SB 225002

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Description: Potent and selective CXCR2 antagonist
Chemical Name: N-(2-Bromophenyl)-N'-(2-hydroxy-4-nitrophenyl)urea
Purity: ≥99% (HPLC)
Citations (12)
Reviews (1)
Literature (1)

Biological Activity for SB 225002

SB 225002 is a potent and selective CXCR2 chemokine receptor antagonist (IC50 = 22 nM) that displays > 150-fold selectivity over CXCR1 receptors. Causes inhibition of IL-8 and GROα-mediated calcium mobilization in HL60 cells (IC50 values are 8 and 10 nM respectively). Prevents IL-8-induced neutrophil chemotaxis in vitro and sequestration in vivo. Inhibits HIV replication in lymphocytes and macrophages.

Licensing Information

Sold for research purposes under agreement from GlaxoSmithKline

Compound Libraries for SB 225002

SB 225002 is also offered as part of the Tocriscreen 2.0 Max and Tocriscreen Antiviral Library. Find out more about compound libraries available from Tocris.

Technical Data for SB 225002

M. Wt 352.14
Formula C13H10BrN3O4
Storage Store at RT
Purity ≥99% (HPLC)
CAS Number 182498-32-4
PubChem ID 3854666
Smiles OC1=CC(=CC=C1NC(=O)NC1=CC=CC=C1Br)[N+]([O-])=O

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 225002

Solvent Max Conc. mg/mL Max Conc. mM
DMSO 35.21 100
ethanol 17.61 50

Preparing Stock Solutions for SB 225002

The following data is based on the product molecular weight 352.14. 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.

Select a batch to recalculate based on the batch molecular weight:
Concentration / Solvent Volume / Mass 1 mg 5 mg 10 mg
1 mM 2.84 mL 14.2 mL 28.4 mL
5 mM 0.57 mL 2.84 mL 5.68 mL
10 mM 0.28 mL 1.42 mL 2.84 mL
50 mM 0.06 mL 0.28 mL 0.57 mL

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Product Datasheets for SB 225002

Certificate of Analysis / Product Datasheet
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References for SB 225002

References are publications that support the biological activity of the product.

White et al (1998) Identification of a potent, selective non-peptide CXCR2 antagonist that inhibits interleukin-8-induced neutrophil migration. J.Biol.Chem. 273 10095 PMID: 9553055

Lane et al (2001) Interleukin-8 stimulates human immunodeficiency virus type 1 replication and is a potential new target for antiretroviral therapy. J.Virol. 75 8195 PMID: 11483765

Catusse et al (2003) Characterization of the molecular interactions of interleukin-8 (CXCL8), growth related oncogen a (CXCL1) and a non-peptide antagonist (SB 225002) with the human CXCR2. Biochem.Pharmacol. 65 813 PMID: 12628493

If you know of a relevant reference for SB 225002, please let us know.

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Keywords: SB 225002, SB 225002 supplier, Potent, selective, CXCR2, antagonists, Chemokine, Receptors, SB225002, GlaxoSmithKline, GSK, CXC, 2725, Tocris Bioscience

12 Citations for SB 225002

Citations are publications that use Tocris products. Selected citations for SB 225002 include:

Yuen et al (2012) Angiogenic dysfunction in bone marrow-derived early outgrowth cells from diabetic animals is attenuated by SIRT1 activation. J Clin Invest 1 921 PMID: 23283553

Saika (2018) Chemokine CXCL1 is responsible for cocaine-induced reward in mice. NeurosciPharm Reports 38 145 PMID: 30175527

Grabner et al (2015) Disruption of STAT3 signalling promotes KRAS-induced lung tumorigenesis. PLoS One 6 6285 PMID: 25734337

Devapatla et al (2015) CXCR2 Inhibition Combined with sora. Improved Antitumor and Antiangiogenic Response in Preclinical Models of Ovarian Cancer. Stem Cells Transl Med 10 e0139237 PMID: 26414070

Jang et al (2011) CXCL1 and its receptor, CXCR2, mediate murine sickle cell vaso-occlusion during hemolytic transfusion reactions. Sci Rep 121 1397 PMID: 21383500

Lourenco et al (2015) Macrophage migration inhibitory factor-CXCR4 is the dominant chemotactic axis in human mesenchymal stem cell recruitment to tumors. J Immunol 194 3463 PMID: 25712213

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

Karim et al (2019) Analogues of ERβ ligand chloroindazole exert immunomodulatory and remyelinating effects in a mouse model of multiple sclerosis. Sci Rep 9 503 PMID: 30679747

Chen et al (2019) Cancer-Derived VEGF-C Increases Chemokine Production in Lymphatic Endothelial Cells to Promote CXCR2-Dependent Cancer Invasion and MDSC Recruitment. Cancers (Basel) 11 PMID: 31390756

Raccosta et al (2013) The oxysterol-CXCR2 axis plays a key role in the recruitment of tumor-promoting neutrophils. J Exp Med 210 1711 PMID: 23897983

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

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

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Reviews for SB 225002

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Used for Migration assays.
By Anonymous on 07/01/2020
Assay Type: In Vitro
Species: Human
Cell Line/Tissue: A549 or MDAMB231

Receptor antagonists (SB225002: for CXCR2, AMD3465: for CXCR4, RS504393: for CCR2 and Maraviroc: for CCR5) at 10 μM

We ordered this product, combining with another inhibitor, to confirm the migration.To confirm that tested product induces migration, we also screen all MAPK inhibitors and MIF receptor antagonists

PMID: 25712213
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Literature in this Area

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 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.