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Biological Activity for SB 332235
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.
Compound Libraries for SB 332235
Technical Data for SB 332235
|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.
Solubility Data for SB 332235
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions for SB 332235
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 for SB 332235
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
If you know of a relevant reference for SB 332235, please let us know.
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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
Citations for SB 332235
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Reviews for SB 332235
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Literature in this Area
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Rheumatoid Arthritis Poster
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.