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Temozolomide is a DNA methylating, chemotherapeutic agent. Displays antitumor activity against a board spectrum of tumors, including leukemias, lymphomas and solid tumors (IC50 = 5.0 μM for cytotoxicity against mouse TLX5 lymphoma cells). Induces autophagy in malignant glioma cells. Exhibits enhanced activity when used in combination with CHC (Cat No. 5029).
Temozolomide is also offered as part of the Tocriscreen 2.0 Max and Tocriscreen FDA-Approved Drugs. Find out more about compound libraries available from Tocris.
|Storage||Store at RT|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
The following data is based on the product molecular weight 194.15. Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|0.5 mM||10.3 mL||51.51 mL||103.01 mL|
|2.5 mM||2.06 mL||10.3 mL||20.6 mL|
|5 mM||1.03 mL||5.15 mL||10.3 mL|
|25 mM||0.21 mL||1.03 mL||2.06 mL|
References are publications that support the biological activity of the product.
Plowman et al (1994) Preclinical antitumor activity of temozol. in mice: efficacy against human brain tumor xenografts and synergism with 1,3-bis(2-chloroethyl)-1-nitrosourea. Cancer Res. 54 3793 PMID: 8033099
Clark et al (1995) Antitumor imidazotetraazines. 32. Synthesis of novel imidazotetrazinones and related bicyclic heterocycles to probe the mode of action of the antitumor drug temozol. J.Med.Chem. 38 1493 PMID: 7739008
Bodell et al (2003) Formation of DNA adducts and induction of lacI mutations in big blue rat-2 cells treated with temozolomide: implications for the treatment of low-grade adult and pediatric tumors. Cancer Epidemiol.Biomarkers Prevent. 12 545 PMID: 12815001
Kanzawa et al (2004) Role of autophagy in temozolomide-induced cytotoxicity for malignant glioma cells. Cell Death Differ. 11 448 PMID: 14713959
If you know of a relevant reference for Temozolomide, please let us know.
Keywords: Temozolomide, Temozolomide supplier, DNA-methylating, antitumor, agent, Apoptosis, Inducer, NSC362856, CCRG81045, chemotherapeutics, TMZ, NSC, 362856, CCRG, 81045, Inducers, Autophagy, 2706, Tocris Bioscience
Citations are publications that use Tocris products. Selected citations for Temozolomide include:
Canello et al (2014) Antineoplastic effect of decoy oligonucleotide derived from MGMT enhancer. PLoS One 9 e113854 PMID: 25460932
Johannessen et al (2013) The DNA repair protein ALKBH2 mediates temozol. resistance in human glioblastoma cells. Neuro Oncol 15 269 PMID: 23258843
Hu et al (2012) Fibulin-3 promotes glioma growth and resistance through a novel paracrine regulation of Notch signaling. Cancer Res 72 3873 PMID: 22665268
Prabhu et al (2013) Targeting the unfolded protein response in glioblastoma cells with the fusion protein EGF-SubA. PLoS One 7 e52265 PMID: 23284962
Deng et al (2017) Quantitative Analyses of Synergistic Responses between Cannabidiol and DNA-Damaging Agents on the Proliferation and Viability of Glioblastoma and Neural Progenitor Cells in Culture. J Pharmacol Exp Ther 360 215 PMID: 27821713
Pastori et al (2014) BET bromodomain proteins are required for glioblastoma cell proliferation. Epigenetics 9 611 PMID: 24496381
Do you know of a great paper that uses Temozolomide from Tocris? Please let us know.
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Temozolomide was used for the establishment of TMZ-resistant glioma cell lines.
Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* your copy today!
*Please note that Tocris will only send literature to established scientific business / institute addresses.
There are two currently recognized forms of programmed cell death: apoptosis and necroptosis. This poster summarizes the signaling pathways involved in apoptosis, necroptosis and cell survival following death receptor activation, and highlights the influence of the molecular switch, cFLIP, on cell fate.