Follistatin 344
What do these badges mean?
Evidence tier
- AHuman-validated — Human trials showing positive results and good safety.
- BAnimal-grade — No human trials yet, but solid animal/preclinical evidence of effect and safety.
- CAnecdotal — No human or animal trials — only anecdotal/observational reports.
- DInsufficient evidence — No or insufficient evidence (encyclopedia only — never recommended by the builder).
Safety light
- 🟢 Green — Only mild, manageable side effects; reasonable safety data.
- 🟡 Yellow — Needs active management, has a meaningful contraindication/interaction, or has thin long-term data.
- 🔴 Red — Risk of a hospital-level event — treat with serious caution.
Browse-only — not on the protocol builder's curated shortlist, so the builder won't recommend it.
What is it?
Follistatin-344 sits in a completely different lane from every other peptide in this wiki. The GH-axis compounds (Ipamorelin, CJC-1295, Sermorelin, Tesamorelin, MK-677 (Ibutamoren)) all work by adding a growth signal — more GH, more IGF-1. Follistatin works the opposite way: by removing an inhibitor. Your body has a built-in brake on muscle growth called myostatin (technically GDF-8, a member of the TGF-β family). Myostatin’s whole job is to keep muscle from growing past a useful set point. Follistatin is your body’s natural inhibitor of myostatin — when follistatin goes up, myostatin gets sequestered, and the brake comes off.
The proof that this pathway works is dramatic and pre-existed any of the synthetic peptides. Belgian Blue cattle carry a natural myostatin mutation and look like cartoon weightlifters. “Bully whippets” (heterozygous myostatin-mutation dogs) are abnormally muscular. A 2004 German case report described a child with a homozygous myostatin loss-of-function mutation who was visibly hyper-muscular as an infant. Myostatin-knockout mice double their lean mass. The pathway is real and the biology is settled — the question is whether you can pharmacologically replicate the knockout phenotype in an adult human without breaking other things.
A naming note worth understanding: follistatin exists in your body as two main circulating isoforms, FS-288 and FS-315. “Follistatin-344” is the precursor form before signal-peptide cleavage that yields FS-315. In commercial / research-peptide contexts, “Follistatin-344” is the synthetic version typically used because of stability and expression characteristics. For practical purposes, this is the synthetic myostatin-neutralizing peptide most users mean when they say “follistatin.”
What does it do in my body?
Follistatin’s mechanism is sequestration. It binds myostatin (GDF-8), activin A, and other TGF-β-family ligands with high affinity, holding them away from their receptors. Myostatin normally signals through the activin receptor type IIB → SMAD2/3 phosphorylation → inhibition of muscle protein synthesis + promotion of muscle atrophy. Take myostatin out of the equation, and you tip the muscle balance toward growth and away from breakdown [ESTABLISHED pharmacology].
Crucial distinction worth holding: follistatin’s action is at the myostatin-muscle axis. It does NOT raise systemic GH or IGF-1. That’s important for two reasons:
- The benefits and risks don’t overlap with the GH-axis catalog — this is its own mechanism class.
- You can in principle stack follistatin with the GH/IGF-1 secretagogues (different pathways, complementary effects on hypertrophy) — though the safety profile of doing so is unstudied.
The activin problem. Follistatin doesn’t only bind myostatin: it also binds activin A, which has system-wide roles (skin integrity, mucosal healing, reproduction, hematopoiesis). Blocking activin too aggressively is what causes the side-effect signature seen with broad TGF-β-family inhibition: nosebleeds, slow wound healing, mucosal issues, reproductive effects, bleeding events. The “holy grail” in this space (and what big pharma is actually chasing with antibody drugs like trevogrumab and garetosmab) is pure myostatin inhibition without activin inhibition. Follistatin doesn’t deliver that — it hits both.
Homeostatic compensation. Tatem makes a point worth carrying forward: human muscle homeostasis is much more redundant than mouse muscle homeostasis. When you crank up follistatin in a human, the body responds by upregulating other inhibitors in the TGF-β family — myostatin elevation itself, GDF-11, others we haven’t catalogued. Mouse hypertrophy doesn’t cleanly translate to human hypertrophy. That’s why the actual human readouts (when they exist) come in much more modest than the rodent picture would predict.
How can it help me?
