Fenbendazole (commonly referred to as “fenben”) is a benzimidazole antiparasitic medication that has been used for several gastrointestinal parasites including pinworms, giardiasis, roundworms, hookworms, whipworms, and tapeworms in humans. It has also been reported to have antitumor and anticancer properties, inhibiting tubulin polymerization which is similar to the actions of cytotoxic anticancer agents such as vinca alkaloids and taxanes. A recent case report of an 80-year old woman with advanced nonsmall cell lung cancer (NSCLC) who self-administered fenbendazole based on social media reports claiming that it was effective in treating her tumor has drawn attention to this alternative therapy.
A new antitumor treatment involving fenbendazole is becoming increasingly popular as the Joe Tippens protocol, but little scientific data have been published on its effectiveness. This article examines a case of a patient who developed severe liver dysfunction shortly after starting the treatment, which was determined to be due to her self-administration of fenbendazole. This is the first known case where a patient experienced liver injury as a result of using an alternative therapy for cancer.
To investigate the effects of fenbendazole on EMT6 tumor growth and radiation response, BALB/cRw mice were injected with either fenbendazole, a placebo, or both, then stratified by their initial tumor volume. The time to the point where the tumor had grown four times its original volume was then calculated. Results showed that both fenbendazole and placebo did not alter tumor growth or radiation response.
In addition, to examine the effect of fenbendazole on hypoxic cancer cells, cultures were made hypoxic by sealing them in permanox Petri dishes with rubber gaskets, inserting needles for the influx and efflux of gases, then gassing them with a mixture of 95% nitrogen and 5% carbon dioxide containing 1 ppm oxygen. Fenbendazole was then injected into the culture via the septum, while still in hypoxia. The cultures were then sealed, transported to the irradiator, and irradiated.
Despite the fact that fenbendazole is not a hypoxia-selective agent, the culture studies demonstrated that fenbendazole caused an early elevation of cyclin B1 in A549 cells and inhibited mitosis progression through its inhibitory effects on tubulin polymerization. This was likely due to its action on cyclin-dependent kinase 1, an essential protein that binds to and phosphorylates CDK1, enabling the cell to transition from G2 to anaphase. Hypoxia enhanced the ability of fenbendazole to prevent cell-cycle arrest, which suggests that this compound may be useful as a hypoxia-selective cancer drug. However, additional investigations will be necessary to verify this hypothesis. Furthermore, further experiments will be required to determine whether fenbendazole exhibits any synergistic interactions with radiosensitizers or the hypoxia-selective nitroheterocyclic cytotoxins. This research could lead to the development of a novel and effective combination therapy with fenbendazole and other drugs, such as the taxanes and vinca alkaloids. This combination therapy would significantly enhance the effectiveness of current treatments and may improve patient outcomes.fenbendazole cancer
