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Etoposide

产品编号 T0132 CAS 33419-42-0

别名: VP-16-213, 依托泊苷, VP-16, 依托泊甙

Etoposide 通过与拓扑异构酶 II 和 DNA 形成复合物来抑制 DNA 合成 (IC50: 60.3 μM)。

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Etoposide, CAS 33419-42-0

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天然产物信息

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化学信息

存储 & 溶解度

参考文献

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植物来源	天然产物 > 小檗科 > 八角莲属
结构类型	天然产物 > 木脂素

产品描述	Etoposide inhibits DNA synthesis by forming a complex with topoisomerase II and DNA (IC50: 60.3 μM).
靶点活性	Topo II:60.3 μM
体外活性	Etoposide inhibits proliferation of a variety of adenocarcinoma cells (IC50s: 0.005-12,200 μM) and HUVEC cells (IC50: 0.249 μM) [2]. Etoposide is capable of causing cytotoxicity on pancreatic β-cells by inducing apoptosis through the JNK/ERK-mediated GSK-3 downstream-triggered mitochondria-dependent signaling pathway in RIN-m5F cells [1].
体内活性	Etoposide (25 mg/kg) reduces tumor growth in a Ma human embryonal carcinoma mouse xenograft model [3]. Etoposide (10 mg/kg/day, i.v.) with ifosfamide and carboplatin, reduces the tumor volume in the hepatoblastoma cell injected NMRI nude mice [4].
激酶实验	Nuclear extracts are prepared, and nuclei are isolated. The activity of topoisomerase II is calculated from the percentage of decatenation obtained. Tritiated kinoplast DNA (KDNA 0.22 μg) is used as a substrate. Etoposide and topoisomerase II are incubated for 30 min at 37 ℃ and are stopped with 1% sodium dodecyl sulfate (SDS) and proteinase K (100 μg/mL). The percentages of decatenation and inhibition of topoisomerase II by Etoposide are obtained [5].
细胞实验	After the Etoposide treatment, cells are removed from the dish with phosphate-buffered saline (PBS) containing 0.03% trypsin and 0.27 mM ethylenediaminetetraacetic acid (EDTA) and are diluted into culture dishes in appropriate numbers to yield between 20 and 200 colonies. After 12 days, cultures are fixed with methanol-acetic acid, stained with crystal violet, and scored for colonies containing more than 50 cells [5].
动物实验	The in vivo model for nude mice HB (NMHB) has been established. Only HB cells with embryonal components are grafted and reproduced successfully in this model. Each NMHB subsequently is transplanted into 50 mice for treatment groups. Treatment is initiated when the majority of the tumors reach a volume of 50-100 mm3. The mice are stratified according to their tumor volume and randomly assigned to groups of ten animals each. The animals injected with tumor are given ifosfamide, cisplatin, doxorubicin, etoposide (10 mg/kg/day, i.v.), and carboplatin as single agents in two blocks. One group of ten animals for each original xenograft served as a control group. After initiation of treatment, the tumor growth is recorded at 5-day intervals for 25-30 days and the relative tumor volumes are calculated. Twenty-four hours before the animals are sacrificed, bromodeoxyuridine (BrdU) is injected intraperitoneally for the semiquantitative determination of proliferation activity of the tumor cells (50 μg of BrdU/g body weight) [4].

别名	VP-16-213, 依托泊苷, VP-16, 依托泊甙
分子量	588.56
分子式	C29H32O13
CAS No.	33419-42-0

存储

Powder: -20°C for 3 years | In solvent: -80°C for 2 years

溶解度

DMSO: 58.9 mg/mL (100 mM)

( < 1 mg/mL refers to the product slightly soluble or insoluble )

