What is the standard Follistatin 344 dosage?

The most commonly reported Follistatin 344 dosage is 100–200 mcg injected subcutaneously once daily for 10–30 day cycles. Some protocols use 100 mcg 1–2 times daily. Higher doses up to 300 mcg have been used, but human clinical data for exogenous peptide injection is extremely limited. These dosages are derived primarily from community protocols and animal research, not from controlled human trials.

Does Follistatin actually inhibit myostatin in humans?

Follistatin absolutely binds and neutralizes myostatin — this is well-established biology. The question is whether exogenous subcutaneous injection of Follistatin 344 peptide achieves sufficient circulating levels for meaningful myostatin inhibition in humans. The dramatic muscle growth seen in myostatin knockout animals and gene therapy studies has not been replicated with peptide injection protocols. The science on myostatin biology is strong; the translation to injectable peptide protocols in humans is unproven.

What is the difference between FS-344, FS-315, and FS-288?

FS-344 is the most common recombinant variant used in research and community protocols. When injected, FS-344 is cleaved in the body to produce FS-315 (the primary circulating serum form) and FS-288 (a tissue-bound form concentrated in the gonads). FS-315 is considered the main systemic myostatin-binding form, while FS-288 preferentially binds activin in reproductive tissues and is involved in FSH regulation. Most injectable Follistatin products are FS-344.

How long should a Follistatin cycle last?

Standard Follistatin 344 cycles run 10–30 days, with most community protocols falling in the 10–20 day range. These are typically run 1–3 times per year with extended off-periods between cycles. Follistatin is not used continuously — the short cycle approach reflects both the cost of the peptide and theoretical concerns about prolonged myostatin suppression and potential reproductive effects from sustained activin binding.

Is Follistatin the same as myostatin inhibitor gene therapy?

No. Follistatin gene therapy (such as AAV-delivered FS-344 in muscular dystrophy trials) produces sustained, high local expression of Follistatin in muscle tissue over months to years. Exogenous peptide injection provides a brief, transient spike in circulating Follistatin with a relatively short half-life. The gene therapy results — including meaningful muscle mass increases in clinical trials — should not be extrapolated to peptide injection protocols. They are fundamentally different delivery methods.

Can Follistatin affect fertility or reproductive hormones?

Yes, this is a legitimate concern. Follistatin binds activin, which plays a critical role in FSH (follicle-stimulating hormone) regulation. In the reproductive system, the activin-follistatin-inhibin axis controls FSH secretion, follicle development, and spermatogenesis. Exogenous Follistatin could theoretically suppress FSH by neutralizing activin. The FS-288 variant is particularly concentrated in gonadal tissue. Short cycles with extended off-periods are recommended in part to minimize potential reproductive effects.

Why is Follistatin so expensive compared to other peptides?

Follistatin 344 is a large, complex glycoprotein (approximately 344 amino acids before processing) that is significantly more difficult and costly to produce than small synthetic peptides like BPC-157 (15 amino acids) or Ipamorelin (5 amino acids). Recombinant production requires mammalian or bacterial expression systems, purification, and quality control. This manufacturing complexity drives the high cost per milligram and is one reason cycles are kept short.

How does Follistatin compare to other myostatin-related approaches?

Follistatin is one of several approaches targeting the myostatin pathway. Others include ACE-031 (a soluble ActRIIB decoy receptor), anti-myostatin antibodies (like domagrozumab), and MSTN gene therapy. Of these, Follistatin peptide injection has the least clinical evidence in humans. ACE-031 and antibody approaches have Phase II trial data. Follistatin gene therapy has promising early results in muscular dystrophy. The injectable peptide remains the least validated approach.

Should I take Follistatin before or after training?

Most community protocols administer Follistatin subcutaneously in the morning, independent of training timing. Unlike acute-acting peptides where timing around workouts matters (e.g., GHRPs), Follistatin’s mechanism is based on sustained myostatin neutralization rather than an acute signaling event. Consistent daily dosing during the cycle is more important than injection timing relative to training sessions.

Can women use Follistatin?

