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Capivasertib

产品编号 T1920 CAS 1143532-39-1

别名: AZD5363

Capivasertib (AZD5363) 是一种广谱的 AKT 抑制剂，对 Akt1、Akt2 和 Akt3 均有抑制活性 (IC50=3/7/7 nM)，具有口服活性。Capivasertib 具有抗肿瘤活性，可以用于治疗乳腺癌。

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Capivasertib, CAS 1143532-39-1

规格	价格/CNY	货期
1 mg	￥ 329	现货
2 mg	￥ 478	现货
5 mg	￥ 788	现货
10 mg	￥ 1,160	现货
25 mg	￥ 1,890	现货
50 mg	￥ 2,660	现货
100 mg	￥ 3,930	现货
1 mL * 10 mM (in DMSO)	￥ 878	现货

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选择批次

纯度: 99.6%

纯度: 99.48%

纯度: 99.29%

纯度: 99.13%

纯度: 98.96%

纯度: 97.59%

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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	Capivasertib (AZD5363) is a broad-spectrum AKT inhibitor with inhibitory activity against Akt1, Akt2, and Akt3 (IC50=3/7/7 nM) with oral activity. Capivasertib has antitumor activity for the treatment of breast cancer.
靶点活性	Akt3:7 nM (cell free), p70 S6K:6 nM (cell free), PKA:7 nM (cell free), Akt2:7 nM (cell free), Akt1:3 nM (cell free)
体外活性	方法：六株人胃癌细胞用 Capivasertib (40 nM-50 µM) 处理 72 h，使用 SRB Assay 检测细胞活力。结果：Capivasertib 对 HGS27、AGS、N87、SNU-1、MKN45、MGC803 细胞的 IC50 分别为 4.6/0.1/14.18/24.04/30.0/44.4 µM。[1] 方法：乳腺癌细胞 BT474c 和前列腺癌细胞 LNCaP 用 Capivasertib (0.03-10 µmol/L) 处理 2 h，使用 Western Blot 检测靶点蛋白表达水平。结果：Capivasertib 有效地抑制了细胞系中 S6 和 4E-BP1 的磷酸化，而它在 ser473 和 thr308 处增加了 AKT 的磷酸化。[2]
体内活性	方法：为检测体内抗肿瘤活性，将 Capivasertib (100-300 mg/kg，10% DMSO 25% w/v Kleptose HPB buffer) 灌胃给药给携带乳腺癌肿瘤 BT474c 的 nude 小鼠，每天两次，持续两周。结果：Capivasertib 在体内剂量依赖性抑制人肿瘤异种移植物的生长。[2] 方法：为检测体内抗肿瘤活性，将 Capivasertib (100-300 mg/kg，10% DMSO 25% w/v Kleptose HPB buffer) 灌胃给药给 PDGCX 小鼠模型，每天两次，持续二十天。结果：Capivasertib 单药治疗的肿瘤生长抑制率为 60%。[3]
激酶实验	The ability of AZD5363 to inhibit the activity of AKT1, AKT2 and AKT3 was evaluated by the Caliper Off-Chip Incubation Mobility Shift Assay. Active recombinant AKT1, AKT2, or AKT3 were incubated with a 5-FAM-labeled custom-synthesized peptide substrate together with increasing concentrations of inhibitor. Final reactions contained 1 to 3 nmol/L AKT1, AKT2, or AKT3 enzymes; 1.5 μmol/L peptide substrate; ATP at Km for each AKT isoform; 10 mmol/L MgCl2, 4 mmol/L dithiothreitol (DTT), 100 mmol/L HEPES, and 0.015% Brij-35. The reactions were incubated at room temperature for 1 hour and stopped by the addition of a buffer containing 100 mmol/L HEPES, 0.015% Brij-35 solution, 0.1% coating reagent, 40 mmol/L EDTA, and 5% DMSO. Plates were then analyzed using a Caliper LC3000, allowing for separation of peptide substrate and phosphorylated product by electrophoresis with subsequent detection and quantification of laser-induced fluorescence. To determine the kinase selectivity profile, AZD5363 was also tested against PKA, ROCK1, ROCK2, and P70S6K. PKA, ROCK1, and ROCK2 activity were determined by Caliper Off-Chip Incubation Mobility Shift Assay, as described earlier. Final reaction conditions for measuring ROCKI activity were 5 nmol/L active recombinant ROCK1, 1.5 μmol/L fluorescein isothiocyanate (FITC)-labeled custom peptide substrate, 7 μmol/L ATP, 1 mmol/L DTT, 5 mmol/L MgCl2, 100 mmol/L HEPES, 0.015% Brij-35, and 5 mmol/L β-glycerophosphate; final reaction for measuring ROCK2 activity contained 7.5 nmol/L active recombinant ROCK2, 1.5 μmol/L FAM-labeled custom peptide substrate, 7.5 μmol/L ATP, 1 mmol/L DTT, 10 mmol/L MgCl2, 100 mmol/L HEPES, 0.015% Brij-35, and 5 mmol/L β-glycerophosphate; and protein kinase A (PKA) activity was measured in a final reaction containing 0.0625 nmol/L PKA, 3 μmol/L FITC-labeled custom peptide substrate, 4.6 μmol/L ATP, 1 mmol/L DTT, 10 mmol/L MgCl2, 110 mmol/L HEPES, and 0.015% Brij-35.P70S6K activity was measured by a radioactive (33P-ATP) filter-binding assay. Recombinant S6K1 (T412E) was assayed against a substrate peptide (KKRNRTLTV) in a final volume of 25.5 μL containing 8 mmol/L MOPS, 200 μmol/L EDTA, 100 μmol/L substrate peptide, 10 mmol/L magnesium acetate, 20 μmol/L γ-33P-ATP (50–1,000 cpm/pmol), and increasing concentrations of AZD5363. The reactions were incubated for 30 minutes at room temperature and terminated by the addition of 0.5 mol (3%) orthophosphoric acid. Reactions were then harvested onto a P81 UniFilter and product formation quantified. IC50 values for all enzyme assays were obtained by fitting data in Origin 7.0.
细胞实验	A high-throughput screening cell-based assay was developed to measure cellular AKT activity using the MDA-MB-468 breast cancer cell line. Cells were exposed to AZD5363 at concentrations ranging from 3 to 0.003 μmol/L. After a 2-hour treatment, cells were fixed with formaldehyde, washed, permeabilized with 0.5% polysorbate 20 and then probed with a phospho-specific antibody against GSK3βser9. Levels of phosphorylated GSK3βser9 were measured with an Acumen Explorer laser scanning cytometer and IC50 values estimates by fitting data in Origin 7.0.
动物实验	When mean tumor sizes reached approximately 0.2 cm^3, the mice were randomized into control and treatment groups. The treatment groups received varying dose schedules of AZD5363 solubilized in a 10% DMSO 25% w/v Kleptose HPB buffer by oral gavage, docetaxel solubilized in 2.6% ethanol in injectable water by intravenous injection once on day 1 at 15 or 5 mg/kg once weekly. When administered in combination, docetaxel was administered 1 hour before the oral dose of AZD5363. The control group received the DMSO/Kleptose buffer alone, twice daily by oral gavage. Tumor volumes (measured by caliper), animal body weight, and tumor condition were recorded twice weekly for the duration of the study. Mice were sacrificed by CO2 euthanasia. The tumor volume was calculated (taking length to be the longest diameter across the tumor and width to be the corresponding perpendicular diameter) using the formula: (length × width) × √(length × width) × (π/6). Growth inhibition from the start of treatment was assessed by comparison of the differences in tumor volume between control and treated groups. Because the variance in mean tumor volume data increases proportionally with volume (and is therefore disproportionate between groups), data were log transformed to remove any size dependency before statistical evaluation. Statistical significance was evaluated using a one-tailed, 2-sample t-test.

