Anecdotal reports of a cancer patient going into remission while taking fenbendazole have been making the rounds on social media, but there’s simply not enough evidence for it to be considered an established treatment. While research is ongoing, there are other ways to get into remission that don’t involve the risky side effects of the drug.
An anti-parasitic drug commonly used in animals to treat parasitic worms may also have some benefits for humans with certain cancers, according to researchers at Panjab University in India. The team’s study found that fenbendazole (FEN), a benzimidazole, could kill cancer cells in cell cultures and animals. The findings were published in the journal Scientific Reports.
The team observed that fenbendazole, or mebendazole, had a profound effect on cancer cells by inhibiting their phosphorylation of the PI3K-Akt pathway. This led to the downregulation of a number of tumor-suppressor genes. In turn, the cell cycle was interrupted, and apoptosis was triggered. The effect did not depend on the status of p53, which is typically increased by apoptosis-inducing drugs such as 5-fluorouracil. However, apoptosis and ferroptosis were enhanced by fenbendazole in cells with wild-type p53, but not those with mutant p53.
For their animal studies, the scientists gave EMT6 tumor-bearing mice three daily i.p. injections of fenbendazole or a placebo, and then subjected the tumors to 10 Gy of x-ray radiation. The growth of untreated tumors was not changed by fenbendazole, but the growth of irradiated tumors was significantly inhibited by fenbendazole. The results suggest that fenbendazole might enhance the effectiveness of radiation therapy by reducing resistance to irradiation and enhancing the induction of apoptosis and ferroptosis.
To test the effect of fenbendazole on hypoxic cells, the team cultured them in permanox Petri dishes (MP Biomedicals, Solon, Ohio) that are sealed with rubber gaskets and needles for the influx and outflow of gases. The cultures were made hypoxic by exposing them to 95% nitrogen and 5% carbon dioxide for 2 h before treatment, then treating the cells with either fenbendazole or an oxygen-selective compound, rapamycin (Sigma, St Louis, MO).
When treated with fenbendazole, the cells experienced significant decreases in proliferation, phosphatidyl serine, and total protein content, but not in total cellular viability, as assessed using a colorimetric assay. The hypoxic cells were more sensitive to rapamycin than nonhypoxic cells, suggesting that fenbendazole might improve the effectiveness of hypoxia-selective nitroheterocyclic cytotoxins and radiosensitizers, which have been shown to be enhanced by rapamycin (9, 10). Moreover, fenbendazole did not induce autophagy or ferroptosis in normal cells. However, the team is still examining these results further to understand the mechanisms of action. (FEN) Tara Williamson, Michelle Carvalho de Abreu, Dimitri G. Trembath, Cory Brayton, Thais Biude Mendes, Paulo Pimentel de Assumpcao, and Janet M. Cerutti, all of Johns Hopkins University, are inventors on intellectual property related to mebendazole and have financial interests in Benizole Therapeutics, PBC. The research was supported by the National Institutes of Health (NIH) and the American Cancer Society. fenbendazole for humans cancer