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Selumetinib

产品编号 T6218 CAS 606143-52-6

别名: ARRY-142886, 司美替尼, AZD6244

Selumetinib (AZD6244) 是一种高效选择性的，非 ATP 竞争性的MEK1/2抑制剂，抑制 MEK1 的IC50为14 nM。它抑制 MEK1/2 磷酸化水平。

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Selumetinib, CAS 606143-52-6

规格	价格/CNY	货期
25 mg	￥ 349	现货
50 mg	￥ 498	现货
100 mg	￥ 813	现货
200 mg	￥ 995	现货
500 mg	￥ 2,150	现货
1 g	￥ 3,330	现货
1 mL * 10 mM (in DMSO)	￥ 228	现货

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其他形式的 Selumetinib:

Selumetinib sulfate
询价
L-708906
询价

选择批次

纯度: 99%

纯度: 98.73%

纯度: 98.1%

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生物活性

化学信息

存储 & 溶解度

参考文献

相关产品

产品描述	Selumetinib (AZD6244) (AZD6244) is an effective, specific inhibitor of MEK1 and ERK1/2 phosphorylation (IC50: 14/10 nM).
靶点活性	MEK1:14 nM (cell free), ERK1/2 phosphorylation:10.3 nM (Malme-3M cells)
体外活性	The IC50 of Selumetinib (AZD6244; ARRY-142886) was 14 nmol/L against purified MEK1. Treatment with ARRY-142886 resulted in the growth inhibition of several cell lines containing B-Raf and Ras mutations but had no effect on a normal fibroblast cell line [1]. For the time course and dose-response experiments, primary 2-1318 cells were treated with vehicle and escalating doses of Selumetinib (AZD6244) for 24 and 48 h. A 50% reduction in cell viability was seen at a dose of <0.5 μmol/L after 48-h incubation [2]. 5 of 31 breast cancer cell lines and 15 of 43 NSCLC cell lines were sensitive against Selumetinib (IC50s: <1 micromol/L) [3].
体内活性	When dosed orally, ARRY-142886 was capable of inhibiting both ERK1/2 phosphorylation and growth of HT-29 xenograft tumors in nude mice. Tumor regressions were also seen in a BxPC3 xenograft model. In addition, tumors remained responsive to growth inhibition after a 7-day dosing holiday [1]. AZD6244, when given p.o. to mice bearing these xenografts, resulted in a dose-dependent inhibition of tumor growth [2]. In vivo administration of AZD6244, doxorubicin, or the combination of AZD6244 and doxorubicin in mice bearing 5-1318 HCC xenografts resulted in approximately 52%, 12%, and 76% growth inhibition, respectively [4].
激酶实验	NH2-terminal hexahistidine tagged, constitutively active MEK1 was expressed in baculovirus-infected Hi5 insect cells and purified by immobilized metal affinity chromatography, ion exchange, and gel filtration. The activity of MEK1 was assessed by measuring the incorporation of [γ-33P]phosphate from [γ-33P]ATP onto ERK2. The assay was carried out in a 96-well polypropylene plate with an incubation mixture (100 μL) composed of 25 mmol/L HEPES (pH 7.4), 10 mmol/L MgCl2, 5 mmol/L β-glycerolphosphate, 100 μmol/L sodium orthovanadate, 5 mmol/L DTT, 5 nmol/L MEK1, 1 μmol/L ERK2, and 0 to 80 nmol/L compound (final concentration of 1% DMSO). The reactions were initiated by the addition of 10 μmol/L ATP (with 0.5 μC k[γ-33P]ATP/well) and incubated at room temperature for 45 min. An equal volume of 25% trichloracetic acid was added to stop the reaction and precipitate the proteins. Precipitated proteins were trapped onto glass fiber B filter plates, excess labeled ATP was washed off with 0.5% phosphoric acid, and radioactivity was counted in a liquid scintillation counter. ATP dependence was determined by varying the amount of ATP in the reaction mixture. The data were globally fitted using SigmaPlot. Values were calculated using the following equation for noncompetitive inhibition: v = [Vmax × S / (1 + I / Ki)] / (Km + S) [1].
细胞实验	Primary HCC cells were plated at a density of 2.0 × 10^4 per well in growth medium. After 48 h in growth medium, the cell monolayer was rinsed twice with MEM. Cells were treated with various concentrations of AZD6244 (0, 0.5, 1.0, 2.0, 3.0, and 4.0 μmol/L) for 24 or 48 h. Cell viability was determined by the MTT assay. Cell proliferation was assayed using a bromodeoxyuridine kit as described by the manufacturer. Experiments were repeated at least thrice, and the data were expressed as mean ± SE [2].
动物实验	HT-29 human colon carcinoma or BxPC3 human pancreatic tumor fragments were implanted s.c. in the flank of nude mice and allowed to grow to 100 to 150 mg. Mice (n = 10 per group) were randomized to treatment groups to receive vehicle (10 mL/kg and 10% ethanol/10% cremophor EL/80% D5W) or ARRY-142886 (10, 25, 50, or 100 mg/kg, oral, BID) on days 1 to 21. Tumors [(W^2 × L) / L] were measured twice weekly. Tumor growth inhibition was calculated as 1 ? (tumor sizetreated / tumor sizevehicle) on each measurement day. Four hours after the last dose on day 21, three mice per group were euthanized to evaluate pharmacokinetic/pharmacodynamic responses. Tumors were excised and flash frozen. Homogenates were analyzed for phospho-ERK1/2 and ERK1/2 expression by Western blotting as described above. For the HT-29 study, monitoring of tumor regrowth was continued for the remaining seven mice per group until tumors reached 1,000 mm^3, when mice would be sacrificed. There were two BxPC3 tumor xenograft studies. For the first study, one group of mice was treated with the clinical standard of care, gemcitabine, at 160 mg/kg, i.p., every 3rd day for a total of four doses. This dose was determined to be the maximum tolerated dose for gemcitabine in the BxPC3 model on this dosing schedule. To evaluate whether previously treated tumors would be refractory to a second cycle of treatment, a second BxPC3 xenograft study was carried out. Mice were treated with vehicle or ARRY-142886 at 25 or 50 mg/kg, BID, for 21 days. Treatment was stopped and tumors were allowed to grow for an additional 7 days before treatment resumed for another 21-day cycle [1].

