body myositis trial · ACE-083 FSHD trial · Duchenne trial results · ACE-083 in healthy volunteers · ACE-083 Charcot-Marie-Tooth trial · Company plasmid study report · Eye-condition case series · Inclusion body myositis trial registry (low-dose group).

What did the human studies find?

StudyWhat researchers reportedWhat it cannot establish
Becker muscular dystrophy, gene therapy, 2015Six men received the gene by injection into both thigh muscles at one of two doses. Walking distance in 6 minutes rose by 58, 125, 108 and 29 metres in four of them and did not improve in two. In two of them, muscle samples showed larger fibres and less scar tissue. [6]Whether the treatment caused the change: there was no comparison group, and everyone took prednisone (a steroid) around the injection.
Inclusion body myositis, gene therapy, 2017Six adults received the gene into both thigh muscles and followed an exercise program. Their median walking distance rose by 56 metres a year, against a median fall of 26 metres a year in eight earlier patients. Four improved by 58–153 metres; two by 5–23 metres. [7]A fair comparison: the "controls" were past patients, not a group followed alongside them, and another expert called the conclusions unfounded. [65]
Duchenne muscular dystrophy, gene therapyThree boys (six were planned) received the gene into several leg and hip muscles. None of the three improved on the 6-minute walk at two years; one improved on a motor-function scale. [8]Anything about benefit: the study was tiny, enrolled only half its planned size, and its results were posted to a registry, not published in a journal.
ACE-083, healthy volunteers, 201858 women past menopause; 42 received 50–200 mg of this engineered follistatin drug into one thigh or shin muscle. The injected muscle grew by up to 14.5% (thigh) and 8.9% (shin) on average, with no significant change in strength. [43]That native follistatin from a vial would do the same: ACE-083 is a different, engineered molecule given in amounts 500 to 2,000 times larger than a 100 mcg vial dose.
ACE-083, two muscle diseases, 2022In facioscapulohumeral muscular dystrophy (95 patients) and Charcot-Marie-Tooth disease (63 patients), injected muscles grew by 9.5–16.4% more than with placebo, but strength gains were inconsistent, function did not improve, and both trials were stopped. [38], [66]That bigger muscles mean better function: in these trials they did not.

Across the gene therapy trials, one research team reported results for 15 people, with no placebo group. They show short-term tolerance and larger muscle fibres in some patients, not restored function, and nothing about vials. [6], [7], [8], [67]

What did the gene therapy trials measure?

In the Becker study, each leg received AAV1 carrying the FS344 gene, at 3 × 10¹¹ or 6 × 10¹¹ vector genomes per kilogram per leg. There were no side effects the researchers linked to the gene transfer, reproductive hormones stayed normal, and two patients showed an immune-cell response against follistatin itself. [6]

The myositis trial used the same product with an exercise program and prednisone (60 mg a day) for a month beforehand. In their reply to the critic, the authors wrote that a combined effect of treatment and exercise was "more realistic". A lower-dose group listed in the trial registry never appeared in either paper. [68], [65], [67]

The US regulator granted the gene therapy orphan designations (a status that supports research into rare diseases) for Duchenne and Becker muscular dystrophy in 2012 and for inclusion body myositis in 2016. A designation is not an approval, and the program did not reach one. [69], [70]

What happened with ACE-083, the injected follistatin drug?

ACE-083 was follistatin joined to part of an antibody so that it would stay in the injected muscle. It is the closest thing to "injected follistatin" ever tested in people, and it worked as designed on muscle size: injected muscles got measurably bigger. [43], [71]

It did not reliably make people stronger or more capable. Each patient trial found a strength gain on one measure, but not consistently. The two trials were stopped because they "did not achieve functional secondary endpoints", and the long-term extension study was terminated too. Many patients also developed anti-drug antibodies, antibodies against the drug itself: about 39% in one trial and 48% in the other. [72], [73], [74], [38], [66]

What about the anti-ageing gene therapy clinics?

A company ran a study in which 43 volunteers aged 23 to 88, at a clinic in a special economic zone in Honduras, received one injection of follistatin plasmid DNA (50 micrograms of DNA, not protein) into belly fat. There was no comparison group, the study was registered only after it had finished, and the report was written by company staff and not peer reviewed. [35], [36]

It reported that blood follistatin rose from 8.58 to 24.03 ng/mL and lean mass by about 2 pounds (1.96 lb) on average, with no severe side effects. Low-density lipoprotein (LDL) cholesterol, the kind linked to heart disease, rose by an average of 8 mg/dL overall, which was not statistically significant, and by an average of 19 mg/dL in about a third of participants. [35]

A well-known self-experimenter who had the treatment published that his follistatin levels rose 160% and his muscle mass 7%, while following many other diet, exercise and drug routines at the same time. A newer trial of an AAV9 follistatin gene therapy for age-related muscle loss is recruiting in Honduras. [37], [47]

Does bigger muscle mean stronger or more capable?

Not necessarily, and this is the most important lesson from the research. Muscle size, strength and everyday function are separate outcomes. A scan can show a bigger muscle; only a strength or function test shows whether a person can do more with it.

ACE-083 enlarged muscles without consistent gains in strength or function. The gene therapy trials reported better walking in some patients, but without a proper comparison group. Across the wider class of drugs that block myostatin or activin, muscle mass rose more reliably than function. [43], [38], [75]

For someone tracking their own results, the same logic applies: useful records separate weight, measured lean mass, strength numbers and how everyday tasks feel, because a quick gain on the scale can be mostly water. [54], [30]

Why is there no approved follistatin medicine?

Drug companies have tried this pathway many times, mostly with engineered antibodies and receptor decoys rather than follistatin itself, and the pattern is consistent: muscle mass goes up, function often does not. [75], [76]

  • Bimagrumab, an antibody against the receptor myostatin uses, did not improve walking in inclusion body myositis. In an obesity trial with semaglutide it helped preserve lean mass, but physical functioning scores were similar across groups. [77], [32]
  • Domagrozumab, an anti-myostatin antibody, did not improve a stair-climb test in Duchenne muscular dystrophy, and the studies were stopped. Landogrozumab added a little lean mass in older people who fall, with mixed results on function. [78], [79], [80]
  • Apitegromab (ISEMBYLD), an antibody against the inactive form of myostatin, became on September 11, 2026 the first drug in this pathway approved by the US regulator to target muscle loss: spinal muscular atrophy, alongside standard treatment, as an IV infusion of 10 mg per kilogram every four weeks. It is not follistatin, and its approval says nothing about vials. [81], [62]

How might follistatin build muscle?

Follistatin works by catching signal proteins outside cells before they reach their receptors. The most important one for muscle is myostatin, but it is not the only one, and that is the source of both its power in animal studies and its risks. [1], [2]

Conceptual illustration of a muscle fiber surface with receptor proteins, free myostatin signal molecules and follistatin molecules wrapped around some of them so they cannot reach the receptors. It represents animal and cell research, not a measured effect of a vial in people.
Myostatin normally docks on receptors on muscle fibers and slows growth. Follistatin wraps around myostatin and related signals so they cannot dock. This generated illustration explains a concept from cell and animal research; it is not microscopy or clinical evidence.

What is myostatin, and what happens without it?

Myostatin is a protein made by muscle that tells muscle to stop growing, a built-in brake. Mice without working myostatin have much larger muscles, and follistatin-rich mice grew even larger ones, which showed that follistatin blocks more than myostatin alone. [27], [82]

The same brake works in people. A child born with a mutation that disabled myostatin had unusually large muscles, a case reported in 2004, and natural myostatin mutations in cattle, sheep and dogs produce heavily muscled animals. Mice engineered to lack myostatin carry about twice the normal muscle mass. [83], [82]

Mice lacking myostatin that also made extra follistatin had about four times the muscle mass of normal mice. That showed follistatin releases more than one brake at once. [82]

How does follistatin block it?

Follistatin wraps around its targets and covers the part that would bind the receptor on the cell. Different sections of the protein handle different targets: one section binds myostatin more strongly, another activin. Researchers could change these sections to make follistatin favour one target over the other. [2], [1]

Its targets include myostatin, the activins (signals that also regulate fertility hormones, healing and scarring), GDF11 and some bone morphogenetic proteins. That broad reach is why follistatin is described as "not selective": it switches off several signals at once. [1], [2]

Is it only about myostatin?

No. In mice, follistatin still enlarged muscles when myostatin was absent, and the growth depended on a muscle-building pathway called mTOR and on the insulin-like growth factor-1 (IGF-1) receptor. Other mouse studies found it increased the stem cells that help muscles grow and repair (satellite cells). [84], [85], [86], [87]

These are animal findings. They explain why researchers are interested, not what a vial does in a person.

Where does the body's own follistatin come from?