The myostatin/activin neutralizer. A 344-amino-acid glycoprotein that removes the brake on muscle growth rather than stepping on the accelerator. Different mechanism class from the GH-secretagogue family — doesn’t touch your GH/IGF-1 axis at all. Real biology behind it (Belgian Blue cattle, the “superchild” mutation, knockout mice that look ridiculous), much thinner human evidence base than the marketing suggests, and a unique commercial wrinkle: the most-publicized form is a one-shot gene-therapy plasmid sold offshore for $25K.
The full evidence — every human, animal, and lab study, graded — is one tap away: use the See the deeper science → toggle at the top.
Is it dangerous? What are the side effects?
The peptide form’s safety surface has a few items worth knowing plainly — none are theoretical.
Documented in clinical / unsupervised-use literature:
- Hepatotoxicity — flagged across multiple secondary sources.
- Endocrine suppression — chronic activin inhibition affects the HPG axis (reproductive hormones).
- Retinal effects — retinal detachment has been documented in clinical trials of injectable myostatin-pathway interventions (the antibody drugs more than follistatin itself, but the class effect applies). This is a class-specific safety surface worth knowing.
- Mucosal / wound-healing effects — downstream of activin blockade; nosebleeds, slow healing.
- Antibody formation — theoretical risk on any multi-week injected peptide; not well-characterized for follistatin specifically.
Mini Circle gene-therapy reported safety: “zero serious AEs” and LDL +8 mg/dL in ~1/3 of patients at 3 months. Vendor-reported, no peer review yet.
Contraindications:
- Active cancer or strong cancer-history risk profile. Myostatin inhibition uncouples a brake on tissue growth — biologically plausible (not proven) concern. Don’t run this with active malignancy.
- Pregnancy, breastfeeding, under-25 developing physiology.
- Active retinal disease given the class signal.
- Active hepatic or renal disease.
Practical management: keep cycles short (8–12 weeks), don’t stack with everything else that promotes growth signaling at once, run baseline + post-cycle labs (LFTs, lipids, ideally a retinal exam if you’re going to do this repeatedly), and treat the foundation — heavy lifting, adequate protein, sleep — as where most of the gain actually comes from.
Regulatory status: Not FDA-approved in either peptide or gene-therapy form. The peptide form sits in the research-chemical gray zone. The plasmid gene-therapy form is delivered exclusively at offshore clinics (Bahamas, Honduras, Panama) — those clinics operate under their own jurisdictions’ frameworks, not US FDA. WADA-banned at all times in sport. Big-pharma activity in the broader myostatin-inhibition space (Regeneron’s trevogrumab, garetosmab antibody drugs targeting myostatin and activin A more selectively) sits separately from the follistatin gray market.
Part 1 — How to reconstitute it
What's used: bacteriostatic water (sterile, preserved water the powder is mixed with) and a separate, larger reconstitution syringe used only for mixing — not the small syringe used for administration.
- Reconstitution math (typical): A 1 mg (1,000 mcg) vial reconstituted with 1 mL bacteriostatic water gives 1,000 mcg/mL. A 150 mcg dose = 0.15 mL = 15 units on a U-100 insulin syringe. (If a 2 mg vial: same logic — 2,000 mcg/mL with 1 mL water; 150 mcg = 7.5 units.)
- Dose: 100–200 mcg per injection.
- Frequency: 2–3× per week.
- Loading-phase variant: Daily injections for week 1, then 2×/week maintenance for the rest of the cycle.
- Cycle: 8–12 weeks on, then a meaningful off period (4–8 weeks) before any rerun.
- Route: Subcutaneous or intramuscular. IM into trained muscle is sometimes used for localized effect, though follistatin’s primary action is systemic.
- Reported gains: “5–10 lb of lean muscle over 8–12 weeks” is the anecdotal vendor framing; the controlled human numbers are far more modest where they exist.
How it's mixed
- The vial is tilted and the bacteriostatic water is added slowly down the inside glass wall — not squirted straight onto the powder.
- It is swirled gently to dissolve. It is never shaken — shaking can damage the peptide.
- The reconstituted vial is stored refrigerated and out of light.
- Reconstituted peptides are commonly used within a few weeks, inside the beyond-use window the source specifies — that window varies by peptide.
The free reconstitution calculator does the concentration math for any vial size and water volume, including the equivalent units on an insulin syringe.
