Side-by-side · Research reference

Follistatin-344vsSelank

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

BHuman-MechanisticAUTO-DRAFTED11/40 cited

Follistatin-344

Myostatin/Activin Antagonist · Research Use

15–25%FST/MSTN ratio ↑

344 AACirculating isoform

ResearchPhase status

Research · No approved protocol

Selank

Anxiolytic + Cognitive · Russian Pharma

150–300 mcg/doseIntranasalZaderej 2014

HumanMechanisticZaderej 2014 Medvedev 2007

~30 minOnset

Intranasal · 2–3×/day during stress / cognitive demand

01Mechanism of Action

Parameter

Follistatin-344

Selank

Primary target

Myostatin (MSTN/GDF-8) and Activin A

Monoamine system (serotonin / GABA modulation) + immunomodulation via tuftsin domainZaderej 2014

Pathway

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

Tuftsin-derived immune signaling + CNS monoamine modulation → reduced anxiety + improved mood / cognitionMedvedev 2007

Downstream effect

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

Anxiolytic + cognitive enhancement; immunomodulation via increased IL-6 + IFN-γMedvedev 2007 Zaderej 2014

Feedback intact?

Yes — indirect antagonist, preserves endogenous regulation

No GABA-receptor binding; no dependence reportedMedvedev 2007

Origin

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

Synthetic 7-AA peptide derived from human tuftsin (immune-system tetrapeptide)Zaderej 2014

Antibody development

Not documented in available trials (endogenous protein)

—

02Dosage Protocols

Parameter

Follistatin-344

Selank

Clinical protocol

None — no approved dosing regimen

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

—

Research context

Endogenous modulation via exercise + nutrition

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

—

Evidence basis

Human observational / biomarker studies

Human-mechanistic + Russian clinical trialsMedvedev 2007

Half-life

Not established

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

Short (minutes plasma); CNS effect lasts ~3 hr

Standard dose

—

150–300 mcg / dose intranasalZaderej 2014

Frequency

—

2–3× per day during stress

Lower / starter dose

—

75 mcg / dose

Duration

—

10–14 day cycles, repeated as needed

Reconstitution

—

Pre-formulated nasal spray (commercial); research vial: bacteriostatic water

Timing

—

Morning + early afternoon preferred

03Metabolic / Fat Loss Evidence

Parameter

Follistatin-344

Selank

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.

—

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

—

04Side Effects & Safety

Parameter

Follistatin-344

Selank

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.

—

Endogenous elevation (exercise)

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

—

Cancer risk (theoretical)

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

—

Regulatory status

Not approved for human use — research peptide only

—

Nasal irritation

—

Mild burning or congestion (transient)

Sedation

—

None — distinct from benzodiazepinesMedvedev 2007

Dependence / withdrawal

—

None reported in clinical useZaderej 2014

Cognitive impairment

—

None — opposite effect (enhancement)

Allergic reaction

—

Rare hypersensitivity

Long-term safety

—

Limited Western RCT data

Pregnancy / OB

—

Avoid — insufficient data

Absolute Contraindications

Follistatin-344

·Active malignancy
·No approved protocol — research use only

Selank

·Pregnancy / breastfeeding
·Hypersensitivity to peptide

Relative Contraindications

Follistatin-344

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

Selank

·Active autoimmune disease (theoretical via immunomodulation)

05Administration Protocol

Parameter

Follistatin-344

Selank

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.

Pre-formulated nasal spray (commercial) or research vial reconstituted with bacteriostatic water.

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.

Intranasal — 1–3 sprays per nostril per dose. Tilt head slightly back.

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.

Morning + early afternoon for cognitive demand; PRN for acute anxiety.

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.

Refrigerate after reconstitution; ≤30 days. Light-protected.

5. Caveat

—

Avoid co-administration with strong sedatives or other anxiolytics initially.

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

Selank

— no documented stacks