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SB 332235 is a potent CXCR2 antagonist (IC50 = 7.7 nM). Exhibits 285-fold selectivity for CXCR2 over CXCR1. Reduces leukocyte numbers in synovial fluid in acute and chronic rabbit arthritis models. Also reduces synovial fluid eicosanoid and cytokine levels in a rabbit chronic arthritis model. Inhibits proliferation of AML cell lines in vitro.
SB 332235 is also offered as part of the Tocriscreen 2.0 Max and Tocriscreen Antiviral Library. Find out more about compound libraries available from Tocris.
|Storage||Store 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 410.66. 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||2.44 mL||12.18 mL||24.35 mL|
|5 mM||0.49 mL||2.44 mL||4.87 mL|
|10 mM||0.24 mL||1.22 mL||2.44 mL|
|50 mM||0.05 mL||0.24 mL||0.49 mL|
References are publications that support the biological activity of the product.
Podolin et al (2002) A potent and selective nonpeptide antagonist of CXCR2 inhibits acute and chronic models of arthritis in the rabbit. J.Immunol. 169 6435 PMID: 12444152
Schinke et al (2015) IL8-CXCR2 pathway inhibition as a therapeutic strategy against MDS and AML stem cells. Blood 125 3144 PMID: 25810490
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Keywords: SB 332235, SB 332235 supplier, SB332235, chemokines, receptors, CXCR2, interleukin-8, IL-8, inflammation, chronic, acute, rheumatoid, arthritis, antagonists, antagonism, Chemokine, CXC, Receptors, 5671, Tocris Bioscience
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Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* your copy today!
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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.