Catalog No.S1237 Synonyms: CCRG81045, NSC 362856
Molecular Weight(MW): 194.15
Temozolomide is a monofunctional SN-1 alkylating agent that can modify nitrogen atoms in the DNA ring and the extracyclic oxygen group, chemically converted to MTIC and degrades to methyldiazonium cation, which transfers methyl groups to DNA at physiologic pH. A DNA damage inducer in L-1210 and L-1210/BCNU cells.
Cited by 8 Publications
5 Customer Reviews
Talazoparib and temozolomide exhibit marked combinatorial efficacy in PDXs. A, Western blot against MGMT by near-infrared imaging in PDX models.
Clin Cancer Res, 2017, 23(2):523-535. Temozolomide purchased from Selleck.
C57BL/6 mice were implanted in the striatum with citrine-GL26-Cherry-HMGB1, which were stably transfected to express the YFP citrine and HMGB1 fused to red fluorescent protein cherry. Fourteen days later, they were treated with saline, Ad-TK+Ad-Flt3L, or Ad-TK+Ad-Flt3L+TMZ (temozolomide). Five days after treatment, the cellular location of cherry-HMGB1 in these cells was assessed by confocal microscopy. Arrows, tumor cells (green) with cytoplasmic HMGB1 (red).
Clin Cancer Res 2014 20(6), 1555-65. Temozolomide purchased from Selleck.
Viability of U87 cells(A) 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 temozolomide (TMZ) and Bliss interaction index (B) 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 400 μM TMZ(A) 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, 104:7-18.. Temozolomide purchased from Selleck.
Establishment of TMZ-resistant (TR) GBM cell lines. a-d, Evaluation of temozolomide resistance in four glioblastoma cell lines. Cells were cultured in the presence of 5-600 μM of TMZ. A dose-dependent association between the survival rate of cells and TMZ concentration can be observed. Each group was cultured for 24 h in the presence of different concentrations of TMZ, followed by an evaluation of IC50 for TMZ inhibited growth in A172-TR/A172, U118-TR/U118, U251-TR/U251 and U87-TR/U87
Neurochem Res, 2016, 41(12):3192-3205. Temozolomide purchased from Selleck.
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|Description||Temozolomide is a monofunctional SN-1 alkylating agent that can modify nitrogen atoms in the DNA ring and the extracyclic oxygen group, chemically converted to MTIC and degrades to methyldiazonium cation, which transfers methyl groups to DNA at physiologic pH. A DNA damage inducer in L-1210 and L-1210/BCNU cells.|
|Features||Methazolastone is a second-generation alkylating agent.|
Methazolastone causes formation of DNA alkali-labile sites which are present in similar amounts and repaired at a similar rate in L-1210 and L-1210/BCNU cell lines. In L-1210 but not in L-1210/BCNU methazolastone induces an arrest of cells in SL-G2-M phases. Methazolastone sensitivity of both chemo-sensitive and resistant cells (D54-R and U87-R) is enhanced significantly under hyperoxia. Both Methazolastone and hyperoxia are associated with increased phosphorylation of ERK p44/42 MAPK (Erk1/2), but to a lesser extent in D54-R cells, suggesting that Erk1/2 activity may be involved in regulation of hyperoxia and Methazolastone-mediated cell death. Hyperoxia enhances Methazolastone toxicity in GBM cells by induction of apoptosis, possibly via MAPK-related pathways.  Methazolastone induces in monocytes the DNA damage response pathways ATM-Chk2 and ATR-Chk1 resulting in p53 activation.  Chronic Methazolastone exposure results in acquired Methazolastone-resistance and elevates miR-21 expression.  Methazolastone treatment triggers endoplasmic reticula (ER) stress with increased expression of GADD153 and GRP78 proteins, and deceases pro-caspase 12 protein. Methazolastone induces autophagy through mitochondrial damage- and ER stress-dependent mechanisms to protect glioma cells. 
|In vivo||After a daily i.p. dose of 40 mg/kg for 5 consecutive days (days 1-5 after tumor transplant), methazolastone increases life-span by 86% in L-1210 and 22% in L-1210/BCNU. In L-1210/BCNU no effect is seen after 100 μM or 200 μM treatment; only 400 μM methazolastone produced an accumulation of cells in premitotic phase but much less than in L-1210. In L-1210/BCNU the maximum accumulation of cells in SL-G2-M is, after 48 hours-72 hours, approximately 30% as compared to 23% in untreated cells. Cells accumulates in SL-G2-M occurred too when L- 1210 leukemia-bearing mice are treated i.v. with methazola stone (40 mg/kg). No such effect is seen on L-1210/BCNU cells from mice given the same drug dose. |
-  Catapano CV, et al. Cancer Res. 1987, 47(18), 4884-4889.
-  Sun S, et al. J Neurooncol. 2012.
-  Bauer M, et al. PLoS One. 2012, 7(6):e39956.
|In vitro||DMSO||38 mg/mL (195.72 mM)|
|In vivo||Add solvents to the product individually and in order:
5% DMSO+30% PEG 300+ddH2O
For best results, use promptly after mixing.
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
|Synonyms||CCRG81045, NSC 362856|
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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT02977780||Recruiting||Glioblastoma||Dana-Farber Cancer Institute|Eli Lilly and Company|Celgene|Puma Biotechnology, Inc.|Accelerate Brain Cancer Cure||February 9, 2017||Phase 2|
|NCT02689336||Recruiting||Glioma|Rhabdomyosarcoma|Osteosarcoma|Medulloblastoma|Neuroectodermal Tumor|Ependymoma|Ewings Sarcoma|Wilms Tumor||Washington University School of Medicine||August 6, 2016||Phase 2|
|NCT02455557||Recruiting||Glioblastoma|Gliosarcoma||Roswell Park Cancer Institute|National Cancer Institute (NCI)||May 5, 2015||Phase 2|
|NCT01473901||Active, not recruiting||Glioblastoma||Novartis Pharmaceuticals|Novartis||December 30, 2011||Phase 1|
|NCT03018288||Not yet recruiting||Glioblastoma||National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC)||January 3, 2017||Phase 2|
|NCT02766270||Recruiting||Grade II/III Glioma||Beijing Tiantan Hospital|Beijing Neurosurgical Institute|Beijing Shijitan Hospital||September 26, 2016||Early Phase 1|
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