Fenbendazole (FZ), a benzimidazole anthelmintic drug used in the treatment of worm infections, has been shown to prevent cancer cell growth. It is a potential candidate for drug repositioning since it has low toxicity in normal human cells. However, its pharmacokinetics and bioavailability in vivo remain unclear. This study aims to evaluate the ability of a commercially available FZ formulation to dissolve in the fluids of the Gastrointestinal tract and be absorbed into the circulation. This is accomplished through dissolution assays and HPLC, LC-MS, NMR analyses. In addition, a comparison of the FZ and a leading brand to determine whether they contain the stated amount of active ingredient on the label is also performed.
FZ induces G2/M arrest and apoptosis in 5-FU-sensitive SNU-C5 and 5-FU-resistant SNU-C5/5-FUR CRC cells. This anti-proliferative effect is accompanied by activation of p53 and p21, and is partly due to ferroptosis and autophagy. Interestingly, fenbendazole is able to increase wild-type but not mutant p53 expression in CRC cells, suggesting that p53-mediated pathways may not be required for fenbendazole-induced cell death in this type of cancer.
Mebendazole, the active ingredient in fenbendazole, is known to disrupt the structure of tubulin, which functions as a microscopic skeleton inside a cell and a highway for transport. In a recent study, Gregory Riggins and his team found that the drug can slow or even stop pancreatic cancer in mice by collapsing tumor cell tubulin. They hope to test the results of their research in human clinical trials. fenbendazole cancer treatment