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Gueiffier, A., et al. (1998) Synthesis of Imidazo[1,2-a]pyridines as Antiviral Agents. Journal of Medical Chemistry, 41, 5108-5112.

has been cited by the following article:

  • TITLE: Trisubstituted Hexahydroimidazo[1,2-α]Pyridine 6 (TIP-6) as a Small-Molecule Inhibitor of Bcl-2 for Inhibition of Proliferation in Hepatoma Cells

    AUTHORS: Wenchao Zhang, Yanlong Pan, Heng Zhou, Xiaofei Gao, Jizu Song, Yuexia Hua, Yuping Du, Jinbo Yang, Xinping Hui, Qin Wang

    KEYWORDS: TIP-6, Antiproliferative, Autophagy, Bcl-2, LC3, Docking

    JOURNAL NAME: Journal of Biosciences and Medicines, Vol.7 No.1, January 4, 2019

    ABSTRACT: Background: Cancer poses a serious threat to human health and survival, and studies had been reported that imidazole or pyridine analogs play as an anti-cancer agent in cancer treatment. Meanwhile, Autophagy plays a dual and substantial role in maintaining cellular homeostasis in cancers, for it is either initiated to rescue cancer cells under stress or executed to promote autophagy cell death under certain circumstances. Objective: TIP-6 was designed and synthesized (7-(4-methoxyphenyl)-5,8α-diphenyl-1,2,3,7,8, 8α-hexahyd-roimidazo[1,2-α]pyridine-6) for evaluation of its biological effects on HepG2 cells and exploring the potential anti-cancer effect. Methods and Results: Chemical synthesis results indicated that the expected compound was obtained. The results of the MTT assay showed that TIP-6 arrested the growth of HepG2 cells in G2/M phase in the cell cycle, showing significant anti-proliferation effect. And analysis of morphological changes and formation of acidic vesicular organelles showed that the autophagy was induced but not apoptosis. The results were further validated by the enhanced expression of LC3I/II, Beclin1and down-regulated expression of Bcl-2in western blot analysis. In addition, the molecular docking predicted that TIP-6 preferentially binds to Bcl-2 and Bcl-xL in the active sites. Conclusion: Overall, this study demonstrated that autophagy cell death was executed in HepG2 cells which were induced by TIP-6.