Most follistatin in the blood comes from the liver, and its level rises and falls with the balance of the hormones glucagon and insulin. Blood levels rose about sevenfold after three hours of hard cycling, peaking a few hours into recovery, and they also rise during fasting and pregnancy. A higher blood level is a normal response to these states, not a sign of muscle growth. [15], [88], [89], [90]

Why do fertility hormones come up?

Follistatin was first discovered because it lowers FSH, a hormone that drives egg and sperm production, and it does so partly by blocking activin, which helps control FSH. That is why fertility is one of the main open safety questions. Could it affect fertility or hormones? covers what is and is not known. [16], [91], [92]

What are the risks and unanswered questions?

Is Follistatin-344 safe?

Its safety in people has not been established, and the one published human harm report tied to vials involves the eyes. No study has given people follistatin protein from a vial, so there is no measured rate of side effects, no known safe amount and no long-term data. [9], [13]

The gene therapy trials reported no serious side effects linked to the treatment, and the ACE-083 trials found it generally well tolerated apart from common injection-site reactions. Those results are real, but they come from different products, small numbers of people and close medical supervision. They cannot be carried over to a vial of uncertain content injected at home. [6], [7], [43]

Fifteen gene therapy patients without treatment-linked serious side effects is useful information, but studies that small and short miss uncommon and slow problems.

What is the eye problem linked to Follistatin-344?

A group of eye doctors in Turkey described 11 male bodybuilders who came to their clinic with worse eyesight after injecting follistatin-344. Scans showed central serous chorioretinopathy (CSCR): fluid collecting under the retina, the light-sensing layer at the back of the eye. [9]

  • Every one of them had injected a whole 1 mg vial subcutaneously into the belly. Eight had injected once; three had injected more than once.
  • Ten had it in one eye, one in both.
  • In the eight who injected once, the fluid cleared and symptoms settled after about 2.3 months on average.
  • All three who had injected more than once had repeat episodes. The summary does not say whether they injected again after the first one.

The authors concluded that follistatin-344 injection "can be considered as a risk factor" for CSCR. A conference report from the same doctors described three men aged 24 to 31 who came to the clinic about 20 days to a month after injecting a single vial, with reduced vision that had started 3 to 10 days earlier; they are probably among the 11. [9], [93]

Conceptual cross-section of the back of the eye showing the retina, the layer of blood vessels beneath it (the choroid) and a small dome of clear fluid lifting the retina near its centre. It explains what central serous chorioretinopathy is; it is not an image from the case series.
In central serous chorioretinopathy, fluid collects under the retina near the centre of vision, which can blur or dim eyesight. This generated illustration explains anatomy; it is not a patient scan or clinical evidence.

This is an uncontrolled report, and it has real limits. Only its summary is publicly available, so it is unknown whether the men also used other drugs, and corticosteroid medicines such as prednisone were the strongest risk factor for CSCR in a study of 312 patients. Nobody knows what the vials actually contained. The report cannot show that follistatin caused the condition or how often it happens. It is still the only published human harm signal from the product people actually buy, and repeat episodes in all three repeat users are hard to dismiss. [9], [94], [10]

None of the public forum threads we reviewed included a first-hand account of vision changes, and neither did the community education groups. That absence cannot show how often eye problems happen.

What side effects do users describe?

In the public forum and Reddit accounts we reviewed, many complaints concerned the injection itself: painful, red, itchy or swollen lumps that sometimes lasted days, and in a few cases red streaks spreading from the site. Several people described flu-like symptoms, fever or shivering, fatigue, and joint or tendon pain, and some stopped because of them. One person described a severe reaction with a large rash, dizziness, fever and weakness after a single 100 mcg injection that improved over the next day. [97], [98], [99], [95], [100], [96]

These are personal accounts from people using products of unknown identity and purity, often alongside other drugs. They cannot tell us how often reactions happen or whether follistatin, a contaminant, another ingredient or the injection itself caused them. The ACE-083 trials also found injection-site reactions common, including in people given placebo. [10], [101], [72]

Could it affect fertility or hormones?

It is a reasonable question with no human answer for vials. Follistatin was discovered because it lowers FSH, and in animals too much or too little follistatin disrupts reproduction. In the 12 gene therapy patients who were checked, reproductive hormones stayed normal; the company plasmid study reported no fall in luteinizing hormone (LH), a hormone that drives testosterone production, or FSH. No one has measured hormones or fertility after repeated protein injections. [16], [102], [103], [6], [35]

A related drug gives a sense of how regulators treat this pathway: the label for sotatercept, an approved medicine that traps activins, warns that it may impair female and male fertility based on animal findings, and can harm an unborn baby. [104]

Does it affect the heart, tendons or blood vessels?

These worries come up often in user discussions, and they have not been studied in people taking follistatin. [29]

  • Heart: no human data. In diabetic mice, extra follistatin reduced heart scarring but also enlarged the heart muscle, and pigs engineered to make human follistatin in muscle had no reported heart enlargement. [105], [106]
  • Tendons: some users describe tendon and joint pain or feeling that training "wear and tear" increased. Tendon effects of blocking this pathway have been studied only in animals: tendons of mice born without myostatin were smaller, had fewer cells and were stiffer and more brittle, while in rats without myostatin, tendons stretched about 20% less before failing but were no smaller, weaker or stiffer. No study has looked at tendons in people using follistatin. [107], [108], [109], [110]
  • Blood vessels and bleeding: broader drugs in this pathway caused nosebleeds and small visible blood vessels (telangiectasia). ACE-031 was stopped in boys with Duchenne muscular dystrophy for this reason, and on the sotatercept label nosebleeds affected 22.1% of patients against 1.9% on placebo. These drugs block activin, as follistatin does, but no human data show that follistatin causes these effects. [111], [104]

What did drug companies see with similar drugs?

The wider class carries safety signals worth knowing, even though none has been shown for follistatin itself. [75]

  • Apitegromab (approved 2026 for spinal muscular atrophy) carries a warning for fractures: 5 of 53 patients (9%) had fractures on the drug against 1 on placebo (2%). [62]
  • Trevogrumab plus garetosmab, two antibodies tested with semaglutide for weight loss: 28.3% of people on the three-drug combination stopped because of side effects, against 4.6% on semaglutide alone, and two people in the combination group died (the company did not attribute the deaths to the drugs). [33]
  • Sotatercept, approved for a lung-blood-vessel disease, lists increased red blood cells, low platelets and serious bleeding among its warnings. [104]

Could product quality change the risk?

Yes, and it may be the biggest practical risk. When anti-doping chemists tested 17 black-market products sold mostly as "follistatin 344", only 9 contained follistatin. Some of the others contained different growth-promoting peptides, such as MGF or GHRP-2. All nine genuine products carried a laboratory tag (a His-tag) and contained a high proportion of clumped molecules. [10]

Follistatin is a large protein that has to be made in living cells, such as bacteria or animal cells, rather than assembled chemically like short peptides. One laboratory supplier's follistatin, for example, is made in bacteria, labelled "For Research Use Only" and sold with an endotoxin limit; that specification says nothing about vials sold as Follistatin-344. [112] Members of the community education groups repeatedly raised this worry: protein made in bacteria can carry bacterial toxins (endotoxin), and we found no published endotoxin test of these vials.

Is Follistatin-344 legal? Is it FDA-approved?

Checked September 23, 2026. Rules differ by country and change quickly.

United States. Follistatin is not an FDA-approved medicine, and FDA has told a pharmacy that it did not qualify for compounding:

  • 2020. FDA warned a compounding pharmacy that had made products with follistatin that the substance had not been nominated for the list of ingredients pharmacies may use. [18]
  • Protein rules. Because follistatin is longer than 40 amino acids, US regulations class it as a protein, which makes it a biological product. [113]
  • 2026. It does not appear on FDA's May 2026 list of ingredients under review for compounding. An FDA briefing in 2026 mentioned "Follistatin-344" only as part of "regenerative combo" products promoted online. [114], [115]

Canada. Health Canada's Drug Product Database lists no product containing follistatin. Its April 2026 advisory on injectable peptides bought online does not name follistatin, but it states that "research use only" labelling "does not make these products legal". [167], [116]

Australia. Follistatin is a prescription-only (Schedule 4) substance and is also listed in Appendix D, clause 5 of the Poisons Standard, which makes possessing it without authority illegal. [11]

United Kingdom and European Union. Anti-doping scientists reported in 2019 that no approved follistatin medicine existed, and we found no UK or EU authorization since, nor any follistatin-specific statement from their medicines regulators. [10]

Is Follistatin-344 banned in sport? Does it show up on a drug test?

