Follistatin-344 Dosage, half-life & reference guide

Week by week.

What to expect in the first 8 weeks

Onset

Unknown in people

Peak effect

Unknown in people; the gene-therapy trials measured at 6 months and a year

Duration

10–30 days per community cycle

1. Day 1–14Community

   The first two weeks are quiet

   Commonly reported: injection-site redness, sometimes mild fatigue, and nothing that separates from training. That is what you would expect from a protein that clears in minutes to hours and has no human efficacy data behind it — and from a market where only 9 of 17 products tested actually contained follistatin.

   The science

   In rats, labelled follistatin given into a vein cleared with an initial half-life of 4 minutes and a terminal one of about 131 minutes, accumulating in the liver (Kogure 1996). Drug developers found native follistatin's pharmacokinetics unsuited to systemic dosing and had to engineer the molecule: Datta-Mannan and colleagues (2013) report that an Fc fusion with the heparin binding removed improved terminal half-life about 100-fold and exposure about 1,600-fold, and only then did weekly dosing do anything in mouse muscle models. Reichel 2019 tested 17 black-market products labelled follistatin: nine contained it, all His-tagged and heavily oligomerized, and some of the rest contained MGF or GHRP-2.

   Sources

   • Kogure et al. (1996)
   • Datta-Mannan et al. (2013)
   • Reichel et al. (2019)

   Updated Oct 2026

2. Day 7–30Clinical

   The eye signal, said plainly

   The only published human series on injected follistatin-344 is an eye one: eleven bodybuilders who injected whole 1 mg vials developed fluid under the retina, which reads as blurred, dim or distorted central vision. In the eight who injected once it cleared on its own over about two months; the three who repeated it had it come back. Worth knowing, and worth an eye exam rather than a wait if your central vision changes.

   The science

   Dağ 2020, a retrospective series from one clinic: 11 male bodybuilders, mean age 36.8, all with a history of injecting complete 1 mg follistatin-344 vials subcutaneously into the abdomen; ten unilateral, one bilateral central serous chorioretinopathy on OCT. Subretinal fluid resolved in 2.3 ± 0.7 months in the eight with a single prior injection, and recurred in the three with multiple injections. The authors put it as follistatin-344 being a possible risk factor worth asking about in anyone presenting with this, not as a proven cause. Note the dose: a whole 1 mg vial in one shot is roughly ten times the 100 mcg a day community guides describe.

   Sources

   • Dağ et al. (2020)

   Updated Oct 2026

3. Day 14–60Clinical

   What follistatin has actually moved in people

   Gene therapy, not an injection. Delivering the follistatin gene into the quadriceps improved six-minute walking distance in four of six men with Becker muscular dystrophy, with no change in the other two, and muscle biopsies showed less fibrosis. That is the human evidence this compound borrows, and it is a different intervention from a vial of protein.

   The science

   Mendell 2015, a phase 1/2a: AAV1.CMV.FS344 injected into both quadriceps of six Becker patients at two dose levels; walking distance gains of 58, 125, 108 and 29 m in four patients and no change in two, with reduced endomysial fibrosis, less central nucleation and more normal fiber-size distribution, and no adverse events attributed to the transfer. A follow-up in six men with sporadic inclusion body myositis reported an annualized six-minute-walk gain of 56.0 m against a 25.8 m decline in eight untreated matched subjects (Mendell 2017) — and drew a published rebuttal arguing the treated group also received high-dose prednisone and supervised exercise while the comparison group received none of those interventions, and that the annualized walk measure was constructed after the fact (Greenberg 2017; Mendell replied). In macaques, the same gene in the quadriceps gave durable size and strength gains with no abnormal organ findings (Kota 2009; an erratum was published in 2026).

   Sources

   • Mendell et al. (2015)
   • Mendell et al. (2017)
   • Greenberg (2017)
   • Kota et al. (2009)

   Updated Oct 2026

4. Day 30–90RCT

   Bigger muscle, unchanged function

   The follistatin drug that did reach proper human trials is the most useful thing in this entry. ACE-083, built to stay in the muscle it was injected into, grew those muscles by roughly 9 to 16% on MRI — and across three trials it did not consistently improve strength, walking or anything patients could feel. Muscle volume and muscle function are not the same endpoint.

   The science

   Glasser 2018, first-in-human in 58 healthy postmenopausal women: injected-muscle volume rose up to 14.5% (rectus femoris) and 8.9% (tibialis anterior) with no significant change in mean strength and no serious adverse events. Statland 2022, randomized phase 2 in facioscapulohumeral dystrophy: total muscle volume +16.4% in biceps and +9.5% in tibialis anterior against placebo, with no consistent functional or patient-reported improvement over up to 12 months. Thomas 2022, randomized phase 2 in Charcot-Marie-Tooth disease: +13.5% muscle volume and better ankle dorsiflexion strength, with the other functional outcomes unchanged. Mild to moderate injection-site reactions were the most common adverse event in all three; development stopped.

