| 包装 | 价格(元) |
| 10mg | 电议 |
| 50mg | 电议 |
| 100mg | 电议 |
| 200mg | 电议 |
| 500mg | 电议 |
Cell lines | Glioma stem cells |
Preparation Method | NVP-BEZ235 was dissolved in DMSO to obtain a stock concentration of 10 mmol/L, which was aliquoted and stored at -20 °C and diluted to the desired final concentration in DMEM/F12 at the time of use. The GSC cells were treated with various concentrations of NVP-BEZ235 for 24, 48, or 72 h. |
Reaction Conditions | 10,20,40,80,160,320µM for 24, 48, or 72 h |
Applications | NVP-BEZ235 treatment significantly increased radiation sensitivity in GSCs, and the inhibition of autophagy by 3-MA blocked NVP-BEZ235-mediated radiosensitization. |
Animal models | male transgenic Tg (Thy1-APPSweLon) 41Ema (T41) mice and their wild-type (WT) littermates. |
Preparation Method | Animals were treated by oral gavage with 5 or 25 mg/kg of NVP-BEZ235, diluted in 1-metyl 2-pirrolidone 10% in PEG 300, or vehicle, once a day for 14 days. According to the genotype (WT or T41) and the treatment (NVP-BEZ235 or vehicle), the animals were divided into five groups: WT + Vehicle, WT + NVP-BEZ235 25 mg/kg (WT + BEZ 25), T41 + Vehicle, T41 + NVP-BEZ235 5 mg/kg (T41 + BEZ 5), and T41 + NVP-BEZ235 25 mg/kg (T41 + BEZ 25). |
Dosage form | 5 or 25 mg/kg, oral |
Applications | BEZ 5 mg/kg significantly reversed this memory impairment in T41 mice. Memory loss is the main sign of Alzheimer's disease (AD) |
| 产品描述 | NVP-BEZ235 is a novel therapeutic agent that targets 2 molecules in thePI3K/Akt/mTOR (phosphatidylinositol 3-kinase) pathway, PI3K and mTOR. It is an ATP-competitive pan-class I PI3K inhibitor that is effective against p110α with hotspot mutations, and likewise inhibits both mammalian target of rapamycin complex 1 (mTORC1) and mTORC2[1]. NVP-BEZ235 antagonizes the PI3K/mTOR signaling pathway and induces cell-cycle arrest, autophagy, and downregulation of vascular endothelial growth factor in glioma cells. NVP-BEZ235 is also an effective radiosensitizer that inhibits ataxia telangiectasia mutated (ATM) and DNA-PK catalytic subunits (DNA-PKcs), arrests cell cycle, and induces apoptosis[2]. NVP-BEZ235 treated colorectal cancer (CRC) cell lines resulted in transient PI3K blockade, sustained decreases in mTORC1/mTORC2 signaling, and a corresponding decrease in cell viability (IC50= 9.0-14.3 nM)[3]. All cell lines with PI3K-activating mutations or Pten deletions (A2780, IGROV1, MOVCAR18, OAW42, and SKOV3) were highly sensitive to NVP-BEZ235 (IC50range 26-70 nM). In contrast, HEYC2, OV167, OV207, and OVCAR5 cells, that lack PI3K-activating mutations or Pten deletions, had an IC50≥ 100 nM (IC50range 100-210 nM) for NVP-BEZ235. Overall, a statistically significant difference between the average NVP-BEZ235 IC50for cell lines with PI3K mutations or Pten deletions (IC50= 48.5 ± 8.1 nM) compared to cell lines that lack these mutations (IC50= 95.9 ± 18.4 nM)[1]. Mouse model of Alzheimer's disease (AD) that expresses a mutant amyloid-β precursor protein (T41 mice) to investigate the effects of NVP-BEZ235. Ten-months-old T41 animals were treated for 14 days with NVP-BEZ235 or vehicle via oral gavage and then submitted to social memory, open field and contextual conditioned fear tests. Hippocampal slices were prepared and Aβ1-42 content, NeuN, Iba-1, CD68 and GFAP were evaluated. Tissues were further processed to evaluate cytokines levels through cytometric bead array. The treatment with NVP-BEZ235 (5 mg/kg) reduced social memory impairment in T41 mice. The drug reduced the CD68/Iba-1 ratio in CA3 region of hippocampus. NVP-BEZ235 diminished IL-10 levels in T41 mice[4]. References: |
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