Yes, it is banned. The World Anti-Doping Agency's 2026 list prohibits "myostatin-binding proteins (e.g. follistatin…)" at all times, in and out of competition, under category S4.3. The 2027 list, which takes effect on January 1, 2027, keeps it. Follistatin has been named on the list since 2019, and drugs that change myostatin function were banned from at least 2008. Gene therapy used to enhance performance is separately banned as gene doping. [12], [117], [118], [119]

Anti-doping chemists published a blood and urine test in 2019 for tagged follistatin. All nine follistatin-containing products they examined carried a laboratory tag, which let the test tell them apart from the body's own protein; the paper does not show a way to do that for an untagged product. Laboratories have also developed tests for the follistatin gene used in gene doping. How long vial use remains detectable has not been published, and we found no public confirmation of routine testing for it. [10], [120]

Does follistatin cause cancer?

Nobody knows, and the animal and cell research points both ways. Follistatin reduced the spread of breast and lung cancer in mouse models, but ovarian cancer cells used follistatin to resist chemotherapy, and high follistatin in patients' ovarian tumours went with worse survival. No long-term cancer study of follistatin vials exists. [121], [122], [123]

Who should be especially cautious?

These groups have no safety data in people. That is a reason for caution, not proof of harm.

  • Pregnancy, breastfeeding and trying to conceive. Follistatin affects fertility hormones and pregnancy in animals, and the related drug sotatercept carries a warning for harm to an unborn baby. [124], [104]
  • Anyone with past eye problems, especially CSCR. The only human harm report involves this condition. [9]
  • People using steroids. Corticosteroid medicines such as prednisone are a major risk factor for CSCR. Many vial users also take anabolic steroids, and the eye case series does not say which other drugs the men used. [94], [9], [54], [125]
  • A history of cancer. Because of the mixed animal findings above. [123]
  • Under 18. No studies include young people. This guide is written for adults.
  • Competitive athletes. It is banned at all times. [12]
  • People taking other medicines. Interactions have not been studied; see the next question.

Has Follistatin-344 been tested alongside other medicines?

Not in people. No study reports how follistatin interacts with prescription medicines, and the pages that list interactions offer opinions, not data. The gene therapy trials gave prednisone around treatment to calm the immune response, which says nothing about combining a vial with other drugs. Bring a complete list of everything you take to a pharmacist or doctor. [6], [7]

What should be monitored while using Follistatin-344?

There is no official monitoring plan, because no regulator has approved a follistatin product or written a label for it. What exists is a record of what the gene therapy and ACE-083 studies measured, and the signals seen in related drugs. It can help you prepare questions for a clinician; it is not a personal testing plan. [6], [43]

What did the studies check?

  • The gene therapy trials took blood at the start, at days 7, 14, 30, 60, 90 and 180, and at one year: a complete blood count, liver and kidney tests, amylase (a pancreas enzyme), creatine kinase (a muscle enzyme) and the hormones FSH, LH, oestrogen and testosterone. They also tested for immune reactions against the virus and against follistatin. [6]
  • The Duchenne gene therapy study added heart tests before treatment (an electrocardiogram and an ultrasound of the heart), plus urine tests, clotting tests and blood follistatin levels, with visits for two years. [126]
  • The ACE-083 trials checked blood counts, blood chemistry, urine, heart rhythm, vital signs, muscle volume on MRI scans and anti-drug antibodies. [43], [38]
  • The company plasmid study tracked blood follistatin, body composition by a low-dose X-ray scan (DEXA), LH and FSH, cholesterol, blood sugar markers and an inflammation marker (hs-CRP). [35]
  • The eye cases were diagnosed with an eye scan (optical coherence tomography). No eye-screening schedule has been tested for follistatin users. [9]

Which signals matter, and why?

Why it mattersWhat studies measured or flaggedTracking category
VisionCSCR in 11 vial users, found after eyesight worsenedSide Effect Burden; Other
Fertility hormonesFSH, LH, oestrogen and testosterone in the gene therapy trials; animal reproductive effectsHormonal Symptoms; Libido
CholesterolLDL rose in about a third of the plasmid study participantsBlood work
Liver, kidney and muscle enzymesLiver and kidney tests and creatine kinase in the gene therapy trialsBlood work
Immune reactions and injection sitesImmune responses to follistatin in two gene therapy patients; anti-drug antibodies with ACE-083; injection-site reactions in trials and user accountsSide Effect Burden; Inflammation
Blood cells and bleedingBlood counts in trials; bleeding, nosebleeds and red-cell changes with related drugsBlood work
BonesFractures with apitegromab, a related antibodyBone Health
The goal you care aboutMuscle volume, strength and walking distanceMuscle Growth; Physical Performance; Daily Functioning

The cholesterol finding comes from an uncontrolled company study of gene therapy, and the bleeding and fracture signals come from different drugs. They show what researchers and regulators paid attention to, not what a person using a vial will experience. [35], [62], [104]

A blood follistatin test is not a practical way to monitor vial use: levels rise naturally with exercise and fasting, and no study has shown that a result tracks muscle growth after a vial. Why a blood test cannot confirm it is working. [127], [88], [89]

What do people in public communities report?

Public discussions of follistatin are dominated by questions, plans and sourcing requests; first-hand results are fewer than the attention suggests. The accounts that exist include quick scale-weight gains, no noticeable change, and injection reactions that made people stop. Most come from people also using steroids, growth hormone or other peptides. [29], [31], [98]

What do the positive reports look like?

The typical positive account describes a fast rise in scale weight, strong "pumps" in the gym and fuller-looking muscles within one or two weeks. One person logging a 10-day course of 100 mcg a day, injected into muscle, in 2011 went from 178 to 183 lb within five injections and then stopped gaining. He had no body-composition test, was in week 8 of a testosterone cycle and was eating about 4,000 calories a day. [25]

Another person on Reddit said they gained 10 pounds of lean muscle in 20 days on 100 mcg a day and later lost only 2 of them, while also on testosterone replacement (150 mg a week) and eating a lot, and without describing how lean mass was measured. A person on a modest routine of two injections a week for five weeks described fuller arms and a "modest" effect, while also training harder and paying more attention to diet. [128], [29]

How long did those changes last?

Follow-ups often change the story. One person who gained 8 pounds in the first two weeks said nothing more happened after that and stopped at three and a half weeks. Retelling it about a year and a half later, he said the gain was mostly lean and he kept it, but that he had started testosterone and another steroid first, so follistatin could not take all the credit. Another said he gained 7 pounds in the first week, "water mostly", and little after that. A third, who took ACE-031 at the same time, said he kept a little weight gained over the next six months, and that he was "very ill and very sore". [30], [54], [129]

These accounts cannot provide an average result or time course. They involve different products, amounts and drug combinations, and people with dramatic stories are more likely to post.

Does everyone describe an improvement?

No. Many people reported nothing: one gained no weight or strength after a week, another had "no effect" after trying twice, a third, who had tried both 344 and 315 years earlier, said he gained and kept nothing, and one commenter wrote that "every bb'er I know that has taken it saw little to no effect". Several suspected their product was fake. [130], [31], [131], [55]

People who had gene therapy also split. Some described gaining 8 to 11 pounds of muscle over a few months, usually without published scan results and sometimes with a commercial link to the treatment; another person who had a follistatin gene therapy abroad later wrote that they "did not get much of anything noticeable" from it. [132], [133], [134]

What about unwanted effects?

The same reports described in the risks section recur here: injection-site reactions, flu-like symptoms, fatigue and joint or tendon pain, with some people stopping because of them. [135], [109], [136]

What do community education groups say?

In the community education groups we reviewed, follistatin is discussed far more than it is used. Educators mostly rank it as a low-evidence, last-resort option, pointing to its short time in the body, its effects on activin and fertility hormones, and the gap between gene therapy results and vials. Only a handful of members described their own results, and those were brief: a small benefit that did not seem worth the price, or no noticeable effect.

Many members said they had bought a vial and never started, citing cost, doubts about what the vial contained or worries about the heart and fertility. More of the first-hand accounts concerned branded products marketed as "modified" or longer-acting follistatin, sold by single sellers without published data on what they contain; the gains described were not measured, and some came from people with a commercial interest in the product. None of the groups discussed the published eye-condition case series.

How can you judge a muscle-gain story?

Useful questions to ask: What exactly was used, from where, and was it tested? How much, how often and for how long? What else changed at the same time: steroids, growth hormone, calories, training? Was the gain measured as scale weight, a body-composition scan or a strength number? What happened a month after stopping?

A quick jump on the scale can come from water and heavy eating rather than muscle, and one long-time forum member put his own early gain down mostly to water. [54] A story with a scan, a strength log and a follow-up tells you far more than "I gained 10 pounds".

How does Follistatin-344 compare with IGF-1 LR3, PEG-MGF and MK-677?