Women can use Follistatin at the same dosages. However, women should be particularly aware of the potential reproductive effects. Follistatin binds activin, which is crucial for follicular development and FSH regulation in women. Disruption of the activin-follistatin axis could theoretically affect menstrual cycles, ovulation, and fertility. Short cycles with extended off-periods are especially important for women. Follistatin is contraindicated during pregnancy and breastfeeding.

Follistatin 344 Dosage Guide

Evidence-based protocols for the myostatin inhibitor — realistic expectations, cycling strategies, stacking with IGF-1 LR3 and MK-677, reproductive considerations, and what the research actually shows.

Compiled by PeptideWiki Editorial Team

What Is Follistatin?

Follistatin 344 (FST-344) is a recombinant form of Follistatin, a naturally occurring glycoprotein that binds and neutralizes members of the TGF-β superfamily — most notably myostatin and activin. By inhibiting myostatin (a powerful negative regulator of muscle growth), Follistatin theoretically removes the “brake” on skeletal muscle hypertrophy, allowing enhanced muscle growth potential.

The science behind myostatin inhibition is compelling. Myostatin knockout animals (notably the “mighty mouse” and Belgian Blue cattle) display dramatically increased muscle mass. Follistatin gene therapy trials in muscular dystrophy patients have shown meaningful improvements in muscle function. However, there is a critical distinction that must be made: the translation from myostatin biology and gene therapy results to exogenous Follistatin peptide injection in humans is far less established. Most human evidence comes from gene therapy, not subcutaneous peptide injection.

Follistatin also plays important roles beyond muscle. It modulates FSH (follicle-stimulating hormone) through activin neutralization, influences inflammation and fibrosis pathways, and participates in tissue remodeling. These broader effects — particularly the reproductive implications — are important safety considerations for anyone using exogenous Follistatin.

Use our Peptide Dosage Calculator to calculate your exact dose based on vial size and concentration.

Important: Follistatin 344 is not FDA-approved for human use. It is classified as a research peptide. Human clinical data for exogenous peptide injection is extremely limited. The dosing information in this guide is derived from animal studies, gene therapy research extrapolation, and community protocols — not from controlled human injection trials. Consult a healthcare provider before using any research peptide.

Evidence reality check: The “myostatin inhibitor” label generates significant hype. The underlying biology is real and well-studied. But injectable Follistatin peptide human data is minimal. This guide presents the available information honestly, distinguishing between what is scientifically established and what remains speculative for this specific delivery method.

Key Characteristics:

Myostatin inhibitor — binds and neutralizes myostatin, removing the primary negative regulator of skeletal muscle growth
Activin binder — also neutralizes activin, affecting FSH regulation, inflammation, and fibrosis pathways
Large glycoprotein — FS-344 is approximately 344 amino acids (before processing) — significantly larger and more complex than typical synthetic peptides
Recombinant production — manufactured through recombinant expression systems, making it one of the most expensive research peptides per milligram
Short half-life — relatively rapid clearance requiring daily dosing during cycles; FS-344 is cleaved in vivo to FS-315 (serum form) and FS-288 (tissue-bound form)
Limited human injection data — strong myostatin biology, promising gene therapy results, but minimal controlled human data for subcutaneous peptide injection protocols

For a complete overview of its mechanism and research, see our full Follistatin 344 profile. New to peptides? Start with the Beginner's Guide to Peptides.

How Follistatin Dosage Is Determined

Unlike peptides with robust human dose-response data (such as Hexarelin or Ipamorelin), Follistatin 344 dosing for subcutaneous injection is not derived from controlled human clinical trials. The commonly cited dosage ranges come from a combination of animal research, gene therapy dose extrapolation, pharmacokinetic estimates, and community experience.

Animal & Preclinical Research

The foundational myostatin research comes from animal models. Lee & McPherron demonstrated that Follistatin overexpression in mice produced significant muscle mass increases — even exceeding the effects of myostatin knockout alone, suggesting Follistatin inhibits additional TGF-β family members beyond myostatin. These studies established the biological rationale but used transgenic overexpression or viral vector delivery, not exogenous peptide injection.

