Powder: -20°C for 3 years | In solvent: -80°C for 1 year
LIT927 (LIT-927) 是一种具有口服活性的 CXCL12 中性配体(对于 CXCL12 与 CXCR4 的结合,Ki:267 nM)。
规格 | 价格/CNY | 货期 | 数量 | |
---|---|---|---|---|
1 mg | ¥ 278 | 现货 | ||
2 mg | ¥ 393 | 现货 | ||
5 mg | ¥ 659 | 现货 | ||
10 mg | ¥ 987 | 现货 | ||
25 mg | ¥ 1,970 | 现货 | ||
50 mg | ¥ 2,930 | 现货 | ||
100 mg | ¥ 4,260 | 现货 | ||
500 mg | ¥ 8,960 | 现货 | ||
1 mL * 10 mM (in DMSO) | ¥ 782 | 现货 |
产品描述 | LIT927 (LIT-927) is an orally active CXCL12 neutraligand (Ki: 267 nM for CXCL12 binding to CXCR4). |
靶点活性 | CXCL12:267 nM (Ki) |
体外活性 | LIT-927 at 10 μM is able to inhibit the increase in intracellular calcium concentration in EGFP-CXCR4+ HEK cells in response to CXCL12, while it has no effect on calcium responses triggered by either CCL17 or CCL22 on EGFP-CCR4+ HEK cells, CCL5 on EGFP-CCR5+ HEK cells, or CCL2 on EGFPCCR2+ HEK cells [1]. |
体内活性 | LIT-927 (350 μmol/kg) inhibited eosinophil infiltration by 54% and 55%. LIT-927 did not exhibit any side effects. In the same murine model of hypereosinophilia, LIT-927 (1400 μmol/kg, P.O.) shows a large and statistically reliable inhibition of eosinophil recruitment (62% inhibition) [1]. |
细胞实验 | HEK EGFP-CXCR4-expressing cells were washed with phosphate-buffered saline (PBS) and detached in PBS-EDTA (5 mM) for 2 min at room temperature. Then cells were carefully resuspended in complete growth medium, pelleted by centrifugation at 320 × g for 5 min, and resuspended in HEPES buffer (137.5 mM NaCl, 6 mM KCl, 1.25 mM CaCl2, 1.25 mM MgCl2, 0.4 mM NaH2PO4, 5.6 mM glucose, 10 mM HEPES (pH 7.4) containing 0.1% BSA. Cells were used at a concentration of 10^6 cells/mL, then the cell suspension (1 mL) was transferred into a quartz cuvette. Time-based recordings of the fluorescence emitted at 510 nm (excitation at 470 nm) were performed at 21 °C using a Fluorolog 3 spectrofluorometer. Fluorescence binding measurements were initiated by adding at t = 150 s, 100 nM CXCL12-Texas Red (TR) to the 1 mL cell suspension. Binding of CXCL12-TR to EGFP-labeled CXCR4 was detected as a reversible decline of emission at 510 nm due to energy transfer from excited EGFP to TR. In the "neutraligand protocol", CXCL12-TR was preincubated for 1 h at room temperature with DMSO or various concentrations of each test compound. Then the premix was added (at t = 150 s), and fluorescence was recorded until equilibrium was reached (300 s). In the "antagonist protocol", DMSO or various concentrations of each test compound were added to EGFP-CXCR4-expressing cells at t = 50 s. Then CXCL12-Texas Red (100 nM) was added at t = 150 s, and fluorescence was recorded until equilibrium was reached (300 s). Dose-response curves of inhibition of CXCL12-TR binding were performed, and the inhibitory constants (Ki) of the different compounds were determined. T134 (20 μM), the CXCR4 receptor antagonist, was used as a control in both "neutraligand" and "antagonist" protocols. |
动物实验 | The activity of each compound was assessed in vivo in an 8 day model of allergic eosinophilic airway inflammation as described previously. Briefly, 9 week-old male Balb/c mice were sensitized by intraperitoneal injection of 50 μg of ovalbumin adsorbed on 2 mg of aluminum hydroxide in 0.1 mL of saline on days 0, 1, and 2. Mice were challenged intranasally [10 μg of OVA in 25 μL of saline (12.5 μL/nostril)] on days 5, 6, and 7. Control mice received intranasal administration of saline alone. Intranasal administrations were performed under anesthesia with intraperitoneal injection of ketamine (50 mg/kg) and xylazine (3.33 mg/kg). Food and water were supplied ad libitum. Two hours before each OVA or saline challenge, compounds in PBS/Cdx were administered intranasally (12.5 μL/nostril), intraperitoneally, or per os as indicated in the figure legends. Bronchoalveolar lavage (BAL) was performed 24 h after the last OVA or saline challenge as described. Mice were deeply anesthetized by intraperitoneal injection of ketamine (150 mg/kg) and xylazine (10 mg/kg). A plastic cannula was inserted into the trachea, and airways were lavaged by 10 instillations of 0.5 mL of ice-cold saline supplemented with 2.6 mM EDTA (saline-EDTA). BAL fluids were centrifuged (300g, 5 min, 4 °C) to pellet cells, and erythrocytes were lysed by hypotonic shock. Cells were resuspended in 500 μL of icecold saline-EDTA, and total cell counts were determined on a hemocytometer. Differential cell counts were assessed on cytological preparations spanning 250 000 cells/mL in ice-cold saline?EDTA, stained with Diff-Quick with counts of at least 400 cells. Counts were expressed as absolute cell numbers or percentage of inhibition of eosinophil recruitment. |
别名 | LIT 927, LIT-927 |
分子量 | 328.75 |
分子式 | C17H13ClN2O3 |
CAS No. | 2172879-52-4 |
Powder: -20°C for 3 years | In solvent: -80°C for 1 year
H2O: Insoluble
DMSO: 25 mg/mL (76.05 mM)
可选溶剂 | 浓度 体积 质量 | 1 mg | 5 mg | 10 mg | 25 mg |
DMSO | 1 mM | 3.0418 mL | 15.2091 mL | 30.4183 mL | 76.0456 mL |
5 mM | 0.6084 mL | 3.0418 mL | 6.0837 mL | 15.2091 mL | |
10 mM | 0.3042 mL | 1.5209 mL | 3.0418 mL | 7.6046 mL | |
20 mM | 0.1521 mL | 0.7605 mL | 1.5209 mL | 3.8023 mL | |
50 mM | 0.0608 mL | 0.3042 mL | 0.6084 mL | 1.5209 mL |
对于不同动物的给药剂量换算,您也可以参考 更多...
请在以下方框中输入您的动物实验信息后点击计算,可以得到母液配置方法和体内配方的制备方法: 比如您的给药剂量是10 mg/kg,每只动物体重20 g,给药体积100 μL,一共给药动物10 只,您使用的配方为5% DMSO+30% PEG300+5% Tween 80+60% ddH2O。那么您的工作液浓度为2 mg/mL。
母液配置方法:2 mg 药物溶于 50 μL DMSO (母液浓度为 40 mg/mL), 如您需要配置的浓度超过该产品的溶解度,请先与我们联系。
体内配方的制备方法:取 50 μL DMSO 主液,加入 300 μL PEG300, 混匀澄清,再加 50 μL Tween 80,混匀澄清,再加 600 μL ddH2O, 混匀澄清。
您可能有的问题的答案可以在抑制剂处理说明中找到,包括如何准备库存溶液,如何存储产品,以及基于细胞的分析和动物实验需要特别注意的问题。
LIT927 2172879-52-4 Autophagy GPCR/G Protein Immunology/Inflammation CXCR LIT 927 LIT-927 Inhibitor inhibitor inhibit