Dear researchers i want to treat U-251 cells with Temozolomide (TMZ) so, i want to know that what should be the minimum DMSO concentration to dissolve the Temozolomide and what should be minimum TMZ stock concentration?
I am not sure about U-251 cells, but typically for in vitro analysis with liver microsomes or hepatocytes, we try to keep [DMSO]
I agree with Kevin that, in general, you always want to minimize the amount of DMSO in your assay. Different cells have different tolerances for DMSO. I would make sure that you run a control that introduces DMSO to the U-251 cells at the same concentration.
But Temozolomide is very soluble in DMSO. According to Sigma, you can make solutions that are greater than 20 mg/mL. That is greater than 100 mM. Now that you know what your starting concentration of Temozolomide is, you can determine how much DMSO is present in any particular if you know the volume of the assay and the concentration of Temozolomide that you want in your assay. If you want to have Temozolomide at concentrations of 250 uM or less, you are ready to go with a 20 mg/mL stock.
Other solvents (e.g., methanol) may also work.
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T2577 - Temozolomide
T2577 SIGMATemozolomide
≥98% (HPLC)
Synonym: 3,4- Dihydro- 3- methyl- 4- oxoimidazo[5,1-d] - 1,2,3,5- tetrazine- 8- carboxamide, 3- Methyl- 4- oxo- 8- imidazolo[5,1-d] [1,2,3,5] tetrazinecarboxamide, 4- Methyl- 5- oxo- 2,3,4,6,8- pentazabicyclo[4.3.0] nona- 2,7,9- triene- 9- carboxamide, 8- Carbamoyl- 3- methylimidazo[5,1-d] - 1,2,3,5- tetrazin- 4(3H)-one, NSC 362856
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SIMILAR PRODUCTS
CAS Number 85622-93-1
Empirical Formula (Hill Notation) C6H6N6O2
Molecular Weight 194.15
MDL number MFCD00866492
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Safety & Documentation
Protocols & Articles
3
Peer-Reviewed Papers
206
Properties
Related Categories
Apoptosis Inducers, Apoptosis and Cell Cycle, Approved Therapeutics/Drug Candidates, Bioactive Small Molecule Alphabetical Index, Bioactive Small Molecules,More...
assay
≥98% (HPLC)
form
powder
color
white to light brown
solubility
DMSO: soluble10 mg/mL, clear
H2O: insoluble
originator
Schering Plough
storage temp.
2-8°C
Description
Frequently Asked Questions
Frequently Asked Questions are available for this Product.
Packaging
25, 100 mg in glass bottle
Preparation Note
Temozolomide is soluble in DMSO at a concentration that is greater than 20 mg/ml. It is insoluble in water.
Application
Temozolomide has been used for analyzing drug resistance mechanisms in glioblastoma cell lines15,16.
Biochem/physiol Actions
Temozolomide is a DNA methylating agent and drug resistance-modifying agent; anti-tumor and anti-angiogenic. 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.
Features and Benefits
This compound is a featured product for Apoptosis research. Click here to discover more featured Apoptosis products. Learn more about bioactive small molecules for other areas of research at sigma.com/discover-bsm.
This compound was developed by Schering Plough. To browse the list of other pharma-developed compounds and Approved Drugs/Drug Candidates, click here.
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T2577-25MG
Available to ship on 26.10.16 - FROM
8,635.06
T2577-100MG
Available to ship on 21.11.16 - FROM
27,776.31
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Safety Information
Symbol
GHS07, GHS08
Signal word
Danger
Hazard statements
H302-H315-H319-H335-H350-H360
Precautionary statements
P201-P261-P305 + P351 + P338-P308 + P313
Personal Protective Equipment
Eyeshields, full-face particle respirator type N100 (US), Gloves, respirator cartridge type N100 (US),type P1 (EN143) respirator filter, type P3 (EN 143) respirator cartridges
RIDADR
NONH for all modes of transport
WGK Germany
3
RTECS
NJ5927050
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Autophagy in Cancer Promotes Therapeutic Resistance (598 KB)
Structure Search
Articles
Autophagy in Cancer Promotes Therapeutic ResistanceAutophagy is a highly regulated process by which long-lived proteins, organelles, and protein aggregates are captured within autophagosomes, which are then fused with lysosomes for degradation.1 Auto...
