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Protein — Branded Follistatin Construct

FLGR-242

No Data

FLGR242 · recombinant follistatin (branded) · myostatin inhibitor

A follistatin with a codename, sold by the company its promoter co-founded. Human data on FLGR-242 itself: self-reports its promoter has published, starting with his own eight weeks — and he says he runs TRT and growth hormone year-round.

Reconstituting this? Do the math.
Molecular Weight
~40 kDa (seller’s figure)
Construct
Modified follistatin-344 + albumin-binding peptide (seller)
Half-life
Not published (19 days stated)
Route
SubQ only, per its promoter
FDA Status
Not approved · on no FDA list
Published Studies
0 on FLGR-242 itself
Human Studies
None · promoter-published self-reports
WADA Status
Prohibited (S4.3, follistatin)
Evidence Strength
FLGR-242: none published
Follistatin: gene therapy, animal
Cost & Access
Research chemical (BioLongevity Labs)

Research only · not on any FDA 503A list · Tell me if this changes →

The other four questions

What does it do? The seller and Campbell say it blocks myostatin, the body’s brake on muscle growth, without touching activin, and that it has a 19-day half-life. None of that has been published.
Who uses it? People following Campbell’s protocols. The published accounts cover Campbell, the CEO of two peptide companies, and a competing bodybuilder.
Does the evidence hold up? There is no study of FLGR-242: no independent analysis of the product, no pharmacokinetic data, no controlled human trial. Follistatin’s own human evidence is two small published gene-therapy trials; the rest is animal work.
Bottom line? The documents describe a product. What is in the vial is the one thing none of them shows.

Dosing from the Literature

Published for muscle: no dose at all; the table is its promoter's stated regimens, 1.25 to 15 mg a week. Not published: any study giving it to anyone.

No study has given FLGR-242 to anyone at any dose. The table records Jay Campbell’s stated regimens as he published them, by date. They are his stated regimens, not recommendations, and they differ: stated weekly amounts run from 1.25 mg to 15 mg, and the 2025 article said there was no need to cycle while the 2026 documents set cycles.

SourceStated AmountFrequencyCycleNotes
jaycampbell.com, Nov 22, 20255 mg, or 2.5 mg (“normal use”); 5 mg (“advanced users seeking maximum hypertrophy”)Every two weeks (5 mg) or weekly (2.5 mg); weekly (5 mg, advanced)“There’s no need to cycle on-and-off”SubQ in the abdomen; “DO NOT INJECT RECOMBINANT FOLLISTATIN INTRAMUSCULARLY.” His stack version is 5 mg weekly, “(Double the recommended dose).”
Substack, Jun 5, 2026Men 1.5–15 mg “depending on their training experience”; women 1–2 mgWeeklyMen six months on, two off; women 3–4 months on, one off“Start at the lower end and progressively titrate up your dose over time.” Women who are not competitive bodybuilders or figure athletes are pointed to SlimAssist (2 mg FLGR242 per vial).
Longevity protocol page, jaycampbell.com (2026)2.5–5 mgOnce every two weeks, morning12–16 weeks on, 8 weeks off“Start at 2.5mg for your first cycle and assess tolerance before moving up. SubQ only — this is not negotiable with FLGR-242.”
jaycampbell.com, Sep 3–4, 20261.25–2.5 mg to startWeekly12–24 weeks on, 6–12 weeks off“Injected subcutaneously only.” The September 2 post says follistatin-344-style frequent dosing “produces a massive cumulative overexposure.”
Dosing Disclaimer

No dose of FLGR-242 has been tested in a study, and no pharmacokinetic data link any dose to blood levels. These rows document one promoter’s published statements; they are not a dosing guide. Always work with a licensed healthcare provider.

→ Peptide Calculator — vial-to-syringe math

What It Is

FLGR-242 is the codename Jay Campbell gave to a follistatin-based protein: “We gave it the codename FLGR242” (Campbell, June 5, 2026). BioLongevity Labs sells it as FLGR242, freeze-dried in 5 mg vials sold in pairs, and describes it as “INTENDED AS A RESEARCH CHEMICAL ONLY” (product page). Campbell describes BioLongevityLabs.com as “the company I co-founded” and calls FLGR-242 “my company’s answer” (Campbell, September 1, 2026). He also sells it in a blend, SlimAssist, which “contains 2mg FLGR242 and 500mcg of a Vitamin B complex per vial,” and points women who are not competitive bodybuilders or figure athletes to it (Campbell, June 5, 2026).

