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Saracatinib

Saracatinib

产品编号 T6078   CAS 379231-04-6
别名: AZD0530, 塞卡替尼

Saracatinib (AZD0530) 是一种有效的 Src 抑制剂,抑制 c-Src、Lck、c-YES、Lyn、Fyn、Fgr 和 Blk 的 IC50值在 2.7 到 11 nM 之间,对其他酪氨酸激酶具有选择性。

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Saracatinib Chemical Structure
Saracatinib, CAS 379231-04-6
规格 价格/CNY 货期 数量
10 mg ¥ 426 现货
25 mg ¥ 759 现货
50 mg ¥ 1,179 现货
100 mg ¥ 2,213 现货
1 mL * 10 mM (in DMSO) ¥ 472 现货
其他形式的 Saracatinib:
产品目录号及名称: Saracatinib (T6078)
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选择批次  
纯度: 99.63%
纯度: 98.55%
纯度: 98.31%
纯度: 98.03%
纯度: 98%
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生物活性
化学信息
存储 & 溶解度
参考文献
产品描述 Saracatinib (AZD0530) (AZD0530) is an effective Src inhibitor (IC50: 2.7 nM), and effective to Lck, Fyn, Lyn, Blk, Fgr and c-Yes.
靶点活性 c-YES:4 nM (cell free), EGFR L858R:5 nM (cell free), EGFR L861Q:4 nM (cell free), c-Src:2.7 nM (cell free), Lyn:5 nM (cell free), Lck:<4 nM (cell free)
体外活性 Saracatinib (AZD0530) potently inhibited the in vitro proliferation of Src3T3 mouse fibroblasts and demonstrated variable antiproliferative activity in a range of human cancer cell lines containing endogenous Src. Sub-micromolar growth inhibition of five of the human cancer cell lines tested with AZD0530 (tumor types: colon, prostate, lung, and leukemia) was observed with IC50 values of 0.2–0.7μM. In 3‐day MTS cell proliferation assays, AZD0530 inhibited in vitro proliferation of the Bcr–Abl‐driven human leukemia cell line K562 with an IC50 of 0.22μM [1]. VS cells were cultured with cabozantinib (2 μmol/L) and saracatinib (2 μmol/L), alone or in combination, for 48 hours. For both VS01 and VS02, the combination treatment reduced VS cell viability by approximately 35%–40% compared with vehicle (0.3% DMSO) and was significantly more effective than saracatinib alone [2]. In DU145 and PC3, AZD0530 inhibited Src activation in a dose-dependent manner. Src inhibition by AZD0530 was also rapid, within 5 min of treatment. A single treatment with AZD0530 resulted in a dose-dependent decrease in the number of cells in all cell lines. LAPC-4 is the most resistant against AZD0530 among prostate cancer cell lines. Immortalized nonmalignant cell lines PZ-HPV7 and RWPE-1 are also on average more resistant to Src inhibition than cancer cell lines [3].
体内活性 AZD0530 treatment potently inhibited the proliferation of subcutaneously transplanted Src3T3 fibroblasts in mice and rats in a dose‐dependent manner. In both models, significant inhibition of tumor growth was seen at doses ≥6mg/kg/day (60% inhibition in mice and 98% inhibition in rats versus animals treated with vehicle) and, at the maximum doses investigated, complete tumor growth inhibition was observed (100% inhibition at 25mg/kg/day in mice and 10mg/kg/day in rats) [1]. Mice were assigned into vehicle, cabozantinib (12.5 mg/kg/day), saracatinib (25 mg/kg/day), and combination (cabozantinib and saracatinib at 12.5 mg/kg/day and 25 mg/kg/day, respectively) treatment cohorts. bioluminescence imaging (BLI) showed that grafts in the combination-treated group had a significantly slower growth rate compared with those in the single-agent groups. Although the vehicle-treated allografts had a 160-fold increase in BL signal over 14 days, the grafts treated with saracatinib or cabozantinib had a 50- and 60-fold increase in BL signal, respectively. Significantly, the allografts from the combination group had only a 25-fold increase in BL signal after 14 days of treatment [2].
激酶实验 Inhibition of tyrosine kinase activity was examined using an ELISA with recombinant catalytic domains of a panel of receptor and non‐receptor tyrosine kinases (in some cases only part of the catalytic domain was used). This method has been described previously. AZD0530 dose ranges varied depending on the activity versus the particular kinase tested, but were typically 0.001–10μM. Specificity assays against a panel of serine/threonine kinases were performed using a filter capture assay with 32P. Briefly, multidrop 384 plates containing 0.5μL AZD0530 or controls (DMSO alone or pH 3.0 buffer controls) were incubated with 15μL of enzyme plus peptide/protein substrate for 5min before the reaction was initiated by the addition of 10μL of 20mM Mg.ATP. For all enzymes the final concentration was approximated to the Michaelis constant (Km). Assays were carried out for 30min at room temperature before termination by the addition of 5μL orthophosphoric acid. After mixing, the well contents were harvested onto a P81 Unifilter plate, using orthophosphoric acid as the wash buffer. Microcal Origin software was used to interpolate IC50 values by nonlinear regression [1].
细胞实验 Cell proliferation was assessed using a colorimetric 5‐bromo‐2′‐deoxyuridine (BrdU) Cell Proliferation ELISA kit, as described previously. Briefly, cells were plated onto 96‐well plates (1.5×10^4 cells/well), the following day 0.039–20μM AZD0530 in DMSO (at a final concentration of 0.5%) was added and the cells were incubated for 24h. The cells were pulse-labeled with BrdU for 2h and fixed. Cellular DNA was then denatured with the provided solution and incubated with anti-BrdU peroxidase for 90min. Following three washes with phosphate‐buffered saline, tetramethylbenzidine substrate solution was added and the plates were incubated on a plate shaker for 10–30min until the positive control absorbance at 690nm was approximately 1.5 absorbance units [1].
动物实验 Female athymic mice (nu/nu: Alpk) and rats (RH‐rnu/rnu) were housed and maintained as previously described. Src3T3 and human tumor lines (as indicated in Table 3) were inoculated subcutaneously in the left flank of animals. Tumor growth was monitored by bi‐dimensional caliper measurements twice weekly. The tumor volume was calculated by the following formula: (length×width)×√(length×width)×(π/6) and supported by excision and weighing of tumors at the end of the studies. Dosing started when the average tumor volume reached 0.2–0.5cm3 (except MDA‐MB‐231 and HT29). Animals were treated once daily by oral gavage with either vehicle alone or AZD0530 6.25–50mg/kg for 10–91 days. Tumor growth inhibition was calculated as described previously. For pharmacokinetic and pharmacodynamic analysis animals were humanely sacrificed and samples (plasma and tumor) were collected. Tumor samples were homogenized with 5 volumes of water and extracted with chloroform. Plasma and tumor samples were analyzed for AZD0530 concentration using high‐performance liquid chromatography with tandem mass spectrometric detection after solid‐phase extraction [1].
别名 AZD0530, 塞卡替尼
分子量 542.03
分子式 C27H32ClN5O5
CAS No. 379231-04-6

