Follistatin-344

Myostatin-antagonist protein · real biology, hype borrowed from gene therapy · WADA-banned

Follistatin-344 is where solid biology meets an untrustworthy product story. Follistatin itself is a genuine, important protein: it is a high-affinity antagonist of several TGF-β-family signaling molecules — it binds and neutralizes activin A, myostatin (GDF-8), and GDF-11 — and myostatin is the body's main brake on muscle growth, so blocking it allows muscle to grow. That much is real and well-established. The problem is what the market does with it. The famous evidence for follistatin and muscle comes almost entirely from genetics (myostatin-deficient 'double-muscled' Belgian Blue cattle, a hypermuscular human child with a myostatin mutation, follistatin-overexpressing mice) and from gene-therapy trials — not from any tested injectable follistatin peptide. Crucially, the well-known human follistatin studies (in Becker muscular dystrophy and inclusion body myositis) used AAV gene therapy: a virus was injected to make the patient's own muscle produce follistatin internally. That is categorically not the same thing as the 'Follistatin-344' protein vials sold to bodybuilders. There are essentially no controlled human trials of injected follistatin-344 protein as a muscle-building drug, no validated dose, and the identity and purity of grey-market product is unverified. To add confusion, '344' is an isoform/precursor name (the 344-residue splice variant), not a peptide brand. One more hard fact: follistatin is explicitly banned in sport by WADA. Net: trustworthy mechanism, untrustworthy product.

The short version

To understand follistatin-344, start with what your body normally does. Muscle growth is held in check by a protein called myostatin — think of it as a built-in brake that stops muscles getting too big. Follistatin is a natural protein that binds to myostatin (and to a few related signaling molecules, like activin A and GDF-11) and neutralizes them, effectively releasing that brake. This is genuine, well-established biology, and it is why follistatin is interesting for muscle at all.

The dramatic 'proof' people cite, though, comes from genetics and gene therapy — not from injecting follistatin. The hyper-muscular Belgian Blue cattle, the famous case of a child born with extraordinary muscle, and the 'mighty mice' all involve genes being missing or overexpressed from birth, not a peptide someone injected. And the well-known human studies — in the muscle-wasting diseases Becker muscular dystrophy and inclusion body myositis — used gene therapy: doctors injected a virus carrying the follistatin gene so the patient's own muscle would manufacture the protein internally. That is a completely different thing from buying a vial labeled 'Follistatin-344.'

Here is the honest bottom line. There are essentially no controlled human trials of injected follistatin-344 protein as a muscle-building drug. There is no validated human dose. The grey-market product's identity and purity are unverified, and the name itself is confusing ('344' refers to a protein isoform, not a brand). On top of all that, follistatin is explicitly banned in sport by the World Anti-Doping Agency at all times — using it is a doping violation. So the mechanism is real and fascinating, but the marketed product borrows credibility from research it was never part of.

Molecular identity

Specs

Gene: FST (Follistatin)
UniProt accession: P19883 (FST_HUMAN)
Canonical length / weight: 344 aa; 38,007 Da

Type: Single-chain secreted glycoprotein (TGF-β-ligand antagonist) — a PROTEIN, not a small moleculeUniProt P19883
Isoforms: FST344 = precursor (incl. 1–29 signal peptide); FST315 = mature secreted form; FST288 = cell-surface-binding formUniProt P19883; NCBI Gene 10468
Molecular target: High-affinity antagonist of TGF-β-family ligands: binds/neutralizes activin A, myostatin (GDF-8), GDF-11, and BMPsUniProt P19883
Molecular formula / single PubChem CID: Not applicable — it is a glycoprotein, not a defined small moleculeBy definition (protein, UniProt P19883)
Half-life: ~4 min initial / ~131 min terminal (rat IV, circulating follistatin protein); no human injectable PK publishedPMID 8690405Half-life curve →
Regulatory status: Not approved as an injectable peptide drug anywhere; gene-therapy programs are investigational onlyRegulatory record; PMID 25322757
WADA status: PROHIBITED at all times — S4.3, follistatin named explicitlyWADA Prohibited List S4.3

Plain English

Mechanism

Follistatin is a secreted protein that acts as a high-affinity, largely irreversible antagonist of several TGF-β superfamily ligands. In practical terms, it grabs hold of these signaling molecules and blocks them from reaching their receptors, shutting down their downstream signaling. The muscle-relevant targets are myostatin (GDF-8) and the related ligands activin A and GDF-11 — all of which normally restrain muscle growth — plus some bone-morphogenetic proteins (BMPs).