别名	ARRY-142886, 司美替尼, AZD6244
分子量	457.68
分子式	C17H15BrClFN4O3
CAS No.	606143-52-6

存储

store at low temperature　|　Powder: -20°C for 3 years | In solvent: -80°C for 1 year

溶解度

DMSO: 84 mg/mL (183.5 mM)

Ethanol: < 1 mg/mL (insoluble or slightly soluble)

H2O: < 1 mg/mL (insoluble or slightly soluble)

溶液配制表

可选溶剂	浓度体积质量	1 mg	5 mg	10 mg	25 mg
DMSO	1 mM	2.1849 mL	10.9247 mL	21.8493 mL	54.6233 mL
	5 mM	0.437 mL	2.1849 mL	4.3699 mL	10.9247 mL
	10 mM	0.2185 mL	1.0925 mL	2.1849 mL	5.4623 mL
	20 mM	0.1092 mL	0.5462 mL	1.0925 mL	2.7312 mL
	50 mM	0.0437 mL	0.2185 mL	0.437 mL	1.0925 mL
	100 mM	0.0218 mL	0.1092 mL	0.2185 mL	0.5462 mL

计算器

摩尔浓度计算器

稀释计算器

配液计算器

分子量计算器

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容积

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容积 (起始)

浓度 (终)

