Fenbendazole cancer treatment is an example of drug repurposing, in which drugs that were originally developed for use against one condition are found to be effective treating another. This approach is particularly useful for cancers, as it can be extremely expensive to discover a new drug and take it through the clinical trials required to receive FDA approval.

Fenbendazole was first used as an antiparasitic agent to treat pinworms, giardiasis, roundworms, hookworms and Taenia solium. It works by binding to and inhibiting the polymerization of tubulin, which makes up the microtubules in cells. Microtubules provide structure and support to cell cytoplasm, and if their function is disrupted by a chemotherapeutic agent, cancer cells may be unable to survive.

A number of studies using human and mouse cancer cells have demonstrated that fenbendazole reduces the viability of cancer cells. Some of these effects are similar to those observed with the cytotoxic anticancer agents, vinca alkaloids and taxanes, and fenbendazole exhibits minimal toxicity in normal cells when given at high doses.

In addition to affecting microtubules, fenbendazole can cause cancer cells to undergo apoptosis and/or necrosis. This is partly due to its sensitivity to p53 (p21), which is a tumor suppressor gene that regulates cell cycle progression and DNA repair. This effect is seen in colorectal cancer cells, where fenbendazole induces apoptosis via mitochondrial injury and caspase-3-poly (ADP-ribose) polymerase pathways. Moreover, fenbendazole can induce ferroptosis in colorectal cancer cells by activating glutathione peroxidase 4 (GPX4). fenbendazole cancer treatment

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