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Potent CXCR2 antagonist (IC50 = 1 nM); attenuates oxaliplatin-induced NF-κB activation, increases oxaliplatin cytotoxicity, and potentiates oxaliplatin-induced apoptosis in AIPC cells. Reduces the numbers of neutrophils infiltrating into tumors in both in vitro and in vivo models and delayed tumor growth. Orally bioavailable.
|Storage||Store at -20°C|
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|
Preparing Stock Solutions
The following data is based on the product molecular weight 400.88. 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||2.49 mL||12.47 mL||24.95 mL|
|5 mM||0.5 mL||2.49 mL||4.99 mL|
|10 mM||0.25 mL||1.25 mL||2.49 mL|
|50 mM||0.05 mL||0.25 mL||0.5 mL|
References are publications that support the biological activity of the product.
Wilson et al (2008) Chemotherapy-induced CXC-chemokine/CXC-chemokine receptor signaling in metastatic prostate cancer cells confers resistance to oxalip. through potentiation of nuclear factor-kappaB transcription and evasion of apoptosis. J.Pharmacol.Exp.Ther. 327 746 PMID: 18780829
Walters et al (2008) Evaluation of a series of bicyclic CXCR2 antagonists. Bioorg.Med.Chem.Lett. 18 798 PMID: 18240390
Tazzyman et al (2011) Inhibition of neutrophil infiltration into A549 lung tumors in vitro and in vivo using a CXCR2-specific antagonist is associated with reduced tumor growth. Int.J.Cancer 129 847 PMID: 21328342
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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.