Fenbendazole (Fenbendazole, Pancur) is a benzimidazole class antiparasitic drug that presents broad spectrum anthelmintic effect against worms in human and animals. It is used under veterinary medicine against various gastrointestinal parasites such as pinworms, roundworms, hookworms, whipworms and the Taenia genus of tapeworms in cattle, sheep, fish, dogs, cats, goats, horses and rabbits. It is also widely used as an animal feed additive against nematodes and trematodes in domestic food-animal species, such as pheasants (Syngamus trachea).
In humans, this medication is typically prescribed for parasite infections of the liver and digestive tract. However, there is growing interest in using fenbendazole to treat cancer. This is because a patient with stage four nonsmall cell lung cancer (NSCLC) has been reported to have experienced tumor shrinkage following the use of this drug, which is being used in conjunction with other natural products, in what is known as the Joe Tippens Protocol.
The underlying mechanism by which fenbendazole and other drugs in this class kill parasites is through interference with microtubules, structures that are vital to cell function. In particular, during cell division (mitosis), the even separation of chromosomes is achieved by the elongation of a mitotic spindle made from microtubules. Drugs that interfere with the activity of these microtubules inhibit important cellular processes and thus inhibit cell growth.
Although fenbendazole is approved for human use, it has not been studied extensively in cancer patients and the effects of its long-term use on humans remain to be determined. It has been shown, however, to induce G2/M arrest and apoptosis in colorectal cancer cells, suggesting that it may have anti-cancer properties. In addition, fenbendazole is known to activate p53 and p21 in normal human cells but decrease mutant p53 expression in cancer cells.
We therefore investigated whether fenbendazole-induced cell death in 5-FU-sensitive SNU-C5 and SNU-C5/5-FUR CRC cells was mediated via the formation of oxidative stress by glutathione peroxidase 4 (GPX4)-dependent ferroptosis. We found that fenbendazole treatment significantly reduced the viability of both cells and induced GPX4-dependent ferroptosis, a process characterized by the accumulation of free iron and mitochondrial dysfunction.
This case study highlights the potential risks of extra-label use of medications in humans and the need for physicians to be aware of this type of behavior among patients who may seek medical advice online. Future studies are needed to determine the extent to which GPX4-dependent ferroptosis is involved in fenbendazole-induced tumor suppression in cancer cells. These findings can also help in the design of more effective therapeutic strategies for chemoresistant NSCLC. The pharmacokinetics of fenbendazole need to be determined in order to assess how conservative withdrawal intervals should be in light of extra-label drug use. This is particularly important in the context of the widespread practice of alternative medicine in the treatment of cancer. fenbendazole for humans