These compounds are discussed together for muscle growth, sold by the same suppliers and sometimes combined. The table compares what each one is and how much human evidence exists. The route column describes how each is used in studies or on protocol websites, not tested doses.

CompoundWhat it isRoute and scheduleHuman evidenceApproval and sport status
Follistatin-344 (this guide)A natural protein (315 building blocks when mature) that blocks myostatin and activins [1]Subcutaneous injection, usually 100 mcg a day for about 10 days, on protocol websites [3]None for vials; gene therapy in 15 patients with muscle diseases [6], [7], [8]Not approved; banned in sport (WADA S4.3) [12]
IGF-1 LR3A lab-made, longer-acting version of insulin-like growth factor-1 that acts on the IGF-1 receptorSubcutaneous injection, daily, on protocol websites [137]None for IGF-1 LR3 itself; native IGF-1 (mecasermin) is an approved medicine for a rare growth disorder in children [138]Not approved; banned in sport (WADA S2.3) [12]
PEG-MGFA lab-made fragment of a muscle form of IGF-1 (mechano growth factor) with a polymer attached to slow its clearanceSubcutaneous injection, 200–400 mcg 2–3 times a week, on protocol websites [139]None; FDA says it has not identified any human exposure data [140]Not approved; FDA placed it among compounding ingredients with possible significant safety risks before its nomination was withdrawn; banned in sport (WADA S2.3) [140], [12]
MK-677 (ibutamoren)A small molecule taken by mouth that makes the body release growth hormoneBy mouth, once daily, usually 25 mg in trials [141]Several randomized trials: lean mass rose about 1.1 kg over a year in older adults without strength gains, and a hip-fracture trial was stopped early for a heart-failure signal [141], [142]Not approved; FDA lists significant safety risks, and its advisory committee voted 1 to 13 against allowing compounding; banned in sport (WADA S2.2) [140], [143], [12]

MK-677 is the only one with randomized trials of the compound itself, and those showed more lean mass without more strength. No study has compared any of these with follistatin, so the table cannot say which works better. [141], [144], [6]

Common questions about Follistatin-344

How long does Follistatin-344 take to work?

There is no reliable answer. No study has measured what a follistatin vial does over time in people. Forum users who report a change usually describe scale-weight gains or "pumps" within the first one to two weeks, which is also when water and stored carbohydrate shift with heavy eating; others notice nothing at all. In the gene therapy trials, changes in walking distance were measured over six months to a year. [30], [31], [6] See what people reported over time.

Is Follistatin-344 a peptide or a steroid?

Neither, strictly. It is a full-sized protein of 315 amino acids once mature, far larger than the short peptides it is sold alongside, and US rules class proteins of this size as biological products. It is not a steroid: anabolic steroids are small ring-shaped molecules that act on hormone receptors, while follistatin works by capturing signal proteins outside cells. It is still banned in sport. [1], [113], [12]

Is Follistatin-344 the same as follistatin gene therapy?

No. In the human research, FS344 was a gene delivered once into muscle by a modified virus, so the muscle kept making follistatin for months or years. A vial sold as Follistatin-344 contains protein that is injected repeatedly, if it contains follistatin at all, and how long it lasts in people has never been measured. Results from gene therapy cannot be used as evidence for vials. [6], [13], [10] See the gene therapy and vial comparison.

Can epicatechin or YK-11 raise follistatin instead?

Not in a way shown to build muscle reliably. Epicatechin, a plant compound found in cocoa and tea, raised the ratio of blood follistatin to myostatin in a one-week study of six people without a comparison group, and raised blood follistatin in a small trial in Becker muscular dystrophy. In an 8-week trial in 62 older men with muscle loss, epicatechin alone improved a muscle-mass measure compared with placebo, but the biggest strength changes came when it was combined with resistance training. These studies are too small to show dependable muscle growth. YK-11 is a different kind of drug (a selective androgen receptor modulator, or SARM) whose link to follistatin comes from one study of mouse cells in a dish; it is banned in sport and FDA has warned sellers about it. [145], [146], [147], [148], [12], [149]

Can a blood test show whether Follistatin-344 is working?

Not reliably. A blood follistatin test is offered mainly for research and drug trials, and different test methods can measure different forms of follistatin, which makes results hard to compare. Levels also rise naturally, about sevenfold after long exercise, by about 155% during a three-day fast, and in pregnancy, so a higher number does not show muscle growth. No published study has measured blood follistatin before and after a vial injection. [127], [168], [150], [88], [89], [90] See what to monitor.

Why do online guides often mention 100 mcg?

Because it has been repeated for years, not because it was tested. The "100 mcg a day for 10 days" pattern uses exactly one 1 mg vial, appears in a forum log from 2011, and is repeated across many dosing pages today. No study has tested any amount of injected follistatin protein in people. [25], [3], [4] See where the numbers come from.

Is it legal to buy Follistatin-344?

It depends on where you live, but it is not an approved medicine anywhere we checked. In Australia, possessing it without authority is illegal. In the United States, FDA told a pharmacy that follistatin did not qualify for compounding, and Canada's drug database lists no follistatin product. A "research use only" label does not make a product legal or safe for human use. See the dated legal-status summary. [11], [18], [167], [116]

What is FLGR242, or "long-acting follistatin"?

It is a branded product, not a studied medicine. One seller markets FLGR242 as a modified, fragmented version of follistatin that it says does not bind activin and lasts longer in the blood. [151] A promotional blog post that credits the seller's scientists says an albumin-binding attachment gives it a 19-day half-life. The post gives 2.5 mg once a week or 5 mg every two weeks, injected subcutaneously into the belly (5 mg a week for "advanced users"), and says breaks are not needed. [170] Each of those injections is 25 to 50 times the common 100 mcg Follistatin-344 amount. We found no published study, trial registration or independent analysis showing what it contains, how long it lasts or whether it avoids activin, so the 19-day figure is a marketing claim, not a measurement. In the community education groups we reviewed, the results users described were not measured. See how to judge these accounts.

Glossary

Plain explanations of the route, dosing and research terms used in this guide. Underlined terms in the text link here.

AAV (adeno-associated virus)
A small virus that does not cause disease, modified to carry a gene into cells. The follistatin gene therapy trials used AAV to deliver the follistatin gene into muscle.
Activin
A family of signal proteins that help control fertility hormones, healing, scarring and muscle. Follistatin binds activins as well as myostatin.
Adverse event
A harmful or unwanted medical event reported after someone used a treatment. A report alone does not prove the treatment caused it.
Aggregation
Protein molecules clumping together. Tested black-market follistatin products contained a high share of clumped molecules.
Amino acid
A small chemical building block. Chains of amino acids make up peptides and proteins.
Animal study
Research in animals such as mice, rats or monkeys. It shows what a substance does in a living body, but results in people can differ.
Anti-drug antibodies
Antibodies the immune system makes against a medicine. They can weaken the medicine or cause reactions. Many patients given ACE-083 developed them.
Bioavailability
How much of a dose reaches the bloodstream in a usable form. It depends heavily on the route and has never been measured for follistatin vials in people.
Biological product (biologic)
A medicine made from living cells, such as a protein or an antibody. In the US, proteins longer than 40 amino acids, including follistatin, are regulated as biologics.
Cell study (in vitro)
Research on cells grown in a dish. It gives early clues about biology, but it is far from proof of benefit in people.
Compounding
When a pharmacy prepares a customized medicine from individual ingredients. In the US, federal lists control which bulk ingredients pharmacies may use.
Controlled trial
A study that compares people who receive a treatment with a similar group who do not, often receiving a placebo instead. Randomly assigning people to each group makes the comparison fairer.
Course and cycle
A course is the period of repeated use, such as 10 days. A cycle is a course plus a planned break before any further use.
Central serous chorioretinopathy (CSCR)
An eye condition in which fluid collects under the retina, often blurring or dimming central vision. It was reported in 11 bodybuilders after follistatin-344 injections.
Daily total
All the amounts given in one day, added together. For example, 100 mcg twice daily is a 200 mcg daily total.
Dose (amount each time)
The amount given on one occasion. A protocol lists both the dose and how often it is given.
FSH (follicle-stimulating hormone)
A hormone from the pituitary gland that drives egg development in women and sperm production in men. Follistatin was first discovered because it lowers FSH.
Freeze-dried (lyophilized)
Dried by freezing and removing the water, leaving a powder. Follistatin vials are sold this way and mixed with liquid before injection.
Gene therapy
A treatment that delivers a gene into cells so the body makes a protein itself. The follistatin gene therapy trials gave one injection into muscle; it cannot be stopped once given.
Half-life
The time it takes for the measured level of a substance in the blood to fall by half. It is not the same as how long an effect lasts.
Intramuscular (IM)
Injected into a muscle.
Intravenous (IV)
Given directly into a vein, so it enters the bloodstream immediately.
Investigational
Still being studied and not approved by a regulator, such as the FDA, to treat any condition.
Loading phase
Starting with a higher amount for a short period, then lowering it. One follistatin page uses 200 mcg a day for three days, then 100 mcg a day.
mcg and mg
Micrograms and milligrams. 1 mg equals 1,000 mcg. Follistatin vials usually hold 1 mg, and protocol amounts are written in mcg.
Myostatin
A protein made by muscle that limits muscle growth, like a built-in brake. Follistatin binds it and stops it from working.
Orphan designation
A US status that supports development of a treatment for a rare disease. It is not an approval.
Peptide
A short chain of amino acids. Follistatin, at 315 amino acids when mature, is a full-sized protein rather than a peptide.
Pharmacokinetics
How the body absorbs, moves, breaks down and removes a substance. It has not been studied for follistatin protein in people.
Placebo
A dummy treatment with no active ingredient, used as a comparison in studies.
Plasmid
A small ring of DNA that cells can read to make a protein. One company gave a follistatin plasmid as a single injection into belly fat.
Preclinical research
Studies done before research in people: cell studies and animal studies.
Reconstitution
Mixing a freeze-dried powder with a liquid so it can be measured and injected. The amount of liquid sets how much follistatin each unit holds.
Research use only
A label on products sold for laboratory research. It does not mean a product is approved, tested for human use or legal to sell as a medicine.
Satellite cells
Stem cells that sit on muscle fibers and help muscles grow and repair.
Schedule 4 (Australia)
Australia's prescription-only medicine category. Follistatin is listed there and in Appendix D, which makes possession without authority illegal.
Subcutaneous (SC)
Injected into the fatty layer just under the skin. This is the route most follistatin protocol descriptions use.
Syringe units
Markings on an insulin syringe that measure volume. On a U-100 syringe, 100 units equal 1 mL. The amount of follistatin per unit depends on how the vial was mixed.
Titration
Adjusting a dose in steps, either starting lower and increasing or starting higher and reducing.
Vector genomes (vg)
A count of virus particles carrying a gene, used to dose gene therapy. It cannot be converted into micrograms of protein.
WADA
The World Anti-Doping Agency, which publishes the list of substances banned in sport. Follistatin is on it under category S4.3.
Withdrawal and rebound
Withdrawal effects are symptoms caused by stopping a substance. A rebound is a problem returning worse than before after stopping. Neither has been studied for follistatin vials.