What the seller says it is: “a novel fragmented, modified version of Follistatin-344 (FST-344) that does not bind to the protein activin,” which “also contains a patented albumin binder.” The product page gives the binder as GGSGGSGGSGGRLIEDICLPRWGCLWEDD, the molecular weight as ~40 kDa and the construct’s albumin affinity as “<20 nM Kd.” Campbell’s first article adds that the base is “a variation of Follistatin (FS I-I)” and gives a serum half-life of 19 days (Campbell, November 22, 2025).

The named parts exist in the literature. FS I-I is a follistatin-derived myostatin inhibitor described in 2008 (Nakatani et al., 2008). The last 18 residues of the binder, RLIEDICLPRWGCLWEDD, are SA21, an albumin-binding peptide published by Genentech scientists in 2002; the rest is a glycine-serine linker (Dennis et al., 2002). Follistatin-344 is the longer of the two precursor forms the human follistatin gene makes by alternative splicing (Shimasaki et al., 1988). The native protein has its own page: Follistatin-344.

What has not been published: the construct’s full sequence, how it is made, its glycosylation, its binding to myostatin or activin, its half-life in any species, and any analysis of the product by a laboratory independent of the seller. PubMed and ClinicalTrials.gov returned no record for FLGR242 or FLGR-242 on September 28, 2026.

Mechanism of Action

No mechanism study of FLGR-242 exists. What follows is the published biology of its parts, and what the seller says the construct does.

  • Myostatin (GDF-8) → activin type II receptors (the brake) — Myostatin is a TGF-β family member expressed in skeletal muscle (McPherron et al., 1997). Purified myostatin binds the activin type II receptors ActRIIB and, to a lesser extent, ActRIIA (Lee & McPherron, 2001). Mice without the gene have individual muscles weighing 2–3 times normal (McPherron et al., 1997).
  • Follistatin as a ligand trap — Follistatin blocks myostatin binding to ActRIIB (Lee & McPherron, 2001). In crystal structures, two follistatin molecules encircle activin and bury a third of its residues, receptor sites included (Thompson et al., 2005). Bound to myostatin, follistatin’s N-terminal domain rearranges, and the complex binds heparin more strongly, which increases myostatin degradation at the cell surface (Cash et al., 2009).
  • Activin and FSH (why selectivity matters) — Follistatin was first isolated as a protein that suppresses FSH release (Ueno et al., 1987) and then identified as the activin-binding protein; activin stimulates FSH release (Nakamura et al., 1990). Native follistatin binds activin more tightly than myostatin: dissociation constants of 1.72 nM and 12.3 nM (Nakatani et al., 2008).
  • FS I-I (a myostatin-selective follistatin) — FS I-I bound activin with a dissociation constant of 64.3 µM and myostatin with 46.8 nM: more than a thousandfold selective for myostatin, and about four times weaker on myostatin than native follistatin (Nakatani et al., 2008). The seller says FLGR-242 “does not bind to the protein activin”; no binding data for FLGR-242 are published.
  • Cell-surface binding (where follistatin acts) — The follistatin isoforms bind activin with similar affinity but differ in cell-surface binding (FST288 > FST303 > FST315), and that binding tracked how well each neutralized activin, myostatin and BMPs in cells (Sidis et al., 2006). Campbell writes that the construct offsets “the binding to heparin that Follistatin demonstrates” (Campbell, November 22, 2025); no data are published.
  • Albumin binding (SA21) — SA21 binds serum albumin at a site distinct from known small-molecule sites, with dissociation constants of 266, 320 and 467 nM for rat, rabbit and human albumin. A related sequence fused to an antibody fragment extended its half-life 26-fold, to 10.4 hours, in mice and 37-fold, to 32.4 hours, in rabbits: 25–43% of albumin’s own half-life in those animals (Dennis et al., 2002). Campbell writes that FLGR-242 “inherits” albumin’s roughly 19-day half-life (Campbell, September 2, 2026). No half-life of FLGR-242 has been measured in a publication.

What the Research Shows

The research below is on myostatin, native follistatin and the construct’s parts. None of it tested FLGR-242.

