Aurora Kinase Inhibitor II
(Synonyms: 4-(4-Benzamidoanilino)-6,7-dimethoxyquinazoline) 目录号 : GC40667Blocks Aurora A kinase activity
Cas No.:331770-21-9
Sample solution is provided at 25 µL, 10mM.
Quality Control & SDS
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- Purity: >99.00%
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- SDS (Safety Data Sheet)
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The Aurora kinases are a family of serine/threonine kinases that are key regulators of mitosis and cytokinesis. Aurora kinase inhibitor II is a cell-permeable anilinoquinazoline that blocks the activity of Aurora A (IC50 = 0.39 µM). In MCF-7 cells, it blocks proliferation with an IC50 value of 1.25 µM.
Cas No. | 331770-21-9 | SDF | |
别名 | 4-(4-Benzamidoanilino)-6,7-dimethoxyquinazoline | ||
Canonical SMILES | COC1=C(OC)C=C(C(NC2=CC=C(NC(C3=CC=CC=C3)=O)C=C2)=NC=N4)C4=C1 | ||
分子式 | C23H20N4O3 | 分子量 | 400.4 |
溶解度 | DMF: 0.25 mg/ml,DMF:PBS(pH7.2) (1:2): 0.33 mg/ml,DMSO: 2.5 mg/ml | 储存条件 | 4°C, protect from light |
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。 |
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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 | 2.4975 mL | 12.4875 mL | 24.975 mL |
5 mM | 0.4995 mL | 2.4975 mL | 4.995 mL |
10 mM | 0.2498 mL | 1.2488 mL | 2.4975 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 | ||||||||||
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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。
miR-331-3p and Aurora Kinase Inhibitor II co-treatment suppresses prostate cancer tumorigenesis and progression
Oncotarget 2017 Jun 27;8(33):55116-55134.PMID:28903407DOI:10.18632/oncotarget.18664.
RNA-based therapeutics could represent a new avenue of cancer treatment. miRNA 331-3p (miR-331-3p) is implicated in prostate cancer (PCa) as a putative tumor suppressor, but its functional activity and synergy with other anti-tumor agents is largely unknown. We found miR-331-3p expression in PCa tumors was significantly decreased compared to non-malignant matched tissue. Analysis of publicly available PCa gene expression data sets showed miR-331-3p expression negatively correlated with Gleason Score, tumor stage, lymph node involvement and PSA value, and was significantly down regulated in tumor tissue relative to normal prostate tissue. Overexpression of miR-331-3p reduced PCa cell growth, migration and colony formation, as well as xenograft tumor initiation, proliferation and survival of mice. Microarray analysis identified seven novel targets of miR-331-3p in PCa. The 3'-untranslated regions of PLCγ1 and RALA were confirmed as targets of miR-331-3p, with mutation analyses confirming RALA as a direct target. Expression of miR-331-3p or RALA siRNA in PCa cells reduced RALA expression, proliferation, migration and colony formation in vitro. RALA expression positively correlated with Gleason grade in two separate studies, as well as in a PCa tissue microarray. Co-treatment using siRALA with an Aurora Kinase inhibitor (AKi-II) decreased colony formation of PCa cells while the combination of AKi-II with miR-331-3p resulted in significant reduction of PCa cell proliferation in vitro and PCa xenograft growth in vivo. Thus, miR-331-3p directly targets the RALA pathway and the addition of the AKi-II has a synergistic effect on tumor growth inhibition, suggesting a potential role as combination therapy in PCa.