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Citation: Tang M, Hu X, Wang Y, Yao X, Zhang W, Yu C, Cheng F, Li J, Fang Q. Ivermectin, a potential anticancer drug derived from an antiparasitic drug. Pharmacol Res. 2021 Jan;163:105207. doi:10.1016/j.phrs.2020.105207. PMID: 32971268; PMCID: PMC7505114.

Ivermectin (IVM) is a macrolide antiparasitic drug with a 16-membered ring structure, derived from a natural compound called avermectin. It belongs to a drug family that also includes selamectin, doramectin, and moxidectin. For decades it has been a frontline treatment for parasitic diseases like river blindness, elephantiasis, and scabies. Its discoverers, Satoshi Ōmura and William C. Campbell, won the 2015 Nobel Prize in Physiology or Medicine for it.

Because ivermectin is already FDA-approved, cheap, and has a well-established human safety profile, it's an attractive candidate for "drug repurposing" — finding new medical uses for existing drugs, which can skip years of safety testing that a brand-new compound would require.

Ivermectin has powerful antitumor effects, including inhibiting cancer cell proliferation, metastasis, and angiogenic (blood vessel-forming) activity across a variety of cancer types. Much of this appears connected to ivermectin's action on a protein called PAK1. On top of blocking tumor growth, ivermectin also promotes several forms of programmed cancer cell death — apoptosis, autophagy, and pyroptosis — and these death pathways appear to interact with and regulate one another in complex ways that aren't yet fully understood.

Evidence in cell culture and animal models spans a wide range of cancer types, including: colon cancer, breast cancer, ovarian cancer, melanoma, leukemia (including chronic myeloid leukemia), glioblastoma, esophageal squamous cell carcinoma, gastric cancer, cholangiocarcinoma, and renal cell carcinoma.

Important caveat: essentially all of this evidence is preclinical — lab dishes and mice — not large-scale human clinical trials.

PAK1 (p21-activated kinase 1) is overactive in a large share of human cancers. It sits at a crossroads of several growth-signaling pathways (RAS, MAPK/ERK, and Akt/mTOR), so cancer cells rely heavily on it to keep dividing and surviving. Ivermectin tags PAK1 for destruction through ubiquitination (the cell's "marked for the trash" labeling system). Because PAK1 sits at that crossroads, degrading it disrupts multiple downstream growth pathways at once — a big part of why ivermectin seems to attack cancer cells from several angles rather than through one narrow mechanism.

Apoptosis (programmed cell death)Triggered mainly through mitochondrial stress. Ivermectin increases reactive oxygen species (ROS) and lowers mitochondrial membrane potential. It tips the balance of pro-death protein Bax over survival protein Bcl-2, causes cytochrome C to be released into the cytosol, and activates a caspase-9/caspase-3 cascade. Activated PARP and caspase-3 finish the job, executing the cell.

AutophagyNormally, autophagy is a cellular "recycling" process that helps stressed cells survive. Ivermectin instead pushes autophagy into a cytostatic mode — one that halts proliferation rather than aiding survival. Mechanism: ivermectin degrades PAK1 → this shuts down Akt/mTOR signaling → which allows a protein complex (Beclin-1/PtdIns3K) to form → which drives this growth-halting form of autophagy, working largely independent of the apoptosis pathway above.

PyroptosisA more inflammatory form of cell death. Ivermectin promotes ROS release via P2X4/P2X7 receptors on the cell surface. This activates the NLRP3 inflammasome, a multi-protein "alarm" complex containing a pattern-recognition receptor, ASC, and pro-caspase-1. This causes pro-caspase-1 to self-cleave into active caspase-1, which does two things: (1) triggers pyroptosis via a protein called GSDMD, and (2) separately drives secretion of the inflammatory signaling molecules IL-1β and IL-18.

How these interact: The paper stresses that apoptosis and autophagy are not fully independent — they mutually regulate each other — and that the exact molecular relationship between them still needs further study.

• Cancer stem cells: A small subpopulation of cells within tumors that resist standard treatment and drive relapse after therapy. Ivermectin has been shown to suppress "stemness" markers in these cells — relevant because killing the bulk tumor while leaving stem cells intact is a common reason cancers recur.
• Multidrug resistance (MDR): Ivermectin appears able to reverse mechanisms that let cancer cells pump out or neutralize chemotherapy drugs, potentially restoring their sensitivity to existing treatments.

The authors emphasize that ivermectin's anticancer effect is generally strongest when combined with conventional chemotherapy agents, rather than used as a standalone treatment. This suggests it may function best as an adjunct or sensitizer to existing therapies rather than as a replacement for them.