  • Myostatin loss in mice — Myostatin-null mice have muscles 2–3 times normal weight, from both more and larger fibers (McPherron et al., 1997). Mice engineered to make extra follistatin in muscle gained muscle mass comparable to the knockouts (Lee & McPherron, 2001).
  • FS I-I in mice — Transgenic mice expressing FS I-I in skeletal muscle had more muscle mass and strength. Crossed with mdx mice, a Duchenne model, their muscles were larger, showed less cell infiltration and recovered strength (Nakatani et al., 2008).
  • Follistatin gene delivery in animals — A single AAV1 injection of myostatin-inhibitor genes raised muscle mass and strength for more than two years in normal and dystrophic mice, with the largest gains from follistatin-344, and worked in aged dystrophic mice too (Haidet et al., 2008). In cynomolgus macaques, AAV1-FS344 injected into the quadriceps produced “pronounced and durable increases in muscle size and strength,” with no abnormal changes in key organs (Kota et al., 2009; an erratum was published in 2026).
  • A child without myostatin (NEJM, 2004) — A boy with a splice-site mutation in both copies of the myostatin gene. At six days old his quadriceps cross-section was 7.2 standard deviations above age-matched controls (6.72 vs 3.13 cm²) and his fat layer 2.88 below; at 4.5 years he could hold two 3-kg dumbbells in horizontal suspension with his arms extended. No myostatin propeptide was detected in his serum. His mother, a former professional athlete, carried one copy. His heart was checked every six months and was normal, but the authors wrote that he was “still too young for such abnormalities to be ruled out definitively” (Schuelke et al., 2004).
  • Mouse results translate poorly — A 2017 study notes that circulating myostatin “is at least 50 times higher in mice than in humans,” and found the myostatin pathway turned down in patients with muscle-wasting diseases: less myostatin, more follistatin (Mariot et al., 2017). The NEJM authors found myostatin hard to detect in human serum, “presumably because humans have lower circulating myostatin levels” (Schuelke et al., 2004). In primates, activin A does more of the braking: blocking GDF8 alone grows muscle prominently in mice but less in monkeys and people (Latres et al., 2017).
  • Myostatin-pathway drugs in people — MYO-029, a myostatin antibody, in 116 adults with muscular dystrophy: no improvement in strength or function in a study not powered for efficacy, and skin hypersensitivity at 10 and 30 mg/kg (Wagner et al., 2008). ACE-031, a decoy receptor: one 3 mg/kg dose raised lean mass 3.3% and thigh muscle volume 5.1% at day 29 in healthy postmenopausal women (Attie et al., 2013); its trial in boys with Duchenne muscular dystrophy stopped over nosebleeds and telangiectasias (Campbell C et al., 2017). ACE-083, a follistatin-based protein injected into one muscle: volume up 14.5% and 8.9% in the two muscles tested, with no significant change in strength (Glasser et al., 2018).
Research Limitations — None of This Is FLGR-242

Every result above is on myostatin, on follistatin delivered as a gene, on FS I-I made inside transgenic mice, or on an albumin-binding peptide attached to an antibody fragment. No study in any species has tested the FLGR-242 construct, and results in mice have translated poorly to people.

Human Data

No controlled human study of FLGR-242 exists. No pharmacokinetic data on FLGR-242 have been published, so its 19-day half-life is a stated figure, not a measurement. No independent characterization of the product (what the protein is, how pure it is, whether it is active) has been published. Campbell: “Large human clinical trials on FLGR-242 do not exist yet” (Campbell, September 3, 2026).

What exists are self-reports, all published by Campbell:

  • His own eight weeks (jaycampbell.com, November 22, 2025) — “Speaking from my N-of-1 experience … here are my quick observations from 8 weeks of use” (the same article also says “just 7 weeks of usage”). He describes big pumps, prominent veins, getting leaner, “very grainy and separated” arms, abdominal swelling and post-injection pain “moderate at worst,” and scale weights of 219.5 lb on November 18 and 221.9 lb on November 21. He writes that his training, diet and sleep were off during the period, and that he did not measure myostatin before or after. In June 2026 he listed testosterone and HGH among the “fundamentals I AM excited about and running year-round” (Campbell, June 5, 2026).
  • Sixteen weeks, two users (X, February 19, 2026) — A photo of Campbell and the CEO of two peptide companies, “two of the people using FLGR-242 (Recombinant Follistatin) for the last 16 weeks.” The post’s readable text ends “Both of us are up 10+ pounds of pure skeletal…”. No method of measurement is given.
  • A bodybuilder’s contest prep (Substack interview, June 26, 2026) — An IFBB professional’s 10-week log: FLGR-242 at 2.5 mg a week, then 5 mg a week, then 1 mg a day in peak week. Weight 193 lb at both check-ins; body fat 12% to 4% and lean mass ~170 to ~185 lb from January 28 to April 5, 2026, with no method stated. He describes a TRT prescription and his current testosterone use, lists TB-500 and AOD-9604 in the same regimen, and says he pushed cardio harder this time. Campbell’s posts describe FLGR-242 as “the only variable he changed.” The post carries a discount code in the athlete’s name.