Its original discovery context, worth knowing, was reproductive: follistatin was first identified as a gonadal protein that suppresses the pituitary's release of follicle-stimulating hormone (FSH), which it does indirectly by sequestering activin. So follistatin is not a muscle-specific molecule — it acts broadly across the activin/TGF-β system, which is both why it is potent and why it carries theoretical risks.

The reason follistatin is even more interesting than a pure myostatin blocker is that it neutralizes multiple muscle-restraining ligands at once. In mice, follistatin overexpression produces more muscle growth than knocking out myostatin alone, and a follistatin transgene on a myostatin-null background quadrupled muscle mass. But that is the crucial honesty boundary: those results are from genetic overexpression in animals (and gene therapy in patients), not from microgram injections of follistatin protein in healthy people — and the leap between the two is not supported by trial data.

Sources:UniProt P19883 PMID 11459935 PMID 17726519

Why people reach for it

Potential benefits

Follistatin-344 is reached for as a myostatin-pathway 'brake release' for muscle growth. The mechanism is real and well-established — but the famous proof comes from genetics and gene therapy, not from an injectable protein, so read its appeal with that gap in mind.

Release the body's main brake on muscle — Its central draw. Follistatin is a genuine high-affinity antagonist that binds and neutralizes myostatin (GDF-8) — the body's primary brake on muscle growth — which is why blocking it is reached for to let muscle grow past its normal ceiling.
Blocks several muscle-restraining signals at once — Beyond myostatin it also neutralizes activin A and GDF-11, so it removes multiple brakes together — in mice, follistatin overexpression grew more muscle than knocking out myostatin alone.
Backed by striking genetics — The pathway's power is real: myostatin-deficient 'double-muscled' cattle, a hypermuscular child with a myostatin mutation, and 'mighty mice' all show what removing this brake can do — proof of the mechanism, even though it's genetics, not a drug.
Pairs with a growth signal, not another brake — Its most coherent stack is a different lever — IGF-1 LR3 adds an anabolic growth signal while follistatin removes the brake (brake-off plus signal-on).
Honest caveat: the injectable is unproven — Essentially no controlled human trials test injected follistatin-344 protein, the famous human studies used gene therapy (a virus making muscle produce it internally), grey-market identity and purity are unverified, and it's explicitly WADA-banned — so this is a real mechanism attached to an untrustworthy product.

Sources:PMID 17726519 PMID 9356471 PMID 15215484 UniProt P19883

What people reach for Follistatin-344 for, drawn from genuine myostatin-pathway biology and genetics (not from any tested injectable protein) and how it's used — not proven outcomes or medical claims.

Implied timing

Best time to dose

Implied best time

Anytime (consistent)

There's no meaningful time-of-day for Follistatin-344 — myostatin suppression is a slow systemic shift, so users just pick a consistent daily time and hold it across the run.

Follistatin works by ligand sequestration — it binds and neutralizes myostatin and related ligands — rather than pulsing with a hormonal rhythm, so there's no circadian window to hit. The effect is a gradual, system-wide change in the muscle-growth brake, not a time-locked event.
Because it's a slow systemic shift, the value is in steady day-to-day coverage, so a fixed daily time (held consistently across the cycle) is what matters — not the specific hour.
Its subcutaneous protein delivery is independent of meals, so food timing doesn't pin the dose to any part of the day either.
Honest limit: this is a timing convention for a compound with no validated human injectable dose and no PK data — there's no studied schedule to anchor to, and any documented use is a WADA violation regardless of timing.

No study establishes an ideal time of day for Follistatin-344 — this is reasoned from its sequestration mechanism and how it's used. Most peptide dosing lands in the midday-to-evening window; for follistatin time of day is essentially irrelevant, so consistency across the run is what counts.

Sources:UniProt P19883

How to run it

Dosing & protocol

Follistatin-344 is dosed here as a subcutaneous injection — the form sold as a research peptide and the route the on-page calculator is built for. What follows is how the bodybuilding/research community actually runs injectable FST-344. Read it as a map of convention — not evidence. The most important fact on this page: there is no validated human injectable dose, no pharmacokinetic data, no dose-finding study, and no clinical protocol for injected follistatin protein.