Gene Therapy Trials

Mendell et al. conducted AAV-delivered Follistatin gene therapy trials in patients with Becker muscular dystrophy and inclusion body myositis. These trials demonstrated measurable improvements in muscle function and the 6-minute walk test. However, gene therapy produces sustained, high local expression of Follistatin in muscle tissue over extended periods — a fundamentally different pharmacokinetic profile from a transient subcutaneous injection.

Community-Derived Dosing

The 100–200 mcg daily dosage range used in community protocols is based on pharmacokinetic estimates, affordability constraints (Follistatin is expensive), and user-reported experiences. There are no published human dose-response studies for subcutaneous Follistatin 344 injection. The dosing is essentially empirical — community consensus rather than clinical evidence.

Strength of evidence: LIMITED for peptide injection. The myostatin biology is strong (extensive animal and in vitro data). Gene therapy trials show promise in muscular dystrophy. But human data for exogenous subcutaneous Follistatin 344 peptide injection is minimal. Dosing protocols are based on extrapolation and community experience, not controlled clinical trials. Treat all dosing as experimental.

Standard Follistatin 344 Dosage Ranges

Follistatin 344 is administered by subcutaneous injection, typically once daily during short cycles. The most commonly reported dosage range is 100–200 mcg per day. Some protocols use twice-daily dosing at 100 mcg each. Higher doses up to 300 mcg daily have been reported but carry more unknowns with no established benefit ceiling.

Dosage by Experience Level

Level	Dose per Day	Frequency	Cycle Length	Notes
Conservative	100 mcg	1x daily (SubQ)	10–14 days	Assess tolerance; lowest risk starting point
Standard	100–200 mcg	1x daily (SubQ)	10–20 days	Most common community protocol; balances cost and exposure
Aggressive	200–300 mcg	1–2x daily (SubQ)	20–30 days	Higher exposure; more unknowns; significantly higher cost

Administration Notes

Route: Subcutaneous injection (abdomen, thigh, or upper arm)
Timing: Most protocols use morning administration; timing relative to meals is less critical than with GHRPs
Consistency: Daily dosing during the cycle is more important than specific time-of-day timing
Reconstitution: Add bacteriostatic water gently down the side of the vial — do not spray directly onto the powder or shake. Swirl gently.
Storage: Refrigerate after reconstitution (2–8°C). Do not freeze reconstituted solution. Use within 14–21 days.

No established dose ceiling: Unlike GHRPs where dose-response curves are well-characterized in humans, there is no human dose-response data for Follistatin 344 injection. The commonly used ranges are empirical, not clinically validated. More is not necessarily better, and higher doses carry more unknowns. Conservative dosing is prudent given the evidence limitations.

Follistatin Variants Explained

Follistatin exists in multiple isoforms, each with different tissue distribution, binding properties, and biological activity. Understanding the variants is important because the form you inject (FS-344) is not the same as the form that circulates systemically or acts in reproductive tissue.

Variant	Amino Acids	Distribution	Key Properties
FS-344	344 (precursor)	Injected form; cleaved in vivo	Most common research/community variant; processed to FS-315 and FS-288 after injection
FS-315	315	Primary circulating serum form	Main systemic myostatin-binding form; does not bind heparan sulfate proteoglycans, so it circulates freely
FS-288	288	Tissue-bound; concentrated in gonads	Binds heparan sulfate proteoglycans on cell surfaces; predominantly involved in gonadal activin regulation and FSH modulation

Why FS-344 Is the Standard Variant

FS-344 is the precursor form that the body naturally processes into the functional variants. When injected subcutaneously, FS-344 is cleaved to produce both FS-315 (which enters circulation and can bind myostatin systemically) and FS-288 (which localizes to tissues, particularly the gonads). Using FS-344 as the injectable form allows the body to generate both functional variants through its natural processing pathways.

The Reproductive Connection (FS-288 & Activin)

The FS-288 variant produced from FS-344 processing concentrates in reproductive tissue, where it binds activin. This activin binding modulates FSH secretion, which is critical for both female follicular development and male spermatogenesis. This is why Follistatin use carries theoretical reproductive considerations — the FS-288 produced from injected FS-344 directly affects the gonadal activin-follistatin axis.