None of these is a study: no control group, no blinding, no measurement of what was injected, and both users who describe their other drugs say they use testosterone. The evidence meter on the FLGR-242 card reads “No data” because it counts published studies of the compound, and there are none.

Follistatin’s own human evidence is gene therapy. In the Becker muscular dystrophy trial, AAV1.CMV.FS344 was injected into both quadriceps of six patients: four walked farther on the 6-minute walk test (by 58, 125, 108 and 29 m) and two did not change; no adverse effects were seen (Mendell et al., 2015). In sporadic inclusion body myositis, six treated patients improved a median +56.0 m/year against −25.8 m/year in eight untreated patients (p = 0.01) (Mendell et al., 2017). These trials put a follistatin gene into thigh muscle; they did not inject follistatin protein. ClinicalTrials.gov lists these and other follistatin gene-therapy trials (NCT01519349; NCT02354781; NCT07443826, recruiting in 2026) and no trial of FLGR-242.

Reconstitution & Storage

FLGR-242 is sold as freeze-dried powder in 5 mg vials; the product page says “We do not use any fillers in this process.” None of the documents gives a mixing volume, a storage temperature or a use-by time after mixing for FLGR-242, and no stability data on the construct are published. The table is arithmetic only: how volume maps to milligrams in the vial size the seller lists (U-100 insulin syringe: 100 units = 1 mL). It is not a recommendation.

Vial SizeWater AddedConcentration1.25 mg2.5 mg5 mg
5 mg1 mL5 mg/mL25 units (0.25 mL)50 units (0.50 mL)100 units (1.0 mL, whole vial)
5 mg2 mL2.5 mg/mL50 units (0.50 mL)100 units (1.0 mL)2.0 mL (whole vial)
  • Route in the documents — Subcutaneous only. Campbell’s first article: “DO NOT INJECT RECOMBINANT FOLLISTATIN INTRAMUSCULARLY UNDER ANY CIRCUMSTANCES!”, because “the albumin will expand” inside the muscle and “It will be extremely painful” (Campbell, November 22, 2025).
  • Needle — Campbell’s November 2025 posts say 31/32-gauge insulin syringes “work better” than 28/29-gauge for post-injection pain and swelling.
  • Storage — No FLGR-242-specific storage instructions appear in the documents read for this page.

→ Peptide Calculator — vial-to-syringe math

Side Effects & Risks

What This Page Cannot Tell You

What is in the vial. No laboratory independent of the seller has published an analysis of FLGR-242. The product page names the laboratories behind its certificates (MDx BioAnalytical Laboratory, BioRegen, SafeCert Labs) and lists what a certificate reports: UHPLC-MS purity, mass identification and content, endotoxin where applicable, and appearance. Binding, biological activity and half-life are not on that list. Everything on this page describes documents; none of it describes the contents of a vial.

No study has recorded side effects of FLGR-242. What exists is what its promoter has posted, and what is known about the pathway:

