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Mebendazole, a benzimidazole antiparasitic drug, was developed in 1971 by Janssen Pharmaceutica in Belgium. Initially introduced as a veterinary anthelmintic, it was later approved for human use to treat parasitic worm infestations such as pinworm, roundworm, and hookworm. Its broad-spectrum efficacy made it a cornerstone of global parasite control, earning a place on the World Health Organization's List of Essential Medicines.
Preclinical studies suggest mebendazole inhibits cancer cell growth, migration, and metastasis while inducing apoptosis and disrupting tumor angiogenesis. In animal models, it has shown potential to reduce tumor size and prevent metastasis, though robust human clinical data is still lacking.
Based on preclinical research, mebendazole has shown potential effects against the following cancers. Note that these findings are preliminary and lack confirmation from human clinical trials:
Mebendazole binds to the colchicine-sensitive site of β-tubulin in parasites, inhibiting microtubule polymerization. This disrupts glucose uptake and cellular transport, leading to parasite immobilization and death, particularly effective against nematodes.
In cancer cells, mebendazole disrupts microtubule dynamics, arresting the cell cycle at the G2/M phase. It also inhibits key oncogenic pathways such as Hedgehog, Wnt/β-catenin, and NF-κB, slowing tumor proliferation in preclinical models.
Mebendazole promotes apoptosis by depolarizing mitochondrial membranes and releasing cytochrome c, alongside increasing reactive oxygen species (ROS) levels. It also induces autophagy, contributing to cancer cell death in vitro.
By inhibiting P-glycoprotein efflux pumps, mebendazole reduces multidrug resistance in cancer cells. It may also modulate the tumor microenvironment, enhancing immune responses and sensitizing tumors to conventional therapies in experimental studies.