Back to Shop
TB-500
Out of Stock

TB-500 5mg

Recovery

$89

4.0 (24 reviews)

Synthetic fragment of Thymosin Beta-4 that promotes tissue repair, reduces inflammation, and accelerates healing of muscle, tendon, and ligament injuries.

5mg per vial, lyophilized powder
Thymosin Beta-4 derived peptide
Third-party tested for purity and potency
Requires reconstitution with bacteriostatic water
1
Third-party tested

Overview

TB-500 is a synthetic version of the naturally occurring peptide Thymosin Beta-4, found in high concentrations at injury sites. It promotes actin regulation, cellular migration, and angiogenesis to accelerate tissue repair. TB-500 has been studied in equine and rodent models for its ability to heal tendons, heart tissue, skin wounds, and corneal injuries.

Lab Results — 5mg

Every batch is independently tested. Results below are from the Certificate of Analysis for the 5mg batch.

Test
Result
Status
Identity (HPLC-MS)
Confirmed TB-500
Pass
Purity
98.7%
Pass
Heavy Metals (Pb)
< 0.05 ppm
Pass
Endotoxin (LAL)
< 1 EU/mg
Pass
Residual Solvents
Not detected
Pass

Scientific Details

Molecular Formula

C₂₁₂H₃₅₀N₅₆O₇₈S

Molecular Weight

~4.9 kDa

Form

Lyophilized peptide powder

Solubility

Soluble in bacteriostatic water

Dosage Range

2–5mg twice weekly (research context)

Plasma Half-Life

~5–6 hours

Bioavailability

~85% subcutaneous

Resources

Key peer-reviewed studies supporting the efficacy and safety of this compound.

Thymosin beta-4 and cardiac repair

Bock-Marquette I. et al.Nature (2004)

Key FindingThymosin Beta-4 activated cardiac progenitor cells and significantly improved cardiac function after myocardial infarction in mouse models.

Thymosin beta-4 promotes corneal wound healing

Sosne G. et al.Experimental Eye Research (2001)

Key FindingTB-4 accelerated corneal epithelial wound closure and reduced inflammatory infiltrate in multiple animal models.

Anti-inflammatory mechanism of thymosin beta-4

Sosne G. et al.Annals of the New York Academy of Sciences (2007)

Key FindingTB-4 suppressed NF-κB signaling and reduced pro-inflammatory cytokine expression in corneal and systemic inflammatory models.