SB 225002
目录号 : GC16465
SB 225002是一种有效的选择性CXCR2趋化因子受体拮抗剂，可抑制125I-IL-8（125I标记的白细胞介素8）和CXCR2的结合，IC50值为22nM。
Cas No.:182498-32-4
Sample solution is provided at 25 µL, 10mM.
;)
,-1-7$$$37316672.jpg');)
;)
;)
$$$36806353.jpg');)
;33(7)%EF%BC%9A546-561$$$37156877.jpg');)
;)
;)
;)
%201124-1138.$$$35908550.jpg');)
%20766-780.$$$37100057.jpg');)
%20418-432.$$$36893736.jpg');)
%EF%BC%9A-240-255.$$$35108512.jpg');)
533-545$$$36543525.jpg');)
%201-13.$$$36600053.jpg');)
;)
Quality Control & SDS
- View current batch:
- Purity: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
| Cell experiment [1]: | |
Cell lines | WHCO1 cells |
Preparation Method | SB 225002 (400nM) was added to cells and 0.001% DMSO (solvent) was added as a control. Detection of cell viability using MTT assay. |
Reaction Conditions | 400nM, 1-6 day |
Applications | Blocking CXCR2 signaling in WHCO1 cells with 400nM SB 225002 significantly decreased cell proliferation by ∼40% to 50%. |
| Animal experiment [2]: | |
Animal models | Wildtype mice (C57BL/6J) fed with normal chow (normolipidemic) or ApoE−/− mice fed with high cholesterol diet (hyperlipidemic) |
Preparation Method | Wildtype mice fed with a normal chow and ApoE knockout mice fed with a high cholesterol diet were exposed to middle cerebral artery occlusion (MCAO). CXCR2 was blocked using the selective antagonist SB 225002 (2mg/kg) or neutralizing CXCR2 antiserum. |
Dosage form | 2mg/kg, 0、24 and 48h, i.p. |
Applications | Administration of the selective CXCR2 inhibitor SB 225002 did not affect ischemic brain injury in normolipidemic wildtype mice, but reversed the increased brain injury in hyperlipidemic ApoE−/− mice. |
References: | |
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.
SB 225002是一种有效的选择性CXCR2趋化因子受体拮抗剂，可抑制125I-IL-8（125I标记的白细胞介素8）和CXCR2的结合，IC50值为22nM[1]。
在HL60细胞中，SB 225002有效阻止IL-8和GROα诱导的中性粒细胞趋化性。在主要表达CXCR2（~80%）和少量表达CXCR1（~20%）受体的细胞中，SB 225002对IL-8和GROα介导的钙动员产生浓度依赖性抑制，IC50值分别为8和10nM[1]。GROβ通过细胞外信号调节激酶1/2（ERK1/2）途径增强EGR-1的转录，该途径可被SB 225002阻断。400nM的SB 225002可阻断WHCO1细胞中的CXCR2信号，可显著降低细胞增殖（40%-50%）[2]。
在中性粒细胞隔离兔子模型中SB 225002（1.39-5.5μg/kg/min）选择性阻断IL-8诱导的中性粒细胞边缘化[1]。SB 225002（2mg/kg）不会影响血脂正常的野生型小鼠的缺血性脑损伤，但逆转了高脂血症ApoE −/−小鼠中增加的脑损伤[3]。在LPS致敏HI（缺氧缺血）脑白质损伤的幼鼠模型中，SB 225002（1或3mg/kg）显著减轻小胶质细胞活化、BBB损伤和LPS致敏HI后白质中的星形胶质细胞增生[4]。
| Cas No. | 182498-32-4 | SDF | |
| 化学名 | 1-(2-bromophenyl)-3-(2-hydroxy-4-nitrophenyl)urea | ||
| Canonical SMILES | OC1=C(NC(NC2=CC=CC=C2Br)=O)C=CC([N+]([O-])=O)=C1 | ||
| 分子式 | C13H10BrN3O4 | 分子量 | 352.14 |
| 溶解度 | ≥ 15.9mg/mL in DMSO | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
||
| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 2.8398 mL | 14.1989 mL | 28.3978 mL |
| 5 mM | 0.568 mL | 2.8398 mL | 5.6796 mL |
| 10 mM | 0.284 mL | 1.4199 mL | 2.8398 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。