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参考文献

1. Yeh TC, et al. Biological characterization of ARRY-142886 (AZD6244), a potent, highly selective mitogen-activated protein kinase kinase 1/2 inhibitor. Clin Cancer Res. 2007 Mar 1;13(5):1576-83. 2. Huynh H, et al, Targeted inhibition of the extracellular signal-regulated kinase kinase pathway with AZD6244 (ARRY-142886) in the treatment of hepatocellular carcinoma. Mol Cancer Therapy, 2007, 6 (1), 138-146. 3. Garon EB, et al. Identification of common predictive markers of in vitro response to the Mek inhibitor selumetinib (AZD6244; ARRY-142886) in human breast cancer and non-small cell lung cancer cell lines. Mol Cancer Thera, 2010, 9 (7), 1985-1994. 4. Huynh H, et al. AZD6244 and doxorubicin induce growth suppression and apoptosis in mouse models of hepatocellular carcinoma. Mol Cancer Ther. 2007 Sep;6(9):2468-76. 5. Zhang Q, Le K, Xu M, et al. Combined MEK inhibition and tumor-associated macrophages depletion suppresses tumor growth in a triple-negative breast cancer mouse model[J]. International Immunopharmacology. 2019, 76: 105864.

文献引用

1. Zhang G M, Huang S S, Ye L X, et al. Reciprocal positive regulation between BRD4 and YAP in GNAQ-mutant uveal melanoma cells confers sensitivity to BET inhibitors. Pharmacological Research. 2022: 106464. 2. Boos S L, Loevenich L P, Vosberg S, et al Disease Modeling on Tumor Organoids Implicates AURKA as a Therapeutic Target in Liver Metastatic Colorectal Cancer. Cellular and Molecular Gastroenterology and Hepatology. 2021 3. Zhang Q, Le K, Xu M, et al. Combined MEK inhibition and tumor-associated macrophages depletion suppresses tumor growth in a triple-negative breast cancer mouse model. International Immunopharmacology. 2019, 76: 105864. 4. Meng Y, Lv T, Zhang J, et al.Temporospatial inhibition of Erk signaling is required for lymphatic valve formation.Signal Transduction and Targeted Therapy.2023, 8(1): 342. 5. Yang N, Fan Z, Sun S, et al.Discovery of highly potent and selective KRASG12C degraders by VHL-recruiting PROTACs for the treatment of tumors with KRASG12C-Mutation.European Journal of Medicinal Chemistry.2023: 115857. 6. Xu H, Tan M, Hou G Q, et al.Blockade of DDR1/PYK2/ERK signaling suggesting SH2 superbinder as a novel autophagy inhibitor for pancreatic cancer.Cell Death & Disease.2023, 14(12): 811.

剂量换算

对于不同动物的给药剂量换算，您也可以参考 更多...

体内实验配液计算器

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。

第一步：请输入动物实验的基本信息

剂量

mg/kg

每只动物体重

给药体积

μL

动物数量

第二步：请输入动物体内配方组成，不同的产品配方组成不同，如有配方需求，可先联系我们提供正确的体内配方。

% DMSO+

% +

% Tween 80+

% ddH₂O

%DMSO+

计算重置

计算结果如下:

工作液浓度: mg/ml;

母液配置方法: mg 药物溶于 μL DMSO (母液浓度为 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 μL DMSO 主液，加入 μL PEG300，混匀澄清，再加 μL Tween 80，混匀澄清，再加 μL ddH₂O, 混匀澄清。

备注:

要按顺序从左向右依次添加助溶剂。可配合物理方法，如涡流、超声波或热水浴使之帮助溶解。

技术支持

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。

Keywords

Selumetinib 606143-52-6 Apoptosis MAPK ERK MEK inhibit ARRY142886 AZD 6244 MAP2K ARRY-142886 ARRY 142886 司美替尼 MAPKK Mitogen-activated protein kinase kinase AZD6244 Inhibitor AZD-6244 inhibitor

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Selumetinib

存储

溶解度

溶液配制表

计算器

输入分子式，点击计算，可计算出产品的分子量。

参考文献

文献引用

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剂量换算

体内实验配液计算器

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