TB-500 (Thymosin Beta-4)
Thymosin β4 fragment · Research-grade reference material
Identity
- Molecular formula
- C212H350N56O78S
- Molecular weight
- 4963.44 g/mol
- CAS number
- 77591-33-4
Research Background
“TB-500” is used inconsistently across the research-compound market. Some vendors sell a short synthetic fragment corresponding to the actin-binding region of the protein, as small as 7 amino acids. The material referenced on this site is the full 43-amino-acid thymosin beta-4 protein, naturally occurring in nearly every nucleated cell type in the body except red blood cells, first isolated from thymus tissue and later found to be one of the most abundant intracellular peptides in mammalian cells.
Thymosin beta-4 was identified in 1991 as biochemically identical to “Fx,” a previously isolated actin-sequestering factor from platelets, establishing it as the primary G-actin buffering protein in most mammalian cell types (Safer, Elzinga, and Nachmias). Since then it has been studied across wound healing, cell migration, cardioprotection, and, notably, in an actual human clinical development program: RegeneRx Biopharmaceuticals has advanced an ophthalmic formulation containing full-length thymosin beta-4, branded RGN-259, through Phase III human trials for a rare corneal condition. RGN-259 holds FDA Orphan Drug Designation for that indication (granted 2013) but has not received FDA marketing approval.
Lab-tested research material
TB-500 (Thymosin Beta-4)
From $59.00 · HPLC purity 99.16% · Batch AC-TB-1 COA
View current batch and sizes →Mechanism
Thymosin beta-4 binds G-actin, the monomeric building block of the cell’s structural scaffolding, and sequesters it, controlling how much is available for rapid filament assembly (Safer, Elzinga, and Nachmias). That buffering function is what allows cells to reorganize their cytoskeleton quickly, which is directly relevant to directed cell migration: research has shown the protein stimulates directional migration of human endothelial cells (Malinda, Goldstein, and Kleinman) and accelerates wound reepithelialization and collagen deposition in animal models (Malinda et al.).
Thymosin β4 is the principal intracellular G-actin–sequestering molecule in eukaryotic cells, regulating the actin cytoskeleton that governs cell shape, motility and migration. TB-500 (its active region) has been studied in preclinical tissue-repair research across wound-healing, cardiovascular, corneal and musculoskeletal models since the late 1990s–2000s. Findings below derive from animal and cell-culture systems. They are not established effects in humans.
Actin sequestration (foundational). High-affinity 1:1 binding to monomeric G-actin (reported Kd ≈ 0.5–0.7 µM), influencing polymerization and cell migration.
Cell migration & re-epithelialization. Promotes keratinocyte and fibroblast migration in preclinical wound models.
Angiogenesis. Endothelial migration and tubule formation; the LKKTET motif is implicated (mutation reduces activity).
Anti-inflammatory modulation. NF-κB-associated modulation of inflammatory signaling in injury models.
Proposed pathways investigated in preclinical (animal / in-vitro) models. Schematic only; not a claim of established human effect.
State of the Evidence
Full-length thymosin beta-4 has a deeper evidence base than most compounds in this category, including a genuine human Phase III randomized controlled trial. That trial is worth reading carefully rather than citing as a blanket endorsement: it tested a specific eye-drop formulation in a rare corneal condition, enrolled only 18 total participants (10 treated, 8 placebo) after the study was terminated early due to slow recruitment, and its primary endpoint showed a strong efficacy trend but fell just short of conventional statistical significance (p = 0.0656). Secondary endpoints did reach significance. None of this generalizes to how research-grade material would be used or dosed outside that specific trial context.
1. In Vitro / Biochemical — “Thymosin Beta 4 and Fx, an Actin-Sequestering Peptide, Are Indistinguishable,” Journal of Biological Chemistry, 1991. Vol. 266, pp. 4029-4032
2. In Vitro / Animal — “Thymosin Beta4 Stimulates Directional Migration of Human Umbilical Vein Endothelial Cells,” FASEB Journal, 1997.
3. Animal — “Thymosin Beta4 Accelerates Wound Healing,” Journal of Investigative Dermatology, 1999.
4. Human — “0.1% RGN-259 (Thymosin ß4) Ophthalmic Solution…Phase III Clinical Trial,” International Journal of Molecular Sciences, 2023. In an 18-patient Phase III trial, 6 of 10 patients treated achieved complete corneal healing at 4 weeks, versus 1 of 8 on placebo. DOI 10.3390/ijms24010554
What the Literature Supports — and What It Doesn’t
The actin-sequestration mechanism and preclinical wound-healing / angiogenesis findings are documented across multiple laboratories. A key nuance: most primary evidence concerns full-length thymosin β4, not the TB-500 fragment as sold by reagent vendors.
Evidence at a glance
Most robust evidence concerns full-length Tβ4; sequence and quality vary between vendor sources of “TB-500.”
The legitimate clinical path is RGN-259 (a Tβ4-based ophthalmic candidate) — as of 2026 at phase 3, with no approved marketed product.
No human randomized controlled trial supports systemic use for musculoskeletal injury; no regulatory approvals for therapeutic use.
Appropriate characterization: a well-studied actin-regulating peptide with substantial preclinical tissue-repair literature and one active pharmaceutical program (ophthalmology), awaiting approved clinical outcomes.
Regulatory & status notes
Selected references
- 1. Thymosin Beta-4 and TB-500 in Tissue Healing, Regeneration, and Musculoskeletal Repair: A Scoping Review. Applied Sciences (MDPI). 2026;16(12):6202.
- 2. Goldstein AL, Kleinman HK. Thymosin β4 in tissue repair and wound healing (foundational literature).
- 3. Bock-Marquette I, et al. Thymosin β4 mediates cardioprotective effects (porcine MI model).
- 4. Malinda KM, et al. Thymosin β4 accelerates wound healing. J Invest Dermatol. 1999.
Safety Information
Research-use compound with limited human data. Evidence strength varies — see the Evidence section above.
No established clinical contraindications. This is an investigational compound with limited human data and has not been evaluated by the FDA for safety in this context. Consult a qualified clinician. For research and educational purposes only, not for human or veterinary use.
Related Compounds
For research and educational purposes only. Not for human or veterinary use.