TB-500 Fragment (17-23) 10mg

Thymosin Beta-4 Fragment (17–23), also known as fequesetide (LKKTETQ), is a synthetic heptapeptide corresponding to a conserved actin-interaction domain derived from the larger thymosin beta-4 polypeptide. This fragment is utilized in laboratory research settings as a molecular probe for investigating cytoskeletal organization, actin dynamics, and intracellular signaling processes.

All observations associated with this peptide originate from in-vitro systems and controlled in-vivo animal models. No clinical, diagnostic, or therapeutic interpretations are implied.

Amino Acid Sequence: LEU-LYS-LYS-THR-GLU-THR-GLN (LKKTETQ)
Chemical Formula: C36H66N10O13
Molecular Weight: 846.97 g/mol
PubChem CID: 10169788
CAS Number: 476014-70-7
Synonyms: Fequesetide; Thymosin Beta-4 (17–23)

The peptide lacks disulfide bonds and exhibits physicochemical properties suitable for aqueous laboratory systems. Structural simplicity enables reproducible synthesis and analytical verification.

Thymosin Beta-4 Fragment (17–23) is employed exclusively in research environments to examine:

• Actin monomer sequestration and filament assembly
• Cellular migration and cytoskeletal remodeling
• Intracellular signal transduction pathways
• Protein–protein interaction dynamics
• Regulation of inflammatory mediators in animal models

All applications are limited to non-clinical experimental models.

Mechanistic investigations indicate that the fragment participates in modulation of actin polymerization processes. Interaction with actin-regulatory complexes such as Arp2/3 has been explored in preclinical models, highlighting its utility for studying branched actin network formation.

Downstream signaling pathways associated with cytoskeletal organization, including focal adhesion kinase–related cascades and PI3K/Akt-associated signaling, have been examined in vitro using this peptide as a research tool.

Published preclinical literature describes investigation of thymosin beta-4–derived fragments in rodent and cellular systems. Experimental observations include modulation of fibroblast migration, endothelial cell organization, and cytokine signaling under controlled laboratory conditions.

Additional studies in neural and musculoskeletal animal models have explored molecular responses related to cytoskeletal plasticity, inflammatory mediator balance, and cellular differentiation markers. These findings are presented strictly as experimental observations without clinical extrapolation.

This product is supplied as a lyophilized synthetic peptide produced via solid-phase peptide synthesis. Each batch is characterized using high-performance liquid chromatography and mass spectrometry to confirm identity and purity.

Analytical documentation supports reproducibility for laboratory workflows.

The above literature was researched, edited and organized by Dr. Logan, M.D. Dr. Logan holds a doctorate degree from Case Western Reserve University School of Medicine and a B.S. in molecular biology.

Geoffrey M. Cooper is being referenced as one of the leading scientists involved in the research and development of TB-500 Fragment (17-23). In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between Peptide Sciences and this doctor. The purpose of citing the doctor is to acknowledge, recognize, and credit the exhaustive research and development efforts conducted by the scientists studying this peptide. Geoffrey M. Cooper is listed in [2] under the referenced citations.

