Catalog No.S1225 Synonyms: VP-16, VP-16213
Molecular Weight(MW): 588.56
Etoposide is a semisynthetic derivative of podophyllotoxin, which inhibits DNA synthesis via topoisomerase II inhibition activity.
Cited by 14 Publications
6 Customer Reviews
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.
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.
(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.
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|Description||Etoposide is a semisynthetic derivative of podophyllotoxin, which inhibits DNA synthesis via topoisomerase II inhibition activity.|
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.  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).  Etoposide treated for 6 hr inhibits colonies of tetraploid variant of the human leukemic lymphoblast line CCRF-CEM with IC50 of 0.6 μM.  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.  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. 
|In vivo||Etoposide administrated as a single agent is found to been ineffective in many xenografts growth, such as Heterotransplanted Hepatoblastoma NMHB1, and NMHB 2,  human neuroblastoma xenograft,  and human gastrointestinal cancer xenograft,  while the dose of 10 mg/kg i.p. Etoposide inhibits murine angiosarcoma cell ISOS-1 tumors in 36% of controls.  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. |
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.
-  van Maanen JM et al, J Natl Cancer Inst, 1988, 80(19), 1526-1533.
-  Ma G, et al. J Dermatol Sci, 2000, 24(2), 126-133.
-  Kalwinsky DK, et al. Cancer Res, 1983, 43(4), 1592-1597.
-  Slater LM, et al. Cancer Chemother Pharmacol, 2001, 48(4), 327-332.
-  Beauchesne P, et al. Cancer Chemother Pharmacol, 1998, 41(2), 93-97.
-  Fuchs J, et al. Cancer, 1998, 83(11), 2400-2407.
-  Kaneko M, et al. Gan To Kagaku Ryoho, 1991, 18(7), 1155-1161.
-  Nagai S, et al. J Surg Oncol, 1993, 54(4), 211-215.
-  Slater LM, et al. Cancer Chemother Pharmacol, 2001, 48(4), 327-332.
|In vitro||DMSO||100 mg/mL (169.9 mM)|
|In vivo||Add solvents to the product individually and in order:
5% DMSO+30% PEG 300+H2O
For best results, use promptly after mixing.
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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT03036904||Not yet recruiting||Diffuse Large B-Cell Lymphoma|High Grade B-Cell Lymphoma||Weill Medical College of Cornell University|Genentech, Inc.|Massachusetts General Hospital|M.D. Anderson Cancer Center||February 6, 2017||Phase 1|
|NCT02432274||Recruiting||Tumors|Solid Malignant Tumors|Osteosarcoma|Differentiated Thyroid Cancer (DTC)||Eisai Limited|Eisai Inc.||December 29, 2014||Phase 1|Phase 2|
|NCT02385110||Recruiting||Leukemia||M.D. Anderson Cancer Center||September 23, 2015||Phase 2|
|NCT03007147||Not yet recruiting||B Acute Lymphoblastic Leukemia With t(9;22)(q34.1;q11.2); BCR-ABL1|BCR-ABL1 Fusion Protein Expression|Minimal Residual Disease|Philadelphia Chromosome Positive|T Acute Lymphoblastic Leukemia|Untreated Adult Acute Lymphoblastic Leukemia|Untreated Childhood Acute Lymphoblastic Leukemia||Childrens Oncology Group|National Cancer Institute (NCI)||July 2017||Phase 3|
|NCT03016871||Not yet recruiting||CD (Cluster of Differentiation) 30-Positive Neoplastic Cells Present|Recurrent Hodgkin Lymphoma|Refractory Hodgkin Lymphoma||City of Hope Medical Center|National Cancer Institute (NCI)||June 2017||Phase 2|
|NCT03041311||Not yet recruiting||Small Cell Lung Cancer||G1 Therapeutics, Inc.||May 2017||Phase 2|
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Frequently Asked Questions
Regarding the Etoposide S1225, do you have any data of the inhibition sepcificity of this product? It will inhibit other enzymes other than TOP2A?
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.