Flubendazole is a widely used anthelmintic drug belonging to benzimidazole group. The molecular mechanism of action of flubendazole is based on its specific binding to tubulin, which results in disruption of microtubule structure and function, and in the interference with the microtubule-mediated transport of secretory vesicles in absorptive tissues of helminths[3]. In animals, flubendazole has good oral bioavailability from an ASD formulation ranging from 15% in dogs, 27% in rats to more than 100% in jirds. Regarding genotoxicity, flubendazole was negative in the Ames test, but positive in the in vivo micronucleus test[4]. Flubendazole exerts anti-proliferation and pro-apoptosis effects in Glioma through affecting the cell cycle and intrinsic apoptotic signaling[5]. Flubendazole is a novel small molecule inhibitor of not only melanoma growth and spread but also of PD-1(programmed cell death protein-1) and MDSC (myeloid-derived suppressor cell) [6]. Flubendazole inhibited the cell survival of different ESCC (esophageal squamous cell carcinoma) cells and induced cell apoptosis in both EC9706 and TE1 cells. In addition, flubendazole also showed a synergistic effect on ESCC cells when combined with doxorubicin[7].
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