Supporting research: muscle, fertility and other animal studies

Explore the muscle, fertility, metabolism and cancer experiments

The useful question is narrower than "Does follistatin build muscle?" Most of the striking results come from animals that were engineered to make extra follistatin all the time, or given the gene by a virus. That is not the same as injecting a small amount of protein.

Muscle size and strength

Mice engineered to make extra follistatin in muscle had increases in muscle mass comparable to mice without myostatin, and mice lacking myostatin that also made extra follistatin had about four times normal muscle mass. A single gene injection kept mouse muscles larger and stronger for more than two years, even in old mice, and in 24-month-old mice it improved the connections between nerves and muscle. [27], [82], [28], [152]

In six monkeys, gene therapy into one thigh increased thigh size and strength, with the treated muscle still making follistatin 15 months later and no organ problems reported. A correction to that paper was published in 2026. Pigs engineered to make human follistatin in muscle had leaner carcasses (72.95% versus 69.18% lean meat). [49], [153], [106]

Muscle diseases in animals

Follistatin gene therapy improved strength in mouse models of Duchenne and facioscapulohumeral muscular dystrophy, and follistatin protein given to mice with spinal muscular atrophy extended average lifespan by 30%. It helped muscles heal after injury in mice. But given at the moment a nerve was cut, it did not prevent the muscle from wasting; it only preserved muscle when given two weeks beforehand. [154], [155], [156], [157], [158]

Fertility and development

Mice born without follistatin had muscle, skin and skeletal defects, could not breathe and died within hours of birth. Mice making too much follistatin had small testes, arrested sperm production and infertility, or blocked egg development. Mice with only one form of follistatin had shortened fertility, and follistatin in the womb was needed for embryos to attach. Too much follistatin in the male reproductive ducts left sperm immotile. [159], [102], [160], [161], [124], [103]

Metabolism and fat

The direction depends on the model. In obese mice, one week of follistatin injections reduced weight gain and improved insulin sensitivity, with some effects lasting after injections stopped. Extra follistatin made in mouse muscle improved how muscle used sugar. But follistatin released from the liver worsened blood sugar control in other mouse models, and reducing it helped. [39], [162], [40]

Cancer, scarring, wounds and bone

Follistatin blocked the spread of breast and lung cancer in mouse models and made breast cancer cells less invasive in a dish, yet ovarian cancer cells used it to resist chemotherapy. In diabetic mice it reduced heart scarring but also enlarged the heart muscle; it reduced radiation scarring in mouse legs, but mice making extra follistatin in their skin healed wounds more slowly. In a rat skull-defect model, it did not improve bone healing. [121], [122], [163], [123], [105], [164], [165], [166]

None of these experiments used the vials sold online, and none can be converted into a human amount.

How this guide was researched

This guide is built from a thorough review of the sources cited throughout it: published scientific studies, registered clinical-trial plans, regulatory documents and published protocol descriptions. We also reviewed public online forums and community education groups where people describe their own experiences with Follistatin-344.

The guide cites 170 sources, including 77 original scientific papers. Each type of source answers a different question. Studies show what researchers measured. Protocol descriptions show how Follistatin-344 is typically used. Personal accounts show what individual people experienced. Every numbered citation links to its entry below, labeled by source type.

How this guide was made

Research and drafting were AI-assisted. Every cited source was checked against the original, and the guide was reviewed and edited by Doserly before publication. It has not had an independent clinical review, and Doserly does not currently have medical reviewers. Doserly makes a medication and health-tracking app and runs Doserly Academy, both of which are promoted in this guide. Read our editorial policy for how guides are researched, updated and corrected.

This guide is for educational purposes. It summarizes what the reviewed sources report so the research is easier to understand; it is not medical advice. For a deeper dive, or to check any point for yourself, go straight to the cited sources.

Explore the sources

These are the documents cited in this guide. Studies, website advice and personal accounts answer different questions. A source being listed does not mean every statement on its page is endorsed.

Showing 170 sources

  1. 01

    FST: Follistatin (Homo sapiens), UniProtKB P19883 ↗

    Protein database

    Selected original full-text sections reviewed.

  2. 02

    Differential antagonism of activin, myostatin and growth and differentiation factor 11 by wild-type and mutant follistatin. ↗

    Cell / animal research

    Original abstract reviewed.

  3. 03

    Follistatin-344 (1 mg) Dosage Protocol ↗

    Dosing website

    Selected original page sections reviewed; protocol-source claim, not a tested dose.

  4. 04

    Follistatin 344 Research, Dosing & Protocols ↗

    Dosing website

    Selected original page sections reviewed; protocol-source claim, not a tested dose.

  5. 05

    Follistatin 344 Dosage Guide ↗

    Dosing website

    Selected original page sections reviewed; protocol-source claim, not a tested dose.

  6. 06

    A phase 1/2a follistatin gene therapy trial for becker muscular dystrophy. ↗

    Human report

    Selected original full-text sections reviewed.

  7. 07

    Follistatin Gene Therapy for Sporadic Inclusion Body Myositis Improves Functional Outcomes. ↗

    Human report

    Selected original full-text sections reviewed.

  8. 08

    Clinical Intramuscular Gene Transfer of rAAV1.CMV.huFollistatin344 Trial to Patients With Duchenne Muscular Dystrophy ↗

    Study registry

    Registry record and posted results checked; no journal publication found.

  9. 09

    Central serous chorioretinopathy associated with high-dose follistatin-344: a retrospective case series. ↗

    Human report

    Original abstract reviewed; the full text was not accessible, so co-used drugs are unknown.

  10. 10

    Detection of black market follistatin 344. ↗

    Laboratory testing study

    Original abstract reviewed.

  11. 11

    Poisons Standard June 2026 ↗

    Regulatory source

    Selected original full-text sections reviewed.

  12. 12

    The 2026 Prohibited List ↗

    Regulatory source

    Selected original full-text sections reviewed.

  13. 13

    Intravenous administration of follistatin: delivery to the liver and effect on liver regeneration after partial hepatectomy. ↗

    Cell / animal research

    Original abstract reviewed; rat study, not human data.

  14. 14
  15. 15

    Circulating Follistatin Is Liver-Derived and Regulated by the Glucagon-to-Insulin Ratio. ↗

    Human study (related drug or measure)

    Original abstract reviewed.

