The anthelmintic fenben is currently used to treat parasites in animals. It is a synthetic benzimidazole carbamate that belongs to a class of medications called metronidazoles. It is FDA-approved for human use and is available at pharmacies in the United States. However, no peer-reviewed study has found that fenben can cure cancer. It is also not approved by Health Canada for the treatment of humans. There are a number of reasons why fenben does not cure cancer, including its relatively low solubility and the fact that the drug is excreted by the lungs. In addition, the drug is known to have side effects such as liver toxicity and allergic reactions in some people.
However, there is evidence that fenben may have anti-tumor activity. In a recent study published in Scientific Reports, researchers observed that fenben inhibited proliferation and promoted cell death in cancer cells in vitro. The authors also demonstrated that fenben affected the kinetics of mitotic catastrophe, a key event in cell division. Moreover, the authors found that fenben enhanced p53 translocation to mitochondria and blocked glucose uptake and expression of the glycolytic enzyme hexokinase II in cancer cells.
To assess the impact of fenben on microtubule dynamics, cultured A549 cells were treated with varying concentrations of fenben and examined by fluorescent imaging. The results showed that fenbendazole treatment significantly reduced the length of time that mitotic spindles remained in prophase, metaphase and anaphase. It also reduced the number of metaphase-plates and anaphase-plates. Furthermore, fenbendazole treatment significantly increased the amount of cyclin B1 that was acetylated by CDK1. Acetylation of tubulin is required for a normal progression of the cell cycle.
In addition, fenbendazole enhanced the sensitivity of cultured cancer cells to radiation. To test this hypothesis, cultures were treated with different doses of fenbendazole and then exposed to irradiation in aerobic or hypoxic conditions. The survival of these cultures was then assayed using a colony formation assay. The results indicated that fenbendazole had a similar radiation sensitizing effect on aerobic and hypoxic cancer cells.
To further characterize the radiosensitizing properties of fenbendazole, its interaction with the P-gp transporter was investigated. The P-gp inhibitor verapamil was added to the culture medium of cells treated with fenbendazole in order to determine whether or not it interacts with the transporter. However, neither the presence nor the absence of fenbendazole affected the ability of the drug to increase the uptake of the reference P-gp substrate rhodamine 123 (Rho123). These results indicate that fenbendazole does not bind to tubulin at the colchicine binding site and is therefore not a P-gp inhibitor. fenben