Fenbendazole for cancer is a promising drug that can help with various cancer types. It works by inhibiting glucose uptake and starving the cancer cells of energy. This leads to cell death through multiple mechanisms, including apoptosis and ferroptosis.
In a study published in Scientific Reports, researchers found that fenbendazole, an antiparasitic medication used in the veterinary industry, could effectively kill cancer cells. It did so by disrupting microtubules, stabilizing p53, and interfering with glucose metabolism.
Inhibition of glucose uptake
Fenbendazole is a commonly used drug that has been found to cause cancer cells to die in laboratory tests. The drug is also used to treat parasites and worms in animals. It is believed to inhibit the growth of tumors by blocking their ability to take up glucose. It also prevents cellular proliferation and induces cell death in cancer cells by killing the tumor forming stem cells.
The drug is not approved for use in humans, and there is no evidence it will cure cancer. A specialist cancer information nurse at the UK’s Cancer Research UK said that although studies in cells and animal models can sometimes look promising, a drug only proves its effectiveness (and safety) when it is tested in human patients.
In 5-FU-sensitive SNU-C5 and SNU-C5/5-FUR colorectal cancer cells, fenbendazole inhibits glucose uptake by inducing apoptosis and autophagy, and p53 is activated through mitochondrial injury or caspase-3 poly (ADP-ribose) polymerase. It also induces ferroptosis in these cells via glutathione peroxidase 4 (GPX4) inhibition, which results in lipid peroxidation. Moreover, the expression of LC3-I and Atg7 was increased significantly in fenbendazole treated cells.
This is the primary mechanism behind chemoresistance, which is when cancer cells develop resistance to chemotherapy drugs by expressing genes that produce enzymes that fight those drugs. In addition, most cancer cells are able to excrete drugs from themselves using special drug efflux pumps known as P-glycoproteins. This limits the amount of chemotherapeutic drugs that can reach cancer cells.
Induction of apoptosis
Apoptosis is the natural way that our bodies destroy cancerous cells. It is caused by a process called ferroptosis, which is characterized by lipid peroxidation and the inactivation of glutathione peroxidase 4. This is an important part of the cell’s cellular defence system. It is also a part of the process that prevents aging and keeps cells healthy.
A recent study found that fenbendazole, the main ingredient in the Joe Tippens protocol, can kill cancer cells by disrupting microtubules. Microtubules provide structure to all living things, including cancer cells. When they are disrupted, it stops the proper division of chromosomes during cell mitosis. This can lead to the formation of chromosome gaps, which eventually leads to cell death. The study also found that fenbendazole can kill cancer cells by targeting multiple pathways.
It can cause apoptosis by stabilizing p53 and interfering with glucose metabolism. It also cleaves PARP, an enzyme that is crucial for cell signaling and mitochondrial function. It can also prevent cellular reprogramming and inhibit telomerase activity, which is involved in cell cycle progression.
It can also reduce the proliferation of cancer cells by inhibiting the formation of a mitotic spindle. It can also reduce the expression of cyclin D1 and cyclin E, and prevent cell cycle entry into G2/M phase. In addition, fenbendazole can reduce the phosphorylation of ERK and STAT3. It also decreases the expression of caspase-3 and -8.
Inhibition of cell proliferation
The drug is believed to act by interfering with microtubules, a crucial protein required for cell division. During mitosis, chromosomes are evenly separated by a structure called the spindle, which is made from microtubules. When fenbendazole interferes with the formation of the spindle, it causes cells to divide more slowly and thus suppresses cancer growth.
It is also believed to induce ferroptosis, a form of programmed cell death that destroys invading cancer cells. This is believed to be one of the pathways by which fenbendazole reduces tumor size in mice. However, researchers say that fenbendazole also targets other cell processes that are involved in tumorigenesis. They believe that drugs that target multiple cellular targets will have improved efficacy and may overcome the resistance that often occurs to single-target cancer treatments.
In the lab, fenbendazole caused SNU-C5 and SNU-C5/5-FUR colorectal cancer cells to enter G2/M phase arrest and induced apoptosis via p53-p21 pathways in vitro. It also inhibited proliferation and increased the level of cytochrome-C in human colon cells.
While fenbendazole has been shown to slow the growth of cancer in cell cultures and animals, there is no evidence that it can cure cancer in humans. It is not a conventional cancer treatment and would need to undergo extensive clinical trials in humans to determine whether it is safe and effective.
Inhibition of DNA synthesis
The anti-parasitic drug fenbendazole blocks the formation of microtubules, which are part of the protein scaffolding in cells. The structures establish cell shape and help transport cellular cargo. The drug also interferes with RNA synthesis, inhibiting gene expression and inhibiting DNA replication. As a result, the cell is prevented from repairing itself and growing, and it will die.
Scientists have tested fenbendazole in human cancer cells and animal models. The drug appears to reduce the growth of some types of cancers, but it doesn’t seem to cure them. In addition, the drug isn’t known to be safe for humans. A specialist cancer information nurse at Cancer Research UK told Full Fact that “there is insufficient evidence that fenbendazole can cure cancer. The drug has not gone through any clinical trials to find out if it is a safe or effective treatment.”
In a series of experiments, researchers examined the effects of fenbendazole on unirradiated EMT6 tumors in BALB/c mice. The growth of the tumors was measured in three-week intervals until they reached a volume four times their initial size. The results show that fenbendazole didn’t alter the growth of unirradiated tumors, and it did not affect the radiation response of irradiated tumors.
In another set of experiments, researchers investigated the effects of fenbendazole in hypoxic colorectal cancer cells. The cultures were sealed in glass culture bottles, fitted with rubber gaskets and needles for the influx and efflux of gases. Then, a humidified mixture of 95% nitrogen and 5% carbon dioxide was gassed into the bottles for 2 h, and fenbendazole was added. The cells were exposed to varying concentrations of the drug, and survival curves were plotted.