Keywords: Apoptosis, Autophagy, Cancer, Degradations, Metabolites, transformation
Discover Bioactive Small Molecules for ApoptosisApoptosis, or programmed cell death (PCD), is a selective process for the removal of unnecessary, infected or transformed cells in various biological systems. As it plays a role in the homeostasis of...
Keywords: Apoptosis, Bioactive small molecules, Cancer, Clinical, Diseases, Ligands, Neurodegenerative Diseases
Discover Bioactive Small Molecules for Cell Cycle ResearchIn proliferating cells, the cell cycle consists of four phases. Gap 1 (G1) is the interval between mitosis and DNA replication that is characterized by cell growth. Replication of DNA occurs during t...
Keywords: Apoptosis, Bioactive small molecules, Cancer, Cell division, Cell proliferation, DNA replication, Diseases, Genetic
Peer-Reviewed Papers
Did you use this product in your Paper? If so click here.
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READ ABSTRACT
1. Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
Zhichao Liu et. al
PLoS computational biology, 7(12), e1002310 (2011)
Drug-induced liver injury (DILI) is a significant concern in drug development due to the poor concordance between preclinical and clinical findings of liver toxicity. We hypothesized that the DILI types (hepatotoxic side effects) seen in the clinic ...Read More
READ ABSTRACT
2. Reversing the Warburg effect as a treatment for glioblastoma.
Ethan Poteet et. al
Journal of Biological Chemistry, 288(13), 9153-9164 (2013)
Glioblastoma multiforme (GBM), like most cancers, possesses a unique bioenergetic state of aerobic glycolysis known as the Warburg effect. Here, we documented that methylene blue (MB) reverses the Warburg effect evidenced by the increasing of oxygen...Read More
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3. Rationale for poly(ADP-ribose) polymerase (PARP) inhibitors in combination therapy with camptothecins or temozolomide based on PARP trapping versus catalytic inhibition.
Junko Murai et. al
Journal of Pharmacology and Experimental Therapeutics, 349(3), 408-416 (2014)
We recently showed that poly(ADP-ribose) polymerase (PARP) inhibitors exert their cytotoxicity primarily by trapping PARP-DNA complexes in addition to their NAD(+)-competitive catalytic inhibitory mechanism. PARP trapping is drug-specific, with olap...Read More
READ ABSTRACT
4. p53 effects both the duration of G2/M arrest and the fate of temozolomide-treated human glioblastoma cells.
Y Hirose et. al
Cancer Research, 61(5), 1957-1963 (2001)
Temozolomide (TMZ) is a DNA-methylating agent that has recently been introduced into Phase II and III trials for the treatment of gliomas. TMZ produces O6-methylguanine in DNA, which mispairs with thymine during the next cycle of DNA replication. Su...Read More
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5. Combined treatment with temozolomide and poly(ADP-ribose) polymerase inhibitor enhances survival of mice bearing hematologic malignancy at the central nervous system site.
Lucio Tentori et. al
Blood, 99(6), 2241-2244 (2002)
Temozolomide (TZM) is a DNA-methylating agent that has recently been introduced into various clinical trials for treatment of solid or hematologic neoplasias, including brain lymphomas. In the current study, we have investigated whether the antitumo...Read More
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6. FoxM1 inhibition sensitizes resistant glioblastoma cells to temozolomide by downregulating the expression of DNA-repair gene Rad51.
Nu Zhang et. al
Clinical Cancer Research, 18(21), 5961-5971 (2012)
Recurrent glioblastoma multiforme (GBM) is characterized by resistance to radiotherapy and chemotherapy and a poor clinical prognosis. In this study, we investigated the role of the oncogenic transcription factor FoxM1 in GBM cells' resistance to al...Read More
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7. Drugs targeting the mitochondrial pore act as cytotoxic and cytostatic agents in temozolomide-resistant glioma cells.
