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TB-500
Derived from a naturally occurring protein involved in cellular structure and mobility, TB-500 is studied for its role in actin regulation and cell migration research. A widely referenced compound in tissue and repair pathway studies.
$50.00
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Derived from a naturally occurring protein involved in cellular structure and mobility, TB-500 is studied for its role in actin regulation and cell migration research. A widely referenced compound in tissue and repair pathway studies.
About TB-500
TB-500 is derived from Thymosin Beta-4, a 43-amino acid protein first identified in thymus tissue and subsequently found to be expressed across a remarkably broad range of biological contexts. Unlike many peptides with narrow tissue-specific activity, Thymosin Beta-4 and its analogues have been studied across skin, muscle, cardiac, and neural signaling pathways, making TB-500 one of the more broadly applicable synthetic research peptides in regenerative biology. It was developed as a laboratory research tool for investigating the regenerative and repair-associated properties of this peptide class in controlled research settings.
The primary studied mechanism of TB-500 centers on its interaction with actin, one of the most fundamental structural proteins involved in cellular function. Actin is essential not only to cellular contraction but to the ability of cells to move, divide, and reorganize during repair processes. By regulating actin dynamics, TB-500 has been studied for its potential to accelerate the movement of repair-associated cells to sites of tissue damage, a process that underlies wound closure, new tissue formation, and recovery-related signaling in preclinical research models.
Beyond its role in cell migration research, TB-500 has been investigated for its pro-angiogenic signaling properties, specifically its potential to stimulate the formation of new blood vessels in ischemic and damaged tissue models. Adequate vascular signaling is a prerequisite for tissue repair pathway activity, and researchers have studied TB-500 for its ability to support this vascular component across multiple tissue signaling contexts, including skin, muscle, tendon, and cardiac repair models.
Mechanism of Action
- TB-500 has been studied for its regulation of actin polymerization, the process by which individual actin proteins link together to form the structural framework cells use to move and reorganize. By modulating this process, TB-500 has been investigated for its ability to accelerate the migration of repair-associated cells to sites of tissue damage, a foundational step in wound closure and tissue regeneration signaling in controlled research settings.
- Studies have examined TB-500’s effects on keratinocyte and fibroblast migration specifically, two primary cell types involved in rebuilding skin and connective tissue signaling pathways following damage. Research has investigated whether accelerating the movement of these cells in laboratory research models leads to more organized and efficient tissue formation at the cellular level.
- TB-500 has been investigated for its pro-angiogenic signaling activity, specifically its potential to stimulate endothelial cells to form new capillary structures in areas of damaged or oxygen-deprived tissue models. New vessel formation is considered a critical component of sustained tissue repair signaling, as it supports the nutrient and oxygen supply that regenerating cells require in structured research environments.
- Research has examined TB-500’s anti-inflammatory signaling properties in acute injury research models, with studies investigating its potential to modulate inflammatory pathway activity at wound sites. Investigators have studied whether this modulation influences the transition between productive acute inflammation and chronic inflammatory signaling states in vitro.
- TB-500 has also been studied in cardiac repair research models, where investigators have examined its potential to support cardiomyocyte survival signaling, new vessel formation, and scar tissue reduction following ischemic injury models in controlled laboratory settings.
Research Highlights
TB-500 has been extensively studied in wound healing research models across multiple tissue signaling contexts. Research has examined its effects on wound closure rates, re-epithelialization, and the structural organization of newly formed tissue at the cellular level, with investigators noting measurable changes in collagen organization in treated research models.
Studies have investigated TB-500's effects on muscle, tendon, and ligament repair signaling pathways in preclinical research models. Research has examined its potential to reduce fibrotic scarring and support collagen fiber alignment, with tendon repair studies reporting changes in mechanical recovery markers in TB-500 treated models.
TB-500 has been studied for its pro-angiogenic signaling properties in wound healing and cardiovascular repair research contexts. Research has examined its potential to stimulate new capillary formation in ischemic and damaged tissue models, with investigators studying whether improved vascularization influences overall tissue repair pathway activity.
TB-500 has been investigated for its ability to modulate inflammatory signaling in acutely injured tissue research models. Studies have examined its effects on inflammatory marker production at wound sites, with researchers studying whether its anti-inflammatory pathway activity works in concert with its cell migration and angiogenic signaling properties in controlled research environments.
Product Specifications
- Molecular Formula
- C₂₁₂H₃₅₀N₅₆O₇₈S
- Molecular Weight
- 4,963.5 g/mol
- CAS #
- 77591-33-4
- Sequence
- Ac-Ser-Asp-Lys-Pro-Asp-Met-Ala-Glu-Ile-Glu-Lys-Phe-Asp-Lys-Ser-Lys-Leu-Lys-Lys-Thr-Glu-Thr-Gln-Glu-Lys-Asn-Pro-Leu-Pro-Ser-Lys-Glu-Thr-Ile-Glu-Gln-Glu-Lys-Gln-Ala-Gly-Glu-Ser
- Purity
- ≥99% (HPLC verified)
- Form
- Lyophilized powder
- Appearance
- White to off-white powder
- Solubility
- Universal Solvent
- Storage
- -20°C (lyophilized), 2-8°C (after preparation)
Reference
- Goldstein, A. L., Hannappel, E., Sosne, G., & Kleinman, H. K. (2012). Thymosin β4: A multi-functional regenerative peptide. Expert Opinion on Biological Therapy, 12(1), 37–51.
- Philp, D., Scheremeta, B., Sibliss, K., et al. (2006). Thymosin beta4 promotes matrix metalloproteinase expression during wound repair. Journal of Cell Science, 119(Pt 6), 1101–1108.
- Bock-Marquette, I., Saxena, A., White, M. D., Dimaio, J. M., & Srivastava, D. (2004). Thymosin beta4 activates integrin-linked kinase and promotes cardiac cell migration, survival and cardiac repair. Nature, 432(7016), 466–472.
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