1. V. Papalazarou and L. M. Machesky, “The cell pushes back: The Arp2/3 complex is a key orchestrator of cellular responses to environmental forces,” Curr. Opin. Cell Biol., vol. 68, pp. 37–44, Feb. 2021, doi: 10.1016/j.ceb.2020.08.012.
2. G. M. Cooper, “The Cytoskeleton and Cell Movement,” in The Cell: A Molecular Approach. 2nd edition, Sinauer Associates, 2000. Accessed: Apr. 10, 2024. [Online]. Available: https://www.ncbi.nlm.nih.gov/books/NBK9893/
3. “18.1: Introduction,” Biology LibreTexts. Accessed: Apr. 10, 2024. [Online]. Available: https://bio.libretexts.org/Under_Construction/Cell_and_Molecular_Biology_(Bergtrom)/18%3A_The_Cytoskeleton_and_Cell_Motility/18.01%3A_Introduction
4. PubChem, “Lkktetq.” Accessed: Apr. 10, 2024. [Online]. Available: https://pubchem.ncbi.nlm.nih.gov/compound/10169788
5. S. Lv, H. Cai, Y. Xu, J. Dai, X. Rong, and L. Zheng, “Thymosin-β 4 induces angiogenesis in critical limb ischemia mice via regulating Notch/NF-κB pathway,” Int. J. Mol. Med., vol. 46, no. 4, pp. 1347–1358, Oct. 2020, doi: 10.3892/ijmm.2020.4701.
6. G. Sosne, P. Qiu, and M. Kurpakus-Wheater, “Thymosin beta-4 and the eye: I can see clearly now the pain is gone,” Ann. N. Y. Acad. Sci., vol. 1112, pp. 114–122, Sep. 2007, doi: 10.1196/annals.1415.004.
7. S. S. Iyer and G. Cheng, “Role of Interleukin 10 Transcriptional Regulation in Inflammation and Autoimmune Disease,” Crit. Rev. Immunol., vol. 32, no. 1, pp. 23–63, 2012.
8. A. Carracedo and P. P. Pandolfi, “The PTEN-PI3K pathway: of feedbacks and cross-talks,” Oncogene, vol. 27, no. 41, pp. 5527–5541, Sep. 2008, doi: 10.1038/onc.2008.247.
9. G. Song, G. Ouyang, and S. Bao, “The activation of Akt/PKB signaling pathway and cell survival,” J. Cell. Mol. Med., vol. 9, no. 1, pp. 59–71, Jan. 2005, doi: 10.1111/j.1582-4934.2005.tb00337.x.
10. J. P. Alao, “The regulation of cyclin D1 degradation: roles in cancer development and the potential for therapeutic invention,” Mol. Cancer, vol. 6, p. 24, Apr. 2007, doi: 10.1186/1476-4598-6-24.
11. Y. Xiong et al., “Neuroprotective and neurorestorative effects of thymosin β4 treatment following experimental traumatic brain injury,” Ann. N. Y. Acad. Sci., vol. 1270, pp. 51–58, Oct. 2012, doi: 10.1111/j.1749-6632.2012.06683.x.
12. D. C. Morris et al., “A dose-response study of thymosin β4 for the treatment of acute stroke,” J. Neurol. Sci., vol. 345, no. 1–2, pp. 61–67, Oct. 2014, doi: 10.1016/j.jns.2014.07.006.
13. J. Zhang et al., “Thymosin beta4 promotes oligodendrogenesis in the demyelinating central nervous system,” Neurobiol. Dis., vol. 88, pp. 85–95, Apr. 2016, doi: 10.1016/j.nbd.2016.01.010.
14. M. Santra et al., “Thymosin β4 up-regulation of microRNA-146a promotes oligodendrocyte differentiation and suppression of the Toll-like proinflammatory pathway,” J. Biol. Chem., vol. 289, no. 28, pp. 19508–19518, Jul. 2014, doi: 10.1074/jbc.M113.529966.
15. M. Severa et al., “Thymosins in multiple sclerosis and its experimental models: moving from basic to clinical application,” Mult. Scler. Relat. Disord., vol. 27, pp. 52–60, Jan. 2019, doi: 10.1016/j.msard.2018.09.035.

ALL ARTICLES AND PRODUCT INFORMATION PROVIDED ON THIS WEBSITE ARE FOR INFORMATIONAL AND EDUCATIONAL PURPOSES ONLY.

The products offered on this website are furnished for in-vitro studies only. In-vitro studies (Latin: in glass) are performed outside of the body.  These products are not medicines or drugs and have not been approved by the FDA to prevent, treat or cure any medical condition, ailment or disease.  Bodily introduction of any kind into humans or animals is strictly forbidden by law.

For Laboratory Research Only. Not for human use, medical use, diagnostic use, or veterinary use.