Cancer treatment has always been a moving target. Chemotherapy, radiation, and surgery remain the pillars of oncology — but for decades, researchers have been quietly building a parallel body of literature around compounds that may support, enhance, or complement those conventional approaches. Some are repurposed drugs that have been in clinical use for years. Others are natural compounds with centuries of traditional use now being examined under rigorous scientific methodology.

This is not a list of cancer cures. It is a survey of what the current research shows about compounds generating legitimate scientific interest — and why physicians, researchers, and informed patients are paying closer attention to them.

Best known as an antiparasitic, ivermectin has accumulated a substantial body of preclinical research suggesting anticancer properties. Studies indicate it may disrupt tumor blood supply by inhibiting angiogenesis — effectively starving cancer cells of the oxygen and nutrients they need to grow. It has also shown activity in reversing multidrug resistance, potentially restoring the effectiveness of chemotherapy agents, and promoting cancer cell death via autophagy (programmed cellular self-destruction).

Note: For cancer treatment, Ivermectin is not FDA-approved, not standard of care, and ASCO and the American Cancer Society advise against its use outside a clinical trial.

Another antiparasitic with a growing oncology research profile. Mebendazole disrupts microtubule formation — the cellular scaffolding cancer cells depend on to divide. It inhibits new blood vessel formation to tumors, down-regulates proteins that shield cancer cells from apoptosis, and has shown synergistic effects with conventional chemotherapy and radiation in multiple cancer models. A 2019 review in Cancers characterized it as a serious candidate for drug repurposing in oncology.

Note: For cancer treatment, Mebendazole is not FDA-approved, not standard of care, and ASCO and the American Cancer Society advise against its use outside a clinical trial.

Both Reishi (Ganoderma lucidum) and Turkey Tail (Trametes versicolor) have been used in traditional East Asian medicine for centuries. The underlying mechanisms are now better understood. Bioactive compounds in these mushrooms bind to receptors on immune cells — activating natural killer cells, T cells, and macrophages — and enhance cytokine production, improving the immune system’s ability to identify and clear abnormal cells. Reishi compounds have additionally shown anti-angiogenic and anti-metastatic activity in research models.

Rich in polyphenols — particularly oleuropein — olive leaf extract has demonstrated potent anti-inflammatory activity and antioxidant properties relevant to cancer biology. Free radical damage contributes to both the initiation and progression of many cancers; the extract’s ability to neutralize oxidative stress makes it an area of ongoing interest, particularly in hormone-related malignancies.

Epigallocatechin gallate (EGCG), the primary active catechin in green tea, has been one of the most extensively studied natural compounds in cancer research. It selectively induces apoptosis in cancer cells while leaving healthy cells relatively unaffected, blocks pro-cancer signaling pathways that drive cell replication, and inhibits angiogenesis in tumors. The selectivity profile — affecting malignant cells preferentially — is what makes EGCG particularly interesting to researchers.

Originally developed as an antimalarial, methylene blue is now being studied in the context of photodynamic therapy — a treatment modality that uses light activation to destroy cancer cells. Its mechanism involves flooding cells with oxygen (cancer cells frequently exploit low-oxygen microenvironments), reducing oxidative stress, protecting mitochondrial function, and supporting healthy cell survival signaling. Current research is focused on optimizing its use as a photosensitizing agent in oncology.

Found in goldenseal, barberry, and Oregon grape, berberine is often discussed for its metabolic effects — it’s sometimes called “nature’s metformin” for its insulin-sensitizing properties. That metabolic activity is directly relevant to cancer: berberine modulates proliferation signaling pathways, induces cancer cell death, inhibits tumor blood supply, and regulates gut microbiota in ways that may support immune function. It has also shown enhancement of other anti-tumor agents in combination studies.

Curcumin, the active compound in turmeric, requires co-administration with piperine (black pepper) to achieve meaningful bioavailability — a critical practical point. With adequate absorption, curcumin has demonstrated the ability to downregulate cancer-promoting signaling cascades, reduce chronic inflammation (a recognized driver of malignancy), modulate immune and oxidative stress markers, and mitigate DNA damage caused by radiation — making it relevant to patients undergoing radiotherapy.

The most widely prescribed antidiabetic drug in the world has a compelling parallel research profile in oncology. Metformin lowers circulating insulin levels (elevated insulin is a tumor growth promoter), inhibits mTOR and AMPK pathways central to cancer cell proliferation, suppresses cancer stem cells — a population associated with treatment resistance and metastasis — and reduces tumor blood supply. Multiple large observational studies have shown reduced cancer incidence and improved outcomes in diabetic patients on metformin.

