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JMS 17-2 hydrochloride is a chemokine CX3CR1 (fractalkine receptor) antagonist. Inhibits fractalkine-induced ERK phosphorylation and decreases migration of breast cancer cells in vitro. Also inhibits circulating tumor cells from seeding into bone and reduces overall tumor burden in a breast cancer metastasis model.
Sold under license from Drexel University.
JMS 17-2 hydrochloride is also offered as part of the Tocriscreen Antiviral Library. Find out more about compound libraries available from Tocris.
|Storage||Desiccate at RT|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
The following data is based on the product molecular weight 456.41. Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|1 mM||2.19 mL||10.96 mL||21.91 mL|
|5 mM||0.44 mL||2.19 mL||4.38 mL|
|10 mM||0.22 mL||1.1 mL||2.19 mL|
|50 mM||0.04 mL||0.22 mL||0.44 mL|
References are publications that support the biological activity of the product.
Shen et al (2016) Novel small-molecule CX3CR1 antagonist impairs metastatic seeding and colonization of breast cancer cells. Mol. Cancer Res. 14 518 PMID: 27001765
If you know of a relevant reference for JMS 17-2 hydrochloride, please let us know.
Keywords: JMS 17-2 hydrochloride, JMS 17-2 hydrochloride supplier, JMS17-2, hydrochloride, HCl, 1380392-05-1, fractalkine, receptor, antagonists, antagonism, cx3cr1, chemokines, Other, Chemokine, Receptors, 6378, Tocris Bioscience
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Rheumatoid arthritis (RA) is a chronic destructive inflammatory autoimmune disease that results from a breakdown in immune tolerance, for reasons that are as yet unknown. This poster summarizes the pathology of RA and the inflammatory processes involved, as well as describing some of the epigenetic modifications associated with the disease and the potential for targeting these changes in the discovery of new treatments.