靶点：Autophagy 通路：Autophagy 背景说明：CA-5f 是一种有效的晚期巨自噬/自噬抑制剂，通过抑制自噬体-溶酶体融合起作用。CA-5f 能够增加 LC3B-II (一种监控自噬的标记物) 和 SQSTM1 蛋白水平，促进 ROS 的产生。 生物活性：CA-5f是一种有效的自噬晚期（late-stage autophagy）抑制剂，通过抑制自噬体-溶酶体融合发挥作用。[1] In Vitro：CA-5f neither impairs the hydrolytic function nor the quantity of lysosomes. Treatment of human umbilical vein endothelial cells(HUVECs)with CA-5f for 1 h suppresses the levels of cytoskeletal proteins and membrane traffic proteins. CA-5f exhibits strong cytotoxicity against A549 non-small cell lung cancer(NSCLC)cells，but low cytotoxicity to normal human umbilical vein endothelial cells(HUVECs)，by increasing mitochondrial-derived reactive oxygen species(ROS)production. CA-5f inhibits autophagic flux by blocking autophagosome-lysosome fusion instead of affecting the pH and hydrolytic function of lysosomes[1]. In Vivo：CA-5f effectively suppresses the growth of A549 lung cancer xenograft as a single agent with an excellent tolerance in vivo. It inhibits autophagic flux，induced apoptosis，and does not affect the level of CTSB(cathepsin B)and CTSD(cathepsin D)in vivo[1]. 细胞实验：A549 cells or HUVECs are seeded into E-Plate 16-well plates overnight and then treated with DMSO or CA-5f and continuously monitored for 96 h. The changes of cell index can be used to monitor cell viability.[1] 动物实验：Animal Models: Four-week-old BALB/c nude mice(subcutaneous injection of A549 cells at the right scapula); Dosages: 40 mg/kg; Administration: injected via caudal vein[1] 数据来源文献：[1] Zhang L， et al. Autophagy. 2019， 15(3):391-406.
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