An unlikely entry, but one with emerging data. Dandelion root extract has demonstrated the ability to activate multiple apoptotic signaling pathways in colorectal cancer cells and suppress gastric cancer cell proliferation and migration in laboratory studies. Its profile as a non-toxic agent with low side effect burden makes it a candidate for integration into broader cancer support protocols, particularly where drug-resistant disease is a concern.

 *Disclaimer: This article is for educational purposes and does not constitute medical advice. Always seek professional guidance. This protocol and use is not FDA-approved, not standard of care, and that ASCO and the American Cancer Society advise against it outside a clinical trial.

In the evolving landscape of cancer research, Dr. William Makis, a Canadian radiologist, oncologist, and researcher with over 100 peer-reviewed publications, has proposed an innovative “hybrid orthomolecular” protocol that repurposes antiparasitic medications such as ivermectin and mebendazole/fenbendazole. This approach draws on preclinical (in-vitro and animal studies) evidence suggesting these drugs may exhibit anticancer properties, including the induction of apoptosis, disruption of mitochondrial function, and targeting of cancer stem cells (CSCs). While promising, it remains experimental and lacks large-scale clinical validation. This article provides an educational overview of the protocol, including its scientific rationale, detailed regimens, supporting evidence, and key considerations for readers interested in alternative therapeutic strategies.

Conceptual Foundation of the Protocol

Makis’ protocol centers on the mitochondrial-stem cell connection (MSCC) in cancer biology. Malignant cells often rely on anaerobic fermentation for energy (the Warburg effect), evading efficient oxidative phosphorylation. Dr. Makis’ method seeks to restore mitochondrial efficiency, deprive tumors of fermentable substrates like glucose and glutamine, and eliminate CSCs, which contribute to metastasis and treatment resistance.

Key agents include ivermectin, an antiparasitic with anti-inflammatory and antiviral effects, and benzimidazoles (mebendazole for human use or fenbendazole, its veterinary equivalent). Preclinical studies indicate these compounds may inhibit tumor growth more effectively than certain chemotherapeutics in specific models. Dr. Makis has highlighted their potential against “turbo cancers”—rapidly progressing malignancies he associates with mRNA COVID-19 vaccines—reporting a 75% response rate in combination therapy.

Detailed in a September 19, 2024, publication in the *Journal of Orthomolecular Medicine* co-authored with Dr. Ilyes Baghli and Dr. Paul Marik, the protocol integrates drug repurposing with orthomolecular interventions (nutrient-based therapies).

It is typically administered:

• over three months in cycles of three weeks on and one week off 
• regular monitoring of liver and kidney function
• bioavailability is enhanced by consuming doses with fatty meals

Makis’ Dosages are stratified by cancer grade: low (early-stage, indolent), intermediate (moderately progressive), or high (aggressive or metastatic). Personalization is essential, with adjustments based on patient response and tolerability.

Makis states that Ivermectin promotes autophagy and apoptosis through mitochondrial pathways, suppresses glycolysis, and selectively targets CSCs. In vitro and animal studies demonstrate its ability to reduce tumor volume, sometimes surpassing agents like paclitaxel.

Dosage Guidelines *This protocol and use is not FDA-approved, not standard of care, and that ASCO and the American Cancer Society advise against it outside a clinical trial.*
(weight-based; e.g., 1 mg/kg for a 70 kg individual equates to 70 mg):

• Low-grade cancers, remission maintenance, or prophylaxis: 0.5 mg/kg, three times weekly (e.g., Monday, Wednesday, Friday).
• Intermediate-grade cancers: 1 mg/kg, three times weekly, or 0.5–1 mg/kg daily for more challenging cases.
• High-grade or turbo cancers: 1–2 mg/kg daily, escalating to 2.5 mg/kg in severe metastatic scenarios (monitor for transient visual disturbances).

Administration: Six days on, one day off; ingest with food. Long-term use at up to 2 mg/kg daily is reported as safe.

Case examples illustrate potential efficacy: A patient with Stage 3 ovarian cancer experienced complete tumor resolution within two months on 12 mg daily alongside chemotherapy. An 83-year-old with Stage 3 follicular lymphoma achieved near-total remission in six months at 1 mg/kg daily. A 54-year-old with recurrent prostate cancer reached remission in four months at 1.5 mg/kg daily.

These benzimidazoles impair microtubule assembly, restrict glucose and glutamine uptake, and activate the p53 tumor suppressor pathway, with particular activity against CSCs. Their synergy with ivermectin enhances overall response rates.

