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Submit ReviewReparixin L-lysine salt is a potent and noncompetitive CXCR1 and CXCR2 allosteric antagonist (IC50 = 1 nM for inhibition of CXCL8-induced human polymorphonuclear cell migration). Also inhibits migration of rodent neutrophils induced by CXCL1, CXCL2, CXCL8 and CINC-1. Inhibits vascular permeability and neutrophil recruitment in in vivo models of mild and severe ischemia/reperfusion injury. Also selectively depletes cancer stem cells in human breast cancer cell lines and xenograft models.
M. Wt | 429.58 |
Formula | C14H21NO3S.C6H14N2O2 |
Storage | Store at -20°C |
Purity | ≥98% (HPLC) |
CAS Number | 266359-93-7 |
PubChem ID | 9932389 |
InChI Key | JEJFWWFZAQBZMJ-GVKMLHTLSA-N |
Smiles | NCCCC[C@H](N)C(O)=O.CC(C)CC1=CC=C(C=C1)[C@@H](C)C(=O)N[S](C)(=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.
References are publications that support the biological activity of the product.
Bertini et al (2004) Noncompetitive allosteric inhibitors of the inflammatory chemokine receptors CXCR1 and CXCR2: prevention of reperfusion injury. Proc.Natl.Acad.Sci.U.S.A. 101 11791 PMID: 15282370
Souza et al (2004) Repertaxin, a novel inhibitor of rat CXCR2 function, inhibits inflammatory responses that follow intestinal ischaemia and reperfusion injury. Br.J.Pharmacol. 143 132 PMID: 15302676
Ginestier et al (2010) CXCR1 blockade selectively targets human breast cancer stem cells in vitro and in xenografts. J.Clin.Invest. 120 485 PMID: 20051626
Keywords: Reparixin L-lysine salt, Reparixin L-lysine salt supplier, repertaxin, CXCR1, CXCR2, chemokine, receptor, antagonists, antagonism, allosteric, noncompetitive, IL-8, CXCL8, interleukin, 8, Repertaxin, L-lysine, salt, Chemokine, CXC, Receptors, Cancer, Stem, Cells, 6957, Tocris Bioscience
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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.