  • Injection-site pain and swelling — Campbell on X, November 11, 2025: “We tested our new recombinant Follistatin (FLGR242) and noticed some post injection pain and swelling initially … Our chemist diluted the formulation.” His November 22 article calls the swelling and pain “moderate at worst, but never severe.” By his account, the formulation changed after the first users.
  • Intramuscular injection — Campbell warns against it: the albumin would “expand” inside the muscle, and “It will be extremely painful” (Campbell, November 22, 2025).
  • Undereating — Campbell: “When you inhibit myostatin significantly, your body’s caloric demand will rise sharply. If you fail to eat an appropriate amount of calories to meet this new energetic demand, you WILL lose muscle” (Campbell, June 5, 2026).
  • Overexposure — Campbell: frequent dosing on top of a 19-day half-life “produces a massive cumulative overexposure to an aggressively anabolic compound” (Campbell, September 2, 2026).
  • Heart — Myostatin is also expressed in the heart. The NEJM authors monitored the myostatin-null boy’s heart and found no cardiomyopathy or conduction disturbance by 4.5 years, but said abnormalities could not yet be ruled out (Schuelke et al., 2004). No cardiac data on FLGR-242 exist.
  • Reproductive hormones — Follistatin suppresses FSH release and activin stimulates it (Ueno et al., 1987; Nakamura et al., 1990). The seller says FLGR-242 does not bind activin; that is unpublished. Campbell: men on TRT or fertility-preserving protocols “should still monitor their blood work as baseline FSH is already a managed variable” (Campbell, September 2, 2026).
  • Signals from related drugs — Blocking this pathway has had effects outside muscle in trials: nosebleeds and telangiectasias stopped the ACE-031 trial in boys with Duchenne (Campbell C et al., 2017), and MYO-029 caused skin hypersensitivity at high doses (Wagner et al., 2008). These are different molecules, and FLGR-242 has had no trial in which such effects could be recorded.
  • Immune response — FLGR-242 is a fusion protein injected repeatedly; no immunogenicity data on it are published.
  • WADA prohibited — WADA prohibits follistatin at all times under S4.3 (myostatin-binding proteins). By its seller’s description, FLGR-242 is a follistatin. Athletes subject to testing should not use it.
  • Drug interactions — Unstudied.

Bloodwork & Monitoring

No monitoring guidance for FLGR-242 has been published. The documents and the biology point to these:

  • FSH and LH — Follistatin and activin sit on the FSH axis (Ueno et al., 1987; Nakamura et al., 1990), and Campbell’s own note tells men on TRT or fertility protocols to keep watching FSH (Campbell, September 2, 2026).
  • Myostatin — Campbell wrote that measuring myostatin before starting and after 8 weeks is what he would have done “If I really wanted to get down and geeky with the data collection”; he did not (Campbell, November 22, 2025). Research laboratories measure serum myostatin, and levels differ between muscle diseases and healthy controls (Mariot et al., 2017).
  • Body composition — The published accounts give scale weights and body-fat percentages without saying how they were measured (Campbell, November 22, 2025; June 26, 2026).
  • Which tests fit a given person — A question for a licensed healthcare provider. This page can’t answer it.

Commonly Stacked With

Campbell’s published stack for FLGR-242, “The Ultimate Recombinant Follistatin with Klotho Stack” (Campbell, November 22, 2025), recorded as he published it. No study has tested FLGR-242 with anything.

Klotho (BioLongevity Labs)

His company’s Klotho, built with the same albumin-binding construct as FLGR-242 (Campbell, June 5, 2026). Kalios has no Klotho page.

Testosterone

“Therapeutic Testosterone” is in the stack. His God Stack page: “For most men, therapeutic testosterone is the base everything else is built on top of.”

HGH / Tesamorelin / Ipamorelin / CJC-1295

“Growth Hormone and or GH Agonist Peptides (Tesa/Ipa/CJC).” In June 2026 he wrote that he no longer recommends CJC-1295 (Campbell, June 5, 2026).

Retatrutide

Injected every other day in the stack, which he recommends “for any GLP-1 peptide user.”

TB-500

Daily, “until we release our recombinant formulation.”

→ Peptide Calculator — vial-to-syringe math

Legal Status

Current Status — September 2026

Not on any FDA list. FLGR-242 is not FDA-approved, and no follistatin appears on FDA’s 503A bulk drug substances categories list (updated May 14, 2026). It is a research chemical: the product page labels it “INTENDED AS A RESEARCH CHEMICAL ONLY,” for “in vitro testing and laboratory experimentation only,” and says it “is not a drug, food, or cosmetic.”

WADA prohibits follistatin at all times under S4.3, agents preventing activin receptor IIB activation: “Myostatin-binding proteins (e.g. follistatin, myostatin propeptide)” (Prohibited List 2026).

No clinical trial of FLGR-242 is registered on ClinicalTrials.gov (searched September 28, 2026).

Cost & Access

BioLongevity Labs sells FLGR-242 as a research chemical in pairs of 5 mg vials, with a certificate of analysis per batch from laboratories it names. Campbell describes the company as the one he co-founded.

