| SKU | Size | Availability | Price | Qty |
|---|---|---|---|---|
| T408143-1ml | 1ml | Available within 4-8 weeks(?) Items will be manufactured post-order and can take 4-8 weeks. Thank you for your patience! | $52.90 |
| Specifications & Purity | Moligand™, 10mM in DMSO |
|---|---|
| Biochemical and Physiological Mechanisms | Temozolomide (CCRG81045, NSC 362856, TMZ) 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 methy |
| Storage Temp | Store at -80°C |
| Shipped In | Ice chest + Ice pads |
| Grade | Moligand™ |
| Product Description | Information Temozolomide (CCRG81045, NSC 362856, TMZ) 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 methy 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. cell lines： Concentrations：0 μM -100 μM Incubation Time：l hours Powder Purity:≥99% |
| Canonical SMILES | CN1N=NC2=C(N=C[N]2C1=O)C(N)=O |
|---|---|
| Molecular Weight | 194.15 |
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