Unlike other anti-parasitic drugs, fenben is also a powerful anticancer drug. It kills cancer cells and it also inactivates a significant number of normal stem cells in the small intestine.
It does so by disrupting microtubule dynamics, inhibiting p53 expression and modulating multiple pathways that lead to cell cycle arrest, apoptosis and ferroptosis. Moreover, it inhibits glucose uptake through down regulation of GLUT transporters and hexokinase, the key glycolytic enzyme.
1. It kills cancer cells
Unlike chemo, which floods your body with toxic chemicals that destroy all cells—including healthy ones—fenbendazole targets only cancerous cells. It does this by interfering with the formation of microtubules, a protein scaffold that gives cells shape and structure.
Cells establish their structures through a protein called the cytoskeleton, which is made of microtubules. During cell division, chromosomes are lined up at metaphase and then divided equally at anaphase through the cleavage of microtubules. When a cellular structure is altered, it is often accompanied by the death of that cell.
Benzimidazole compounds have been shown to interfere with energy metabolism in parasites by blocking glucose uptake and depriving the cell of ATP. We tested the ability of fenbendazole to inhibit the glucose uptake of H460 and A549 cells using the fluorescent glucose analogue 2-NBDG and found that it significantly decreased the cellular glucose consumption in both cell lines (Fig. 8a). In addition, anchorage independent growth of the cells was greatly reduced in the presence of fenbendazole.
2. It kills immune cells
There are a number of established treatments for cancer, including chemotherapy, radiation therapy, and surgery. These treatments are effective because they target cancer cells and stop them from dividing and growing. They also destroy any cells that contain mutated genes that may have caused the cancer to begin with.
However, there is an alternative treatment that has been shown to kill cancer cells as well — deworming drugs, such as fenbendazole. These medications work by interfering with microtubules, which are necessary for cell division. They also kill parasites, which might be the origin of some cancers.
Research has shown that fenbendazole is able to kill cancer cells in petri dishes and mice. It has also been found to boost the production of a gene called p53, which can help keep cancer cells in check. The drug also blocks cancer cells’ ability to process sugar, which they need to survive. These effects make fenbendazole a promising candidate for cancer therapy.
3. It kills stem cells
Fenbendazole has been shown to kill cancer stem cells in colorectal cancer (CRC) cell lines and patient-derived colon cancer organoids. It also prevented the proliferation of p53-deficient cells and inhibited the growth of metastases. However, there isn’t enough evidence that fenbendazole can cure cancer in people. The anecdotal story of Joe Tippens, a man whose cancer went into remission after taking fenbendazole on a veterinarian’s recommendation, has received millions of views on social media platforms.
Bendimidazole anthelmintics (BAs) have anticancer activity, but the mechanism of action is not consistent under different culture conditions and at different densities of cells. It induces intracellular changes to promote apoptotic cell death through distinct mechanisms under different growth conditions. Interestingly, the BAs reduce glucose uptake in cancer cells by down regulation of GLUT transporters and key glycolytic enzymes including hexokinase II. This is accompanied by ferroptosis-augmented apoptosis triggered by glutathione peroxidase 4 (GPX4) deficiency in p53-deficient cells. GPX4 is a mitochondrial protein that triggers autophagy to promote cell death.
4. It kills normal cells
A benzimidazole that is used as an anthelmintic to treat parasitic worm infections, fenbendazole (FZ) has been found to disrupt microtubules and cause cancer cells to die. The de-wormer also disrupts the ability of cancer cells to process sugar, which is required for their survival. It also boosts the production of a gene called p53 that can keep cancer cells from proliferating.
Treatment with fenbendazole causes cell cycle arrest and mitotic catastrophe in colorectal cancer cells. It also triggers necroptosis through a mechanism that is independent of p53, which can lead to caspase-8-dependent cell death.
In addition to its mode of action as a moderate microtubule destabilizer, fenbendazole induces apoptosis through other pathways in colorectal cancer cells, including mitochondrial injury and ferroptosis-augmented apoptosis. Moreover, the phenotypic effects of fenbendazole on tumorigenesis are enhanced in 5-fluorouracil-resistant SNU-C5 cells. Immunoblot analysis demonstrated that fenbendazole significantly increased Beclin-1 and LC3-I expression in these cells. It also decreased phosphor/total ERK, p38, and JNK levels. fenben for cancer