Practical takeaway: If you are purchasing Follistatin for research, FS-344 is the standard variant. Be aware that injecting FS-344 produces both systemic (FS-315, myostatin binding) and gonadal (FS-288, activin binding) effects. You cannot selectively get myostatin inhibition without activin modulation when using FS-344.

Calculate Your Follistatin 344 Dose

Follistatin 344 is supplied as a lyophilized (freeze-dried) powder, typically in 1 mg vials (due to cost, larger vials are less common than with other peptides). You reconstitute it with bacteriostatic water, then draw your dose using an insulin syringe. Handle the reconstitution gently — Follistatin is a large protein that can be denatured by vigorous agitation.

Worked Example:

Vial size: 1 mg (1,000 mcg) of Follistatin 344
Bacteriostatic water added: 1 mL
Concentration: 1,000 mcg ÷ 1 mL = 1,000 mcg per mL
Target dose: 100 mcg
Volume to draw: 100 ÷ 1,000 = 0.1 mL = 10 units on an insulin syringe

Quick Reference — 1 mg Vial

Bac Water Added	Concentration	100 mcg Dose	200 mcg Dose
0.5 mL	2,000 mcg/mL	5 units (0.05 mL)	10 units (0.1 mL)
1 mL	1,000 mcg/mL	10 units (0.1 mL)	20 units (0.2 mL)
2 mL	500 mcg/mL	20 units (0.2 mL)	40 units (0.4 mL)

Reconstitution tip: Add the bacteriostatic water slowly, letting it run down the inside wall of the vial. Do not spray it directly onto the lyophilized powder. Once the water is added, gently swirl or roll the vial until dissolved. Never shake a Follistatin vial — the protein can be denatured by vigorous agitation.

Skip the Math — Use Our Calculator

Enter your vial size, water volume, and desired dose — get instant calculations with zero manual math.

Follistatin 344 Dosage by Goal

Follistatin's primary appeal is myostatin inhibition for muscle growth, but its broader TGF-β modulation makes it relevant to other goals as well. The following protocols reflect community experience and theoretical rationale — remember that human injection data is limited for all of these applications.

Muscle Growth & Myostatin Inhibition

The primary use case for Follistatin 344. The goal is to achieve sufficient circulating Follistatin to meaningfully neutralize myostatin and allow enhanced muscle hypertrophy. This requires consistent daily dosing, adequate training stimulus, and proper nutrition. Myostatin inhibition removes a brake — it does not actively build muscle without the training signal.

Dose: 100–200 mcg SubQ daily
Cycle: 10–30 days (most common: 10–20 days)
Cycles per year: 1–3 cycles with extended off-periods
Requirements: Progressive overload training, caloric surplus, adequate protein intake (1.6–2.2 g/kg/day)
Realistic expectations: Do not expect gene therapy or myostatin knockout results. Any effects from peptide injection will be subtle and develop over multiple cycles.

Body Recomposition & Fat Loss Support

Myostatin inhibition may support improved body composition by favoring lean mass retention and potentially enhancing fat oxidation. Follistatin's effects on activin may also influence metabolic pathways. This is a secondary application with even less human evidence than the muscle growth use case.

Dose: 100 mcg SubQ daily
Cycle: 10–20 days
Context: Best used alongside a well-structured training program and moderate caloric deficit
Note: Consider stacking with MK-677 for additional GH-mediated fat loss support (see stacking section)

Recovery & Anti-Fibrosis

Follistatin's TGF-β modulation extends beyond myostatin. By binding activin and other TGF-β ligands involved in fibrosis, Follistatin may support tissue remodeling and recovery. This is a research-stage application with animal model support but minimal human data.

Dose: 100 mcg SubQ daily
Cycle: 10–14 days
Context: May complement a BPC-157 recovery protocol for injury rehabilitation
Evidence level: Preclinical only. Animal models show anti-fibrotic effects. No human injection data for this application.

Muscle Wasting & Sarcopenia (Research Context)

The most medically relevant application of Follistatin is in conditions of pathological muscle wasting — muscular dystrophy, sarcopenia, cachexia, and age-related muscle loss. This is where gene therapy trials have shown the most promise. Peptide injection for this purpose remains speculative but has the strongest theoretical rationale.

