A widely used antihelminth, fenbendazole has recently been shown to have potent cancer-suppressive activity in lab experiments. Its mechanism of action is similar to those of hypoxia-selective nitroheterocyclic cytotoxics/radiosensitizers and taxanes. In this study we used EMT6 mammary tumor cells in cell culture and as solid tumors in mice to examine the cytotoxic and radiotumor effects of fenbendazole, alone and in combination with radiation or paclitaxel. Intensive treatment with fenbendazole was toxic to EMT6 cells, with toxicity increasing with incubation time and under conditions of severe hypoxia. However, fenbendazole did not alter the radiation dose-response curves and did not enhance the antineoplastic effects of either radiation or paclitaxel. In addition, fenbendazole in maximally-intensive regimens did not change the growth of EMT6 tumors in the mouse mammary gland or in lymph nodes and bone marrow.

The cellular concentration of fenbendazole was determined with an AlamarBlue assay and the IC50 values were calculated. LC-MS and NMR were used to check that the amount of fenbendazole measured was the same as the amount claimed on the label. Dissolution experiments were performed to simulate fenbendazole’s ability to dissolve in the fluids of the gastrointestinal tract, be absorbed and reach specific areas of the body. The 2% Sodium Dodecyl Sulfate (SDS) solution was used in the dissolution experiment, and the percentage of dissolved fenbendazole at the different time points was observed.

Both the analytical standard and commercial Brand P had a similar dissolution profile; the percentage of dissolved fenbendazole did not exceed 20% at any of the time points. In contrast, the commercial Brand S had a higher percentage of dissolved fenbendazole. This difference was attributed to the fact that the commercial Brand S had deuterated DMSO added, which enhanced its solubility. fenbendazole for cancer

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