Potent anti-cancer compound. Induces apoptosis in normal and tumor cell lines.
DNA Topoisomerase II activity inhibitor. Increases Topo II-mediated DNA breakage primarily by inhibiting the ability of the enzyme to religate cleaved nucleic acid molecules. Does not lead to immediate block of DNS synthesis, induces a progressive inhibition of DNA replication.p53 activator.
Blocks the cell cycle between the end of the S phase and the early G2 phase.
Oncoprotein Mdm2 synthesis inhibitor.
Apoptosis inducer through the cytochrome c/Apaf-1/caspase-9 pathway and the Fas-mediated death signaling pathway.
Cell cycle checkpoint activator. Affects gene expression at different levels (chromatin remodeling, transcription and alternative splicing).
Chemotherapeutic compound used in cancers.
Used in conditioning regimen prior to a bone marrow or blood stem cell transplantation.
Storage and Stability:
Short-term Storage: +20°C
Long-term Storage: +20°C
Stable for at least 2 years after receipt when stored at +20°C. Store solutions in DMSO at 4°C. After reconstitution, prepare aliquots and store at -20°C.
Purity: >98% (HPLC)
Important Note: This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications without the expressed written authorization of United States Biological.
Product Reference: |
The podophyllotoxin derivatives VP16-213 and VM26: B.F. Issell; Cancer Chemother. Pharmacol. 7, 73 (1982)
Topoisomerase-specific drug sensitivity in relation to cell cycle progression: K.C. Chow & W.E. Ross; Mol. Cell. Biol. 7, 3119 (1987)
Increases in sequence specific DNA binding by p53 following treatment with chemotherapeutic and DNA damaging agents: R.B. Tishler, et al.; Cancer Res. 53, 2212 (1993)
Topoisomerase II-etoposide interactions direct the formation of drug-induced enzyme-DNA cleavage complexes: D.A. Burden, et al.; J. Biol. Chem. 271, 29238 (1996)
Cell death induced by topoisomerase-targeted drugs: more questions than answers: S.H. Kaufmann; Biochim. Biophys. Acta 1400, 195 (1998) (Review)
Etoposide: four decades of development of a topoisomerase II inhibitor: K.R. Hande; Eur. J. Cancer 34, 1514 (1998) (Review)
Differential regulation of p21waf-1/cip-1 and Mdm2 by etoposide: etoposide inhibits the p53-Mdm2 autoregulatory feedback loop: E.L. Arriola, et al.; Oncogene 18, 1081 (1999)
Early caspase activation in leukemic cells subject to etoposide-induced G2-M arrest: evidence of commitment to apoptosis rather than mitotic cell death: R.J. Sleiman & B.W. Stewart; Clin. Cancer Res. 6, 3756 (2000)
Ordering of ceramide formation, caspase activation, and Bax/Bcl-2 expression during etoposide-induced apoptosis in C6 glioma cells: M. Sawada, et al.; Cell Death Differ. 7, 761 (2000)
Distinct pathways for stimulation of cytochrome c release by etoposide: J.D. Robertson, et al.; J. Biol. Chem. 275, 32438 (2000)
Deacetylase activity associates with topoisomerase II and is necessary for etoposide-induced apoptosis: C.A. Johnson, et al.; J. Biol. Chem. 276, 4539 (2001)
Etoposide: discovery and medicinal chemistry: P. Meresse, et al.; Curr. Med. Chem. 11, 2443 (2004) (Review)
Etoposide, topoisomerase II and cancer: E.L. Baldwin & N. Osheroff; Curr. Med. Chem. Anticancer Agents 5, 363 (2005) (Review)
The dispersal of replication proteins after Etoposide treatment requires the cooperation of Nbs1 with the ataxia telangiectasia Rad3-related/Chk1 pathway: R. Rossi, et al.; Cancer Res. 66, 1675 (2006)
Cellular response to etoposide treatment: A. Montecucco & G. Biamonti; Cancer Lett. 252, 9 (2007) (Review)
Chemomobilization with Etoposide is Highly Effective in Patients with Multiple Myeloma and Overcomes the Effects of Age and Prior Therapy: W.A. Wood, et al.; Biol. Blood Marrow. Transplant. 17, 141 (2011)
|Intended for research use only. Not for use in human, therapeutic, or diagnostic applications.|