Dose: 100–200 mcg SubQ daily
Cycle: 20–30 days (longer cycles for therapeutic contexts)
Context: Always under medical supervision for pathological conditions. Not a replacement for standard medical treatment.
Note: Gene therapy delivery (AAV-FS344) has shown meaningful results in clinical trials for Becker muscular dystrophy. Peptide injection results for muscle wasting are unvalidated.

Training is non-negotiable. Myostatin inhibition removes a constraint on muscle growth — it does not create the growth stimulus. Without progressive overload training and adequate nutrition, even complete myostatin elimination would have limited effect on muscle hypertrophy. Follistatin is not a substitute for training.

Cycling Protocols

Follistatin 344 is universally used in short cycles with extended off-periods. This cycling approach reflects multiple considerations: the high cost of the peptide, theoretical concerns about prolonged myostatin suppression, potential reproductive effects from sustained activin binding, and the overall lack of long-term safety data for exogenous injection.

Follistatin is not used continuously. Unlike some peptides that can be used year-round (such as Ipamorelin), Follistatin 344 is cycled in short bursts. Continuous use is not recommended due to cost, lack of long-term safety data, and theoretical reproductive concerns.

Cycling Protocols

Protocol	On-Cycle	Off-Cycle	Cycles/Year	Notes
Short Burst	10 days	20–30 days off	2–3	Most conservative; minimal exposure; good first protocol
Standard	20 days	40–60 days off	2–3	Most common community protocol; balances exposure and cost
Extended	30 days	60–90 days off	1–2	Maximum cycle length; higher cost; more reproductive concerns

Why the Off-Periods Are Long

The extended off-periods between Follistatin cycles serve several purposes:

Reproductive axis recovery: Allow the activin-follistatin-inhibin axis to normalize, particularly FSH regulation
Cost management: Follistatin 344 is one of the most expensive research peptides; short cycles with long breaks are more sustainable
Safety margin: Given the limited human data, longer off-periods provide a margin of safety against unknown long-term effects
Assessment window: The off-period allows you to evaluate what effects, if any, the cycle produced before committing to another

Timing Cycles for Maximum Effect

Many users time their Follistatin cycles to coincide with phases of intensified training or the beginning of a hypertrophy block. The rationale is that reducing myostatin during a period of high training stimulus may maximize the anabolic potential. Others time cycles during a caloric surplus phase to capitalize on the growth-permissive environment.

Blood work consideration: If you are monitoring hormones, check FSH, LH, and testosterone levels before starting a Follistatin cycle and again 4–6 weeks after completion to assess any impact on the reproductive axis. This is particularly important for men concerned about fertility and women monitoring ovulatory function.

Follistatin 344 Stacking Protocols

Follistatin stacking aims to complement myostatin inhibition with other growth-promoting or recovery-supporting mechanisms. The theoretical rationale is that removing the myostatin brake (Follistatin) while simultaneously enhancing growth signals (IGF-1, GH) may produce synergistic effects. However, stacking multiple experimental compounds makes it impossible to attribute effects to any single agent.

Follistatin 344 + IGF-1 LR3 — Growth Factor Synergy

The most theoretically synergistic Follistatin stack. Follistatin 344 inhibits myostatin (removing the growth brake), while IGF-1 LR3 provides a direct anabolic growth signal through the IGF-1 receptor. The combined approach addresses both sides of the growth equation: removing inhibition and enhancing stimulation.

Compound	Dose	Frequency	Purpose
Follistatin 344	100–200 mcg SubQ	1x daily	Myostatin inhibition (remove growth brake)
IGF-1 LR3	20–50 mcg SubQ	1x daily (post-workout or morning)	Direct anabolic growth signal via IGF-1 receptor

Complexity warning: Both Follistatin 344 and IGF-1 LR3 are potent growth factor modulators with limited human safety data for combined use. This stack carries the most theoretical synergy but also the most unknowns. Blood glucose monitoring is recommended as IGF-1 LR3 can cause hypoglycemia. Start conservatively.