   Sources

   • Glasser et al. (2018)
   • Statland et al. (2022)
   • Thomas et al. (2022)

   Updated Oct 2026

5. Any dayAnimal

   What Follistatin-344 is built on

   Strong biology, real human trials of other things, and nothing on the vial itself. Follistatin as a molecule has decades of solid work: it binds myostatin and activin, and mice over-expressing it grow like myostatin-knockout mice. What it does not have is a single efficacy study of the injected peptide in people — the human record is gene therapy in two rare muscle diseases, an engineered follistatin drug that grew muscles without improving function, and one eye case series.

   The science

   Lee & McPherron 2001: follistatin blocks myostatin binding to the activin type IIB receptor, and transgenic mice over-expressing it in muscle showed dramatic increases in mass comparable to myostatin-knockout mice. Lee 2010 and Winbanks 2012 showed the effect is not myostatin-only — activin A is part of it — and Kalista 2012 showed the hypertrophy needs the IGF-1 receptor, Akt and mTOR, with IGF-1 receptor inhibition blunting it by 63%. Shimasaki 1988 established the two splice precursors (344 and 317 amino acids); Sugino 1993 separated FS-315 from the cell-binding FS-288, which is why the trials chose FS344 (reviewed by Al-Zaidy and colleagues). The human work sits in the cards above: the gene-therapy trials in Becker muscular dystrophy and inclusion body myositis, the second of them rebutted in print; the ACE-083 trials, which grew muscle volume without consistent functional gains; and the retinal case series (Dağ 2020). Nothing published tests a vial of follistatin-344 injected for muscle.

   Sources

   • Lee & McPherron (2001)
   • Lee et al. (2010)
   • Winbanks et al. (2012)
   • Kalista et al. (2012)
   • Shimasaki et al. (1988)
   • Sugino et al. (1993)
   • Al-Zaidy et al. (2015)
   • Dağ et al. (2020)

   Updated Oct 2026

6. With HGH, IGF-1 LR3 and MK-677Community

   Why it ends up next to the GH peptides

   The pairing has a mechanism behind it: in mice, follistatin's muscle growth needs the IGF-1 receptor and the Akt–mTOR pathway, which is the arm GH, IGF-1 analogues and secretagogues push on. So the stack is a brake released and a throttle pressed. Nothing has tested the combination in any species, and the glucose risk in such a stack comes from the IGF-1 side.

   The science

   Kalista 2012: in mice, a dominant-negative IGF-1 receptor cut follistatin-induced fiber hypertrophy by 63%, blocking Akt cut it by 65%, and rapamycin cut it by 36% — the hypertrophy runs through IGF-1 receptor, Akt and mTOR. GH works largely by raising IGF-1, and MK-677 lifted IGF-1 into the young-adult range in older adults (Chapman 1996). Follistatin also binds activin A and GDF11, so it is not a myostatin-only tool (Lee 2010). No study has combined follistatin with GH, MK-677 or an IGF-1 analogue.

   Sources

   • Kalista et al. (2012)
   • Chapman et al. (1996)
   • Lee et al. (2010)

   Updated Oct 2026

Swipe for more ›

After week 8

1. Day 60+Community

   Past a month or two, nothing is mapped

   Community cycles stop between 10 and 30 days and take weeks off, so this window is mostly repeat courses — and repeat injection is exactly where the retinal cases came back. There is no long-term data on the injected protein in people. The gene-therapy trials ran for years, but they delivered one isoform into one muscle, which is a different thing.

   The science

   The three patients in Dağ 2020 with multiple prior injections had recurrent central serous chorioretinopathy, against spontaneous resolution in the eight single-injection cases. No toxicology or repeat-dose study of injected follistatin has been published. The gene-therapy safety window is a year of normal blood counts, organ panels and pituitary hormones in six Becker patients (Mendell 2015) and up to 15 months of normal histology and function in macaques (Kota 2009) — reassuring about the isoform, silent about weeks of systemic protein.

   Sources

   • Dağ et al. (2020)
   • Mendell et al. (2015)
   • Kota et al. (2009)

   Updated Oct 2026

Mixing and a typical run.

Safety.

Goes with.

• HGH
• IGF-1 LR3
• MK-677

Questions people ask.

Research.

Reference.

Cadence

Daily

Half-life

Not measured in people: no human pharmacokinetic study of injected follistatin has been published. In rats, labelled follistatin given into a vein cleared in two phases, about 4 minutes then about 2 hours, and collected in the liver (Kogure 1996). Drug companies that tried to develop it found native follistatin cleared too fast to work as an injection and had to engineer around it. The 90-minute figure community guides quote has never been measured; the rat terminal value is about 131 minutes.

Research basis

●●● Emerging

Primarily preclinical / limited human data