Fenbendazole is an antiparasitic drug that’s used to treat gastrointestinal parasites in animals. Some studies have found that it may also reduce cancer cell growth in laboratory tests.
The researchers found that fenbendazole reduced oxidative stress in triple-negative breast cancer cells (MDA-MB-231 and MCF-7). The drug also triggered ferroptosis and inhibited glucose uptake.
A benzimidazole compound used to treat parasites in dogs, fenbendazole (FZ) has shown cytotoxicity against cancer cells. It works by targeting microtubules in cancer cells, causing them to break apart and lose structure. It also interferes with the way cancer cells use glucose. This combination makes fenbendazole an excellent candidate for cancer therapy.
Researchers in the US have found that fenbendazole can slow down cancer growth in cells and mice. However, there is insufficient evidence that fenbendazole can cure cancer in humans.
In colorectal cancer cells, fenbendazole can inhibit cell proliferation and trigger apoptosis. In addition to causing G2/M arrest and increasing p53 expression, it also triggers ferroptosis, which is a form of cell death triggered by decreased mitochondrial function. This is mediated by decreased expression of Beclin-1 and GPX4 and increased caspase-3 activity.
Researchers have also found that fenbendazole, which is a type of anthelmintic drug, can reduce the number of lung metastases in mice. They injected the drug into the mice and then irradiated them. The researchers found that the fenbendazole-treated mice had significantly fewer lung tumors than the control mice. They also found that fenbendazole was not toxic to healthy lung tissue. Nevertheless, this anecdotal data isn’t enough to recommend fenbendazole for cancer patients. In fact, the anecdotal data may be misleading, and it is important to perform randomized controlled trials to verify these results.
Inhibition of glucose uptake
Fenbendazole may inhibit the uptake of glucose by cancer cells, and this could be a potential mechanism for its anticancer effects. However, it’s important to note that a lot of cancer research is done in animal models, and these findings don’t necessarily translate to humans. In addition, other evidence suggests that fenbendazole isn’t as effective in fighting cancer as it’s often claimed.
A 2022 study published in Scientific Reports found that fenbendazole could reduce cancer cell growth in vitro, and it also caused apoptosis in colorectal cancer cells. It also inhibited the growth of tumors in mice. The results of this study were consistent with earlier studies, which had shown that fenbendazole could cause cell cycle arrest in cancer cells.
Another study found that fenbendazole can induce necroptosis in 5-fluorouracil-resistant colorectal cancer cells. This is a form of cell death that involves activation of RIP and pMLKL, an enzyme that triggers mitochondrial dysfunction and oxidative stress. The study also found that fenbendazole significantly inhibited the autophagy process in 5-fluorouracil-resistant cancer cells.
A specialist cancer information nurse at Cancer Research UK told Full Fact that there’s no evidence that fenbendazole cures cancer. The drug hasn’t been tested in clinical trials to see if it works, and it’s not an established treatment for cancer. However, there are many other ways to treat cancer, and there’s no reason why anyone should avoid conventional treatment.
Induction of apoptosis
Scientists have discovered that fenbendazole can destroy cancer cells in the laboratory by stopping the proper growth of microtubules. The proteins that make up microtubules give cells their structure and shape. They also provide a scaffolding for transporting organelles. However, fenbendazole interferes with the formation of these proteins and prevents the cell from growing and dividing. The drug is already an ingredient in dog wormers and may have similar effects on human cancer cells. However, turning these laboratory tests into an approved drug is a long process.
Cancer cells often develop resistance to single-target drugs, so multi-target treatments are more likely to work. Researchers found that fenbendazole can cause multiple cellular changes to inhibit tumorigenesis and reduce tumour size in mice. Scientists believe that this effect is mediated by several different pathways.
The results showed that fenbendazole can trigger necroptosis in colorectal cancer cells by activating p53-dependent apoptosis and autophagy. It can also increase oxidative stress in these cells by increasing the expression of Beclin-1 and decreasing the expression of GPX4. This is accompanied by apoptosis, mitochondrial injury and caspase-3-poly (ADP-ribose) polymerase activity.
A spokesperson for Cancer Research UK told Full Fact that there is insufficient evidence that fenbendazole can cure cancer. The drug has not been tested in humans and hasn’t gone through clinical trials. It’s also not an NHS-approved medicine.
Inhibition of proliferation
Fenbendazole is a drug that has been used for many years to treat parasites and worms in animals. It has also been suggested that it may help prevent cancer in humans. A number of studies show that it can slow the growth of cancer cells in cell cultures and in animal models. However, the evidence for these claims is limited. Scientists need to conduct more clinical trials to confirm that fenbendazole can treat human cancer.
The research by Kyung-Sun Kang and Da-Hyun Kim, published in the American Association for Cancer Research, suggests that fenbendazole can cause apoptosis in colorectal cancer cells by targeting mitochondria. It can also increase p53 expression and induce oxidative stress-related pathways such as autophagy and ferroptosis. In addition, it can trigger apoptosis in 5-fluorouracil-resistant SNU-C5/5-FUR cells without affecting wild-type p53. The researchers found that fenbendazole activates apoptosis by inhibiting mitochondrial fission and increasing the expression of LC3, Atg7, and active caspase-8. Moreover, it suppresses GPX4 expression and augments ferroptosis-augmented apoptosis in these cells.
These results indicate that fenbendazole can target different cancers by triggering multiple pathways, including mitochondrial injury and caspase-3-poly (ADP-ribose) polymerase pathway activation. It can also interfere with glucose metabolism, thereby inhibiting cell proliferation and promoting apoptosis. This is a promising strategy for preventing tumor growth in cancer patients. In addition, fenbendazole has been shown to be safe in animals.