Follistatin 344 + MK-677 — Myostatin Inhibition + GH Elevation

Combines Follistatin's myostatin inhibition with MK-677 (Ibutamoren)'s sustained GH and IGF-1 elevation. MK-677 is an oral GH secretagogue that raises baseline GH and IGF-1 levels, complementing Follistatin's myostatin-blocking mechanism. This is a more accessible stack since MK-677 is oral.

Compound	Dose	Frequency	Purpose
Follistatin 344	100–200 mcg SubQ	1x daily (during 10–20 day cycle)	Myostatin inhibition
MK-677	12.5–25 mg oral	1x daily (continuous; before bed)	Sustained GH and IGF-1 elevation; improved sleep

Protocol note: MK-677 can be run continuously (it does not require cycling like Follistatin). Many users run MK-677 as a baseline and add Follistatin cycles on top of it 1–3 times per year. Monitor appetite and blood glucose — MK-677 increases both.

Follistatin 344 + BPC-157 (Growth Modulation + Tissue Repair)

Combines Follistatin's TGF-β modulation and anti-fibrotic potential with BPC-157's well-documented tissue repair and angiogenesis effects. This stack is oriented toward recovery and rehabilitation rather than pure muscle growth, leveraging Follistatin's broader biological activities beyond myostatin inhibition.

Compound	Dose	Frequency	Purpose
Follistatin 344	100 mcg SubQ	1x daily (during 10–14 day cycle)	TGF-β modulation, anti-fibrotic support
BPC-157	250 mcg SubQ	1–2x daily (near injury site)	Localized tissue repair, angiogenesis, growth factor upregulation

Follistatin 344 + GH Secretagogue Stack (Comprehensive Growth Support)

For users seeking maximum growth support, Follistatin can be combined with a GHRP + GHRH stack to simultaneously inhibit myostatin and elevate GH/IGF-1 through pituitary stimulation. This is the most comprehensive approach but also the most complex and expensive.

Compound	Dose	Frequency	Purpose
Follistatin 344	100–200 mcg SubQ	1x daily (during 10–20 day cycle)	Myostatin inhibition
Ipamorelin	200–300 mcg SubQ	2–3x daily (fasted)	Clean GH pulse (minimal side effects)
CJC-1295 (no-DAC)	100 mcg SubQ	At each Ipamorelin injection	Amplifies and sustains GH pulse (GHRH mechanism)

Complexity and attribution: Stacking multiple compounds with limited individual human evidence makes it impossible to determine which agent is responsible for observed effects or side effects. When possible, introduce one compound at a time to establish baseline response before adding additional agents. This is especially important with Follistatin given its limited human injection data.

Explore more combinations with our Peptide Stack Builder or browse the Top 10 Peptide Stacks guide.

Safety, Side Effects & Contraindications

Safety Data Is Limited: Follistatin 344 has minimal human safety data for subcutaneous peptide injection. Most safety information is extrapolated from Follistatin biology, gene therapy safety monitoring, and community reports. The side effects listed below are a combination of theoretical concerns based on mechanism, animal model observations, and anecdotal community reports. Approach with appropriate caution.

Reported & Theoretical Side Effects

Community-reported (generally well-tolerated at standard doses):

Injection site reactions — redness, soreness, or minor swelling (common with SubQ injection of any peptide)
Mild fatigue or lethargy — reported by some users, usually transient
Temporary joint discomfort — reported infrequently; mechanism unclear
Mild headache — usually resolves within the first few days

Theoretical concerns (based on mechanism of action):

FSH suppression: Follistatin binds activin, which is critical for FSH regulation. Prolonged activin neutralization could suppress FSH, affecting fertility in both men (spermatogenesis) and women (follicular development, ovulation)
Reproductive axis disruption: The FS-288 variant produced from FS-344 concentrates in gonadal tissue. Short cycles mitigate but may not eliminate this concern
Potential for unchecked cell proliferation: TGF-β family members regulate cell growth. Chronic suppression of activin and myostatin could theoretically promote unwanted cell proliferation. This is a long-term concern, not an acute risk
Effects on wound healing and fibrosis: TGF-β signaling is important for wound healing. Excessive TGF-β suppression could theoretically impair healing, though Follistatin's anti-fibrotic effects may be beneficial in some contexts

The honest assessment: Most community reports describe Follistatin 344 as well-tolerated during short cycles at standard doses. The theoretical concerns above are based on mechanism, not observed adverse events from peptide injection. However, the absence of observed side effects is not proof of safety — it reflects the limited monitoring and short duration of community use. Short cycles with extended off-periods are the primary risk mitigation strategy.