Dosage Guidelines (generally flat doses) *This protocol and use is not FDA-approved, not standard of care, and that ASCO and the American Cancer Society advise against it outside a clinical trial.*

• Low-grade: Mebendazole 200 mg daily or fenbendazole 222 mg, three times weekly  (complement with vitamin E 800 IU, curcumin 600 mg, and CBD oil 25 mg daily).
•  Intermediate-grade: Mebendazole 400 mg or fenbendazole 222 mg, six days weekly.
• High-grade: Mebendazole up to 1,500 mg or fenbendazole 444–1,000 mg daily, six days weekly (higher for patients over 200 lb or extensive disease; up to 4 g mebendazole reported as tolerable).

Administration: Post-meal intake with milk thistle (250–350 mg) for hepatoprotection; regular blood monitoring advised.

Illustrative cases: A pancreatic cancer patient showed marked improvement with the combination. Stage 4 renal cell carcinoma resulted in a 71% reduction in lung metastases over six months on high-dose fenbendazole.

Preclinical data from the 2024 publication and related studies support superior outcomes in models compared to standard chemotherapy. A 2025 PubMed case series on fenbendazole documents tumor regressions in self-administered cases. Dr. Makis’ clinic reports hundreds of testimonials, including remissions in prostate, lymphoma, and pancreatic cancers.

Makis reports, however, evidence is predominantly anecdotal and preclinical. Mainstream critiques emphasize the absence of randomized controlled trials, potential biases in testimonials, and risks of unverified claims. Fact-checking resources classify these approaches as unproven, with warnings against scams.

This protocol represents a possible cost-effective, accessible option for adjunctive cancer management but is not approved by regulatory bodies like the FDA for oncology. Potential adverse effects include gastrointestinal discomfort or, rarely, organ toxicity at elevated doses. Many of the anecdotal successes reported are in conjunction with a traditional cancer treatment protocol or after such attempts have failed. Consultation with a qualified healthcare provider is imperative for monitoring, sourcing from reputable pharmacies, and integration with conventional therapies.

For further reading, explore peer-reviewed sources and patient forums. This overview aims to inform and educate, fostering informed discussions on emerging cancer strategies.

*Disclaimer: This article is for educational purposes and does not constitute medical advice. Always seek professional guidance.*

 The Gerson Therapy is an alternative medical framework developed in the 1920s and 1930s by German-born physician Dr. Max Gerson. Unlike mainstream oncology, which targets specific tumors locally, Gerson's theory treats cancer as a systemic, whole-body disease. The fundamental hypothesis is that cancer arises from two primary pathological states: toxicity (the accumulation of environmental and dietary poisons) and deficiency (the severe depletion of essential nutrients and cellular minerals). 

 Central to the Gerson theory is the concept of a cellular sodium-potassium imbalance. Dr. Gerson posited that damaged cells lose their ability to retain potassium, allowing sodium and water to flood in, which ultimately degrades cellular metabolism and damages the liver. To reverse this, the therapy utilizes an intensive three-part regimen: a strict organic plant-based diet alongside 13 freshly pressed juices daily to flood the body with potassium; an extensive regimen of targeted supplements (such as Lugol's iodine, potassium compounds, and thyroid hormones); and frequent coffee enemas. The enemas are theorized to cause the bile ducts to dilate, stimulating the liver to rapidly filter and eliminate the toxins released by broken-down tumor tissue. 

 The Gerson Institute, co-founded in 1977 by Dr. Gerson’s daughter, Charlotte Gerson, operates as a non-profit organization dedicated to preserving, teaching, and promoting this methodology. Based in San Diego, California, the institute does not directly operate its own clinical facilities due to strict regulatory laws surrounding alternative cancer therapies in the United States. Instead, it provides educational programs, trains home-treatment caretakers, and licenses external clinics—most notably in Mexico and Europe—where patients can legally receive the therapy in an inpatient setting. 

https://gerson.org/

• Dosing Standards: Ivermectin is approved strictly for short-interval, weight-based dosing (150–200 mcg/kg). There is no medically validated timeline for extended high-dose use.
• Pharmacokinetics: The drug has a plasma half-life of 12 to 36 hours, clearing systemic circulation in 3 to 7 days. Because it is highly fat-soluble, high doses cause prolonged accumulation in adipose tissues.
• Toxicity Profile: Over dosage results in acute neurotoxicity (hallucinations, confusion, ataxia, seizures, coma) and systemic compromise (severe gastrointestinal distress, hypotension).
• Clinical Protocol: Immediate and permanent cessation is mandatory upon symptom onset. Symptom resolution may take weeks. Therapy should only be re-initiated at corrected, standard doses under direct medical supervision after complete physiological recovery.