Side-by-side · Research reference

Follistatin-344vsProstamax

Side-by-side comparison across mechanism, dosage, evidence, side effects, administration, and stack synergies. Citations on every claim where available.

AHuman-MechanisticHUMAN-REVIEWED4/58 cited

BAnimal-MechanisticHUMAN-REVIEWED11/38 cited

Follistatin-344

Myostatin/Activin Antagonist · Research Use

15–25%FST/MSTN ratio ↑

344 AACirculating isoform

ResearchPhase status

Research · No approved protocol

Prostamax

Khavinson Bioregulator · Tissue-Specific Peptide

0.05 ng/mLActive concentrationZakutskiĭ 2006

2.5×SCE frequency increaseDzhokhadze 2012

4 AAPeptide length

SQ · Protocol per Khavinson tradition

01Mechanism of Action

Parameter

Follistatin-344

Prostamax

Primary target

Myostatin (MSTN/GDF-8) and Activin A

Chromatin in prostatic cells — pericentromeric heterochromatin regions

Pathway

FST-344 binds MSTN/Activin → prevents ActRIIB receptor engagement → disinhibits muscle anabolism

Epigenetic modulation → heterochromatin decondensation → transcriptional derepressionDzhokhadze 2012

Downstream effect

Elevated follistatin/myostatin ratio, increased muscle protein synthesis, attenuated muscle atrophy signalingJeong 2026

Increased sister chromatid exchange, Ag-NOR activation, reduced C-heterochromatin condensation; tissue-specific regenerative stimulation in prostate organotypic culturesDzhokhadze 2012 Zakutskiĭ 2006

Feedback intact?

Yes — indirect antagonist, preserves endogenous regulation

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Origin

Endogenous glycoprotein, 344-AA isoform lacking heparin-binding domain (vs FST-315)

Synthetic tetrapeptide modeled on naturally occurring protein-derived bioregulators isolated between lysine-arginine motifs in long-lived speciesKhavinson 2017

Antibody development

Not documented in available trials (endogenous protein)

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02Dosage Protocols

Parameter

Follistatin-344

Prostamax

Clinical protocol

None — no approved dosing regimen

Follistatin-344 measured as endogenous biomarker, not administered exogenously in cited trials.

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Research context

Endogenous modulation via exercise + nutrition

Resistance training + EAA intake elevated FST/MSTN ratio by 15–25% in 12-week RCT (older women).

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Evidence basis

Human observational / biomarker studies

Animal / organotypic cultureZakutskiĭ 2006 Dzhokhadze 2012

No randomized controlled trials in humans.

Half-life

Not established

Circulating isoform; lacks tissue-binding domain of FST-315.

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Effective concentration (in vitro)

—

0.05 ng/mLZakutskiĭ 2006

Organotypic culture model; demonstrated tissue-specific stimulation.

Human clinical dose

—

Not established

No published human trials; dosing extrapolated from Russian clinical tradition (not peer-reviewed).

Age groups studied

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Young (3-week) and aged (18-month) rats; elderly humans (75–86 years) in vitroZakutskiĭ 2006 Dzhokhadze 2012

Duration

—

Not specified

Khavinson protocols typically 10–20 days per cycle; no long-term safety data.

03Metabolic / Fat Loss Evidence

Parameter

Follistatin-344

Prostamax

Primary target

Muscle mass preservation, not direct lipolysis

—

Indirect fat effect

Increased lean mass → elevated resting metabolic rate

Not primary mechanism. Muscle-sparing during deficit.

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Clinical evidence

Lorcaserin trial (6 mo) showed no MAFI axis changes during fat lossRamirez-Cisneros 2026

Suggests follistatin not primary driver of fat loss in weight-reduction interventions.

—

GLP-1RA studies

Liraglutide (35 days) — no significant MAFI axis modulation despite fat/lean changes

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04Side Effects & Safety

Parameter

Follistatin-344

Prostamax

Clinical safety data

None — no human exogenous administration trials in literature

—

Theoretical risks

Excessive myostatin inhibition → muscle overgrowth, impaired glucose tolerance

Based on myostatin-null animal models and clinical myostatin inhibitor trials.

