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CAY10594 是磷脂酶 D2 抑制剂 (体外IC50=140 nM,细胞IC50=110 nM)。它在体外显著阻碍乳腺癌细胞的侵袭性迁移,并调节磷酸化 GSK-3β/JNK 轴改善扑热息痛诱导的急性肝损伤。
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CAY10594 是磷脂酶 D2 抑制剂 (体外IC50=140 nM,细胞IC50=110 nM)。它在体外显著阻碍乳腺癌细胞的侵袭性迁移,并调节磷酸化 GSK-3β/JNK 轴改善扑热息痛诱导的急性肝损伤。
规格 | 价格 | 库存 | 数量 |
---|---|---|---|
1 mg | ¥ 629 | 现货 | |
5 mg | ¥ 1,230 | 现货 | |
10 mg | ¥ 1,990 | 现货 | |
25 mg | ¥ 3,370 | 现货 | |
50 mg | ¥ 4,890 | 现货 | |
100 mg | ¥ 6,860 | 现货 | |
1 mL x 10 mM (in DMSO) | ¥ 1,680 | 现货 |
产品描述 | CAY10594 is a potent phospholipase D2(PLD2) inhibitor. CAY10594 ameliorates acetaminophen-induced acute liver injury by regulating the phosphorylated-GSK-3β/JNK axis. |
体内活性 | CAY10594的给药显著以剂量依赖的方式阻断了急性肝损伤,8mg/kg的CAY10594几乎完全抑制了损伤。在急性肝损伤的病理进程中,GSH水平降低,而CAY10594在APAP挑战后6小时给药显著恢复了这一点。GSK-3β (Serine 9)/JNK的磷酸化主要参与APAP引起的肝损伤。CAY10594给药强烈阻断了APAP诱导的急性肝损伤模型中的GSK-3β (Serine 9)/JNK磷酸化。一致地,CAY10594处理的小鼠中,肝细胞的细胞质和线粒体中持续的JNK激活也有所减少。多种类型的免疫细胞也涉及APAP引起的肝损伤。然而,与APAP挑战的车辆处理组和CAY10594处理组的小鼠相比,中性粒细胞和单核细胞群体没有差异。CAY10594的治疗性给药也显著减轻了APAP挑战引起的肝损害,提高了生存率[1]。 |
动物实验 | Mice were fasted for 16?hours before APAP injection. APAP (500?mg/kg) was administered with oral gavage in mice. CAY10594 (N-[2-(4-oxo-1-phenyl-1,3,8-triazaspiro[4,5]dec-8-yl)ethyl]-2-naphthalene carboxamide)23 was dissolved in 1% DMSO and intraperitoneally administered to mice 30?minutes prior to APAP injection for examining protective effects or after 3?hours from APAP challenge for investigating therapeutic effects of CAY10594[1]. |
分子量 | 428.53 |
分子式 | C26H28N4O2 |
CAS No. | 1130067-34-3 |
Smiles | O=C(NCCN1CCC2(CC1)N(CNC2=O)c1ccccc1)c1ccc2ccccc2c1 |
密度 | 1.29 g/cm3 (Predicted) |
存储 | Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice. | |||||||||||||||||||||||||
溶解度信息 | DMSO: 20 mg/mL (46.7 mM) | |||||||||||||||||||||||||
溶液配制表 | ||||||||||||||||||||||||||
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