Fenbendazole (also known as fenben or Pancur) is a common veterinary medication used to treat parasites and worms in animals. It is now being used in cancer patients as part of the Joe Tippens Protocol.
Fenbendazole targets the billions of cells lining the small intestine that transport nutrients into blood via tubulin-constructed beltways. It does this by interfering with glucose uptake.
Fenbendazole has been found to have anticancer activity in both cell cultures and animals. It acts through moderate microtubule disruption, p53 stabilization, and interference with glucose metabolism, leading to the preferential elimination of cancer cells in vitro and in vivo. It also causes inhibition in glucose uptake by downregulating glycolytic enzymes and GLUT transporters, starving them of the sugar they need to grow and multiply.
The drug also stimulates apoptosis in 5-fluorouracil-resistant SNU-C5 cells, and it increases ferroptosis and caspase-8 activation, but does not require p53. In this way, it may be a useful alternative treatment for patients with multi-drug resistant cancers.
It is important to remember that fenbendazole/Panacur is an animal anthelmintic, and only has limited experience with human use. Moreover, Tippens’ anecdotal experience with the drug could be a statistical outlier and isn’t likely to be replicated in randomized controlled trials. Therefore, further research is needed before fenbendazole/Panacur can be considered a viable option for humans with cancer.
Inhibition of glucose uptake
Fenbendazole is an anti-parasitic drug that also has powerful anti-cancer properties. It reactivates the p53 gene, which is known to suppress tumor development. In addition, it inhibits the proliferation of cancer cells by blocking their glucose uptake. This is especially important for malignant cancers, which depend on glucose for growth and survival.
Bendimidazole anthelmintics (BAs) have recently gained attention for their antitumor activity. The antitumor effects of FZ are mediated by multiple intracellular changes, including disruption of microtubule dynamics, p53 activation, and induction of apoptosis. It has been shown that FZ inhibits the growth of human cancer cells by reducing glycolytic enzymes and inhibiting the expression of the glucose transporter GLUT 4. In addition, it starves cancer cells of their primary energy source.
The aim of this study was to estimate the human risk associated with consuming tissues from pheasants treated with fenbendazole. The risk assessment was based on a deterministic approach. It calculated the FDA liver tolerances, EMA liver MRLs, and the LODs for pheasant liver fenbendazole sulfone for different tissues.
The anthelmintic benzimidazole carbamates (MBZ, albendazole, and mebendazole) have shown anti-cancer activity against cancer cells. These drugs inhibit glucose uptake and induce cell death by oxidative stress. They also disrupt microtubule dynamics and cause mitochondrial dysfunction.
The researchers studied fenbendazole in the human leukemia cells HL-60. They found that fenbendazole suppresses cellular growth and triggers apoptosis in a dose-dependent manner. The morphological changes were analyzed by phase-contrast and fluorescent microscopy. In addition, the levels of specific protein markers for apoptosis and autophagy were determined.
In addition to p21 induction, FZ also up-regulated apoptotic proteins such as cleaved caspase-3 and PARP, while the expression of anti-apoptotic bcl-2 was reduced. Furthermore, the effects of FZ were not affected by the pharmacological inhibition of mitogen-activated protein kinases. Furthermore, glucose consumption and lactate production were inhibited by FZ treatment. These results indicate that FZ can trigger apoptosis in cancer cells through the oxidative stress-induced cell cycle arrest and mitochondrial apoptosis pathways.
Fenbendazole is an animal anthelmintic and has a long track record of safety in humans. It has been used to treat parasites including ascaris, hookworm and trichuris for more than 40 years. It is also effective against tapeworms. Recently, a cancer patient claimed that he was cured of his small cell lung cancer using this anti-parasitic drug. Moreover, researchers have found that this benzimidazole carbamate is able to kill cancer cells in vitro and in mice.
It was also discovered that FZ inhibited the growth of HL-60 leukemia cells. It caused tubulin depolymerization, inhibited glycolysis and reduced ATP formation in the cell. In addition, it induced ROS accumulation in the cells. This toxicity was reversed by N-acetyl cysteine, which is an inhibitor of ROS production.
To determine the effect of hypoxia on fenbendazole cytotoxicity, cultures were grown in glass culture bottles sealed with rubber gaskets and needles for influx and efflux of gases. The gasses were replaced with a mixture of 95% nitrogen and 5% carbon dioxide containing 1 ppm oxygen. After 2-h treatments with fenbendazole, cell numbers were determined.fenben for humans