SB 225002 |
| Catalog No.GC16465 |
SB 225002, un antagoniste puissant, sélectif et non peptidique de CXCR2, inhibe la liaison de 125I-IL-8 à CXCR2 avec une IC50 de 22 nM.
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Cas No.: 182498-32-4
Sample solution is provided at 25 µL, 10mM.
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SB 225002 is a potent and selective CXCR2 chemokine receptor antagonist that inhibits the binding of 125I-IL-8 (125I-labeled interleukin 8) and CXCR2 with an IC50 value of 22nM[1].
In HL60 cells, SB 225002 potently prevented IL-8 and GROα-induced neutrophil chemotaxis. In cells expressing predominantly CXCR2 (~80%) and to a lesser extent CXCR1 (~20%) receptors, SB 225002 produces concentration-dependent inhibition of IL-8 and GROα-mediated calcium mobilization, with IC50 values of 8 and 10nM, respectively[1]. GROβ enhances transcription of EGR-1, via the extracellular signal-regulated kinase 1/2 (ERK1/2) pathway, which can be blocked by an antagonist of CXCR2 (SB 225002). 400nM of SB 225002 blocked CXCR2 signaling in WHCO1 cells and significantly reduced cell proliferation (40%-50%)[2].
SB 225002 (1.39-5.5μg/kg/min）selectively blocks IL-8-induced neutrophil marginalization in a neutrophil sequestration rabbit model[1]. SB 225002 (2mg/kg) did not affect ischemic brain damage in lipid-normal wild-type mice, but reversed the increased brain damage in hyperlipidemic ApoE-/- mice[3]. In a young rat model of lipopolysaccharide (LPS)-sensitized hypoxic-ischemic (HI) cerebral white matter injury, SB 225002 (1 or 3mg/kg) significantly attenuated microglia activation, blood-brain barrier (BBB) injury, and astrocyte hyperplasia in the white matter after LPS-sensitized HI[4].
References:
[1] White J R, Lee J M, Young P R, et al. Identification of a potent, selective non-peptide CXCR2 antagonist that inhibits interleukin-8-induced neutrophil migration[J]. Journal of Biological Chemistry, 1998, 273(17): 10095-10098.
[2] Wang B, Hendricks D T, Wamunyokoli F, et al. A growth-related oncogene/CXC chemokine receptor 2 autocrine loop contributes to cellular proliferation in esophageal cancer[J]. Cancer research, 2006, 66(6): 3071-3077.
[3] Herz J, Sabellek P, Lane TE, Gunzer M, Hermann DM, Doeppner TR. Role of Neutrophils in Exacerbation of Brain Injury After Focal Cerebral Ischemia in Hyperlipidemic Mice. Stroke. 2015 Oct;46(10):2916-25.
[4] Wang LY, Tu YF, Lin YC, Huang CC. CXCL5 signaling is a shared pathway of neuroinflammation and blood-brain barrier injury contributing to white matter injury in the immature brain. J Neuroinflammation. 2016 Jan 6;13:6.
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