An antiparasitic drug, fenbendazole (FZ) interferes with microtubule activity and disrupts cell division. It is a member of the benzimidazole class of drugs and has been studied as a potential cancer treatment.

While research in cells and animals can look promising, no peer-reviewed study has found evidence that fenbendazole can cure cancer in humans. This is important because without evidence, a medicine cannot be approved for use in people.

Microtubule Inhibition

Developing new drugs for cancer is often time-consuming and expensive. Repurposing existing veterinary medicines that have shown promising results for human use can save significant time and money and accelerate the development process. Fenbendazole is a common anthelmintic drug used to treat parasites and worms in animals (common brands include Pancur, Safe-Guard) and has been found to be effective against certain cancers in humans.

Some studies show that fenbendazole can slow down cancer cell growth in cell cultures and animals. However, there isn’t enough evidence from randomized clinical trials showing that fenbendazole can cure cancer in humans. Moreover, anecdotal reports from people who claim to have cured their cancer by using fenbendazole aren’t reliable and could be due to other factors that aren’t being accounted for.

Fenbendazole is known to interfere with the microtubule polymerization process and inhibit the progression of cells through mitosis. By preventing the binding of cyclin B1 to CDK1, fenbendazole can prevent cell division and induce mitotic catastrophe. In addition, fenbendazole also causes oxidative stress by inducing the expression of pro-oxidants such as COX-2 and iNOS.

Fenbendazole also inhibits the expression of glucose transporters and hexokinase, a glycolytic enzyme that is necessary for cancer cell proliferation. Collectively, the microtubule disruption effect, p53 stabilization and interference with glucose metabolism lead to preferential elimination of cancer cells by multiple cellular pathways.

Inhibition of Glucose Uptake

Fenbendazole is an antiparasitic drug used to treat parasitic worms in animals like horses. It has been shown to slow down cancer cell growth in animal studies, but there is no evidence that it can cure humans with cancer. The claim that fenbendazole can cure cancer is based on an anecdotal story of Joe Tippens, who claimed that his melanoma went into remission after he started taking fenbendazole. However, he was also receiving conventional cancer treatments at the same time that could have also contributed to his remission.

According to a study published in Scientific Reports, fenbendazole can inhibit glucose uptake by cancer cells. This is because cancer cells require a lot of glucose for energy and to grow. By binding to tubulin, a key component of the microtubule protein, fenbendazole blocks its ability to function, which in turn stops cancer cells from getting the nutrients they need to grow and survive.

Additionally, fenbendazole targets multiple proteins and pathways that are involved in the cell cycle and apoptosis. This may make it more effective than single-target drugs, which often have limited efficacy and can lead to drug resistance. For example, fenbendazole can cause G2/M arrest in cancer cells by affecting the p53 pathway. It can also induce apoptosis through necrosis, autophagy, and ferroptosis. This means that fenbendazole can effectively kill cancer cells while avoiding any toxicity to normal cells.

Inhibition of P53 Stabilization

In contrast to popular depictions of cells that appear to be various organelles floating in an amorphous bag of liquid, cells establish their shape and structure through a protein scaffold called the cytoskeleton. The cytoskeleton is made of microtubules, which themselves are made of a polymer called tubulin. Like other cytotoxic anticancer drugs, fenbendazole interferes with the formation of microtubules by binding to and destabilizing tubulin.

A study published in 2022 found that fenbendazole can inhibit the growth of cancer cells in cell cultures and in mice. The drug also reduced the size of tumors in mice. The researchers attributed the effects to a reduction in oxidative stress and the inhibition of cellular signaling pathways.

The research was conducted on colorectal cancer cells and patient-derived colon cancer organoids. The authors found that fenbendazole inhibited glucose uptake and caused the cell cycle to arrest in G2/M phase in both cell lines. It also induced apoptosis through the p53 and p21 pathways. In addition, fenbendazole induced ferroptosis in SNU-C5 and SNU-C5/5-FUR cells. Ferroptosis is a form of autophagy that can be triggered by high levels of free iron, and it is known to lead to mitochondrial injury and caspase-3-PARP activation.

While fenbendazole has been shown to kill cancer cells in laboratory tests, there is no evidence that it can cure cancer in humans. It is unlikely that the anecdotal experience of Tippens could be replicated, and randomized controlled trials would need to be performed before any conclusions can be drawn.

Induction of Apoptosis

Unlike most other cancer drugs that target only one specific pathway of tumorigenesis, fenbendazole blocks several pathways. As such, it is able to prevent the development of resistance in cancer cells. This may also explain why it is effective against multiple types of cancers.

To determine the anti-cancer effects of fenbendazole, researchers treated human cancer cells with it. They found that it caused partial alteration of the microtubule network in the cell nucleus, resulting in apoptosis. They also found that it interfered with glucose uptake, inhibiting the energy supply to the cancer cells.

The team next tested fenbendazole for its ability to induce autophagy in colorectal cancer cells. They found that the drug significantly increased the expression of Beclin-1 and LC3-I, two important markers of autophagy. Moreover, it induced ferroptosis in the cells. Ferroptosis is a form of programmed cell death that involves the release of mitochondrial oxidative stress and reactive oxygen species.

Overall, the findings of the study suggest that fenbendazole can effectively eliminate cancer cells both in vitro and in vivo. The team also notes that the mechanism of action is multifaceted, involving moderate microtubule disruption, p53 stabilization, and interference with glucose metabolism. These results are promising, but there is no evidence that fenbendazole can cure cancer in humans. For this, randomized controlled trials involving large numbers of patients are needed. fenbendazole for cancer