No validated human injectable dose exists. Grey-market FST-344 has no confirmed identity or purity. WADA explicitly prohibits follistatin by name (S4.3) at all times. Any protocol here is community-invented from mechanism, not trial-proven.

Tiered dose ranges

Community convention anchors to the bodybuilding grey-market range; no clinical dose-finding study has been conducted. These numbers carry no pharmacokinetic or safety validation.

Low / trial:: 50–100 mcg once daily — the range most often cited for first exposure; some users stay here for a full run to limit unknown unknowns.
Standard:: 100 mcg once daily — the most commonly reported maintenance range in bodybuilding communities. More is not known to be better; no dose-response curve exists.
Higher range:: Up to ~200 mcg once daily — used by some, no supporting rationale beyond anecdote. Gene-therapy trials used viral genomes/kg, a measure impossible to convert to a protein microgram dose — those numbers do not anchor this range.

Subcutaneous administration

FST-344 is injected into subcutaneous fat. The protein's large size (~38 kDa glycoprotein) means subcutaneous absorption is slow and systemic bioavailability from SC injection is uncharacterized.

Injection site:: The abdomen (staying a couple of inches clear of the navel), the love-handle area, or the outer thigh. Rotate sites between doses — one spot used repeatedly risks local irritation. For muscle-focused goals, some users inject near the target muscle group, though SC protein absorption is not local in the way peptide injections can be.
Measuring the dose:: Drawn on a U-100 insulin syringe from the reconstituted vial. At the default mix (10 mg vial + 2 mL bacteriostatic water = 5,000 mcg/mL): 50 mcg = 1 IU · 100 mcg = 2 IU · 200 mcg = 4 IU. The calculator does this live for any vial size.
Time of day:: No circadian rationale applies — follistatin works by ligand sequestration (it binds myostatin, it does not pulse with a hormonal rhythm), so time of day is essentially irrelevant. Pick a consistent daily time and hold it across the run — see Best time to dose above.
Food window:: Subcutaneous protein injection does not compete with food for absorption. Inject independently of meals.

Cycle & washout

No clinical cycle guidance exists. The community convention below reflects the 'pulsed use' logic applied to all anabolic/anti-catabolic agents to prevent chronic systemic suppression of TGF-β/activin signaling.

Cycle length:: 10–30 days is the most common community range — often described as a short, concentrated run rather than a continuous course. The theoretical concern is chronic, broad activin/TGF-β suppression in a system that governs tissue growth across many organs.
Washout:: At minimum an equal-length break; many users hold 2–3 months between runs. There is no established clearance data for the protein.
Honest limit:: Cycle conventions for an unproven, uncharacterized protein are invented. The washout rationale is precautionary, not evidence-based. WADA status makes documented use a doping violation independent of any health framing.

Reconstitution at a glance

The on-page calculator does this live. Quick reference for the default 10 mg vial:

Mixing:: 10 mg vial + 2 mL bacteriostatic water = 5,000 mcg per mL. On a 100-unit (1 mL) insulin syringe: 50 mcg = 1 IU · 100 mcg = 2 IU · 150 mcg = 3 IU · 200 mcg = 4 IU.
Protein fragility note:: At ~38 kDa, follistatin is a large glycoprotein — significantly more fragile than small peptides like BPC-157. Do not shake the vial; swirl gently. This applies to mixing math only; the calculator page covers handling.

Sources:PMID 25322757 PMID 28279643 UniProt P19883

Substrate the signal needs

Nutritional cofactor precision

Follistatin's proposed benefit is brake-removal — binding myostatin and related ligands so muscle growth can exceed its normal ceiling. But releasing a brake builds nothing on its own; you still need fuel, a stimulus, and an honest ceiling of a different kind. The three cofactor groups below are muscle-growth physiology applied to the brake-removal frame — not follistatin-nutrition data, because no such data exists.

Reasoned from the brake-removal mechanism and general resistance-training nutrition — not a follistatin cofactor study. No nutrient can supply the proof or purity the injectable product lacks.

SUPPLY the substrate: protein + leucine + calorie surplus

Releasing the myostatin brake means nothing if the raw materials for muscle protein synthesis are absent. This is where most FST-344 users leave the most on the table.