  16. 16
  17. 17
  18. 18

    Tailor Made Compounding LLC - 594743 - 04/01/2020 ↗

    Regulatory source

    Selected original full-text sections reviewed.

  19. 19

    Follistatin-344 Evidence Summary ↗

    Dosing website

    Selected original page sections reviewed; protocol-source claim, not a tested dose.

  20. 20

    FOLLISTATIN – 344 ↗

    Dosing website

    Selected original page sections reviewed; protocol-source claim, not a tested dose.

  21. 21

    Follistatin-344 ↗

    Dosing website

    Selected original page sections reviewed; protocol-source claim, not a tested dose.

  22. 22

    Follistatin-344 Protocol ↗

    Dosing website

    Selected original page sections reviewed; protocol-source claim, not a tested dose.

  23. 23

    Follistatin 344 Peptide: Myostatin Blocker ↗

    Dosing website

    Selected original page sections reviewed; protocol-source claim, not a tested dose.

  24. 24

    Follistatin 344 Protocol: Myostatin-Inhibitor Dosing & Cycling ↗

    Dosing website

    Selected original page sections reviewed; protocol-source claim, not a tested dose.

  25. 25

    Follistatin 344 10 day log ↗

    Community discussion

    Public thread reviewed; a personal account, not clinical evidence.

  26. 26

    Follistatin 344 5mg Vial Dosage Protocol ↗

    Dosing website

    Selected original page sections reviewed; protocol-source claim, not a tested dose.

  27. 27

    Regulation of myostatin activity and muscle growth. ↗

    Cell / animal research

    Original abstract reviewed.

  28. 28

    Long-term enhancement of skeletal muscle mass and strength by single gene administration of myostatin inhibitors. ↗

    Cell / animal research

    Original abstract reviewed.

  29. 29

    Has anyone here tried follistatin... if so, with what results? ↗

    Community discussion

    Public thread reviewed; a personal account, not clinical evidence.

  30. 30

    AAS paired with Myostatin Inhibitor ↗

    Community discussion

    Public thread reviewed; a personal account, not clinical evidence.

  31. 31

    Myostatin... ? ↗

    Community discussion

    Public thread reviewed; a personal account, not clinical evidence.

  32. 32

    Bimagrumab plus semaglutide alone or in combination for the treatment of obesity: a randomized phase 2 trial. ↗

    Human study (related drug or measure)

    Selected original full-text sections reviewed.

  33. 33

    Interim Results from Ongoing Phase 2 COURAGE Trial Confirm Potential to Improve the Quality of Semaglutide (GLP-1 receptor agonist)-induced Weight Loss by Preserving Lean Mass ↗

    Company statement

    Original company release reviewed; interim results.

  34. 34

    Tirzepatide - a better semaglutide? (GIP + GLP1 agonism). Also LY3437943 ↗

    Community discussion

    Public thread reviewed; a personal account, not clinical evidence.

  35. 35

    Plasmid delivery of follistatin gene therapy safely improves body composition and lowers extrinsic epigenetic age in sex- and age-diverse adult human subjects ↗

    Human report

    Selected original full-text sections reviewed; company-written and not peer reviewed.

  36. 36

    Phase I: Safety and Efficacy of an Injectable Follistatin Plasmid Gene Therapy in Humans ↗

    Study registry

    Registry record checked; registered after the study ended; no results posted.

  37. 37

    I edited my DNA on a secret island ↗

    Self-published account

    Public thread reviewed; a personal account, not clinical evidence.

  38. 38

    Randomized phase 2 study of ACE-083, a muscle-promoting agent, in facioscapulohumeral muscular dystrophy. ↗

    Human trial

    Selected original full-text sections reviewed.

  39. 39

    Intraperitoneal administration of follistatin promotes adipocyte browning in high-fat diet-induced obese mice. ↗

    Cell / animal research

    Selected original full-text sections reviewed.

  40. 40

    Inactivating hepatic follistatin alleviates hyperglycemia. ↗

    Cell / animal research

    Original abstract reviewed.

  41. 41

    Follistatin-344 — mechanism, protocols & dosing ↗

    Dosing website

    Selected original page sections reviewed; protocol-source claim, not a tested dose.

  42. 42

    FOLLISTATIN 344 Dosing Protocol | Research Guide ↗

    Dosing website

    Selected original page sections reviewed; protocol-source claim, not a tested dose.

  43. 43

    Locally acting ACE-083 increases muscle volume in healthy volunteers. ↗

    Human trial

    Selected original full-text sections reviewed.

  44. 44

    Follistatin 315 Research, Dosing & Protocols ↗

    Dosing website

    Selected original page sections reviewed; protocol-source claim, not a tested dose.

  45. 45

    Follistatin 315 Dosage Guide: How Much Should You Take? (2026) ↗

    Dosing website

    Selected original page sections reviewed; protocol-source claim, not a tested dose.

  46. 46

    Follistatin-344 (FST-344): Research Evidence & Safety Profile ↗

    Dosing website

    Selected original page sections reviewed; protocol-source claim, not a tested dose.

  47. 47

    CALM-AF-AI: Counteracting Age-related Loss of Muscle With AAV-Follistatin Combined With Angiogenesis-Inducing VEGF Plasmid Gene Therapy ↗

    Study registry

    Registry record checked. Registration is not a published result.

  48. 48

    Safety and Efficacy of Klotho and Follistatin Gene Therapy ↗

    Study registry

    Registry record checked. Registration is not a published result.

  49. 49

    Follistatin gene delivery enhances muscle growth and strength in nonhuman primates. ↗

    Cell / animal research

    Selected original full-text sections reviewed.

  50. 50

    Increasing lean muscle mass in mice via nanoparticle-mediated hepatic delivery of follistatin mRNA. ↗

    Cell / animal research

    Selected original full-text sections reviewed.

  51. 51

    Follistatin Protein Enhances Satellite Cell Counts in Reinnervated Muscle. ↗

    Cell / animal research

    Selected original full-text sections reviewed.

  52. 52

    Stop Taking Follistatin-344 — Timing, Risks, and Protocols ↗

    Dosing website

    Selected original page sections reviewed; seller claims, contradicted by the same seller elsewhere.

  53. 53

    Follistatin-344 Cycle Length — Research Timing Guide ↗

    Dosing website

    Selected original page sections reviewed; seller claims, contradicted by the same seller elsewhere.

  54. 54

    5 days into researching follistatin 344 untagged ↗

    Community discussion

    Public thread reviewed; a personal account, not clinical evidence.

  55. 55

    Ace 031. Has anybody tried Ace 31 in any capacity? It seems interesting but was curious if anybody has done a cycle of it. ↗

    Community discussion

    Public thread reviewed; a personal account, not clinical evidence.

  56. 56
  57. 57

    Protein Engineering on Human Recombinant Follistatin: Enhancing Pharmacokinetic Characteristics for Therapeutic Application. ↗

    Cell / animal research

    Original abstract reviewed.

  58. 58

    Systemic administration of follistatin288 increases muscle mass and reduces fat accumulation in mice. ↗

    Cell / animal research

    Selected original full-text sections reviewed.

  59. 59

    Follistatin 344 Dosage, Reconstitution & Mixing Trends ↗

    Dosing website

    Selected original page sections reviewed; protocol-source claim, not a tested dose.

  60. 60

    Follistatin-344 · Wirkung, Dosierung & Studien ↗

    Dosing website

    Selected original page sections reviewed; protocol-source claim, not a tested dose.

  61. 61

    A single ascending-dose study of muscle regulator ACE-031 in healthy volunteers. ↗

    Human study (related drug or measure)

    Selected original page sections reviewed.

  62. 62

    ISEMBYLD (apitegromab-mstn) injection, for intravenous use ↗

    Regulatory source

    Selected original label sections reviewed.

  63. 63

    Follistatin-288-Fc Fusion Protein Promotes Localized Growth of Skeletal Muscle. ↗

    Cell / animal research

    Original abstract reviewed.

  64. 64

    How to Reconstitute Follistatin-344? (Lab Protocol) ↗

    Dosing website

    Selected original page sections reviewed; seller claims.

  65. 65

    Unfounded Claims of Improved Functional Outcomes Attributed to Follistatin Gene Therapy in Inclusion Body Myositis. ↗

    Published critique

    Original full-text letter reviewed; a published critique of the inclusion body myositis trial.

  66. 66

    Randomized Phase 2 Study of ACE-083 in Patients With Charcot-Marie-Tooth Disease. ↗

    Human trial

    Selected original full-text sections reviewed.

  67. 67

    Follistatin Gene Transfer to Patients With Becker Muscular Dystrophy and Sporadic Inclusion Body Myositis ↗

    Study registry

    Registry record checked. Registration is not a published result.

  68. 68

    Reply to Letter to the Editor. ↗

    Authors' reply

    Original full-text reply reviewed; the trial authors' response to the critique.