参考文献

1. Chen GL, et al. Nonintercalative antitumor drugs interfere with the breakage-reunion reaction of mammalian DNA topoisomerase II. J Biol Chem. 1984 Nov 10;259(21):13560-6. 2. Drevs J, et al. Antiangiogenic potency of various chemotherapeutic drugs for metronomic chemotherapy. Anticancer Res. 2004 May-Jun;24(3a):1759-63. 3. Osieka R, et al. Enhancement of etoposide-induced cytotoxicity by cyclosporin A. Cancer Chemother Pharmacol. 1986;18(3):198-202. 4. Fuchs, J., et al. Comparative activity of cisplatin, ifosfamide, doxorubicin, carboplatin, and etoposide in heterotransplanted hepatoblastoma. Cancer, 1998. 83(11): p. 2400-7. 5. Beauchesne P, et al. Etoposide sensitivity of radioresistant human glioma cell lines. Cancer Chemother Pharmacol. 1998;41(2):93-7. 6. Lee KI, et al. Etoposide induces pancreatic β-cells cytotoxicity via the JNK/ERK/GSK-3 signaling-mediated mitochondria-dependent apoptosis pathway. Toxicol In Vitro. 2016 Jul 26. pii: S0887-2333(16)30147-3. 7. Calvani M, det al. Etoposide-Bevacizumab a new strategy against human melanoma cells expressing stem-like traits. Oncotarget. 2016 Jun 9. doi: 10.18632/oncotarget.9939. 8. Zhang J, Hirst A J, Duan F, et al. Darren Robinson, 3 Mark Jones, 2 Le Li, 4 Peizhe Wang, Peng Jiang, 4 Peter W. Andrews, 2 Ivana Barbaric, 2,* and Jie Na[J]. Anti-apoptotic Mutations Desensitize Human Pluripotent Stem Cells to Mitotic Stress and Enable Aneuploid Cell Survival. Stem Cell Reports. 9. Ruan C, Wang C, Gong X, et al. An integrative multi-omics approach uncovers the regulatory role of CDK7 and CDK4 in autophagy activation induced by silica nanoparticles[J]. Autophagy. 2020. 10. Weizhe Li, Hong-Yan Wang, Xiaolu Zhao, Hongguo Duan, Binghua Cheng, Yafei Liu, Mengjie Zhao et al. A methylation-phosphorylation switch determines Plk1 kinase activity and function in DNA damage repair [J]. Science Advances. 2019 Mar 6;5(3):eaau7566.

文献引用

1. Yang C, Xu H, Yang D, et al.A renal YY1-KIM1-DR5 axis regulates the progression of acute kidney injury.Nature Communications.2023, 14(1): 4261. 2. Qu Y Q, Song L L, Xu S W, et al.Pomiferin targets SERCA, mTOR, and P-gp to induce autophagic cell death in apoptosis-resistant cancer cells, and reverses the MDR phenotype in cisplatin-resistant tumors in vivo.Pharmacological Research.2023: 106769. 3. Wang D, Wang Y, Di X, et al.Cortical tension drug screen links mitotic spindle integrity to Rho pathway.Current Biology.2023 4. Ruan C, Wang C, Gong X, et al. An integrative multi-omics approach uncovers the regulatory role of CDK7 and CDK4 in autophagy activation induced by silica nanoparticles. Autophagy. 2020 5. Yang G, Wan P, Xiang Q, et al. E3 Ubiquitin Ligase ASB17 Promotes Apoptosis by Ubiquitylating and Degrading BCLW and MCL1. Biology-Basel. 2021, 10(3): 234. 6. Feng J, Xi Z, Jiang X, et al. Saikosaponin a enhances Docetaxel efficacy by selectively inducing death of dormant prostate cancer cells through excessive autophagy. Cancer Letters. 2022: 216011. 7. Li W, Wang H Y, Zhao X, et al. A methylation-phosphorylation switch determines Plk1 kinase activity and function in DNA damage repair. Science Advances. 2019, 5(3): eaau7566 8. Zhang J, Hirst A J, Duan F, et al. Darren Robinson, 3 Mark Jones, 2 Le Li, 4 Peizhe Wang, Peng Jiang, 4 Peter W. Andrews, 2 Ivana Barbaric, 2,* and Jie Na[J]. Anti-apoptotic Mutations Desensitize Human Pluripotent Stem Cells to Mitotic Stress and Enable Aneuploid Cell Survival. Stem Cell Reports. 2019, 12(3): 557-571 9. Kong Y, Liu Y, Li X, et al.Palmitoylation landscapes across human cancers reveal a role of palmitoylation in tumorigenesis.Journal of Translational Medicine.2023, 21(1): 1-19. 10. Wu X, Yi X, Zhao B, et al.The volume regulated anion channel VRAC regulates NLRP3 inflammasome by modulating itaconate efflux and mitochondria function.Pharmacological Research.2023: 107016.

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。

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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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浓度

容积

分子量

浓度 (起始)

容积 (起始)

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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

Etoposide 33419-42-0 Apoptosis Autophagy DNA Damage/DNA Repair Microbiology/Virology Mitophagy Antibiotic Antibacterial Topoisomerase P388 HCT116 p53 chemotherapy Mitochondrial Autophagy FBXW Inhibitor anti-cancer VP-16-213 inhibit VP 16 Bacterial 依托泊苷 VP-16 prodrug 依托泊甙 VP16 leukemia inhibitor

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Etoposide

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