While there is some evidence that fenbendazole can stop cancer cells from proliferating in cell cultures, there is no proof that it cures people with cancer. The Joe Tippens protocol has been criticized for its lack of controls and anecdotal nature.
Researchers are looking at repurposing drugs for use as anti-cancer agents, including the broad-spectrum anthelmintic fenbendazole. It’s already used in veterinary medicine and has a wide safety margin in animals.
Inhibition of glucose uptake
Inhibition of glucose uptake by cancer cells is an important mechanism of action for anticancer drugs. Cancer cells require more glucose for energy than normal cells. This can lead to drug resistance in cancer therapy. The drugs that interfere with microtubules can prevent this process and help kill cancer cells.
Fenbendazole is a benzimidazole compound that is used as an antiparasitic drug in humans and other animals. It acts by binding to b-tubulin microtubule subunits and disrupting their polymerization. The drug has similar effects to cytotoxic anticancer agents that act on microtubules. These include the vinca alkaloids and taxanes.
Cells rely on microtubules to provide structure and shape. They also use them for cell division, which involves separating the even-numbered chromosomes into two identical copies. This is accomplished through a structure called the mitotic spindle, which is made of microtubules. Drugs that interfere with microtubules can inhibit the function of the mitotic spindle, preventing chromosome separation.
Researchers tested fenbendazole’s effect on human cancer cells in petri dishes and mice. They found that fenbendazole prevented cancer cells from taking up glucose and led to their preferential elimination. However, this effect was not enough to overcome the growth of tumors in these studies. These experiments were performed in mice with injected tumors, and the growth of the tumors was measured every week until they reached a volume of 1000 mm3. Tumors were then irradiated, and the number of lung metastases observed at necropsy was recorded.
Induction of apoptosis
Fenbendazole is a broad-spectrum antiparasitic drug used to treat parasitic worm infections in animals. It has been shown to reduce cancer cell growth in laboratory cultures. It also induces apoptosis in cancer cells and blocks glucose uptake, a major energy source for cancer cell proliferation. However, there is not enough evidence from randomized clinical trials to prove that fenbendazole cures cancer in humans.
Recently, posts on Facebook and TikTok claiming that a dog deworming medication called fenbendazole can cure cancer have gained traction online. These posts cite the story of Joe Tippens, an American man with lung cancer who took fenbendazole on a veterinarian’s recommendation and experienced dramatic improvements in his health. While these stories may be inspiring, there is insufficient evidence that fenbendazole cures lung cancer.
The benzimidazole carbamate compound fenbendazole has anthelmintic effects by binding to b-tubulin microtubule subunits and disrupting their polymerization. It has also been shown to have anticancer properties, but only at low concentrations.
A study by researchers at the National Centre for Human Genome Studies and Research (NCHGSR) in India found that fenbendazole could inhibit the growth of colorectal cancer cells. This was because it interfered with microtubules, which are important for the movement of cellular organelles. This mechanism of action is similar to that of hypoxia-selective nitroheterocyclic cytotoxins and radiosensitizers, such as paclitaxel and vinca alkaloids.
Inhibition of cell proliferation
Fenbendazole, which is also known as Pancur and Safe-Guard, is a benzimidazole anthelmintic that has long been used to treat parasites in humans (roundworms, hookworms, whipworms, and some tapeworms). More recently, it has been reported to have anti-cancer effects. It appears to inhibit cell proliferation by disrupting the microtubules that are involved in cell division. It also interferes with glucose uptake, which is a common energy source for cancer cells.
These effects are similar to those of paclitaxel and vincristine, two drugs that have been shown to be effective against some types of cancer. However, unlike these drugs, fenbendazole targets multiple mechanisms of tumorigenesis. Moreover, its multi-targeting action makes it less likely to cause drug resistance.
In addition to its effects on cellular proliferation, fenbendazole has an anti-tumor effect in leukemia and myeloma cells. It reduced their viability with a concentration of only 1mM in 8 of the eight myeloma and 4 of 6 leukemia cell lines tested.
In another experiment, a group of mice with EMT6 tumors were randomized to receive either three i.p. injections of fenbendazole or a placebo plus 10 Gy of x-rays. They were then monitored for tumor growth until they reached four times their original volume. The data show that fenbendazole did not alter the growth of unirradiated tumors, nor did it significantly affect the response to x-rays.
Inhibition of cell migration
The drug works by interfering with the formation of microtubules, a protein scaffold that gives cells their shape and structure. Cells also use this protein to transport organelles and cargo around the body. Textbook depictions of cells often show them as amorphous bags of liquid, but the reality is much different. In fact, a highly dynamic protein scaffold called the cytoskeleton gives each cell its shape and structure. It is a crucial mechanism for many aspects of cell function, including mitosis. When fenbendazole interferes with the formation of these microtubules, it blocks essential functions in the cell. The resulting cell cycle arrest prevents the cell from reproducing and leads to apoptosis.
Several studies have shown that fenbendazole can inhibit the growth of cancer cells in cell cultures and animals. However, these findings are preliminary and should be interpreted cautiously. They may be the result of other factors not accounted for, such as the conventional cancer treatments Joe Tippens received. Furthermore, these studies were conducted without randomized controlled trials.
The researchers found that 2- and 24-h treatments of fenbendazole significantly reduced the number of cells in monolayer cultures, and their clonogenicity was suppressed. In addition, fenbendazole caused G2/M cell-cycle arrest in 5-FU-sensitive SNU-C5 and SNU-C5/5-FUR cells, and induced apoptosis in both types of cells through the p21-mediated pathway and a combination of autophagy, necrosis, and fenbendazole for humans cancer