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Cat. No. M2129
Temozolomide Structure

NSC362856, CCRG81045

Size Price Availability Quantity
Free Sample (0.5-1 mg)  USD 0 In stock
10mM/1mL In DMSO USD 65 In stock
100mg USD 140 In stock
500mg USD 240 In stock
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Biological Activity

Temozolomide (NSC 362856, CCRG 81045) is a DNA methylating agent used for the treatment of Grade IV astrocytoma. Temozolomide exhibits schedule-dependent antineoplastic activity by interfering with DNA replication. Temozolomide 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). Temozolomide induces G2/M arrest and apoptosis through adduction of a methyl group to O6 position of guanine in genomic DNA and functional inactivation of DNA repair protein O(6)-alkylguanine DNA alkyltransferase (AGT) in base excision repair (BER) pathway. Temozolomide treatment triggered ER stress with increased expression of GADD153 and GRP78 proteins, and deceased pro-caspase 12 protein. Temozolomide is currently in a phase II clinical trial in the treatment of melanoma.

Product Citations
Customer Product Validations & Biological Datas
Source Cell Death Dis (2018). Figure 3. Temozolomide (Abmole Bioscience)
Method Glucose starvation sensitizes glioblastoma cells to chemotherapies
Cell Lines U87 and U251 cells
Concentrations 200 μM
Incubation Time 5 d
Results Treatment with either temozolomide or carboplatin induced about 50 and 80% GBM cell death under normal and glucose starvation conditions, respectively
Source Cell Death Dis (2018). Figure 1. Temozolomide (Abmole Bioscience)
Method Glucose starvation sensitizes glioblastoma cells to chemotherapies
Cell Lines U87 and U251 cells
Concentrations 200 μM
Incubation Time 5 d
Results The cytotoxic effect was progressive and by day 5, temozolomide or carboplatin treatment caused 40–60% cell loss in U87 and U251 cells. Glucose starvation nearly doubled the cell loss to 70–90%.
Source Cancer letters (2016). Figure 6.Temozolomide was obtained from AbMole (Houston, TX, USA)
Method western blot
Cell Lines U87 or U251 cells
Concentrations 200 μM for U87, 50 μM for U251
Incubation Time 48 h
Results TMZ treatment induces the expression of HDAC6 and EGFR (Fig. 6D). Combination use of HDAC6 inhibitors and TMZ abolishes TMZ mediated EGFR and ERK phosphorylation (Fig. 6G).
Source Cancer letters (2016). Figure 5.Temozolomide was obtained from AbMole (Houston, TX, USA)
Method cell viability assay and cell apotosis(flow cytometry)
Cell Lines U87 or U251 or A172 cells
Concentrations 200, 400 and 800µM or 50, 100 and 200µM or 100, 200 and 400µM
Incubation Time 48 h
Results These data suggest that the combination treatment of HDAC6 inhibitors and TMZ displayed an additive therapeutic effect on glioblastoma.
Source Cancer letters (2016). Figure 3.Temozolomide was obtained from AbMole (Houston, TX, USA)
Method cell viability assay and cell apotosis(flow cytometry)
Cell Lines U87 or U251 cells
Concentrations 400, 800 and 1200µM or 50, 100 and 200µM
Incubation Time 48 h
Results Our results suggest that the overexpression of HDAC6 in glioblastoma might be an intrinsic mechanism that confers resistance to TMZ.
Cell Experiment
Cell lines A2058, A375, M238 and M249 cell lines
Preparation method Colony formation assay Depending on the cell line (and plating efficiency), 200–1000 cells were seeded into each well of a 6-well plate and treated as described in detail previously. In the case of primary melanoma cells, 1000 cells were seeded and let grow for 24 days in the presence or absence of drug treatment; because only small colonies formed, the stained colonies were counted under the microscope.Survival of melanoma cells after drug treatment. Five different melanoma cell lines (as indicated), as well as a culture of primary melanoma tissue cells (labeled ‘primary’) were exposed to increasing concentrations of TMZ (diamonds) or NEO212 (circles) for 48 hours, and long-term survival was determined via colony formation assay (CFA).
Concentrations 0, 25, 50, 75, 100µM
Incubation time 48 h
Animal Experiment
Animal models A375 cells subcutaneous tumor growth model
Formulation 45% glycerol, 45% ethanol, 10% DMSO
Dosages 50 mg/kg
Administration subcutaneous injection
Conversion of different model animals based on BSA (Value based on data from FDA Draft Guidelines)
Species Mouse Rat Rabbit Guinea pig Hamster Dog
Weight (kg) 0.02 0.15 1.8 0.4 0.08 10
Body Surface Area (m2) 0.007 0.025 0.15 0.05 0.02 0.5
Km factor 3 6 12 8 5 20
Animal A (mg/kg) = Animal B (mg/kg) multiplied by  Animal B Km
Animal A Km

For example, to modify the dose of resveratrol used for a mouse (22.4 mg/kg) to a dose based on the BSA for a rat, multiply 22.4 mg/kg by the Km factor for a mouse and then divide by the Km factor for a rat. This calculation results in a rat equivalent dose for resveratrol of 11.2 mg/kg.

Chemical Information
Molecular Weight 194.15
Formula C6H6N6O2
CAS Number 85622-93-1
Purity 99.92%
Solubility DMSO 30 mg/mL
Storage at -20°C

Human monocytes undergo excessive apoptosis following temozolomide activating the ATM/ATR pathway while dendritic cells and macrophages are resistant.
Bauer M, et al. PLoS One. 2012;7(6):e39956. PMID: 22768182.

Inhibition of mitochondria- and endoplasmic reticulum stress-mediated autophagy augments temozolomide-induced apoptosis in glioma cells.
Lin CJ, et al. PLoS One. 2012;7(6):e38706. PMID: 22745676.

Preclinical antitumor activity of temozolomide in mice: efficacy against human brain tumor xenografts and synergism with 1,3-bis(2-chloroethyl)-1-nitrosourea.
Plowman J, et al. Cancer Res. 1994 Jul 15;54(14):3793-9. PMID: 8033099.

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Keywords: Temozolomide, NSC362856, CCRG81045 supplier, Autophagy, inhibitors

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