Protein intake:: 1.8–2.2 g per kg of body weight per day (roughly 0.8–1.0 g per pound). The higher end is appropriate for users in a calorie surplus who are training hard. Leucine is the amino acid that most directly triggers the mTOR pathway (the cell's anabolic switch) — distribute protein across 3–4 meals, each with ≥2.5–3 g leucine, to keep the synthesis signal elevated.
Calorie surplus:: You cannot grow into a released ceiling in a calorie deficit. A modest surplus of 250–500 kcal/day over maintenance is the practical target — enough to fuel new tissue without excessive fat gain. Track it for at least the first two weeks of any FST-344 cycle.
Timing:: Post-training protein (within ~2 hours) captures the training-amplified synthesis window. Casein or a mixed protein before sleep slows overnight catabolism during the long fasting window.

AMPLIFY the stimulus: resistance training + creatine

Follistatin is not a stimulus — it removes a restraint. Progressive resistance training is the signal that tells the body where to put the released growth potential. Without it, a lifted myostatin ceiling has nowhere to go.

Resistance training:: Progressive overload — increasing load, volume, or mechanical tension over time — is the non-negotiable stimulus. In animal models, follistatin-transgenic mice that were trained had greater fiber hypertrophy than untrained transgenics. Train 3–5 days per week, targeting the muscle groups the goal is to grow.
Creatine monohydrate:: 3–5 g per day. The best-supported training aid in the literature: it raises intramuscular phosphocreatine (resynthesizes ATP faster), allowing heavier sets and more volume — which is a stronger stimulus. This is ordinary sports-nutrition biochemistry layered on top of the brake-removal frame, not a follistatin claim.
Timing:: Creatine: any time daily — consistency matters more than timing. Training: during the FST-344 cycle, the window of hypothetical brake-removal is the window to drive the highest-stimulus sessions.

MITIGATE / honest limit: what no cofactor can fix

This is the anti-cofactor card. Before stacking supplements on top of FST-344, name what they cannot address.

No nutrient validates the injectable:: Eating perfectly and training hard optimizes a mechanism (myostatin suppression) that has never been demonstrated to operate from a subcutaneous protein injection. The genetic and gene-therapy evidence is real; the injectable-protein-does-the-same-thing assumption is not proven. Cofactors optimize around a gap, not through it.
No cofactor addresses purity:: Grey-market FST-344 has unverified identity — the vial may contain the full protein, a fragment, a short derived peptide, or a mislabeled substance entirely. No supplement addresses this. Purity verification requires third-party testing of the actual lot.
No cofactor offsets broad TGF-β suppression:: Follistatin inhibits activin, GDF-11, and BMPs systemically — a broader footprint than myostatin alone. TGF-β/activin signaling is tumor-suppressive in many tissues. No nutritional intervention selectively narrows this. The theoretical risk is structural to the molecule.

Combinations + timing

Stacking notes + timing windows

Follistatin operates on one specific lever: neutralizing myostatin, activin A, and related TGF-β ligands that brake muscle growth. The genuinely complementary stacks hit a different lever — adding an anabolic growth signal (GH or IGF-1 axis) rather than doubling the same brake removal. One entry below is a caution, not a recommendation.

User combinations reasoned from complementary mechanisms — not regimens studied head-to-head. Every compound here carries its own proof gap. WADA prohibits follistatin by name (S4.3) at all times — any stack including FST-344 is a doping violation in sport.

FST-344 + ACE-031 — CAUTION: same lever, not a complement

This is the stack to avoid, not to run. ACE-031 is a soluble activin receptor IIB (ActRIIB) trap — it captures the same myostatin/activin ligands that follistatin neutralizes, via a different binding mechanism but the same pathway.

Why it is redundant:: Both FST-344 and ACE-031 block activin-receptor signaling. Stacking them doubles coverage of one pathway (myostatin/activin suppression) while adding nothing to a different anabolic axis — muscle growth does not compound proportionally because you have already removed the brake; blocking it twice does not remove it further.
Why it compounds risk:: ACE-031's clinical program was halted after bleeding events attributable to broad activin-receptor inhibition (the same TGF-β/vascular off-target load follistatin carries). Combining two agents on the same pathway doubles that vascular and TGF-β off-target burden without additive muscle benefit.
Outcome:: Do not stack. If the goal is myostatin suppression, one agent on that pathway is the maximum justified by any logic available. Choose one.

FST-344 + IGF-1 LR3

The most mechanistically coherent FST-344 pairing — different lever, same goal. IGF-1 LR3 adds a growth signal; FST-344 removes the brake. Brake-off + signal-on is the theory.