Pricing and availability vary and are set by the seller. Kalios does not sell compounds.

References

  1. Campbell J. Recombinant Follistatin: The Future Of True Muscle Growth. jaycampbell.com/blog/recombinant-follistatin-the-future-of-true-muscle-growth/. Last updated November 22, 2025. (The eight-week N-of-1 report, the first stated regimen, the “FS I-I” base and the 19-day half-life figure.)
  2. Campbell J. Post on X, November 11, 2025. x.com/JayCampbell333/status/1988064323562770816. (Injection pain and swelling; “Our chemist diluted the formulation.”)
  3. Campbell J. Post on X, February 19, 2026. x.com/JayCampbell333/status/2024585669306171888. (Sixteen weeks, two users; the readable text ends “up 10+ pounds of pure skeletal…”.)
  4. Campbell J. The 2026 Jay Campbell GOD Stack For High-Performance Men & Women. jaycampbell333.substack.com/p/the-2026-jay-campbell-god-stack-for. June 5, 2026. (“We gave it the codename FLGR242”; stated regimens for men and women; testosterone and HGH “running year-round.”)
  5. Campbell J. A Real-World Case Study Of Follistatin (FLGR242): Exclusive Interview With IFBB Pro Alex Padron. jaycampbell333.substack.com/p/a-real-world-case-study-of-follistatin. June 26, 2026.
  6. Campbell J. FLGR-242: 7 Follistatin Myths That Don’t Hold Up. jaycampbell.com/blog/follistatin-myths/. Last updated September 1, 2026. (“the company I co-founded.”)
  7. Campbell J. FLGR-242 vs Follistatin 344: Albumin Binding Changes Everything. jaycampbell.com/blog/flgr242-vs-follistatin-344/. Last updated September 2, 2026.
  8. Campbell J. What FLGR-242 Is an Alternative To: Replacing HGH, IGF-1 LR3, and SARMs for Lean Mass. jaycampbell.com/blog/flgr242-alternative/. Last updated September 3, 2026.
  9. Campbell J. Follistatin vs Myostatin Inhibitors: FLGR-242, YK-11, and Ace-031 Compared. jaycampbell.com/blog/follistatin-vs-myostatin-inhibitors/. Last updated September 4, 2026.
  10. Campbell J. Jay Campbell’s Longevity Protocol. jaycampbell.com/protocols/longevity-protocol/. Read September 28, 2026.
  11. Campbell J. The God Stack. jaycampbell.com/protocols/god-stack/. Read September 28, 2026. (The public page; the full protocol is sent by email.)
  12. BioLongevity Labs. FLGR242 (10mg) product page. biolongevitylabs.com/product/follistatin/. Read September 28, 2026.
  13. Ueno N, Ling N, Ying SY, Esch F, Shimasaki S, Guillemin R. Isolation and partial characterization of follistatin: a single-chain Mr 35,000 monomeric protein that inhibits the release of follicle-stimulating hormone. Proc Natl Acad Sci USA. 1987;84(23):8282-8286. PMID: 3120188.
  14. Shimasaki S, Koga M, Esch F, et al. Primary structure of the human follistatin precursor and its genomic organization. Proc Natl Acad Sci USA. 1988;85(12):4218-4222. PMID: 3380788.
  15. Nakamura T, Takio K, Eto Y, Shibai H, Titani K, Sugino H. Activin-binding protein from rat ovary is follistatin. Science. 1990;247(4944):836-838. PMID: 2106159.
  16. McPherron AC, Lawler AM, Lee SJ. Regulation of skeletal muscle mass in mice by a new TGF-beta superfamily member. Nature. 1997;387(6628):83-90. PMID: 9139826.
  17. Lee SJ, McPherron AC. Regulation of myostatin activity and muscle growth. Proc Natl Acad Sci USA. 2001;98(16):9306-9311. PMID: 11459935.
  18. Thompson TB, Lerch TF, Cook RW, Woodruff TK, Jardetzky TS. The structure of the follistatin:activin complex reveals antagonism of both type I and type II receptor binding. Dev Cell. 2005;9(4):535-543. PMID: 16198295.
  19. Sidis Y, Mukherjee A, Keutmann H, Delbaere A, Sadatsuki M, Schneyer A. Biological activity of follistatin isoforms and follistatin-like-3 is dependent on differential cell surface binding and specificity for activin, myostatin, and bone morphogenetic proteins. Endocrinology. 2006;147(7):3586-3597. PMID: 16627583.
