More On Repurposing Ivermectin To Treat Cancers

Written by Justus R Hope on August 3, 2026. Posted in Current News

While looking at before-and-after pictures of stubborn toe fungus treated with topical ivermectin, I could not help wondering: how are fungi similar to cancers? And why would agents that we find kill cancers also kill fungi?

The same toe, after worsening for two years under standard care, cleared dramatically in just seven weeks with once-weekly topical ivermectin applications.

Although ivermectin is generally considered to have only weak antifungal activity, the results were striking.

That personal observation led me deeper into a larger biological pattern that keeps appearing in the scientific literature: many compounds effective against pathogenic fungi also show potent anticancer activity, and vice versa.

This is not coincidence. Cancer cells and pathogenic fungi face nearly identical survival challenges inside a human host.

Both must grow aggressively, survive immune attacks, adapt to low oxygen and scarce nutrients, invade tissues, and resist chemical assault.

Not surprisingly, when we look at the agents that suppress cancer, we often see those same agents also suppress fungi. For example, let us review the agents that comprise the ROOT protocols that Dr. Marik and I published as powerfully preventing cancer. Most had notable anti-fungal activity.

Shared Survival Strategies: How Fungi and Cancer Cells Outmaneuver the Host

Researchers have documented more than a dozen mechanistic parallels between fungal pathogens (especially yeasts such as Candida and Cryptococcus, and molds such as Aspergillus) and malignant cells.

Here are the most important ones, ranked roughly by strength of experimental evidence:

Aerobic glycolysis (Warburg-like metabolism): Both cancer cells and many fungi preferentially ferment glucose even when oxygen is abundant. Classic yeast studies of the Crabtree effect showed that Saccharomyces cerevisiae converts glucose to ethanol under aerobic conditions when sugar is plentiful. Pathogenic fungi such as Candida albicans similarly maintain high glycolytic flux. This rapid ATP production supports fast growth in both systems.
Resistance to programmed cell death: Cancer cells disable apoptosis pathways. Fungi possess analogous anti-apoptotic machinery that allows them to survive oxidative stress, antifungal drugs, and host immune attack.
Multidrug resistance (MDR) efflux pumps: Both deploy ATP-binding cassette transporters and other pumps that eject toxins, chemotherapy drugs, and antifungal agents from the cell.
Hypoxia adaptation: Tumors develop hypoxic cores; fungi invading tissue or biofilms experience low-oxygen microenvironments. Both activate hypoxia-responsive pathways and shift metabolism accordingly.
Extracellular matrix (ECM) protection and biofilm/stroma formation: Cancer-associated fibroblasts and dense extracellular matrix shield tumor cells. Fungi form biofilms with protective matrices that limit drug penetration and immune cell access. Cryptococcus even produces a polysaccharide capsule that functions like a personal fortress.
Persistent dormant or “persister” cell subpopulations: Both maintain small populations of slow-growing, quiescent cells that tolerate therapy and later repopulate the disease. In cancer, these dormant cells are known as Cancer Stem Cells (CSCs); in fungal infections, they take the form of persister cells or spores. Both utilize these low-metabolism ‘sleeper cells’ to hide from drugs and the immune system, waiting for the optimal moment to reactivate.
Immune evasion strategies: Cancer cells downregulate antigen presentation, secrete immunosuppressive cytokines, and recruit regulatory immune cells.

Pathogenic fungi mask surface molecules, inhibit complement, and modulate macrophage and neutrophil responses.

Invasion and tissue dissemination: Cancer cells undergo epithelial-mesenchymal transition (EMT) and invade. Fungi switch between yeast and hyphal forms, secrete proteases, and penetrate epithelial barriers.
Mitochondrial dysfunction and alternate energy strategies: Both exhibit flexible metabolism, can operate with damaged mitochondria, and exploit alternative carbon sources or host metabolites.
Exploitation of host inflammation: Chronic inflammation fuels tumor progression. Fungi often thrive in inflamed tissues and can further amplify or manipulate the inflammatory response for their benefit.
Secretion of niche metabolites and signaling molecules: Both release factors that remodel the local microenvironment—altering pH, nutrient availability, and neighboring cell behavior—to favor their own survival.

Additional parallels include genomic instability under stress, phenotypic plasticity, and the ability to enter latent or dormant states that later reactivate. These shared strategies mean that the same molecular vulnerabilities appear in both systems.

Why the Same Drug Classes Hit Both Targets

Because their survival toolkits overlap so extensively, certain classes of compounds reliably damage both cancer cells and fungi. This shared vulnerability explains why antiparasitic and antifungal drugs like Ivermectin and Mebendazole have emerged as some of the most promising repurposed cancer agents of the past decade.

Membrane-active agents
Fungi rely on ergosterol; mammalian cells (including cancer cells) rely on cholesterol. Agents that disrupt sterol-rich membranes—such as polyenes (amphotericin B), azoles (itraconazole), and allylamines (terbinafine)—create lethal membrane instability. Cancer cells with altered membrane composition or high metabolic membrane turnover are often unusually sensitive to the same physical disruption.

Microtubule-targeting agents
Cell division requires functional microtubules. Benzimidazoles (mebendazole, fenbendazole, albendazole) bind fungal and mammalian tubulin, disrupting mitosis in much the same way that traditional chemotherapy drugs like taxanes (Taxol) and vinca alkaloids do.