Part 2 — Typical dosing
Educational context only — talk to a licensed medical provider before any protocol. What follows describes the doses and schedules most commonly reported in the research and by practitioners, shared so you can have an informed conversation. These compounds are sold for research use only, are not FDA-approved drugs, and this is not medical advice.
Administration as reported. Reported practice is subcutaneous administration (into the fat just under the skin) using a 0.3 mL U-100 insulin syringe, with sites rotated.
Two delivery paths exist and they’re genuinely different products:
| Path | Peptide injection | Gene-therapy plasmid |
|---|---|---|
| What you inject | Recombinant follistatin protein | A circular DNA plasmid that encodes follistatin |
| Frequency | 2–3× per week, 8–12 weeks per cycle | Single SubQ injection lasting ~1 year |
| Cost model | Recurring per-vial | Lump sum (offshore clinic, ~$25K) |
| Access | Research-peptide market | Bahamas / Honduras / Panama travel-medicine clinics |
| Regulatory | Gray-market research chemical | Not FDA-approved; offshore only |
| Genome integration | N/A (it’s a protein) | No: plasmid stays extra-chromosomal, doesn’t integrate |
| Half-life | Hours-range (the peptide) | Plasmid persists ~1 year inside cells |
Not a research peptide — it’s an experimental gene-therapy procedure delivered at a clinic. OHM can cover it as content (it’s genuinely interesting biotech) but there’s no affiliate path.
What should I avoid combining — and what's synergistic?
Stacking: Different mechanism class from GH/IGF-1, so people do combine follistatin with Ipamorelin / CJC-1295 / Ipamorelin (additive hypertrophy logic across pathways) and with IGF-1 LR3 / MGF (direct downstream growth signal on top of removed brake). The safety profile of those stacks is unstudied — the activin off-target risks compound with anything that pushes growth signaling hard.
Where do people source this?
OHM does not sell or handle any compound. Research-use-only material is sold by third-party vendors; our vetting notes and disclosures are on the Where to buy page. If you'd rather have a physician in the loop, see the telehealth option. Whatever the route, the supply chain is the real risk: only consider vendors that publish batch-level third-party Certificates of Analysis.
The myostatin/activin neutralizer. A 344-amino-acid glycoprotein that removes the brake on muscle growth rather than stepping on the accelerator. Different mechanism class from the GH-secretagogue family — doesn’t touch your GH/IGF-1 axis at all. Real biology behind it (Belgian Blue cattle, the “superchild” mutation, knockout mice that look ridiculous), much thinner human evidence base than the marketing suggests, and a unique commercial wrinkle: the most-publicized form is a one-shot gene-therapy plasmid sold offshore for $25K.
| Class | Glycoprotein myostatin (GDF-8) + activin A neutralizer; TGF-β family inhibitor |
| Mechanism (one-liner) | Binds and sequesters myostatin → removes the brake on muscle protein synthesis → hypertrophy |
| Route | SubQ or IM injection (peptide form); single SubQ plasmid injection (gene-therapy form, offshore) |
| Half-life | Short (hours-range commonly cited) — needs 2–3×/week dosing in peptide form |
| Evidence | Genetic-knockout proof of concept across species; abundant rodent + large-animal hypertrophy studies; Mini Circle 2024 vendor preprint, n≈500; Liz Parrish / BioViva 2015 n=1 self-experiment |
| Regulatory status | Not FDA-approved. Research-chemical classification for the peptide form. Gene-therapy plasmid form delivered only at offshore clinics (Bahamas, Honduras, Panama). WADA-banned. |
| Primary OHM use case | Honest education on a genuinely novel mechanism (myostatin inhibition) with an editorially-rich gene-therapy parallel — high-traffic content lane, low conversion lane |
What it is
Follistatin-344 sits in a completely different lane from every other peptide in this wiki. The GH-axis compounds (Ipamorelin, CJC-1295, Sermorelin, Tesamorelin, MK-677 (Ibutamoren)) all work by adding a growth signal — more GH, more IGF-1. Follistatin works the opposite way: by removing an inhibitor. Your body has a built-in brake on muscle growth called myostatin (technically GDF-8, a member of the TGF-β family). Myostatin’s whole job is to keep muscle from growing past a useful set point. Follistatin is your body’s natural inhibitor of myostatin — when follistatin goes up, myostatin gets sequestered, and the brake comes off.
