FENBENDAZOLE & IVERMECTIN VS CHEMOTHERAPY – ANIMAL STUDIES

A growing body of preclinical work in animals and in vitro, is examining ivermectin and fenbendazole as potential anticancer agents in animals. These antiparasitic agents hit cancer cells hard while leaving normal cells largely intact, while currently used chemotherapy agents like taxanes, hit not just the cancer cells but also destroy healthy cells.

A growing body of preclinical work in animals and in vitro, is examining ivermectin and fenbendazole — two inexpensive, widely used veterinary antiparasitcs — as potential anticancer agents in animals. The core finding is striking: these antiparasitic agents hit cancer cells hard while leaving normal cells largely intact, while currently used chemotherapy agents like taxanes, hit not just the cancer cells but they also destroy healthy cells. Understanding why requires looking at several simultaneous mechanisms.

The Microtubule Angle of The Antiparasitics — and Why It's Different From Chemotherapy

Ivermectin and fenbendazole work by binding beta-tubulin and disrupting microtubule cell structure (the cell scaffolding) — the same structural target exploited by major chemotherapy classes. But the similarity ends there. While traditional chemotherapeutic agents such as taxanes, inhibit the depolymerization of already-formed microtubules, antiparasitics like ivermectin and fenbendazole target a different binding site on beta-tubulin, blocking pre-polymerization — two distinct mechanisms of action, both resulting in microtubule dysfunction.

Compared to the known chemotherapeutic microtubule-disrupting agents like taxanes, ivermectin and fenbendazole show relatively mild tubulin depolymerizing activity (on the cell scaffolding). This moderate activity of ivermectin and fenbendazole may be part of why normal cells tolerate ivermectin and fenbendazole better. This moderate activity, however, is enough to obliterate the scaffolding of cancer cells, effectively causing the cells’ death.

The Chemotherapy Drug-Resistance Problem — Solved with Ivermectin and Fenbendazole A major limiting factor of chemotherapeutic agents like taxanes and vinca alkaloids is their dose, in attempting to limit their toxicity and susceptibility to multidrug resistance, occurring commonly due to high expression of P-glycoprotein which protects the survivability of cancer cells. Ivermectin and fenbendazole sidestep this problem in a structurally elegant way: targeting the colchicine-binding site in fenbendazole show minimal multidrug resistance, in addition to overcoming the effect of β-tubulin isoform overexpression and inhibiting the P-glycoprotein, thus protecting against cancer-friendly P-glycoprotein from being expressed.

Glucose Starvation and p53 Tumor Suppressor Protein Restoration

Ivermectin and fenbendazole both inhibit glucose uptake needed by cancer cells to survive. Therefore, disrupting glucose transport mechanism by blocking glucose import, is a direct metabolic attack on cancer cells. When the tumor suppressor protein p53 is restored, it prevents the expression and actions of the "glucose gates" in cancer cells. This dual hit on both the transporter and the tumor suppressor pathway that regulates it, works effectively against cancer cells.

The chemotherapeutic agents, such as taxanes, do not work this way against cancer cells.Chemotherapy kills cancer cells along with healthy, non-cancer cells.

The preclinical case for Ivermectin and Fenbendazole is coherent, multi-layered, and increasingly hard to dismiss.

Disclaimer

This information is for educational purposes only and is not intended to diagnose, treat, cure, or prevent any disease, or to replace the advice of a qualified veterinarian. Our PetMectin™️ and PetDazole™️ are indicated for animal use only. These statements have not been evaluated by the Food and Drug Administration.

Virex Health/Virogex Inc.