存储

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

溶解度

DMSO: 33 mg/mL (60.9 mM)

Ethanol: 29 mg/mL (53.5 mM)

溶液配制表

可选溶剂 浓度 体积 质量 1 mg 5 mg 10 mg 25 mg
DMSO / Ethanol 1 mM 1.8449 mL 9.2246 mL 18.4492 mL 46.1229 mL
5 mM 0.369 mL 1.8449 mL 3.6898 mL 9.2246 mL
10 mM 0.1845 mL 0.9225 mL 1.8449 mL 4.6123 mL
20 mM 0.0922 mL 0.4612 mL 0.9225 mL 2.3061 mL
50 mM 0.0369 mL 0.1845 mL 0.369 mL 0.9225 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. Green TP, et al. Preclinical anticancer activity of the potent, oral Src inhibitor AZD0530. Mol Oncol, 2009, 3(3), 248-261. 2. Fuse MA, et al. Combination Therapy With c-Met and Src Inhibitors Induces Caspase-Dependent Apoptosis of Merlin-Deficient Schwann Cells and Suppresses Growth of Schwannoma Cells. Mol Cancer Ther. Mol Cancer Ther. 2017 Nov;16(11):2387-2398. 3. Chang YM, et al. Src family kinase oncogenic potential and pathways in prostate cancer as revealed by AZD0530. Oncogene. 2008 Oct 23;27(49):6365-75.

文献引用

1. Yang S, Yang S, Zhang H, et al. Targeting Na+/K+‐ATPase by berbamine and ouabain synergizes with sorafenib to inhibit hepatocellular carcinoma. British Journal of Pharmacology. 2021 2. Li J, Liu X, Liu Y, et al.Saracatinib inhibits necroptosis and ameliorates psoriatic inflammation by targeting MLKL.Cell Death & Disease.2024, 15(2): 122.
Serclutamab BKI-1369 BEBT-109 EGFR/HER2/DHFR-IN-3 KI8751 EGFR/HER2/DHFR-IN-2 BGB-102 Lapatinib Ditosylate

相关化合物库

该产品包含在如下化合物库中:
酪氨酸激酶分子库 抗癌活性化合物库 神经退行性疾病化合物库 抗癌药物库 抗癌临床化合物库 JAK-STAT 化合物库 经典已知活性库 免疫/炎症分子化合物库 抗卵巢癌化合物库 临床期小分子药物库

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
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g
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
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% ddH2O
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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

Saracatinib 379231-04-6 Angiogenesis Autophagy JAK/STAT signaling Tyrosine Kinase/Adaptors BTK Src EGFR AZD0530 inhibit AZD-0530 Inhibitor 塞卡替尼 AZD 0530 inhibitor

 

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