Why it works:: IGF-1 LR3 activates the IGF-1 receptor → PI3K/Akt/mTOR anabolic signaling axis — entirely separate from the myostatin/TGF-β pathway that FST-344 targets. Releasing the myostatin ceiling (FST-344) while simultaneously amplifying the growth signal (IGF-1 LR3) is complementary: each acts on a different control point of muscle growth regulation.
The protocol:: FST-344 100 mcg subcutaneously once daily + IGF-1 LR3 50–100 mcg subcutaneously within 30 minutes post-training on training days. IGF-1 LR3 is a long-acting analog (roughly 20–30 hour half-life); the post-training window captures the muscle-sensitized state. Both are WADA-prohibited at all times.
Outcome:: The combination users reach for when the goal is maximizing the anabolic environment during a resistance-training cycle. Protein substrate (≥1.8 g/kg/day) and calorie surplus are non-negotiable co-requirements — the signal and the released brake both require raw material.

FST-344 + CJC-1295 / Ipamorelin (GH secretagogue pair)

Adds a different upstream lever — stimulating endogenous GH secretion, which then raises IGF-1. A more conservative entry point than exogenous IGF-1 LR3 for users who want the GH axis without direct IGF-1 injection.

Why it works:: CJC-1295 is a GHRH analog (amplifies GH pulse amplitude); Ipamorelin is a GHRP (amplifies pulse frequency via ghrelin receptor). Together they raise pulsatile GH secretion → liver IGF-1 production. This GH/IGF-1 anabolic axis is entirely distinct from the myostatin/TGF-β brake that FST-344 targets — different signaling cascades, not the same lever twice.
The protocol:: FST-344 100 mcg subcutaneously once daily (morning) + CJC-1295 100 mcg + Ipamorelin 100 mcg subcutaneously at bedtime on an empty stomach (GH pulses are blunted by elevated insulin and somatostatin; the bedtime, fasted window maximizes the GH signal). Both secretagogues are co-injected in the same syringe.
Outcome:: Reached for when users want the GH axis contribution without direct IGF-1 LR3. The combination addresses two separate growth-control nodes simultaneously. All three compounds are WADA-prohibited. Protein and calorie surplus requirements are identical to the IGF-1 LR3 stack above.

Reconstitution math

Reconstitution calculator

Calculated for a 1 mL U-100 insulin syringe (100 units/mL).

Peptide per vial

BAC water added

Desired dose

Units per dose

Draw to this mark on a U-100 syringe

Volume per dose: 0.2 mL
Doses per vial: 10
Concentration: 5 mg/mL

One vial lasts

Daily: 10 days
Every other day: 20 days
5×/week: 14 days

Research use only. Not for human consumption. Outputs are reference values based on research literature — verify all measurements independently.

From the studies

Side effects from research

No controlled human safety data exist for injectable follistatin-344 protein, so the concerns below are mechanism-based and theoretical, not observed product findings. That distinction matters: the reassuring gene-therapy safety data come from local AAV expression in patients with muscle disease, not from systemic protein injection in healthy users.

The central theoretical worry follows from follistatin's breadth: it inhibits activin and other TGF-β-family signaling throughout the body, and TGF-β/activin signaling is tumor-suppressive in many tissues. Chronic broad inhibition therefore raises a theoretical cancer concern (removing a growth-restraining signal) — plausible from the biology, though not demonstrated for the product. Because follistatin's native job is suppressing FSH, exogenous use could also plausibly disturb reproductive and endocrine balance, and its binding of GDF-11 (a ligand with contested roles in heart and blood-vessel health) gives it uncertain cardiac implications.

On top of the biology, grey-market vials carry the usual risks of research-chemical proteins — unverified purity, possible endotoxin contamination, mislabeling, and sterility problems. The honest summary is that human safety is uncharacterized and there are real theoretical reasons for caution.

As reported in literature

Research dosing ranges

There is no human dosing table for injectable follistatin protein, because no such trials exist. The rows below lay out the actual evidence across three tiers — genetics, gene therapy, and the (absent) injectable-peptide trials — so it is unmistakable that the muscle-growth fame rests on genetics and gene therapy, not on a tested peptide drug. Gene-therapy doses are viral genomes per kilogram and are NOT a peptide dose.

