Triple Combination Of Ivermectin, Mebendazole and Fenbendazole For Cancer.
Abstract
✅Background:
Drug repurposing is gaining attention in oncology. Antiparasitic agents such as ivermectin, fenbendazole, and mebendazole have demonstrated preclinical anticancer activity. The potential synergy of these agents as a triple combination is of increasing interest.
✅Objective:
To review mechanistic rationale, preclinical evidence, and human observational data supporting the triple combination of ivermectin, fenbendazole, and mebendazole in cancer and discuss research gaps and limitations.
✅Methods:
Mechanistic studies, preclinical research, and publicly reported case testimonials were reviewed. Human evidence was synthesized using a PRISMA-style framework.
✅Results:
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Preclinical studies demonstrate complementary mechanisms of action across all three agents. 10 publicly reported cases of triple anti-parasitic therapy and one case of quadruple anti-parasitic therapy suggest temporal associations with tumor shrinkage or biomarker improvements, though all are uncontrolled and confounded by prior or concurrent therapies.
✅Conclusion:
While biologically plausible, the ivermectin–fenbendazole–mebendazole combination remains investigational. Observations are hypothesis-generating and warrant controlled preclinical studies and exploratory clinical trials before clinical adoption
✅Mechanistic Rationale: The Triple Combination Approach
The triple combination is based on complementary anticancer mechanisms:
➡️Microtubule Disruption: Fenbendazole and Mebendazole inhibit microtubule polymerization, leading to mitotic arrest and apoptosis (programmed cell death) (OneDayMD, 2026).
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➡️Metabolic Interference: Fenbendazole impairs glucose uptake via GLUT1/hexokinase inhibition, effectively disrupting the energy supply of cancer cells.
➡️Oncogenic Signaling Inhibition: Ivermectin targets STAT3, Wnt/β-catenin, AKT/mTOR, and YAP pathways, potentially enhancing programmed cell death and immune modulation.
➡️Anti-angiogenic Activity: Mebendazole suppresses VEGF-mediated angiogenesis, limiting the tumor's ability to form new blood vessels.
