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(NICD)[2]",{"key":253,"value":254},"体外研究","与其对APP裂解的抑制效力相比,BMS-708163对Notch加工的抑制效力较弱,IC50 = 58±23nM [1]。 BMS-708163(10μM)与吉非替尼联合显着减弱PC9\u002FAB2细胞的集落生长,增加活性caspase 3和PARP的表达,并降低PC9\u002FAB2细胞中Ki-67的表达。 BMS-708163诱导细胞凋亡并增强PC9\u002FAB2细胞中G1期的细胞周期停滞。 BMS-708163处理有效下调PC9\u002FAB2细胞中Notch1,HES1,PI3K和Akt的表达[3]。",{"key":256,"value":257},"体内研究","在整个给药间隔期间,BMS-708163相对于对照在10和100mg\u002Fkg时显着降低血浆和脑Aβ40水平,表明在口服1mg\u002Fkg剂量后8小时Aβ40显着降低,并显着降低CSFAβ40水平。在大鼠中,单次口服剂量后3小时测量3至100 mg\u002Fkg [1]。与单独的吉非替尼相比,BMS-708163(10mg\u002Fkg)单一疗法对PC9\u002FAB2肿瘤生长具有轻微的抑制作用。 BMS-708163单一疗法导致胱天蛋白酶3表达的轻微增加以及体内Ki-67表达的轻微降低。在用BMS-708163加吉非替尼治疗的异种移植肺癌样本中,caspase 3表达显着增加,Ki-67染色减少[3]。",{"key":259,"value":260},"细胞实验","使用来自细胞计数试剂盒8（CCK-8）的基于四唑盐（WST-8）的比色测定来评估细胞活力。将细胞以5×103细胞\u002F孔的初始密度接种到96孔板中并培养24小时，然后用DMSO，增加浓度的吉非替尼或BMS708163，BIBW2992或BMS708163和BMS708163的组合培养细胞。 BIBW2992额外48小时。在加入10μLCCK-8溶液后，在酶标仪中测量A450并孵育1小时。显示相对于未处理对照的生长百分比。",{"key":262,"value":263},"动物实验","用乙醚麻醉4-6周龄雌性Balb \u002F c无胸腺（nu + \u002F nu +）小鼠。使小鼠适应环境一周，然后注射已重悬于200μL基质胶中的1.5×106个PC9 \u002F AB2细胞。当检测到确定的直径约150-300mm3的肿瘤时，将小鼠随机分成组并通过管饲法口服给药（1％甲基纤维素，0.2％吐温80在无菌水中），吉非替尼（3mg \u002F kg稀释）在载体中），BMS-708163（在载体中稀释10mg \u002F kg），或吉非替尼（3mg \u002F kg）和BMS-708163（10mg \u002F kg）的组合，持续5天\u002F周。每个治疗组由8只小鼠组成。使用以下公式每五天测量和计算肿瘤体积：π\u002F 6×（较大直径）×（较小直径）2。 30天后，通过颈椎脱臼杀死小鼠。",{"key":265,"value":266},"参考文献","[1].\nGillman KW, et al. Letter Discovery and Evaluation of BMS-708163, a Potent, Selective and Orally Bioavailable γ-Secretase Inhibitor. Med Chem Lett, 2010, 1 (3), 120-124.\n[2].\nCrump CJ, et al. BMS-708,163 targets presenilin and lacks notch-sparing activity. Biochemistry. 2012 Sep 18;51(37):7209-11.\n[3].\nXie M, et al. γ Secretase inhibitor BMS-708163 reverses resistance to EGFR inhibitor via the PI3K\u002FAkt pathway in lung cancer. J Cell Biochem. 2015 Jun;116(6):1019-27.\n[4].\nBorghys H, et al. A canine model to evaluate efficacy and safety of γ-secretase inhibitors and modulators. 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