  69. 69

    Orphan drug designation: adeno-associated virus transgene of follistatin (Duchenne and Becker muscular dystrophy) ↗

    Regulatory source

    Selected original full-text sections reviewed.

  70. 70

    Orphan drug designation: adeno-associated virus delivered transgene of follistatin (inclusion body myositis) ↗

    Regulatory source

    Selected original full-text sections reviewed.

  71. 71
  72. 72

    A Study of ACE-083 in Patients With Facioscapulohumeral Muscular Dystrophy ↗

    Study registry

    Registry record checked. Registration is not a published result.

  73. 73

    A Study of ACE-083 in Patients With Charcot-Marie-Tooth Disease ↗

    Study registry

    Registry record checked. Registration is not a published result.

  74. 74

    Extension Study to Evaluate the Long-Term Effects of ACE-083 in Patients With Facioscapulohumeral Muscular Dystrophy (FSHD) and Charcot-Marie Tooth (CMT) Disease Types 1 and X (CMT1 and CMTX) ↗

    Study registry

    Registry record checked. Registration is not a published result.

  75. 75
  76. 76

    Downregulation of myostatin pathway in neuromuscular diseases may explain challenges of anti-myostatin therapeutic approaches ↗

    Cell / animal research

    Selected original full-text sections reviewed.

  77. 77

    Safety and efficacy of intravenous bimagrumab in inclusion body myositis (RESILIENT): a randomised, double-blind, placebo-controlled phase 2b trial. ↗

    Human study (related drug or measure)

    Original abstract reviewed.

  78. 78

    Randomized phase 2 trial and open-label extension of domagrozumab in Duchenne muscular dystrophy ↗

    Human trial (related drug)

    Original abstract reviewed.

  79. 79

    Pfizer Terminates Domagrozumab (PF-06252616) Clinical Studies for the Treatment of Duchenne Muscular Dystrophy ↗

    Company statement

    Selected original full-text sections reviewed.

  80. 80

    Myostatin antibody (LY2495655) in older weak fallers: a proof-of-concept, randomised, phase 2 trial. ↗

    Human study (related drug or measure)

    Selected original page sections reviewed.

  81. 81

    FDA Approves First Therapy to Target Muscle Loss in Spinal Muscular Atrophy ↗

    Regulatory source

    Selected original full-text sections reviewed.

  82. 82

    Quadrupling muscle mass in mice by targeting TGF-beta signaling pathways. ↗

    Cell / animal research

    Original abstract reviewed.

  83. 83

    Myostatin mutation associated with gross muscle hypertrophy in a child. ↗

    Human report

    PubMed record checked (no abstract); cited for the existence and title of the case report.

  84. 84

    Follistatin-mediated skeletal muscle hypertrophy is regulated by Smad3 and mTOR independently of myostatin. ↗

    Cell / animal research

    Original abstract reviewed.

  85. 85

    The type 1 insulin-like growth factor receptor (IGF-IR) pathway is mandatory for the follistatin-induced skeletal muscle hypertrophy. ↗

    Cell / animal research

    Selected original page sections reviewed.

  86. 86

    Follistatin induces muscle hypertrophy through satellite cell proliferation and inhibition of both myostatin and activin. ↗

    Cell / animal research

    Original abstract reviewed.

  87. 87

    Role of IGF-I in follistatin-induced skeletal muscle hypertrophy. ↗

    Cell / animal research

    Original abstract reviewed.

  88. 88

    Exercise induces a marked increase in plasma follistatin: evidence that follistatin is a contraction-induced hepatokine. ↗

    Human study (related drug or measure)

    Original abstract reviewed.

  89. 89

    Energy Deprivation Alters in a Leptin- and Cortisol-Independent Manner Circulating Levels of Activin A and Follistatin But Not Myostatin in Healthy Males ↗

    Human study (related drug or measure)

    Original source reviewed.

  90. 90

    Activin A and follistatin are dynamically regulated during human pregnancy. ↗

    Human study (related drug or measure)

    Original abstract reviewed.

  91. 91

    In vivo comparison of the follicle-stimulating hormone-suppressing activity of follistatin and inhibin in ovariectomized rats. ↗

    Cell / animal research

    Original abstract reviewed.

  92. 92
  93. 93

    Follistatin 344 ile İlişkili Santral Seröz Koryoretinopati (Central serous chorioretinopathy associated with follistatin 344) ↗

    Human report

    Selected original full-text sections reviewed.

  94. 94

    Risk factors for central serous chorioretinopathy: a case-control study. ↗

    Human study (related drug or measure)

    Original abstract reviewed.

  95. 95

    [Compounds] [Homebrew] Myostatin Inhibitors = Swole Goals? ↗

    Community discussion

    Public thread reviewed; a personal account, not clinical evidence.

  96. 96

    What peptide did you regret running? ↗

    Community discussion

    Public thread reviewed; a personal account, not clinical evidence.

  97. 97

    Painfull red swelling after Follistatin ↗

    Community discussion

    Public thread reviewed; a personal account, not clinical evidence.

  98. 98

    Follistatin 344 ↗

    Community discussion

    Public thread reviewed; a personal account, not clinical evidence.

  99. 99

    Peptide follistatine qui inhibe la myostatine pour la croissance musculaire ↗

    Community discussion

    Public thread reviewed; a personal account, not clinical evidence.

  100. 100

    Severe pain after Follistatin 344!?!? Help!?! ↗

    Community discussion

    Public thread reviewed; a personal account, not clinical evidence.

  101. 101

    A Study of ACE-083 in Healthy Subjects ↗

    Study registry

    Registry record checked. Registration is not a published result.

  102. 102

    Overexpression of mouse follistatin causes reproductive defects in transgenic mice. ↗

    Cell / animal research

    Original abstract reviewed.

  103. 103

    Overexpression of follistatin in the mouse epididymis disrupts fluid resorption and sperm transit in testicular excurrent ducts. ↗

    Cell / animal research

    Original abstract reviewed.

  104. 104

    WINREVAIR (sotatercept-csrk) for injection, for subcutaneous use ↗

    Regulatory source

    Selected original label sections reviewed.

  105. 105

    Follistatin Attenuates Myocardial Fibrosis in Diabetic Cardiomyopathy via the TGF-β-Smad3 Pathway. ↗

    Cell / animal research

    Original abstract reviewed.

  106. 106

    The transgenic expression of human follistatin-344 increases skeletal muscle mass in pigs. ↗

    Cell / animal research

    Original abstract reviewed.

  107. 107

    Tendons of myostatin-deficient mice are small, brittle, and hypocellular. ↗

    Cell / animal research

    Original abstract reviewed.

  108. 108

    Changes in skeletal muscle and tendon structure and function following genetic inactivation of myostatin in rats. ↗

    Cell / animal research

    Original abstract reviewed.

  109. 109

    Follistatin 315 for the guns. Any tips tricks? Not a good first run. ↗

    Community discussion

    Public thread reviewed; a personal account, not clinical evidence.

  110. 110

    [Compounds] Pre workout combo. ↗

    Community discussion

    Public thread reviewed; a personal account, not clinical evidence.

  111. 111

    Myostatin inhibitor ACE-031 treatment of ambulatory boys with Duchenne muscular dystrophy: Results of a randomized, placebo-controlled clinical trial. ↗

    Human study (related drug or measure)

    Original abstract reviewed.

  112. 112

    Human Follistatin Recombinant Protein, catalog 120-13-20UG ↗

    Supplier product page

    Original product page reviewed; laboratory reagent labelled for research use only.

  113. 113

    21 CFR 600.3: Definitions (including "protein") ↗

    Regulatory source

    Selected original full-text sections reviewed.

  114. 114

    Bulk Drug Substances Used in Compounding Under Section 503A: Categories ↗

    Regulatory source

    Original list reviewed (May 2026); follistatin is not listed.

  115. 115

    FDA Evaluation of KPV-Related Bulk Drug Substances for the Pharmacy Compounding Advisory Committee ↗

    Regulatory source

    Selected original full-text sections reviewed.

  116. 116

    Think twice before injecting peptides bought online: unauthorized products can seriously harm you ↗

    Regulatory source

    Original advisory reviewed; follistatin is not named.

  117. 117

    The 2027 Prohibited List ↗

    Regulatory source

    Original list reviewed; takes effect 1 January 2027.

  118. 118

    The 2019 Prohibited List ↗

    Regulatory source

    Selected original full-text sections reviewed.

  119. 119

    The 2008 Prohibited List ↗

    Regulatory source

    Selected original full-text sections reviewed.

  120. 120

    Multiplex detection of seven transgenes for human gene doping analysis ↗

    Laboratory testing study

    Original source reviewed.