The proof that this pathway works is dramatic and pre-existed any of the synthetic peptides. Belgian Blue cattle carry a natural myostatin mutation and look like cartoon weightlifters. “Bully whippets” (heterozygous myostatin-mutation dogs) are abnormally muscular. A 2004 German case report described a child with a homozygous myostatin loss-of-function mutation who was visibly hyper-muscular as an infant. Myostatin-knockout mice double their lean mass. The pathway is real and the biology is settled — the question is whether you can pharmacologically replicate the knockout phenotype in an adult human without breaking other things.
A naming note worth understanding: follistatin exists in your body as two main circulating isoforms, FS-288 and FS-315. “Follistatin-344” is the precursor form before signal-peptide cleavage that yields FS-315. In commercial / research-peptide contexts, “Follistatin-344” is the synthetic version typically used because of stability and expression characteristics. For practical purposes, this is the synthetic myostatin-neutralizing peptide most users mean when they say “follistatin.”
How it works
Follistatin’s mechanism is sequestration. It binds myostatin (GDF-8), activin A, and other TGF-β-family ligands with high affinity, holding them away from their receptors. Myostatin normally signals through the activin receptor type IIB → SMAD2/3 phosphorylation → inhibition of muscle protein synthesis + promotion of muscle atrophy. Take myostatin out of the equation, and you tip the muscle balance toward growth and away from breakdown [ESTABLISHED pharmacology].
Crucial distinction worth holding: follistatin’s action is at the myostatin-muscle axis. It does NOT raise systemic GH or IGF-1. That’s important for two reasons:
- The benefits and risks don’t overlap with the GH-axis catalog — this is its own mechanism class.
- You can in principle stack follistatin with the GH/IGF-1 secretagogues (different pathways, complementary effects on hypertrophy) — though the safety profile of doing so is unstudied.
The activin problem. Follistatin doesn’t only bind myostatin: it also binds activin A, which has system-wide roles (skin integrity, mucosal healing, reproduction, hematopoiesis). Blocking activin too aggressively is what causes the side-effect signature seen with broad TGF-β-family inhibition: nosebleeds, slow wound healing, mucosal issues, reproductive effects, bleeding events. The “holy grail” in this space (and what big pharma is actually chasing with antibody drugs like trevogrumab and garetosmab) is pure myostatin inhibition without activin inhibition. Follistatin doesn’t deliver that — it hits both.
Homeostatic compensation. Tatem makes a point worth carrying forward: human muscle homeostasis is much more redundant than mouse muscle homeostasis. When you crank up follistatin in a human, the body responds by upregulating other inhibitors in the TGF-β family — myostatin elevation itself, GDF-11, others we haven’t catalogued. Mouse hypertrophy doesn’t cleanly translate to human hypertrophy. That’s why the actual human readouts (when they exist) come in much more modest than the rodent picture would predict.
What the research shows
Tiered honestly — and the tiers really matter here because the marketing for this compound runs far ahead of the controlled data.
Genetic-knockout proof of concept. The strongest evidence for the pathway working comes from natural experiments: Belgian Blue cattle (myostatin loss-of-function), bully whippets (heterozygous myostatin mutation), myostatin-null mice (double muscle mass), and the 2004 German “superchild” case. These prove that shutting down myostatin signaling produces dramatic muscle hypertrophy. They do not prove that injecting follistatin in an adult human does the same thing.
Rodent and large-animal studies. Dramatic muscle hypertrophy with follistatin overexpression or myostatin inhibition across multiple species — well-replicated. First-class evidence that the mechanism does what it claims to do, in the species tested.
Mini Circle 2024 preprint: gene-therapy form. Mini Circle is a company running plasmid follistatin gene therapy out of offshore clinics (Roatan, Honduras + similar). Their April 2024 preprint — not peer-reviewed — reports 3-month outcomes across an n of around 500 patients:
- Lean mass: average +2 lb (fat-free mass).
- Body fat: −0.87% body-fat percentage.
- Reported epigenetic age: −12 years in older participants (via TruDiagnostic).
- Zero serious adverse events reported.
- Most common AE: LDL +8 mg/dL in roughly one-third of patients.
- Mini Circle cites a “Jajyan 2021” mouse study for a 32.5% lifespan extension claim.
