Side-by-side · Research reference

Follistatin-344vsGLP-1 (7-37)

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-MechanisticHUMAN-REVIEWED16/43 cited

Follistatin-344

Myostatin/Activin Antagonist · Research Use

15–25%FST/MSTN ratio ↑

344 AACirculating isoform

ResearchPhase status

Research · No approved protocol

GLP-1 (7-37)

Incretin Hormone · Native Peptide

~2 minHalf-lifeAlavi 2021 Ding 2017

3297.7 DaMolecular weightAlavi 2021

1922Discovery year

Research use only · IV/SC in experimental settings

01Mechanism of Action

Parameter

Follistatin-344

GLP-1 (7-37)

Primary target

Myostatin (MSTN/GDF-8) and Activin A

GLP-1 receptor (class B GPCR)Koole 2015

Pathway

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

GLP-1R activation → cAMP production → PKA signaling → insulin secretion (pancreatic β-cells)Lu 2025 Koole 2015

Downstream effect

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

Glucose-dependent insulin release, glucagon suppression, delayed gastric emptying, reduced food intakeLu 2025 Ding 2017

Feedback intact?

Yes — indirect antagonist, preserves endogenous regulation

Yes — physiological secretion and degradation preserved

Origin

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

Endogenous peptide cleaved from proglucagon in intestinal L cells; secreted postprandially

Antibody development

Not documented in available trials (endogenous protein)

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02Dosage Protocols

Parameter

Follistatin-344

GLP-1 (7-37)

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

—

Half-life

Not established

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

~2 minutes (plasma)Alavi 2021 Ding 2017

Requires continuous infusion for sustained effect.

Clinical use

—

None — native GLP-1 not used therapeutically

Engineered analogues (semaglutide, liraglutide) used clinically.Friedman 2024

Research dosing

—

Variable — 0.1–10 nmol/kg in animal models

Used as reference standard for analogue comparison.

Modified analogues

—

t½ extended to 13 h (liraglutide), 165 h (semaglutide)

Via DPP-4 resistance + fatty acid acylation.

03Metabolic / Fat Loss Evidence

Parameter

Follistatin-344

GLP-1 (7-37)

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.

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GLP-1RA studies

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

—

Mechanism

—

GLP-1R activation in hypothalamic satiety centers (arcuate nucleus) reduces food intakeLu 2025

Effect demonstrated with long-acting analogues (liraglutide).Lu 2025

Native GLP-1 efficacy

—

Minimal — rapid degradation prevents sustained appetite suppression

Gastric emptying

—

Delayed in animal models, contributing to satiety

Body weight impact

—

Not observed with native GLP-1 — requires analogue formulations

04Side Effects & Safety

Parameter

Follistatin-344

GLP-1 (7-37)

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

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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

—

Native GLP-1

—

Well-tolerated in research settings; no prolonged exposure data

Hypoglycemia risk

—

Low — insulin secretion is glucose-dependent

Analogue side effects

—

Nausea, vomiting, diarrhea (GLP-1R agonists)

Not applicable to native GLP-1 due to non-therapeutic use.

GLP-1 resistance

—

High glucose-induced PKCβ overexpression may reduce GLP-1 responsiveness in endothelial cellsPujadas 2016

Absolute Contraindications

Follistatin-344

·Active malignancy
·No approved protocol — research use only

GLP-1 (7-37)

—

Relative Contraindications

Follistatin-344

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

GLP-1 (7-37)

—

05Administration Protocol

Parameter

Follistatin-344

GLP-1 (7-37)

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.

Native GLP-1(7-37) is not formulated for therapeutic use. Administered IV or SC in experimental protocols to study GLP-1R pharmacology and as reference standard for analogue development.

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.

Lyophilised peptide stored at -20°C or below. Reconstituted solutions should be prepared fresh and used immediately due to rapid degradation.

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.

For therapeutic GLP-1R activation, use FDA-approved long-acting analogues: semaglutide (once weekly), liraglutide (once daily), dulaglutide (once weekly), or exenatide (twice daily or once weekly).

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.

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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

GLP-1 (7-37)

— no documented stacks