Fenbendazole cancer is an antiparasitic drug that’s been shown to slow down tumor growth in cell cultures and mice. But it’s not a cure for people. In fact, it hasn’t even been proven to work in human clinical trials. And the anecdotal evidence that it can cure cancer is misleading at best.
A popular online story about Joe Tippens, a cancer patient in the United States, went viral after his claim that he was in remission from lung cancer because of fenbendazole and other alternative medicine treatments. In reality, Tippens was enrolled in a clinical trial at MD Anderson Cancer Center and had also been receiving other conventional cancer treatment at the time of his remission.
The researchers found that fenbendazole caused autophagy and cell death in colorectal cancer cells, but didn’t induce necroptosis or ferroptosis. This was because fenbendazole bound beta-tubulin and disrupted microtubules, which led to G2/M arrest and apoptosis. It also activated p53 and p21 pathways. However, p53 mutant cells showed decreased sensitivity to fenbendazole.
Moreover, the authors observed that fenbendazole enhanced the expression of autophagy proteins Beclin-1 and LC3-I, and decreased the expression of mitotic spindle protein, mitotic checkpoint complex, and anaphase-promoting complex in both SNU-C5 and SNU-C5/5-FUR CRC cells. In addition, fenbendazole increased the phosphor (total form) of p53 in SNU-C5 and SNU-C5/5-FUR cells, whereas ERK, p38, and JNK were not changed. This result indicates that the mechanism by which fenbendazole causes apoptosis in both 5-FU sensitive and resistant colorectal cancer cells is through activating p53-p21 pathways. fenbendazole cancer