Treat these numbers with appropriate skepticism: the data is vendor-published, the trial is uncontrolled, and the −12 years epigenetic age claim is extraordinary and needs peer review before it travels. The directionally-positive lean-mass and body-fat numbers are also genuinely modest — +2 lb of fat-free mass over 3 months is comparable to what a beginner lifter gets from training alone.
Brian Johnson’s published Mini Circle data. Derek from More Plates More Dates reported Johnson’s numbers: at 4 months post-injection, circulating follistatin +160%, but at 6 months only +7% lean mass — and Johnson changed many other variables simultaneously. That’s an honest read: the follistatin elevation is real and durable; the lean-mass outcome is small and confounded. Useful as a data point, not as proof of effect.
Liz Parrish / BioViva 2015. Parrish, the BioViva founder, self-administered combined telomerase + follistatin gene therapy. She reported lean-mass gains in the thighs and telomerase elevation persisting 3+ years. Historically important as the first publicly-disclosed human gene-therapy follistatin self-experiment; not clinical-grade evidence.
The injectable peptide path. Direct injectable Follistatin-344 has even thinner human data than the gene-therapy path — most of what’s reported is community-anecdotal. The mechanism is identical, the dosing is more frequent, the half-life is short, and the same caveats about activin off-target effects apply.
Where the science honestly stands: the pathway is real and well-established; the mechanism (myostatin sequestration → reduced atrophy + increased hypertrophy) is biologically sound; the human readouts so far are modest, vendor-reported, and uncontrolled; and the published per-protocol head-to-head against just lifting heavy and eating protein doesn’t exist. As Tatem put it: “The best myostatin inhibitor remains the same as it was in 1975 — heavy squats and enough protein to kill a small horse.” That’s not a dismissal — it’s the foundation any layer of pharmacology gets added on top of.
The size-vs-strength honest caveat. Even when follistatin reliably drives muscle-fiber cross-sectional area (the hypertrophy mechanism), strength gains don’t scale on the same curve. Dr. Ashley Froese frames it bluntly: “It sounds amazing, but in reality, it’s kind of hard to dose. You get really inconsistent results. You got big old muscles, but you can only lift like a chicken.” The mechanism behind this dissociation is plausible — neuromuscular efficiency (motor-unit recruitment, rate coding), tendon-and-connective-tissue load-bearing capacity, and intramuscular coordination all adapt on training-driven timelines (months-to-years), not on the timeline that myostatin-inhibition-driven fiber hypertrophy operates on (weeks). You can grow a muscle bigger than its supporting infrastructure can productively load. Combined with follistatin’s inconsistent-dosing-results reputation in real-world use, this is the most-glossed honest limit in follistatin content. OHM-customer-facing framing: follistatin is a hypertrophy lever, not a strength-and-performance lever: and the size-strength dissociation is real. It pairs better with a properly-loaded training program than it substitutes for one.
Real-world protocol
The doses and schedules here are for educational and informational purposes only. Follistatin-344 is sold for research use only and is not an FDA-approved drug. This is not medical advice. Consult a qualified physician before beginning any protocol.
Two delivery paths exist and they’re genuinely different products:
| Path | Peptide injection | Gene-therapy plasmid |
|---|---|---|
| What you inject | Recombinant follistatin protein | A circular DNA plasmid that encodes follistatin |
| Frequency | 2–3× per week, 8–12 weeks per cycle | Single SubQ injection lasting ~1 year |
| Cost model | Recurring per-vial | Lump sum (offshore clinic, ~$25K) |
| Access | Research-peptide market | Bahamas / Honduras / Panama travel-medicine clinics |
| Regulatory | Gray-market research chemical | Not FDA-approved; offshore only |
| Genome integration | N/A (it’s a protein) | No: plasmid stays extra-chromosomal, doesn’t integrate |
| Half-life | Hours-range (the peptide) | Plasmid persists ~1 year inside cells |
- Reconstitution math (typical): A 1 mg (1,000 mcg) vial reconstituted with 1 mL bacteriostatic water gives 1,000 mcg/mL. A 150 mcg dose = 0.15 mL = 15 units on a U-100 insulin syringe. (If a 2 mg vial: same logic — 2,000 mcg/mL with 1 mL water; 150 mcg = 7.5 units.)
- Dose: 100–200 mcg per injection.
- Frequency: 2–3× per week.