别名	AZD5363
分子量	428.92
分子式	C21H25ClN6O2
CAS No.	1143532-39-1

存储

Powder: -20°C for 3 years | In solvent: -80°C for 1 year

溶解度

Ethanol: 1 mg/mL

DMSO: 80 mg/mL (186.5 mM)

H2O: Insoluble

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	2.3314 mL	11.6572 mL	23.3144 mL	58.2859 mL
	5 mM	0.4663 mL	2.3314 mL	4.6629 mL	11.6572 mL
	10 mM	0.2331 mL	1.1657 mL	2.3314 mL	5.8286 mL
	20 mM	0.1166 mL	0.5829 mL	1.1657 mL	2.9143 mL
	50 mM	0.0466 mL	0.2331 mL	0.4663 mL	1.1657 mL
	100 mM	0.0233 mL	0.1166 mL	0.2331 mL	0.5829 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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参考文献

1. Wang J, et al. Ceritinib increases sensitivity of AKT inhibitors to gastric cancer. Eur J Pharmacol. 2021 Apr 5;896:173879. 2. Davies BR, et al. Preclinical pharmacology of AZD5363, an inhibitor of AKT: pharmacodynamics, antitumor activity, and correlation of monotherapy activity with genetic background. Mol Cancer Ther. 2012 Apr;11(4):873-87. 3. Li J, et al. The AKT inhibitor AZD5363 is selectively active in PI3KCA mutant gastric cancer, and sensitizes a patient-derived gastric cancer xenograft model with PTEN loss to Taxotere. J Transl Med. 2013 Oct 2;11:241. 4. Weng Q, Zhao M, Zheng J, et al. STAT3 dictates β-cell apoptosis by modulating PTEN in streptozocin-induced hyperglycemia[J]. Cell Death & Differentiation. 2020, 27(1): 130-145.

文献引用

1. Weng Q, Zhao M, Zheng J, et al. STAT3 dictates β-cell apoptosis by modulating PTEN in streptozocin-induced hyperglycemia. Cell Death & Differentiation. 2020, 27(1): 130-145 2. Liu Q, Miao Y, Wang X, et al. Structure-based virtual screening and biological evaluation of novel non-bisphosphonate farnesyl pyrophosphate synthase inhibitors. European Journal of Medicinal Chemistry. 2019: 111905 3. Wang J, Xu X, Wang T, et al. Ceritinib increases sensitivity of AKT inhibitors to gastric cancer. European Journal of Pharmacology. 2021: 173879. 4. Wang J, Xu X, Wang T, et al. Ceritinib increases sensitivity of AKT inhibitors to gastric cancer. European Journal of Pharmacology. 2021: 173879. 5. Bing S, Xiang S, Xia Z, et al.AKT inhibitor Hu7691 induces differentiation of neuroblastoma cells.Acta Pharmaceutica Sinica B.2023 6. Zhang W, Li X, Jiang M, et al.SOCS3 deficiency-dependent autophagy repression promote the survival of early-stage myeloid-derived suppressor cells in breast cancer by activating the Wnt/mTOR pathway.Journal of Leukocyte Biology.2023: qiad020.

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

Capivasertib 1143532-39-1 Autophagy Cytoskeletal Signaling PI3K/Akt/mTOR signaling Tyrosine Kinase/Adaptors Akt PKA mTOR AZD5363 Inhibitor inhibit AZD 5363 PKB AZD-5363 Protein kinase B inhibitor

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Capivasertib

存储

溶解度

溶液配制表

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参考文献

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剂量换算

体内实验配液计算器

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