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Endogenous elevation (exercise)

No adverse effects reported in 12-week resistance + EAA trials

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Cancer risk (theoretical)

Myostatin inhibition may promote tumor growth in malignancy (preclinical data)

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Regulatory status

Not approved for human use — research peptide only

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Published adverse events

—

None reported in available literature

Genotoxicity signals

—

Increased sister chromatid exchange (SCE) — marker of DNA recombination/repair; unclear long-term implications

Metal ion interactions

—

Modulates Cu(II) and Cd(II) chromatin effects; unknown clinical relevance

Human safety data

—

Absent — no published Phase 1/2/3 trials

Absolute Contraindications

Follistatin-344

·Active malignancy
·No approved protocol — research use only

Prostamax

·Active prostate malignancy — epigenetic modulation effects unknown in cancer

Relative Contraindications

Follistatin-344

·Insulin resistance / Type 2 diabetes (monitor glucose)
·Pregnancy / lactation (unknown safety profile)

Prostamax

·History of prostate cancer — theoretical concern re: transcriptional activation
·Undiagnosed prostatic nodules or elevated PSA

05Administration Protocol

Parameter

Follistatin-344

Prostamax

1. Regulatory status

Follistatin-344 is not approved for human administration. All cited studies measure endogenous serum follistatin as a biomarker, not as an exogenous therapeutic agent.

Subcutaneous or intramuscular — per Khavinson bioregulator tradition. No published human pharmacokinetic data.

2. Endogenous modulation

Resistance exercise combined with essential amino acid (EAA) supplementation elevated the follistatin/myostatin ratio by 15–25% in 12-week randomized trials. Protein intake (1.2–1.5 g/kg/day) synergizes with training to upregulate endogenous follistatin.

If lyophilised: reconstitute with sterile water per manufacturer protocol (not standardized in literature).

3. Measurement context

Serum follistatin and follistatin/myostatin ratio are used diagnostically in sarcopenia screening and as biomarkers of muscle anabolic balance in clinical trials.

Typically daily or every-other-day in Russian clinical tradition; duration 10–20 days per cycle.

4. Research consideration

Gene therapy and recombinant follistatin delivery are under preclinical investigation for muscular dystrophy and sarcopenia. No human safety or efficacy data for exogenous FST-344 administration.

No established biomarkers. Theoretical: PSA, prostate imaging, symptom scores (IPSS for BPH).

5. Note

—

All protocols derived from non-peer-reviewed Russian clinical practice; Western regulatory approval absent.

06Stack Synergy

Follistatin-344

+ BPC-157

Multi-pathway

View BPC-157 →

Follistatin-344 (myostatin antagonist) and BPC-157 (tissue repair peptide) address complementary pathways in muscle recovery. FST-344 promotes muscle protein synthesis by disinhibiting myostatin signaling, while BPC-157 accelerates healing of tendons, ligaments, and microtears via angiogenesis and collagen synthesis. Combined, they may support both hypertrophy and structural repair during high-volume training or injury recovery.

Follistatin-344: No approved protocol — endogenous modulation via resistance exercise + EAA
BPC-157: 250–500 mcg SQ · twice daily · near injury site or systemic
Duration: 4–8 weeks
Primary benefit: Muscle hypertrophy + accelerated soft tissue repair

+ TB-500

Moderate

View TB-500 →

TB-500 (thymosin beta-4 fragment) promotes cell migration, angiogenesis, and anti-inflammatory signaling in muscle and connective tissue. Follistatin-344's anabolic signaling may synergize with TB-500's regenerative effects during muscle damage or overtraining, particularly in older adults where both myostatin inhibition and tissue repair are rate-limiting.

Follistatin-344: Endogenous upregulation (resistance training + protein)
TB-500: 2–5 mg SQ · twice weekly · loading phase 4 weeks, then maintenance
Frequency: Twice weekly TB-500, daily training stimulus for FST
Primary benefit: Enhanced recovery, reduced inflammation, muscle growth support

Prostamax

— no documented stacks