- Loading-phase variant: Daily injections for week 1, then 2×/week maintenance for the rest of the cycle.
- Cycle: 8–12 weeks on, then a meaningful off period (4–8 weeks) before any rerun.
- Route: Subcutaneous or intramuscular. IM into trained muscle is sometimes used for localized effect, though follistatin’s primary action is systemic.
- Reported gains: “5–10 lb of lean muscle over 8–12 weeks” is the anecdotal vendor framing; the controlled human numbers are far more modest where they exist.
Stacking: Different mechanism class from GH/IGF-1, so people do combine follistatin with Ipamorelin / CJC-1295 / Ipamorelin (additive hypertrophy logic across pathways) and with IGF-1 LR3 / MGF (direct downstream growth signal on top of removed brake). The safety profile of those stacks is unstudied — the activin off-target risks compound with anything that pushes growth signaling hard.
Not a research peptide — it’s an experimental gene-therapy procedure delivered at a clinic. OHM can cover it as content (it’s genuinely interesting biotech) but there’s no affiliate path.
Side effects & management
The peptide form’s safety surface has a few items worth knowing plainly — none are theoretical.
Documented in clinical / unsupervised-use literature:
- Hepatotoxicity — flagged across multiple secondary sources.
- Endocrine suppression — chronic activin inhibition affects the HPG axis (reproductive hormones).
- Retinal effects — retinal detachment has been documented in clinical trials of injectable myostatin-pathway interventions (the antibody drugs more than follistatin itself, but the class effect applies). This is a class-specific safety surface worth knowing.
- Mucosal / wound-healing effects — downstream of activin blockade; nosebleeds, slow healing.
- Antibody formation — theoretical risk on any multi-week injected peptide; not well-characterized for follistatin specifically.
Mini Circle gene-therapy reported safety: “zero serious AEs” and LDL +8 mg/dL in ~1/3 of patients at 3 months. Vendor-reported, no peer review yet.
Contraindications:
- Active cancer or strong cancer-history risk profile. Myostatin inhibition uncouples a brake on tissue growth — biologically plausible (not proven) concern. Don’t run this with active malignancy.
- Pregnancy, breastfeeding, under-25 developing physiology.
- Active retinal disease given the class signal.
- Active hepatic or renal disease.
Practical management: keep cycles short (8–12 weeks), don’t stack with everything else that promotes growth signaling at once, run baseline + post-cycle labs (LFTs, lipids, ideally a retinal exam if you’re going to do this repeatedly), and treat the foundation — heavy lifting, adequate protein, sleep — as where most of the gain actually comes from.
Regulatory status
Not FDA-approved in either peptide or gene-therapy form. The peptide form sits in the research-chemical gray zone. The plasmid gene-therapy form is delivered exclusively at offshore clinics (Bahamas, Honduras, Panama) — those clinics operate under their own jurisdictions’ frameworks, not US FDA. WADA-banned at all times in sport. Big-pharma activity in the broader myostatin-inhibition space (Regeneron’s trevogrumab, garetosmab antibody drugs targeting myostatin and activin A more selectively) sits separately from the follistatin gray market.
Technical & analytical reference (chemistry & QC)
Molecular identity verified against UniProt (2026-06-23). Follistatin-344 is a secreted glycoprotein, not a synthetic peptide — it’s the 344-amino-acid splice variant of human follistatin (UniProt P19883). PubChem does not catalog full glycoproteins; the verified identity sources are UniProt + DrugBank.
