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Submit ReviewSB 265610 is a potent CXCR2 antagonist that inhibits CINC-1-mediated but not C5a-mediated Ca2+ mobilization (IC50 values are 3.4 and 6800 nM respectively). Inhibits CINC-induced chemotaxis and attenuates neutrophil accumulation in inflammatory lung injury in vivo.
Sold for research purposes under agreement from GlaxoSmithKline
SB 265610 is also offered as part of the Tocriscreen 2.0 Max and Tocriscreen Antiviral Library. Find out more about compound libraries available from Tocris.
M. Wt | 357.16 |
Formula | C14H9BrN6O |
Storage | Store at RT |
Purity | ≥98% (HPLC) |
CAS Number | 211096-49-0 |
PubChem ID | 9841667 |
InChI Key | SEDUMQWZEOMXSO-UHFFFAOYSA-N |
Smiles | O=C(NC3=C(Br)C=CC=C3)NC1=CC=C(C#N)C2=C1NN=N2 |
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 | |
---|---|---|---|
Solubility | |||
DMSO | 35.72 | 100 | |
ethanol | 3.57 | 10 |
The following data is based on the product molecular weight 357.16. 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 | 2.8 mL | 14 mL | 28 mL |
5 mM | 0.56 mL | 2.8 mL | 5.6 mL |
10 mM | 0.28 mL | 1.4 mL | 2.8 mL |
50 mM | 0.06 mL | 0.28 mL | 0.56 mL |
References are publications that support the biological activity of the product.
Auten et al (2001) Nonpeptide CXCR2 antagonist prevents neutrophil accumulation in hyperoxia-exposed newborn rats. J.Pharmacol.Exp.Ther. 299 90 PMID: 11561067
Milatovic et al (2003) Impaired healing of nitrogen mustard wounds in CXCR2 null mice. Wound Repair Regen. 11 213 PMID: 12753603
If you know of a relevant reference for SB 265610, please let us know.
Keywords: SB 265610, SB 265610 supplier, Potent, CXCR2, antagonists, Chemokine, Receptors, SB265610, GlaxoSmithKline, GSK, CXC, 2724, Tocris Bioscience
Citations are publications that use Tocris products. Selected citations for SB 265610 include:
Ha et al (2014) A novel phenylcyclohex-1-enecarbothioamide derivative inhibits CXCL8-mediated chemotaxis through selective regulation of CXCR2-mediated signalling. Br J Pharmacol 171 1551 PMID: 24354854
Bieren et al (2015) Immune Antibodies and Helminth Products Drive CXCR2-Dependent Macrophage-Myofibroblast Crosstalk to Promote Intestinal Repair. PLoS Pathog 11 e1004778 PMID: 25806513
Toh et al (2011) Mesenchymal transition and dissemination of cancer cells is driven by myeloid-derived suppressor cells infiltrating the primary tumor. PLoS Biol 9 e1001162 PMID: 21980263
Halpern et al (2011) Mesenchymal stem cells promote mammary cancer cell migration in vitro via the CXCR2 receptor. Cancer Lett 308 91 PMID: 21601983
Burton et al (2011) Bone morphogenetic protein receptor II regulates pulmonary artery endothelial cell barrier function. Blood 117 333 PMID: 20724539
Jung et al (2016) CXCR2 Inhibition in Human Pluripotent Stem Cells Induces Predominant Differentiation to Mesoderm and Endoderm Through Repression of mTOR, β-Catenin, and hTERT Activities. Stem Cells Dev 25 1006 PMID: 27188501
Lavoie-Lamoureux et al (2010) IL-4 activates equine neutrophils and induces a mixed inflammatory cytokine expression profile with enhanced neutrophil chemotactic mediator release ex vivo. Am J Physiol Lung Cell Mol Physiol 299 L472 PMID: 20639353
He et al (2018) Circadian Expression of Migratory Factors Establishes Lineage-Specific Signatures that Guide the Homing of Leukocyte Subsets to Tissues. Immunity 49 1175 PMID: 30527911
Do you know of a great paper that uses SB 265610 from Tocris? Please let us know.
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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.