Fenbendazole is a medication commonly used to treat parasites and worms (roundworms, hookworms, whipworms, and some tapeworms) in animals. It’s also a common ingredient in a cancer treatment protocol known as the Joe Tippens Cancer Protocol, which claims to cure some types of cancer in humans using a combination of this drug and other antiparasitic supplements. However, scientific evidence shows that fenbendazole doesn’t prevent or treat cancer in humans and it can have dangerous side effects.
The Joe Tippens Cancer Protocol recommends taking 222 mg of fenbendazole (one gram of Panacur C) a day, seven days a week. This dose is not recommended for everyone, and people should follow the instructions on their prescription label to avoid a toxic overdose.
While some studies show that fenbendazole slows tumor growth in cell cultures and mice, there isn’t sufficient evidence to suggest that it could cure cancer in humans. Most of the studies that have been conducted on this topic are anecdotal and based on the experience of one patient who experienced a complete remission after using fenbendazole. This anecdotal information doesn’t take into account that the patient also underwent conventional cancer treatments, which aren’t accounted for in these studies.
Fenbendazole works by interfering with the formation of microtubules, which are part of the protein scaffold in cells. Textbook depictions of cells often portray them as floating bags of amorphous liquid, but the cytoskeleton provides structure and stability to cell structures and organelles. Benzimidazole drugs, including fenbendazole, work by blocking the function of this protein scaffold, which is necessary for cellular growth and activity.
In the study, researchers found that fenbendazole was able to slow the growth of SNU-C5 and SNU-C5/5-FUR colorectal cancer cells in vitro. This effect is believed to be due to a reduction in the proliferation of these cells and increased p21 expression, which promotes cell cycle arrest. Fenbendazole was also found to induce autophagy, augmented by Beclin-1 and LC3-I, in both SNU-C5 and SNU-C5/5-FUR cells. In addition, fenbendazole was a potent inhibitor of the growth of 5-fluorouracil-resistant colorectal cancer cells, suggesting that this drug may be useful for treating resistant tumors.
Aside from its effects on cellular growth, fenbendazole was found to induce apoptosis and necroptosis in both 5-FU-sensitive and 5-FU-resistant colorectal cancer cells. The effect of fenbendazole on apoptosis was associated with its ability to activate p53 and increase p21 expression, but it was independent of the presence or absence of mutant p53 in SNU-C5 cells. The effect of fenbendazole-induced necroptosis was also independent of p53 in both irradiated and unirradiated cancer cells. However, it was more pronounced in irradiated cells than in unirradiated cells. This indicates that the apoptotic and necroptosis-promoting effect of fenbendazole is mainly dependent on its ability to inhibit mitochondrial respiration and block mitosis. fenbendazole for cancer