Recovery & Tissue Repair
TB-500
Synthetic fragment of thymosin beta-4 studied for G-actin sequestration, cell migration and eNOS- and VEGF-linked angiogenesis.
Also known asThymosin Beta-4 · Tβ4
Identity
Residue chain
One bead per amino acid residue, N-terminus to C-terminus. Long chains are shown truncated.
- Molecular weight
- 4963 Da
- Amino acid residues
- 43
- Half-life
- 60–90 min
- CAS number
- 77591-33-4
Monograph
Specifications
- Research area
- Recovery & Tissue Repair
- Half-life
- 60–90 min
- Molecular weight
- 4963 Da
- Amino acid residues
- 43
- CAS number
- 77591-33-4
- Formula
- C₂₁₂H₃₅₀N₅₆O₇₈S
- Sequence
- Ac-Ser-Asp-Lys-Pro (active 4-aa fragment of Thymosin β-4)
- Designation
- Thymosin Beta-4 Fragment 17-23
Pharmacokinetics
- Half-life
- 60–90 min
- T-max
- ~1 h
- Route
- Subcutaneous / intramuscular (research use)
Receptor targets
- G-actin (cytoskeletal target)Sequestration / cell migration
- eNOS pathwayAngiogenic signaling
- NF-κB axisAnti-inflammatory modulation
Signalling cascade
- 1G-actin sequestration
- 2Cytoskeletal remodeling
- 3Cell migration
- 4Tissue repair
- Mechanism of action
- Synthetic fragment of Thymosin Beta-4 that sequesters G-actin to promote cytoskeletal remodeling and cell migration. Upregulates anti-inflammatory gene expression via NF-κB inhibition and stimulates angiogenesis through eNOS and VEGF pathways.
- Storage and handling
- Refrigerate at 2–8 °C after reconstitution. Lyophilized powder is stable at room temperature for up to 24 months.
Research focus
- 01Tissue repair and wound healing acceleration
- 02Cell migration and cytoskeletal dynamics (actin sequestration)
- 03Inflammatory resolution via NF-κB pathway inhibition
- 04Angiogenesis and microvascular remodeling
- 05Cardiac and skeletal muscle recovery in preclinical models
Overview
TB-500 is a synthetic fragment of thymosin beta-4 that sequesters G-actin, driving cytoskeletal remodelling and cell migration. Preclinical work covers angiogenesis through eNOS and VEGF, NF-κB-linked inflammatory resolution, and repair endpoints in cardiac and skeletal muscle models.