TB-500
Also known as: Thymosin Beta-4, Tβ4
TB-500 is a synthetic version of Thymosin Beta-4, an endogenous 43-amino-acid peptide involved in actin sequestration, angiogenesis, and tissue repair. Research documents its role in wound healing and inflammatory modulation.
Sequence Length
43 amino acids
Molecular Weight
4,963 Da
Endogenous Source
Thymic tissue, platelets, wound fluid
Key Domain
LKKTET actin-binding motif
Molecular Target
G-actin, ILK, PINCH
Research Use Only
Not for human or veterinary use
Overview
Thymosin Beta-4 (Tβ4), the endogenous protein on which TB-500 is based, was originally isolated from thymic extracts in the 1960s. It belongs to the beta-thymosin family of actin-monomer-sequestering proteins and is one of the most abundant intracellular peptides in mammals, present at high concentrations in platelets, wound fluid, and inflammatory cells. TB-500 is a synthetic peptide corresponding to the full 43-amino-acid sequence of Tβ4.
The primary biochemical function of Thymosin Beta-4 is regulation of G-actin (globular actin) availability. By sequestering actin monomers, Tβ4 modulates the dynamic assembly and disassembly of actin filaments — a process critical to cell migration, morphology, and division. This actin-regulatory function underlies many of the downstream effects observed in wound healing research, where cell migration is essential for tissue restitution.
Research in animal models has documented TB-500's effects across multiple tissue types. Studies report accelerated repair of cardiac tissue following myocardial injury, improved tendon healing, corneal wound closure, and promotion of hair follicle keratinocyte migration. TB-500 has also been investigated in models of multiple sclerosis, where it appeared to promote oligodendrocyte survival and remyelination — findings that have generated interest in neuroprotection research.
TB-500 is offered for research use only and has not been approved for clinical therapeutic applications. Investigators interested in actin dynamics, wound healing models, or angiogenesis research will find an extensive primary literature base, including work by Huff, Bhatt, and Goldstein documenting structure-activity relationships within the Tβ4 sequence.
Mechanism of Action
The central mechanism of Thymosin Beta-4 involves its LKKTET actin-binding domain, which sequesters G-actin and thereby shifts the actin equilibrium toward a more migratory, dynamic cytoskeletal state. Beyond actin regulation, Tβ4 has been shown to activate ILK (integrin-linked kinase), which mediates Akt phosphorylation and downstream pro-survival signaling.
In vascular research, TB-500 promotes endothelial cell migration and tube formation through mechanisms involving VEGF and MMPs. Research has also identified a nuclear role for Tβ4 in transcriptional regulation, where it appears to interact with PINCH and α-parvin to influence focal adhesion assembly and gene expression programs associated with tissue remodeling.
Research Applications
- Actin dynamics and cytoskeletal biology research
- Cardiac tissue repair and myocardial regeneration models
- Angiogenesis and endothelial migration studies
- Corneal wound closure research
- Tendon and musculoskeletal healing models
- Neuroprotection and remyelination studies
Research Use Only. TB-500 is available for laboratory and research applications only. It is not approved by the FDA or any equivalent regulatory authority for human or veterinary therapeutic use. All information on this page is derived from published preclinical literature and is presented for informational and research context purposes only. Investigators should consult current primary literature and comply with applicable regulations before initiating research.
Order TB-500 for Research →Peptide Family
Tissue Repair Peptides
Structural Protein Synthesis · Angiogenesis · Wound Healing
All Compound Research Overviews