Dose	Route	Model	Outcome	Sources:
Genetic (loss-of-function)	n/a	Cattle — myostatin-null Belgian Blue / Piedmontese ('double-muscled')	Myostatin loss causes the hypermuscular phenotype — foundational genetics, no follistatin injected	PMID 9356471
Genetic (loss-of-function)	n/a	Human — child with homozygous myostatin mutation (Schuelke 2004)	Gross muscle hypertrophy (~2× muscle), normal heart and cognition — proof of the pathway in humans, but it is genetics, not a drug	PMID 15215484
Genetic (overexpression)	n/a	Mouse — follistatin transgene on myostatin-null background (Lee 2007)	~4× muscle mass of wild-type — shows follistatin blocks muscle-restraining ligands beyond myostatin alone (transgenic, not injected)	PMID 17726519
≈3–6×10¹¹ vg/kg/leg	IM gene therapy (AAV)	Human trial — Becker muscular dystrophy (Mendell 2015, n=6)	6-minute walk improved in most; larger fibers, less fibrosis; no serious follistatin-related adverse events over 2 years — but it is AAV gene therapy, not a peptide injection	PMID 25322757
None	n/a	Human — injectable follistatin-344 protein as a muscle drug	Essentially NO controlled human efficacy or safety trials exist; no validated dose; grey-market identity/purity unverified	UniProt P19883

Quick answers

Frequently asked

Are the famous follistatin studies the same as injecting Follistatin-344?

No — this is the key confusion. The well-known human studies (in Becker muscular dystrophy and inclusion body myositis) used gene therapy: a virus carrying the follistatin gene was injected so the patient's own muscle would produce follistatin. That is not the same as injecting a vial of follistatin protein, and the gene-therapy results should not be read as evidence for the injectable product.

Does injecting follistatin-344 build muscle in humans?

There is no controlled human trial evidence that it does. The muscle-growth fame comes from genetics (myostatin-deficient cattle, a hypermuscular child, transgenic mice) and from gene therapy — not from any tested follistatin peptide injection. The leap from those to 'inject this to build muscle' is unsupported.

What does '344' mean?

It refers to a protein isoform, not a brand. The follistatin gene produces splice variants named by their residue count: FST344 is the longer precursor (including a signal peptide), which becomes the 315-residue mature secreted protein (FST315) once released. So 'Follistatin-344' nominally references that longer isoform — but whether a given vial contains the full protein, a fragment, or a short peptide is usually unverifiable.

Is there a known safe dose?

No. There is no validated human injectable dose and no pharmacokinetic or safety data for the protein as a muscle agent. The human gene-therapy doses are measured in viral genomes per kilogram and cannot be converted into a peptide dose. Any microgram protocol online is invented.

Is follistatin banned in sport?

Yes — explicitly. The World Anti-Doping Agency prohibits follistatin by name under the 'agents preventing activin receptor IIB activation' category (myostatin inhibitors), banned at all times, in and out of competition. Using follistatin-344 is a doping violation. Some 'certified-for-sport' follistatin supplements create a dangerous grey area, but the list language still classes follistatin as prohibited.

Primary sources

References

UniProt P19883UniProt P19883 (FST_HUMAN) — follistatin protein: 344 aa, 38,007 Da, signal 1–29, isoforms, activin/myostatin/GDF-11/BMP binding
NCBI Gene 10468NCBI Gene 10468 — FST gene, isoforms FST317/FST344, FSH-inhibiting
PMID 9356471McPherron & Lee, PNAS 1997 — double muscling in cattle from myostatin (GDF8) mutations
PMID 15215484Schuelke et al., NEJM 2004 — myostatin mutation causing gross muscle hypertrophy in a child
PMID 11459935Lee & McPherron, PNAS 2001 — regulation of myostatin activity / follistatin-transgenic mice
PMID 17726519Lee, PLoS ONE 2007 — quadrupling muscle mass by targeting TGF-β pathways (follistatin Tg × myostatin-null)
PMID 25322757Mendell et al., Mol Ther 2015 — follistatin GENE THERAPY (AAV1.CMV.FS344) for Becker muscular dystrophy
PMID 28279643Mendell et al., Mol Ther 2017 — follistatin gene therapy for sporadic inclusion body myositis
WADA S4.3WADA Prohibited List, S4.3 'Agents Preventing Activin Receptor IIB Activation' — follistatin named prohibited at all times

Research use only · Not medical advice · Updated 2026-06-01