  20. Cash JN, Rejon CA, McPherron AC, Bernard DJ, Thompson TB. The structure of myostatin:follistatin 288: insights into receptor utilization and heparin binding. EMBO J. 2009;28(17):2662-2676. PMID: 19644449.
  21. Nakatani M, Takehara Y, Sugino H, et al. Transgenic expression of a myostatin inhibitor derived from follistatin increases skeletal muscle mass and ameliorates dystrophic pathology in mdx mice. FASEB J. 2008;22(2):477-487. PMID: 17893249. (FS I-I.)
  22. Dennis MS, Zhang M, Meng YG, Kadkhodayan M, Kirchhofer D, Combs D, Damico LA. Albumin binding as a general strategy for improving the pharmacokinetics of proteins. J Biol Chem. 2002;277(38):35035-35043. PMID: 12119302. (SA21.)
  23. Schuelke M, Wagner KR, Stolz LE, Hübner C, Riebel T, Kömen W, Braun T, Tobin JF, Lee SJ. Myostatin mutation associated with gross muscle hypertrophy in a child. N Engl J Med. 2004;350(26):2682-2688. PMID: 15215484.
  24. Haidet AM, Rizo L, Handy C, et al. Long-term enhancement of skeletal muscle mass and strength by single gene administration of myostatin inhibitors. Proc Natl Acad Sci USA. 2008;105(11):4318-4322. PMID: 18334646.
  25. Kota J, Handy CR, Haidet AM, et al. Follistatin gene delivery enhances muscle growth and strength in nonhuman primates. Sci Transl Med. 2009;1(6):6ra15. PMID: 20368179. Erratum: Sci Transl Med. 2026;18(861):eaek4223.
  26. Mendell JR, Sahenk Z, Malik V, et al. A phase 1/2a follistatin gene therapy trial for becker muscular dystrophy. Mol Ther. 2015;23(1):192-201. PMID: 25322757.
  27. Mendell JR, Sahenk Z, Al-Zaidy S, et al. Follistatin gene therapy for sporadic inclusion body myositis improves functional outcomes. Mol Ther. 2017;25(4):870-879. PMID: 28279643.
  28. Latres E, Mastaitis J, Fury W, et al. Activin A more prominently regulates muscle mass in primates than does GDF8. Nat Commun. 2017;8:15153. PMID: 28452368.
  29. Mariot V, Joubert R, Hourdé C, et al. Downregulation of myostatin pathway in neuromuscular diseases may explain challenges of anti-myostatin therapeutic approaches. Nat Commun. 2017;8(1):1859. PMID: 29192144.
  30. Wagner KR, Fleckenstein JL, Amato AA, et al. A phase I/II trial of MYO-029 in adult subjects with muscular dystrophy. Ann Neurol. 2008;63(5):561-571. PMID: 18335515.
  31. Attie KM, Borgstein NG, Yang Y, et al. A single ascending-dose study of muscle regulator ACE-031 in healthy volunteers. Muscle Nerve. 2013;47(3):416-423. PMID: 23169607.
  32. Campbell C, McMillan HJ, Mah JK, et al. Myostatin inhibitor ACE-031 treatment of ambulatory boys with Duchenne muscular dystrophy: results of a randomized, placebo-controlled clinical trial. Muscle Nerve. 2017;55(4):458-464. PMID: 27462804.
  33. Glasser CE, Gartner MR, Wilson D, Miller B, Sherman ML, Attie KM. Locally acting ACE-083 increases muscle volume in healthy volunteers. Muscle Nerve. 2018;57(6):921-926. PMID: 29486514.
  34. World Anti-Doping Agency. Prohibited List 2026 (in effect January 1, 2026). S4.3, Agents preventing activin receptor IIB activation. wada-ama.org.
  35. FDA. Bulk Drug Substances Nominated for Use in Compounding Under Section 503A of the Federal Food, Drug, and Cosmetic Act (categories 1–3). Updated May 14, 2026. fda.gov/media/94155/download.
  36. ClinicalTrials.gov. Searches for “FLGR242” and “FLGR-242” (no records) and “follistatin,” September 28, 2026: NCT01519349, NCT02354781, NCT07443826.

Last updated: September 28, 2026  |  Profile authored by Kalios Peptides research team

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