Skip to content
Specimen Atlas of Research Peptides81 plates · MIT
Side-by-side · Research reference

Follistatin-344vsTB-500

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
BPhase 2HUMAN-REVIEWED8/46 cited
Follistatin-344
Myostatin/Activin Antagonist · Research Use
15–25%FST/MSTN ratio ↑
344 AACirculating isoform
ResearchPhase status
Research · No approved protocol
TB-500
Thymosin β4 fragment · Healing
2 mgPer doseGoldstein 2012
Phase 2Evidence levelGoldstein 2012
~2 hrHalf-life
SQ or IM · Multiple sites · 2–3×/week

01Mechanism of Action

Parameter
Follistatin-344
TB-500
Primary target
Myostatin (MSTN/GDF-8) and Activin A
G-actin (sequestering) + cell-surface integrinsGoldstein 2012
Pathway
FST-344 binds MSTN/Activin → prevents ActRIIB receptor engagement → disinhibits muscle anabolism
Actin remodelling → cell migration; integrin-linked signaling → angiogenesis; anti-inflammatory cytokine modulationGoldstein 2012Malinda 1999
Downstream effect
Elevated follistatin/myostatin ratio, increased muscle protein synthesis, attenuated muscle atrophy signalingJeong 2026
Accelerated wound healing, endothelial migration, hair follicle regeneration, cardiac repair (preclinical)Goldstein 2012
Feedback intact?
Yes — indirect antagonist, preserves endogenous regulation
Endogenous protein at baseline; supplementation amplifies
Origin
Endogenous glycoprotein, 344-AA isoform lacking heparin-binding domain (vs FST-315)
17-AA active fragment of endogenous 43-AA thymosin β4 (TMSB4X gene)Goldstein 2012
Antibody development
Not documented in available trials (endogenous protein)

02Dosage Protocols

Parameter
Follistatin-344
TB-500
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
Animal-strong + Phase 2 dermal/ocular trialsGoldstein 2012
Half-life
Not established
Circulating isoform; lacks tissue-binding domain of FST-315.
~2 hours (estimated; tissue uptake longer)
Standard dose
2 mg per injectionGoldstein 2012
Anecdotal community range; clinical Phase 2 trials used 70–840 mcg/kg IV.
Frequency
2× per week (loading); then 1× per week (maintenance)
Lower / starter dose
1 mg per injection
Duration
4–8 weeks loading; longer maintenance for chronic injury
Reconstitution
Bacteriostatic water, 1–2 mL per 5 mg vial
Timing
Evening or pre-rest preferred (anecdotal)

03Metabolic / Fat Loss Evidence

Parameter
Follistatin-344
TB-500
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
TB-500
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
Injection site reaction
Mild erythema, transient pain
GI symptoms
Rare nausea (anecdotal)
Cancer risk
Theoretical via angiogenesis pathway
Lethargy / fatigue
Reported anecdotally during loading phase
Antibody formation
No data (no long-term human trials)
Pregnancy / OB
Avoid
Long-term safety
Unknown beyond Phase 2
Absolute Contraindications
Follistatin-344
  • ·Active malignancy
  • ·No approved protocol — research use only
TB-500
  • ·Active malignancy (theoretical angiogenesis concern)
  • ·Pregnancy / breastfeeding
Relative Contraindications
Follistatin-344
  • ·Insulin resistance / Type 2 diabetes (monitor glucose)
  • ·Pregnancy / lactation (unknown safety profile)
TB-500
  • ·Cancer history
  • ·Concurrent VEGF inhibitor therapy

05Administration Protocol

Parameter
Follistatin-344
TB-500
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.
Add 1–2 mL bacteriostatic water to 5 mg vial → 2.5–5 mg/mL. Roll gently.
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.
SQ near injury site (preferred), or systemic SQ (abdomen). Rotate sites.
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.
Evening or pre-sleep is most common anecdotal timing.
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.
Lyophilised: room temp, light-protected. Reconstituted: refrigerate, ≤30 days.
5. Needle
27–31G, 4–8 mm insulin syringe.

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
TB-500
+ BPC-157
Strong
View BPC-157

TB-500 and BPC-157 cover complementary halves of tissue repair: BPC-157 upregulates VEGFR2-driven angiogenesis and fibroblast outgrowth; TB-500 sequesters G-actin to enable endothelial / epithelial migration. The anecdotal canonical "healing stack" — pairs especially well for tendon and ligament injuries.

TB-500
2 mg SQ · 2× per week
BPC-157
250–500 mcg SQ · daily
Primary benefit
Combined angiogenesis + cell migration for tendon/ligament/muscle repair