Annalisa Lena et. al
Journal of Translational Medicine, 7, 13 (2009)
High grade gliomas are one of the most difficult cancers to treat and despite surgery, radiotherapy and temozolomide-based chemotherapy, the prognosis of glioma patients is poor. Resistance to temozolomide is the major barrier to effective therapy. ...Read More
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8. Inhibition of angiogenesis by non-toxic doses of temozolomide.
Hjalmar Kurzen et. al
Anti-Cancer Drugs, 14(7), 515-522 (2003)
It is well established that certain chemotherapeutic agents have potent antiangiogenic properties which may be part of their antitumor activity. Temozolomide (TMZ) is a lipophilic methylating agent used in the therapy of malignant melanoma and other...Read More
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9. Vorinostat Enhances Cytotoxicity of SN-38 and Temozolomide in Ewing Sarcoma Cells and Activates STAT3/AKT/MAPK Pathways.
Valerie B Sampson et. al
PLoS ONE, 10(11), e0142704 (2015)
Histone deacetylase inhibitors (HDACi) have been evaluated in patients with Ewing sarcoma (EWS) but demonstrated limited activity. To better understand the potential for HDACi in EWS, we evaluated the combination of the HDACi vorinostat, with DNA da...Read More
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10. A New Epigenetic Mechanism of Temozolomide Action in Glioma Cells.
Anna-Maria Barciszewska et. al
PLoS ONE, 10(8), e0136669 (2015)
Temozolomide (TMZ) is an oral alkylating chemotherapeutic agent that prolongs the survival of patients with glioblastoma (GBM). Despite that high TMZ potential, progression of disease and recurrence are still observed. Therefore a better understandi...Read More
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11. ATM regulates 3-methylpurine-DNA glycosylase and promotes therapeutic resistance to alkylating agents.
Sameer Agnihotri et. al
Cancer Discovery, 4(10), 1198-1213 (2014)
Alkylating agents are a first-line therapy for the treatment of several aggressive cancers, including pediatric glioblastoma, a lethal tumor in children. Unfortunately, many tumors are resistant to this therapy. We sought to identify ways of sensiti...Read More
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12. VEGF regulates region-specific localization of perivascular bone marrow-derived cells in glioblastoma.
Kelly Burrell et. al
Cancer Research, 74(14), 3727-3739 (2014)
Glioblastoma multiforme (GBM) is characterized by a pathogenic vasculature that drives aggressive local invasion. Recent work suggests that GBM cells recruit bone marrow-derived progenitor cells (BMDC) to facilitate recurrence after radiotherapy, bu...Read More
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13. Phase I trial of hydroxychloroquine with dose-intense temozolomide in patients with advanced solid tumors and melanoma.
Reshma Rangwala et. al
Autophagy, 10(8), 1369-1379 (2014)
Blocking autophagy with hydroxychloroquine (HCQ) augments cell death associated with alkylating chemotherapy in preclinical models. This phase I study evaluated the maximum tolerated dose (MTD), safety, preliminary activity, pharmacokinetics, and ph...Read More
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14. Progression types after antiangiogenic therapy are related to outcome in recurrent glioblastoma.
Martha Nowosielski et. al
Neurology, 82(19), 1684-1692 (2014)
This retrospective study analyzed whether the type of radiologic progression, classified according to contrast enhancement on MRI T1-weighted sequences and changes in T2-hyperintense signal, is relevant for outcome in patients with progressive gliob...Read More
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15. Optimization of combined temozolomide and peptide receptor radionuclide therapy (PRRT) in mice after multimodality molecular imaging studies.
Sander M Bison et. al
EJNMMI Research, 5(1), 62 (2015)
Successful treatments of patients with somatostatin receptor (SSTR)-overexpressing neuroendocrine tumours (NET) comprise somatostatin-analogue lutetium-177-labelled octreotate ((177)Lu-TATE) treatment, also referred to as peptide receptor radionucli...Read More
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