Fenbendazole is a commonly used medication used to treat parasites and worms in animals. It is also being self-administered by some cancer patients in combination with other natural treatments as part of a cancer treatment method called the Joe Tippens Protocol. The benzimidazole anthelmintic is typically well tolerated by humans.

In the present study, we aimed to investigate the antitumor effect of the anthelmintic drug fenbendazole (FZ) in 5-fluorouracil-resistant colorectal cancer cells. To that end, we performed clonogenic assays to analyze the effects of FZ on cell proliferation and analyzed cell death pathways using flow cytometry. In addition, we assessed whether FZ has synergistic effects when combined with the microtubule targeting drug taxol and the glycolytic inhibitor 2 deoxyglucose (2DG) or dichloroacetate (DCA) – a pyruvate dehydrogenase kinase inhibitor that shifts metabolism towards glucose oxidation over glycolysis.

The results demonstrated that FZ strongly inhibits hepatocellular carcinoma H4IIE cell proliferation, induces apoptosis and alters several pro-apoptotic proteins. However, when compared with control cells in the actively growing phase of the cell cycle, FZ is less effective when treating cells in late stationary phase (Fig. 9a).

Moreover, we observed that FZ reduces glucose uptake by H4IIE cells due to downregulation of the GLUT transporters and key glycolytic enzymes. This effect is related to p53 activation and alteration of microtubule dynamics. Additionally, FZ decreases cellular metabolite production by modulating genes such as hexokinase II, SCO255, TIGAR, and glutaminase 2 (GLS2)53–59. These results suggest that fenbendazole may act as a new antitumor agent by targeting multiple cellular pathways and inducing apoptosis. fenben for cancer

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