  121. 121

    Follistatin is a metastasis suppressor in a mouse model of HER2-positive breast cancer. ↗

    Cell / animal research

    Original abstract reviewed.

  122. 122
  123. 123

    Quiescent Ovarian Cancer Cells Secrete Follistatin to Induce Chemotherapy Resistance in Surrounding Cells in Response to Chemotherapy. ↗

    Cell / animal research

    Selected original page sections reviewed.

  124. 124

    Follistatin is critical for mouse uterine receptivity and decidualization. ↗

    Cell / animal research

    Original abstract reviewed.

  125. 125

    Igf-1 lr3, follistatin 344, gh (morning), test, Npp/deca, and anadrol. ↗

    Community discussion

    Public thread reviewed; a personal account, not clinical evidence.

  126. 126

    Study protocol and statistical analysis plan, NCT02354781 (rAAV1.CMV.huFollistatin344 in Duchenne muscular dystrophy) ↗

    Study registry

    Selected original full-text sections reviewed.

  127. 127

    Weight management drug development & clinical trial support ↗

    Company page

    Original source reviewed.

  128. 128

    Follistatin-344 ↗

    Community discussion

    Public thread reviewed; a personal account, not clinical evidence.

  129. 129

    Super happy with bpc-157 and tb-500. What else should I try? ↗

    Community discussion

    Public thread reviewed; a personal account, not clinical evidence.

  130. 130

    Follistatin 344 Results - Brutal Honesty ↗

    Community discussion

    Public thread reviewed; a personal account, not clinical evidence.

  131. 131

    follistatin 344 ↗

    Community discussion

    Public thread reviewed; a personal account, not clinical evidence.

  132. 132

    Minicircle: This biohacking company is using a crypto city to test controversial gene therapies (MIT Tech Rev) ↗

    Community discussion

    Public thread reviewed; a personal account, not clinical evidence.

  133. 133

    The Coolest, Craziest Peptides & Where To Get Them ↗

    Community discussion

    Public thread reviewed; a personal account, not clinical evidence.

  134. 134

    Follistatin 344 Plasma Gene Therapy, anyone tried it? ↗

    Community discussion

    Public thread reviewed; a personal account, not clinical evidence.

  135. 135

    Anyone here tried Follistatin-344? ↗

    Community discussion

    Public thread reviewed; a personal account, not clinical evidence.

  136. 136

    Follistatin-344 ↗

    Community discussion

    Public thread reviewed; a personal account, not clinical evidence.

  137. 137

    IGF-1 LR3 ↗

    Dosing website

    Selected original page sections reviewed; protocol-source claim, not a tested dose.

  138. 138

    INCRELEX (mecasermin) injection, for subcutaneous use: Prescribing Information ↗

    Regulatory source

    Selected original full-text sections reviewed.

  139. 139

    PEG-MGF Complete dosing & administration guide ↗

    Dosing website

    Selected original page sections reviewed; protocol-source claim, not a tested dose.

  140. 140

    Certain Bulk Drug Substances for Use in Compounding That May Present Significant Safety Risks ↗

    Regulatory source

    Original page reviewed (April 2026 update).

  141. 141

    Effects of an oral ghrelin mimetic on body composition and clinical outcomes in healthy older adults: a randomized trial. ↗

    Human study (related drug or measure)

    Selected original page sections reviewed.

  142. 142

    MK-0677 (ibutamoren mesylate) for the treatment of patients recovering from hip fracture: a multicenter, randomized, placebo-controlled phase IIb study. ↗

    Human study (related drug or measure)

    Original abstract reviewed.

  143. 143

    October 29, 2024 Pharmacy Compounding Advisory Committee Meeting Minutes ↗

    Regulatory source

    Selected original full-text sections reviewed.

  144. 144

    Ibutamoren Mesylate: FDA Presentation for the Pharmacy Compounding Advisory Committee ↗

    Regulatory source

    Selected original full-text sections reviewed.

  145. 145

    Effects of (-)-epicatechin on molecular modulators of skeletal muscle growth and differentiation. ↗

    Human study (related drug or measure)

    Original source reviewed.

  146. 146

    (-)-Epicatechin induces mitochondrial biogenesis and markers of muscle regeneration in adults with Becker muscular dystrophy. ↗

    Human study (related drug or measure)

    Original source reviewed.

  147. 147
  148. 148

    Selective androgen receptor modulator, YK11, regulates myogenic differentiation of C2C12 myoblasts by follistatin expression. ↗

    Cell / animal research

    Original source reviewed.

  149. 149

    TITAN SARMS LLC warning letter ↗

    Regulatory source

    Selected original full-text sections reviewed.

  150. 150

    Determination of free follistatin levels in sera of normal subjects and patients with various diseases. ↗

    Human study (related drug or measure)

    Original abstract reviewed.

  151. 151

    FLGR242 (10mg) ↗

    Seller page

    Selected original page sections reviewed; seller claims, no published data.

  152. 152

    Follistatin-induced muscle hypertrophy in aged mice improves neuromuscular junction innervation and function. ↗

    Cell / animal research

    Original abstract reviewed.

  153. 153
  154. 154

    Micro-dystrophin and follistatin co-delivery restores muscle function in aged DMD model. ↗

    Cell / animal research

    Original abstract reviewed.

  155. 155

    AAV-mediated follistatin gene therapy improves functional outcomes in the TIC-DUX4 mouse model of FSHD. ↗

    Cell / animal research

    Original abstract reviewed.

  156. 156

    Delivery of recombinant follistatin lessens disease severity in a mouse model of spinal muscular atrophy. ↗

    Cell / animal research

    Original abstract reviewed.

  157. 157
  158. 158

    Evaluation of follistatin as a therapeutic in models of skeletal muscle atrophy associated with denervation and tenotomy. ↗

    Cell / animal research

    Original abstract reviewed.

  159. 159

    Multiple defects and perinatal death in mice deficient in follistatin. ↗

    Cell / animal research

    Original abstract reviewed.

  160. 160

    Female infertility and disrupted angiogenesis are actions of specific follistatin isoforms. ↗

    Cell / animal research

    Original abstract reviewed.

  161. 161

    The follistatin-288 isoform alone is sufficient for survival but not for normal fertility in mice. ↗

    Cell / animal research

    Original abstract reviewed.

  162. 162

    Mechanisms involved in follistatin-induced hypertrophy and increased insulin action in skeletal muscle. ↗

    Cell / animal research

    Selected original page sections reviewed.

  163. 163

    Increased Expression of Follistatin in Breast Cancer Reduces Invasiveness and Clinically Correlates with Better Survival. ↗

    Cell / animal research

    Original abstract reviewed.

  164. 164

    Follistatin attenuates radiation-induced fibrosis in a murine model. ↗

    Cell / animal research

    Selected original page sections reviewed.

  165. 165

    Impaired wound healing in transgenic mice overexpressing the activin antagonist follistatin in the epidermis. ↗

    Cell / animal research

    Original abstract reviewed.

  166. 166

    Follistatin Effects in Migration, Vascularization, and Osteogenesis in vitro and Bone Repair in vivo. ↗

    Cell / animal research

    Original abstract reviewed.

  167. 167

    Drug Product Database: search for products containing follistatin (no results) ↗

    Regulatory source

    Database searched by active ingredient through Health Canada's official API; no product containing follistatin is listed.

  168. 168

    Development, validation and application of an ultra-sensitive two-site enzyme immunoassay for human follistatin. ↗

    Human study (related drug or measure)

    Original abstract reviewed.

  169. 169

    Follistatin: Dosage, Benefits & Side Effects (2026) ↗

    Dosing website

    Selected original page sections reviewed; protocol-source claim, not a tested dose.

  170. 170

    Recombinant Follistatin: The Future Of True Muscle Growth ↗

    Promotional page

    Selected original page sections reviewed; promotional claims about a seller product, no published data.

Updates and corrections

Updated September 24, 2026. This version replaces the earlier Follistatin-344 page. It adds a comparison of the protocols websites describe, with their provenance; sections on storage, stopping, monitoring and related compounds; a dated legal-status summary for the United States, Canada and Australia; the September 2026 approval of apitegromab and other drugs in the same pathway; and answers to common questions. It corrects several details carried by the earlier page's sources: the monkey study's 15% figure was thigh circumference, not muscle mass; the Becker trial reduced scarring to 35% and 43% of starting levels in two patients; the 194–327% muscle increases came from engineered mice, not gene injections; and follistatin was first named on the anti-doping list in 2019, while myostatin-blocking agents were banned earlier. The date describes this revision, not a fresh check of every source.

Found an error or a relevant study we missed? Report a correction with the guide title, the specific passage and a supporting source if available. Please leave out personal health records. See our editorial policy for how we handle attribution, evidence limits and corrections.