Fenbendazole, an antiparasitic medication that was first developed to deworm animals, has been shown in recent research to have a host of cancer-fighting properties and could potentially be used as an alternative to current therapies. The drug works by interfering with the glucose intake of cancer cells, starving them of their main source of energy and causing them to die off. Fenbendazole also has a microtubule-destabilizing effect, similar to the vinca alkaloids, which have been known to cause cell death by targeting microtubules and disrupting their formation.
The anthelmintic, which is listed by Health Canada as an animal dewormer, was originally designed to target parasites in ruminants such as sheep and cattle. In recent years, however, researchers have found that it can have other uses as well. Two drugs in the benzimidazole family have entered the clinical trial stage, but turning those trials into an effective human treatment will be a long journey.
In one experiment, a team of scientists at McMaster University discovered that fenbendazole has a host of cancer-fighting properties. In the study, the team tested how different doses of fenbendazole affect the growth and radiation response of EMT6 cancer cells in vitro. The results showed that high doses of fenbendazole significantly reduced the growth and clonogenicity of the cancer cells. The team then looked at the effects of severe hypoxia on fenbendazole toxicity. Severe hypoxia increased the cytotoxicity of fenbendazole, even at low concentrations. The team concluded that fenbendazole’s ability to interfere with the glycolysis of cancer cells, thus depriving them of their primary energy source and leading to their eventual death, is enhanced by hypoxia.
Another way in which fenbendazole may inhibit cancer growth is by blocking a protein called mTOR, which is involved in the proliferation of cancerous cells. MTOR is a signaling protein that regulates cell metabolism, cellular growth and division, and cell fate. Fenbendazole, like other benzimidazoles, interferes with the function of mTOR by binding to tubulin and interfering with its polymerization and stability.
A third method by which fenbendazole may reduce the growth of cancerous cells is by preventing their ability to absorb nutrients, including oxygen. The drug does this by binding to the ring of a molecule in the mitochondria, which causes a blockage of the nutrient transport system and prevents its function.
To test the effectiveness of fenbendazole in combination with radiation, the researchers conducted an experiment that compared the growth of unirradiated EMT6 tumors to their growth after being treated with three daily fenbendazole injections. They also compared the growth of irradiated tumors treated with fenbendazole alone to those that were only irradiated, and found that both treatments significantly decreased tumor growth, as measured by a colony formation assay. They did not, however, find any effect on the number of lung metastases that were present at necropsy in mice that had localized EMT6 tumor irradiation. The research was published in the journal Molecular Oncology. fenben
