Etoposide
製品コードS1225 別名：VP-16, VP-16213
分子量(MW)：588.56
Etoposide is a semisynthetic derivative of podophyllotoxin, which inhibits DNA synthesis via topoisomerase II inhibition activity.
カスタマーフィードバック(6)
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ABT-199 synergizes strongly with lymphoma chemotherapy agents that affect MCL1 levels. Viability and CI vs Fa after 24-h exposure to etoposide alone or in combination with ABT-199 in Riva, U2932 and VavP-Bcl2/c-MYC murine tumor cells. Viability shown at 500 nM.
Leukemia, 2015, 29: 1702–1712. Etoposide purchased from Selleck.
Dox promotes formation of DNA DSBs in primary neurons. (A) Cortical neurons at 28–32 DIV were treated with a vehicle or with Dox (0.1 μ M) or with DNA damaging drug etoposide (5 μ M) overnight, fixed, and stained for a marker of DSBs phosphorylated histone H2A variant X, γ H2A.X (green), MAP2c (red), and with the nuclear Hoechst dye (blue), and imaged. The neuronal nucleus is enlarged on the Dox panel to illustrate the γ H2A.X puncta. Note the green nuclear staining in cells treated with Dox and etoposide. Also note the reduced dendritic arborization in neurons treated with Dox and etoposide. Scale bar is 20 μm.
Sci Rep, 2016, 6:25705.. Etoposide purchased from Selleck.
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Viability of U87 cells(C) assessed by the Alamar blue assay, 72 h after transfection with siRNA anti-survivin (siSURV) or with siMUT and/or cell incubation with the chemotherapeutical drugs etoposide (ETO) and Bliss interaction index (D) determined for the combined effects on cell viability of survivin silencing plus treatment with each drug. Cells were transfected, for 4 h, with (14Ser)2N5/siRNA/HL complexes and, after an additional period of 20 h, cells were incubated with 1.5 μM ETO (C) for 48 h. Results, representative of at least three independent experiments, are expressed as a percentage of the nontreated control cells. Combined treatment (dotted bar) was compared with the single drug treatment (gray bar) (**p < 0.01, ***p < 0.001) and the Bliss interaction index of each combined treatment was compared with the theoretical value expected for an additive effect (1.0) (#p < 0.05, ns, non-significant).
Eur J Pharm Biopharm, 2016, 104:7-19.. Etoposide purchased from Selleck.
Cellular biomarker responses in HT29 cells exposed to various cytotoxic chemotherapeutic agents in combination with the Chk1 inhibitor V158411. HT29 cells were exposed to the combination GI80 of gemcitabine (0.2 uM), camptothecin (0.44 uM), cisplatin (68 uM), oxaliplatin (131 uM), doxorubicin (1.2 uM) or etoposide (59 uM) for 18 hours followed by DMSO (-) or 400 nM V158411 (+) for a further 24 hours. Protein expression was characterized by immunoblotting.
BMC Cancer 2014 14, 483. Etoposide purchased from Selleck.
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(c) and (d) Effects of fractions C4 and C5 on topoisomerase II activity. Topoisomerase II activity was measured by plasmid DNA cleavage assay. DNA bands were visualized using UV light and the intensity of linear DNA band in each lane was measured using imageJ software. Lane 1: plasmid PBR322DNA. Lane 2: control, topoisomerase II + plasmid PBR322DNA. Lanes 3, 4, and 5: 40, 20, and 10 μg/mL fraction C4 + plasmid PBR322DNA, respectively. Lanes 6, 7, and 8: 40, 20, and 10 μg/mL fraction C5 + plasmid PBR322DNA, respectively. Lane 9: 100 μM etoposide + plasmid PBR322DNA. The data in different groups were expressed as the mean ± SD from 3 experiments. Statistical difference between groups was assessed by t-test using SPSS 20.0. ∗∗P < 0.01 versus the control group.
Evid Based Complement Alternat Med, 2017, 2017:1456786. Etoposide purchased from Selleck.
Effects of etoposide on the radiosensitivities of cholangiocarcinoma cell lines. The cell survival curves of (A) KKU-M055 and (B) KKU-M214 cells were obtained from clonogenic survival assays. The cells were treated with X-ray irradiation or etoposide (0.025 or 0.05 µg/ml) alone or pretreated with etoposide for 24 h prior to X-ray irradiation. Survival fractions were determined at day 10 following X-ray irradiation. The dose-response curves depict the mean ± standard deviation of survival fractions of three independent experiments. IR, irradiation.