Contraindications

Active cancer or history of cancer — Follistatin modulates TGF-β signaling pathways involved in cell growth regulation. Use in the presence of active malignancies is contraindicated.
Pregnancy and breastfeeding — Follistatin's effects on activin and the reproductive axis make it strictly contraindicated during pregnancy and nursing. No safety data exists.
Active fertility treatment — Follistatin binds activin, which is crucial for FSH regulation and follicular development. Do not use during IVF cycles, assisted reproduction, or when actively trying to conceive.
Known reproductive hormone disorders — conditions involving FSH, LH, or gonadotropin dysregulation may be worsened by exogenous Follistatin.
Autoimmune conditions — TGF-β family members play roles in immune regulation. Modulating this axis in the presence of autoimmune disease carries unknown risks.
Age under 25 — growth plate closure, hormonal axis development, and reproductive maturation make Follistatin inappropriate for younger individuals.

Monitoring Recommendations

FSH and LH levels: Check before the first cycle and 4–6 weeks after cycle completion to assess reproductive axis impact
Testosterone (men): Monitor alongside FSH/LH to detect any downstream effects on testicular function
Menstrual regularity (women): Track cycle length and regularity before, during, and after Follistatin use
IGF-1 levels: Optional but useful to see if Follistatin (especially when stacked with GH secretagogues) is affecting the GH/IGF-1 axis
General health markers: CBC, CMP, and liver function as a baseline and after the first cycle

Regulatory Status: Follistatin 344 is not FDA-approved for human use. It is classified as a research peptide / research chemical. It has no pharmaceutical-grade manufacturing standard for human injection. Regulations vary by jurisdiction — verify your local laws before purchasing or possessing research peptides.

Common Follistatin Dosing Mistakes

Avoid these common errors to get the most out of your Follistatin protocol:

Expecting gene therapy results from peptide injection

The dramatic muscle growth seen in myostatin knockout animals and Follistatin gene therapy trials cannot be extrapolated to exogenous peptide injection. Gene therapy produces sustained, high local expression in muscle tissue over months. Peptide injection provides a transient circulating spike with a short half-life. Set realistic expectations.

Running excessively long cycles

Follistatin 344 is typically cycled for 10–30 days, not months. Extended cycles increase the theoretical risk of reproductive effects (FSH suppression via activin binding) and other unknowns. The limited human data makes conservative cycling a prudent approach.

Using Follistatin as a standalone muscle-building protocol

Even if Follistatin provides meaningful myostatin inhibition, it does not replace training stimulus, nutrition, and recovery. Myostatin inhibition removes one brake on muscle growth — it does not actively build muscle on its own. Training, adequate protein, and caloric surplus remain the primary drivers of hypertrophy.

Ignoring the evidence gap between biology and application

The biology of myostatin is well-established — knockout animals are dramatically more muscular, and gene therapy trials show promise. But injectable Follistatin peptide human data is minimal. Do not confuse strong mechanistic science with strong clinical evidence for the specific delivery method you are using.

Stacking multiple unproven compounds simultaneously

Some protocols combine Follistatin with IGF-1 LR3, MK-677, and other growth factors all at once. While each has a theoretical rationale, stacking multiple compounds with limited human data makes it impossible to attribute effects or side effects to any single agent. Start with one compound at a time when possible.

Not accounting for the cost-to-evidence ratio

Follistatin 344 is one of the most expensive research peptides per milligram. Given the limited human evidence for peptide injection efficacy, users should weigh the cost against the uncertain benefit. Peptides with stronger human evidence (like GHRPs or GHRHs) may offer a better return on investment for muscle growth goals.

