The antiparasitic drug fenbendazole is commonly used to treat parasitic worms and tapeworms in animals. It has also been found to be effective against cancer in mice and humans. The Joe Tippens Protocol, named for a man who claimed to have cured his own cancer using fenbendazole, has gained significant attention online.
Stanford virologist Jeffrey Glenn didn’t set out to develop drugs to cure cancer, but the work of his lab to thwart viruses like hepatitis and the common cold led to a new collaboration and a drug that appears to shrink tumors in mice. Glenn’s team has discovered that they can block the same cellular processes that allow certain viruses to grow and spread by disrupting normal cellular functions.
One of the key molecules targeted by benzimidazole carbamates is tubulin, which is involved in forming microtubules that form a cage around the nucleus and allow cell division. When tubulin is inhibited, cell-cycle progression stops because cyclin B1 no longer binds to cyclin-dependent kinase 1 (CDK1) to allow a transition from G2 phase to mitosis. The cells can no longer divide and apoptosis is triggered.
To test the hypothesis that fenbendazole might be able to inhibit cancer growth in humans, researchers treated human non-small cell lung cancer (NSCLC) A549 cells with different concentrations of fenbendazole. The cells were then analyzed for cell-cycle and apoptosis status using flow cytometry. Inhibition of tubulin polymerization by fenbendazole was confirmed by immunofluorescence, which showed that the cells were less active than control untreated cells. The apoptosis-inducing activity of fenbendazole was also determined by the increase in expression of caspase-3, poly (ADP-ribose) polymerase and cytochrome-C. A reduction of glucose uptake by the cells was also observed.
The team also looked for signs of autophagy, which is an essential cellular process for maintaining homeostasis in cells. They found that fenbendazole caused a shift in the protein p53, which regulates cell-cycle and apoptosis responses. Finally, they found that fenbendazole could reduce cancer cell survival by blocking the ability of a certain molecule, phosphorylated Akt/PKB, to activate mitosis-promoting complex (MPC) II.
Despite the evidence of in vitro and in vivo tests, the authors note that there is not enough information to support a claim that fenbendazole can prevent or cure cancer in humans. They stress that their research is early and more randomized clinical trials must be conducted before fenbendazole can be considered as an anticancer drug. However, the authors hope that their findings will encourage other scientists to pursue similar studies and develop drugs that use a combination of cellular mechanisms to fight against cancers. These drugs would be more effective than single-targeted approaches that have so far failed to provide substantial benefits to patients. The research was supported by the National Institutes of Health and the Stanford University Cancer Center. fenbendazole cancer