Cryptococcus, a particularly aggressive fungal pathogen, shows striking sensitivity to several of these agents, mirroring the mitotic vulnerability of rapidly dividing cancer cells.

Mitochondrial and metabolic disruptors
Both fungi and cancer cells depend on flexible energy production and must manage high levels of reactive oxygen species. Compounds such as niclosamide, artemisinin derivatives, and anthracyclines interfere with this mitochondrial function, triggering an energy crisis or lethal oxidative stress in both cell types.

Nucleic-acid disruptors and antimetabolites
Agents such as 5-Fluorouracil (and its antifungal relative flucytosine), methotrexate, doxorubicin, and bleomycin interfere with nucleotide metabolism. Because both cancer cells and actively growing fungi ramp up these pathways, they share susceptibility.

These mechanistic overlaps explain why the list of dual-activity compounds keeps growing.

Repurposed and Dual-Activity Agents Showing Anticancer Promise

A growing roster of agents originally developed as antifungals, antiparasitics, antibiotics, or even everyday nutraceuticals now demonstrate anticancer activity in laboratory, animal, and sometimes clinical settings.

Many of them simultaneously suppress pathogenic fungi. Key examples include:

Benzimidazoles: mebendazole, fenbendazole, albendazole — potent microtubule disruptors with documented activity against Cryptococcus and multiple cancer types.
Azoles: itraconazole — a clinical antifungal that also inhibits cancer-related signaling pathways (including Hedgehog) and shows antitumor effects.
Niclosamide — mitochondrial uncoupler and multi-pathway inhibitor with strong preclinical antifungal and anticancer data.
Ivermectin — the agent that cleared the long-standing toe fungus; it exhibits both modest antifungal effects and broader anticancer mechanisms (including effects on signaling pathways and mitochondrial function).
Doxycycline — antibiotic with mitochondrial and anti-angiogenic effects relevant to both systems.
Metformin — metabolic modulator that influences AMPK and mitochondrial pathways.
Berberine, curcumin, EGCG, quercetin, apigenin, steviol/stevioside, garlic extract (allicin) — plant-derived compounds with documented anti-Candida and anticancer activities, often through membrane perturbation, oxidative stress, or signaling pathway interference.
Vitamin D3 — modulates immune responses and cellular differentiation relevant to both host defense against fungi and cancer control.
PSK (polysaccharide-K / Turkey Tail) — immunomodulatory and metabolic effects.
Classic chemotherapeutics with secondary antifungal activity: doxorubicin, paclitaxel (Taxol), methotrexate, bleomycin, and vincristine.

Additional agents that strengthen the dual-activity pattern include amphotericin B, terbinafine, certain artemisinin derivatives, and 5-fluorouracil/flucytosine.

When ranked by combined antifungal and anticancer potency, the strongest cluster includes the classical antifungals (amphotericin B, itraconazole, terbinafine), the benzimidazoles, niclosamide, anthracyclines, garlic/allicin, and selected artemisinins.

The Overlap Is Mechanistic, Not Accidental

Cancer cells and pathogenic fungi are both eukaryotic organisms that have evolved under intense selective pressure to survive inside a hostile mammalian host.

They independently converged on many of the same solutions: rapid glycolytic energy production, robust drug efflux, anti-death machinery, protective extracellular structures, metabolic flexibility, and immune manipulation.

Consequently, a drug that successfully attacks one of these deeply conserved programs in a cancer cell often finds the same vulnerability in a fungal cell.

The Example of Cryptococcus

Take the example of Cryptococcus (specifically C. neoformans and C. gattii). This highly dangerous, encapsulated yeast thrives in the environment (often in bird droppings) and the lungs of vulnerable hosts.

What makes Cryptococcus uniquely difficult to eradicate is its ability to build physical fortresses and exploit hypoxic (low oxygen) environments to hide from both the immune system and antifungal drugs.
Upon entering the host’s lungs, the fungus constructs a massive, gelatinous polysaccharide capsule around itself, creating a walled-off barrier that blocks macrophages from engulfing it and physically limits the penetration of standard antifungal drugs like echinocandins.
When phagocytes do manage to swallow the yeast, Cryptococcus uses the immune cell itself as a ‘Trojan Horse.’ Rather than dying in the harsh, hypoxic, and acidic compartment of the macrophage, it neutralizes the acid with urease, drops its metabolic rate to survive the hypoxia, and hitches a ride inside the immune cell across the blood-brain barrier to cause lethal meningitis.

The Search for New Anti-Cancer Agents

Agents long used against fungi are being re-examined for oncology, and many oncology drugs display measurable antifungal effects in laboratory assays. The pattern holds across membrane disruptors, microtubule poisons, mitochondrial toxins, and antimetabolites.

The observation that began with a stubborn toe fungus clearing under topical ivermectin is not an isolated curiosity.

It points to a broader biological truth: pathogenic fungi and cancer cells rely on overlapping toolkits for survival inside the human body.

Because those toolkits are so similar, agents capable of dismantling them frequently work against both.

This is not chance. It is the predictable consequence of shared evolutionary pressures and conserved eukaryotic biology.

Understanding these parallels helps explain why so many antifungal, antiparasitic, and metabolic compounds are now showing anticancer promise—and why the search for better cancer therapies continues to find unexpected allies among drugs originally developed to fight fungi.

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Header image: ET Health World