Oncol Lett, 2018, 15(3):3895-3903. Etoposide purchased from Selleck.
製品安全説明書
Topoisomerase阻害剤の選択性比較
生物活性
| 製品説明 | Etoposide is a semisynthetic derivative of podophyllotoxin, which inhibits DNA synthesis via topoisomerase II inhibition activity. | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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| 体外試験 |
Etoposide inhibits DNA synthesis by forming a complex with topoisomerase II and DNA, which induces breaks in double stranded DNA and prevents repair by topoisomerase II binding. Accumulated breaks in DNA prevent entry into the mitotic phase of cell division, and lead to cell death. Etoposide acts primarily in the G2 and S phases of the cell cycle. [1] Etoposide inhibits the growth of murine angiosarcoma cell line (ISOS-1) in a 5 days-period with IC50 of 0.25 μg/mL. Cell growth of normal murine microvascular endothelial cells (mECs) is less sensitive to Etoposide with IC50 of 10 μg/mL). [2] Etoposide treated for 6 hr inhibits colonies of tetraploid variant of the human leukemic lymphoblast line CCRF-CEM with IC50 of 0.6 μM. [3] Etoposide treated for 2 hr inhibits growth of human pancreatic cancer cell line Y1, Y3, Y5, Y19, YM. YS, and YT with IC50s of 300 μg/mL, 300 μg/mL, 300 μg/mL, 91 μg/mL, 0.68 μg/mL, 300 μg/mL, 300 μg/mL, and 260 μg/mL, respectively. [4] Etoposide exposed for 1 hr inhibits growth of human glioma cell lines CL5, G142, G152, G111, and G5 with IC50 of 8, 9, 9.8, 10, and 15.8 μg/mL respectively for 12 days. Under same condition, the IC90 value is attained in cell lines CL5, G152, G142, and G111 at 26, 27, 32, and 33 μg/mL. Etoposide inhibition of topoisomerase II is homogeneous for each cell. The average inhibition rates are 15%, 21.8%, 31.8%, 41.5%, and 49.5% for 1, 2, 4, 8, and 16 μg Etoposide, respectively. [5] |
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| 細胞データ |
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| 体内試験 | Etoposide administrated as a single agent is found to been ineffective in many xenografts growth, such as Heterotransplanted Hepatoblastoma NMHB1, and NMHB 2, [6] human neuroblastoma xenograft, [7] and human gastrointestinal cancer xenograft, [8] while the dose of 10 mg/kg i.p. Etoposide inhibits murine angiosarcoma cell ISOS-1 tumors in 36% of controls. [2] Etoposide induces tumor immunity in Lewis lung cancer. A single administration of 50 mg/kg Etoposide i.p., induces a 60% survival of C57B1/6 mice injected with Lewis lung cancer cell (3LL) over 60 days. About 40% of these surviving mice reject a subsequent challenge with 3LL, while none of control mice survive beyond 30 days. 3LL cells which have survived an 90% lethal concentration of Etoposide in vitro kill 75% of recipient mice, but 60% surviving mice reject challenge with 3LL. Splenocytes harvested from tumor rejecting mice protect naive mice injected with 3LL. [9] |
お薦めの試験操作（参考用のみ）
| キナーゼ試験：[5] |
+ 展開
Topoisomerase II activity assay: 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. |
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| 細胞試験： [5] |
+ 展開
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| 動物試験：[2] |
+ 展開
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参考
- [1] van Maanen JM et al, J Natl Cancer Inst, 1988, 80(19), 1526-1533.
- [2] Ma G, et al. J Dermatol Sci, 2000, 24(2), 126-133.
- [3] Kalwinsky DK, et al. Cancer Res, 1983, 43(4), 1592-1597.
- [4] Slater LM, et al. Cancer Chemother Pharmacol, 2001, 48(4), 327-332.
- [5] Beauchesne P, et al. Cancer Chemother Pharmacol, 1998, 41(2), 93-97.
- [6] Fuchs J, et al. Cancer, 1998, 83(11), 2400-2407.
- [7] Kaneko M, et al. Gan To Kagaku Ryoho, 1991, 18(7), 1155-1161.
- [8] Nagai S, et al. J Surg Oncol, 1993, 54(4), 211-215.
- [9] Slater LM, et al. Cancer Chemother Pharmacol, 2001, 48(4), 327-332.