| Field | Value |
|---|---|
| Molecular formula | Not assignable as a single empirical formula (glycoprotein; glycosylation patterns vary by expression system) |
| Average MW | Unglycosylated polypeptide ≈ 37 kDa (mature 344-aa sequence); glycosylated form ≈ 38–42 kDa by SDS-PAGE (varies with HEK293 vs CHO vs E. coli expression) |
| CAS | 80449-31-6 commonly cited for “follistatin” (generic); the FST-344-splice-variant-specific CAS varies across suppliers |
| UniProt | P19883 (human follistatin precursor; FST-344 is the splice variant lacking the C-terminal acidic tail of FST-315) |
| Sequence | 344-amino-acid splice variant of UniProt P19883; full sequence on the UniProt page. Functional domains: N-terminal signal peptide + FS-domain repeats × 3 + C-terminal heparin-binding region (FST-288 lacks this tail; FST-315 retains the longer acidic-tail variant) |
| Class | Secreted glycoprotein TGF-β-superfamily antagonist; binds and neutralizes myostatin, activin A/B, GDF-11, and BMP-2/7 |
| QC identity | SDS-PAGE + Western blot vs. anti-follistatin antibody; potency by myostatin-binding ELISA or activin-A-binding ELISA; purity ≥95% by RP-HPLC for research-grade material |
| Storage / reconstitution | Lyophilized −20 °C (long-term −80 °C); reconstitute in sterile water or PBS; avoid repeated freeze-thaw (irreversible aggregation > 3 cycles) |
| Endotoxin | <1 EU/μg for research-grade material; lower for any clinical-trial material |
| Degradation / stability | Disulfide-bond integrity is the critical QC variable — follistatin’s three FS-domain repeats each have multiple intramolecular disulfides; reduction or scrambling abolishes activity. Heat-sensitive; do not autoclave |
Primary references: Schneyer et al. Endocrinology 2004 (PMID 14764637) — FST-288 vs FST-315 vs FST-344 functional comparison; Sidis et al. Endocrinology 2006 (PMID 16469786) — myostatin/activin binding selectivity; UniProt P19883; DrugBank polypeptide page.
Sources
- Research note — Follistatin-344 + MK-677 muscle cluster (text aggregation, mechanism + Mini Circle preprint + Parrish + safety items).
- Tatem A. “Doctor PREDICTS Future Muscle Drugs: Bimagrumab, Follistatin, Orforglipron & More” (muscle-drugs landscape; Mini Circle critique; “1975 squats” quote).
- Mini Circle 2024 follistatin gene-therapy preprint. https://minicircle.io/wp-content/uploads/2024/04/fstpreprint.pdf
- Sarah Constantin substack — independent analysis of Mini Circle’s follistatin data. https://sarahconstantin.substack.com/p/minicircle-follistatin-gene-therapy
- Fight Aging — BioViva / Parrish follistatin gene therapy data. https://www.fightaging.org/archives/2016/11/data-on-the-effects-of-follistatin-gene-therapy-from-bioviva/
- peptidedossier.com — Follistatin-344 reference. https://peptidedossier.com/peptides/follistatin-344/
- Schuelke M et al. Myostatin mutation associated with gross muscle hypertrophy in a child (the “superchild” case). N Engl J Med. 2004.
- Belgian Blue / whippet myostatin-mutation natural-experiment literature.
See also: MK-677 (Ibutamoren), Ipamorelin, CJC-1295, CJC-1295 / Ipamorelin, IGF-1 LR3 and MGF — the IGF-1 axis muscle cluster, GHRP-2, GHRP-6, and Hexarelin — the injectable ghrelin-receptor GH peptides.
Sources & references
- Research note — Follistatin-344 + MK-677 muscle cluster (text aggregation, mechanism + Mini Circle preprint + Parrish + safety items).
- Tatem A. “Doctor PREDICTS Future Muscle Drugs: Bimagrumab, Follistatin, Orforglipron & More” (muscle-drugs landscape; Mini Circle critique; “1975 squats” quote).
- Mini Circle 2024 follistatin gene-therapy preprint. https://minicircle.io/wp-content/uploads/2024/04/fstpreprint.pdf
- Sarah Constantin substack — independent analysis of Mini Circle’s follistatin data. https://sarahconstantin.substack.com/p/minicircle-follistatin-gene-therapy
- Fight Aging — BioViva / Parrish follistatin gene therapy data. https://www.fightaging.org/archives/2016/11/data-on-the-effects-of-follistatin-gene-therapy-from-bioviva/
- peptidedossier.com — Follistatin-344 reference. https://peptidedossier.com/peptides/follistatin-344/
- Schuelke M et al. Myostatin mutation associated with gross muscle hypertrophy in a child (the “superchild” case). N Engl J Med. 2004.
- Belgian Blue / whippet myostatin-mutation natural-experiment literature.
See also: MK-677 (Ibutamoren), Ipamorelin, CJC-1295, CJC-1295 / Ipamorelin, IGF-1 LR3 and MGF — the IGF-1 axis muscle cluster, GHRP-2, GHRP-6, and Hexarelin — the injectable ghrelin-receptor GH peptides.