Ignoring potential reproductive effects

Follistatin binds activin, which is critical for FSH regulation, follicle development, and spermatogenesis. Short cycles exist partly to limit exposure of the reproductive axis to exogenous Follistatin. Do not dismiss reproductive concerns, especially for women or anyone planning conception.

Improper storage and handling

Follistatin 344 is a large, complex glycoprotein that is more fragile than small synthetic peptides. It must be stored properly (refrigerated after reconstitution, never frozen once in solution). Rough handling, excessive heat, or repeated freeze-thaw cycles can denature the protein and render it inactive. Handle with more care than you would a small peptide.

Not reconstituting gently

When adding bacteriostatic water to the Follistatin vial, let the water run down the side of the vial rather than spraying it directly onto the lyophilized powder. Do not shake the vial — gently swirl or roll it. Follistatin is a large protein that can be denatured by vigorous agitation, unlike smaller peptides that are more robust.

Frequently Asked Questions

Key Takeaways

Follistatin 344 is a myostatin inhibitor — it binds and neutralizes myostatin, theoretically removing the brake on skeletal muscle growth
Standard dose: 100–200 mcg SubQ daily for 10–30 day cycles, 1–3 times per year with extended off-periods
The biology is real; the peptide injection evidence is limited — myostatin science and gene therapy results are strong, but human data for subcutaneous Follistatin peptide injection is minimal
FS-344 is the standard variant — it is processed in vivo to FS-315 (circulating, myostatin-binding) and FS-288 (tissue-bound, gonad-concentrated)
Cycling is essential: 10–30 days on, with off-periods 2–3 times the cycle length. Not used continuously.
Reproductive considerations are real: Follistatin binds activin, which regulates FSH. Monitor reproductive hormones, especially if fertility is a concern
Best stacks: IGF-1 LR3 for growth factor synergy, MK-677 for GH elevation, or BPC-157 for recovery support
Handle with care: Follistatin is a large protein — reconstitute gently (no shaking), refrigerate after reconstitution, use within 14–21 days
Training and nutrition are non-negotiable — myostatin inhibition removes a constraint but does not replace the growth stimulus from progressive overload training and adequate protein
Set realistic expectations: Do not expect gene therapy or myostatin knockout animal results from peptide injection. Effects, if any, will be subtle and develop over multiple cycles.
Not FDA-approved — classified as a research peptide. No pharmaceutical-grade standard exists for human injection. Check local regulations.

This article is for educational and informational purposes only. Follistatin 344 is not approved by the FDA for human use and is classified as a research peptide. Human clinical data for exogenous subcutaneous injection is extremely limited. It is not intended to diagnose, treat, cure, or prevent any disease. Consult a qualified healthcare provider before using any research peptide, especially if you have pre-existing medical conditions, are taking medications, are planning conception, or are pregnant or nursing. See our Medical Disclaimer.

References

Lee SJ, McPherron AC. “Regulation of myostatin activity and muscle growth.” Proc Natl Acad Sci USA. 2001;98(16):9306-9311.
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.
Mendell JR, et al. “A phase 1/2a follistatin gene therapy trial for Becker muscular dystrophy.” Mol Ther. 2015;23(1):192-201.
Mendell JR, et al. “Follistatin gene therapy for sporadic inclusion body myositis improves functional outcomes.” Mol Ther. 2017;25(4):870-879.
Amthor H, et al. “Follistatin complexes myostatin and antagonises myostatin-mediated inhibition of myogenesis.” Dev Biol. 2004;270(1):19-30.
Rodino-Klapac LR, et al. “Inhibition of myostatin with emphasis on follistatin as a therapy for muscle disease.” Muscle Nerve. 2009;39(3):283-296.
Nakatani M, et al. “Transgenic expression of a myostatin inhibitor derived from follistatin increases skeletal muscle mass and ameliorates dystrophic pathology.” FASEB J. 2008;22(2):477-487.
Phillips DJ, de Kretser DM. “Follistatin: a multifunctional regulatory protein.” Front Neuroendocrinol. 1998;19(4):287-322.
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