Fenben lab fenbendazol is a broad-spectrum anthelmintic, approved for use in several animal species. It is an inhibitor of microtubule polymerization and has antitumor properties in human cancer cells with a KRAS mutation. It has also been shown to suppress tumor growth in animal models.5 Despite these promising results, there has been little interest in developing a human version of fenbendazole. Repurposing veterinary drugs with similar activity for human cancer therapy would be cost-effective and time-efficient.
In this case report, a 67-year-old female with advanced NSCLC began taking oral fenbendazole (Fenben(r) lab fenbendazole), an anthelmintic sold as a parasiticide for dogs. This medication was purchased and self-administered by the patient based on information obtained on social media sites that claimed it was effective against cancer.
The drug was administered three times daily as i.p. injections for a total of 12 days, until the tumors reached a volume of 1000 mm3. Neither local invasion of the tumors nor lymph node metastases was observed. Fenbendazole treatment did not affect the growth of unirradiated tumors or of irradiated tumors. The growth curve of irradiated tumors was not altered by three treatments of fenbendazole given one day before, two days before, or one day after irradiation (Figure 3).
Upon further investigation, it was determined that the reason fenbendazole did not significantly inhibit tumor growth in this animal model is that its antitumor effects are mediated by inhibition of cell cycle progression and the phosphorylation of cyclin B1. Cyclin B1 binds to cyclin-dependent kinase 1 (CDK1) to initiate mitosis. Inhibition of tubulin polymerization by fenbendazole causes the release of cyclin B1 from CDK1, which is then targeted for ubiquitination and proteasome-mediated degradation. This leads to a block in cell division and mitosis, thereby preventing the formation of new chromosomes.