溶解度 (25°C)
| 体外 | DMSO | 100 mg/mL (169.9 mM) |
|---|---|---|
| Water | Insoluble | |
| Ethanol | Insoluble | |
| 体内 |
左から（NMPから）右の順に溶剤を製品に加えます(文献ではなく、Selleckの実験によるデータ): 5% DMSO+30% PEG 300+H2O 混合させたのち直ちに使用することを推奨します。 |
15mg/mL |
* 溶解度測定はSelleck技術部門によって行われており、その他文献に示されている溶解度と差異がある可能性がありますが、同一ロットの生産工程で起きる正常な現象ですからご安心ください。
化学情報
| 分子量 | 588.56 |
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| 化学式 | C29H32O13 |
| CAS No. | 33419-42-0 |
| 保管 | 粉 |
| in solvent | |
| 別名 | VP-16, VP-16213 |
便利ツール
モル濃度計算器
求めたい質量、体積または濃度を計算してください。
質量 (g) = 濃度 (mol/L) x 体積 (L) x 分子量 (g/mol)
モル濃度計算器方程式
*貯蔵液を準備するとき、常に、オンであるとわかる製品のバッチに特有の分子量を使って、を通してラベルとMSDS/COA（製品ページで利用可能な）。
希釈計算器
貯蔵液を準備するために必要な希釈率を計算してください。Selleck希釈計算器は、以下の方程式に基づきます：
開始濃度 x 開始体積 = 最終濃度 x 最終体積
希釈の計算式
この方程式は、一般に略語を使われます：C1V1 = C2V2 ( 入力 出力 )
常に貯蔵液を準備するとき、小びんラベルとMSDS/COA（オンラインで利用できる）で見つかる製品のバッチに特有の分子量を使ってください。
分子量计算器
そのモル質量と元素組成を計算するために、合成物の化学式を入力してください：
チップス: 化学式は大文字と小文字の区別ができます。C10H16N2O2 c10h16n2o2
モル濃度計算器
臨床試験
| NCT Number | Recruitment | Conditions | Sponsor/Collaborators | Start Date | Phases |
|---|---|---|---|---|---|
| NCT03583424 | Recruiting | Hematopoietic Cell Transplantation Recipient|Recurrent Diffuse Large B-Cell Lymphoma|Recurrent Grade 1 Follicular Lymphoma|Recurrent Grade 2 Follicular Lymphoma|Recurrent Grade 3 Follicular Lymphoma|Recurrent Marginal Zone Lymphoma|Recurrent Non-Hodgkin Lymphoma|Refractory Diffuse Large B-Cell Lymphoma|Refractory Follicular Lymphoma|Refractory Marginal Zone Lymphoma|Refractory Non-Hodgkin Lymphoma|Refractory Transformed Indolent Non-Hodgkin Lymphoma | Ohio State University Comprehensive Cancer Center|National Cancer Institute (NCI) | July 9 2018 | Phase 1|Phase 2 |
| NCT03126916 | Recruiting | Childhood Ganglioneuroblastoma|Childhood Neuroblastoma|INRG Stage L2|INRG Stage M|INRG Stage MS|NMYC Gene Amplification|Recurrent Neuroblastoma | Children''s Oncology Group|National Cancer Institute (NCI) | May 9 2018 | Phase 3 |
| NCT03519971 | Recruiting | Non-Small Cell Lung Cancer | AstraZeneca | April 9 2018 | Phase 3 |
| NCT03407144 | Recruiting | Hodgkin Lymphoma | Merck Sharp & Dohme Corp. | April 9 2018 | Phase 2 |
| NCT03136146 | Recruiting | Hematopoietic/Lymphoid Cancer|Acute Lymphoblastic Leukemia|Lymphoblastic Lymphoma|Burkitt Leukemia/Lymphoma | M.D. Anderson Cancer Center | August 9 2017 | Phase 2 |
| NCT03432598 | Recruiting | Locally Advanced or Metastatic Lung Cancer | BeiGene | August 9 2017 | Phase 2 |
技術サポート
ストックの作り方、阻害剤の保管方法、細胞実験や動物実験の際に注意すべき点など、製品を取扱う時に問い合わせが多かった質問に対しては取扱説明書でお答えしています。
他に質問がある場合は、お気軽にお問い合わせください。
よくある質問（FAQ）
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質問1：
Regarding the Etoposide S1225, do you have any data of the inhibition sepcificity of this product? It will inhibit other enzymes other than TOP2A?
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回答：
According to the available published data, the inhibition of Etoposide is specific to TOP2A. But there're also two papers showing that Etoposide could inhibit the p34cdc2 Kinase Activity: 1. http://cancerres.aacrjournals.org/content/52/7/1817.short ; 2. http://cancerres.aacrjournals.org/content/50/12/3761.short.
