The Makis Protocol: Repurposed Drugs for Cancer
A comprehensive overview of Dr. William Makis' experimental approach combining ivermectin, fenbendazole, and mebendazole
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⚠️ Critical Disclaimer
- This is NOT medical advice — it is educational content only
- No large-scale randomized controlled trials (RCTs) exist for these treatments
- Evidence is based primarily on preclinical studies, case reports, and anecdotal outcomes
- Always consult a licensed oncologist before making any treatment decisions
- Do not replace conventional cancer treatment with experimental protocols
- Dr. Makis' medical license is currently inactive in the province of Alberta
Protocol Overview
The Makis Protocol is an experimental approach to cancer treatment developed by Dr. William Makis, a physician with training in nuclear medicine and oncology from McGill University who holds an MD and FRCPC designation. He has become a prominent voice on repurposed drugs for cancer.
Dr. Makis' medical license is currently listed as inactive in Alberta, Canada. The protocol he advocates combines three antiparasitic drugs—ivermectin, fenbendazole, and mebendazole—along with targeted supplements. This approach is based on preclinical research showing these drugs have anticancer properties, though clinical validation through large-scale trials remains lacking.
The protocol has gained attention through social media and patient advocacy communities, with anecdotal reports of tumor marker reductions. However, these outcomes have not been verified through controlled clinical trials, and the scientific community emphasizes the need for rigorous study before drawing conclusions.
Core Drugs — The Big 3
The protocol centers on three repurposed antiparasitic drugs, each with distinct mechanisms and preferred applications. No cancer dose has been established for any of these drugs, so this page does not reproduce the doses circulated in protocol material—those come from anecdotal protocols, not from clinical trials or established oncological guidelines.
Ivermectin
Proposed Mechanisms
- PAK1 kinase inhibition
- Akt/mTOR pathway modulation
- Induces apoptosis, autophagy, and pyroptosis
- Immunogenic cell death (HMGB1/calreticulin release)
- Targets cancer stem cells
Fenbendazole
Proposed Mechanisms
- Microtubule disruption → mitotic arrest
- GLUT4 glucose transporter downregulation
- Mitochondrial translocation of p53 (cell studies)
- Mitochondrial dysfunction induction
Key study: Dogra et al. 2018, Scientific Reports — PMID: 30093705
Mebendazole
FDA-approved for human use (antiparasitic) • Studied in a Phase 1 glioma trial
Proposed Mechanisms
- Microtubule disruption similar to fenbendazole
- Anti-angiogenic properties
- Studied in brain tumors (Phase 1 glioma trial)
- G2/M cell cycle arrest
Johns Hopkins Phase 1 trial: NCT01729260 (completed 2021) — PMID: 33506200
Combination Strategy
Most protocols in the Makis approach combine ivermectin with one or both benzimidazoles. The choice of benzimidazole often depends on the cancer type and location, particularly for CNS involvement.
| Cancer Type | Preferred Drug | Rationale |
|---|---|---|
| Brain Cancers / Glioblastoma | Mebendazole | Phase 1 glioma dose/safety trial (efficacy not established) |
| Ovarian Cancer | Mebendazole | Protocol preference (no cited trial) |
| Prostate Cancer | Fenbendazole | Protocol preference (no cited study) |
| Pancreatic Cancer | Fenbendazole | Anecdotal response reports |
| Breast Cancer | Fenbendazole | Protocol preference (no cited study) |
| Lung Cancer | Fenbendazole | Joe Tippens case anecdote |
| Colorectal Cancer | Mebendazole | Recent protocol preference |
| Lymphoma | Fenbendazole | Protocol preference (no cited study) |
| Melanoma / Sarcoma | Fenbendazole | Protocol preference (no cited study) |
| Advanced/Refractory | Hybrid Protocol | Both benzimidazoles + ivermectin |
The 5 Priority Supplements
The protocol emphasizes specific supplements believed to enhance efficacy, protect organs, and support metabolic health during treatment.
Vitamin D3 + K2 + Magnesium
Protocol material pairs vitamin D3 with K2 and magnesium; that pairing has not been tested as a cancer intervention.
Curcumin (with Piperine)
NF-κB and TNF-α suppression. Piperine is added to increase curcumin absorption.
Berberine
AMPK activation, glucose metabolism control. May enhance metabolic stress on cancer cells.
Milk Thistle (Silymarin)
Included for liver support during benzimidazole use. No evidence is cited here that it prevents benzimidazole-related liver injury.
Zinc
Immune function and mitochondrial support. Monitor levels to avoid excess.
Optional Additions
Black seed oil, lactoferrin, turkey tail mushroom, melatonin, high-dose vitamin C, tocotrienols, and bromelain are sometimes included based on individual protocols.
Monitoring & Safety
Regular bloodwork is essential when following any experimental protocol. These tests should be performed at baseline and repeated periodically to detect potential adverse effects early.
Liver Function
ALT/AST, bilirubin, ALP — hepatotoxicity risk with benzimidazoles
Kidney Function
Creatinine, BUN — assess renal clearance
Complete Blood Count
Monitor for anemia and neutropenia
Comprehensive Metabolic Panel
Electrolytes, glucose levels
Tumor Markers
Cancer-specific markers (PSA, CA-125, CEA, etc.)
Vitamin D & Zinc
25(OH)D and serum zinc levels
Optional: CRP & Coagulation
Inflammatory markers and clotting factors
Lifestyle Components
The protocol emphasizes metabolic interventions alongside pharmaceutical approaches, based on the theory that cancer cells rely heavily on glucose metabolism.
- Ketogenic or Low-Carbohydrate Diet — Reduce glucose availability to cancer cells through dietary carbohydrate restriction
- Intermittent Fasting (16:8) — Daily eating window of 8 hours with 16-hour fasting period to enhance metabolic flexibility
- Track Progress — Monitor tumor markers and imaging results to assess any changes over time
Mechanisms of Action
For healthcare professionals and researchers interested in the proposed biological rationale behind these repurposed drugs.
Ivermectin — Multi-Target Pathway Modulation
- PAK1 kinase inhibition — disrupts Ras/MAP kinase and Wnt/β-catenin signaling
- Akt/mTOR pathway suppression — reduces cell survival signaling
- Induces immunogenic cell death via HMGB1 and calreticulin release
- Promotes apoptosis, autophagy, and pyroptosis across multiple cancer cell lines
- May target cancer stem cell populations
Fenbendazole — Tubulin Disruption & Metabolic Interference
- Binds β-tubulin and disrupts microtubule polymerization
- Induces G2/M cell cycle arrest and subsequent apoptosis
- Downregulates GLUT4 glucose transporters and inhibits glucose uptake in cell studies
- Induces mitochondrial translocation of p53 in cell studies
- Induces mitochondrial dysfunction and oxidative stress
Mebendazole — Benzimidazole Studied in Glioma
- Similar microtubule disruption mechanism to fenbendazole
- Studied in CNS malignancies (Phase 1 glioma trial)
- Anti-angiogenic effects — may inhibit tumor blood vessel formation
- FDA-approved safety profile (for antiparasitic use)
Synergistic Combination Theory
- Direct cytotoxicity from microtubule disruption (benzimidazoles)
- Multi-pathway signaling inhibition (ivermectin)
- Metabolic stress via glucose pathway interference
- Proposed adaptive immune system augmentation through immunogenic cell death
- Theoretical synergy may exceed individual drug effects
Key Published Studies
These peer-reviewed publications form part of the scientific basis for investigating these drugs in cancer contexts.
Dogra et al. 2018
"Fenbendazole acts as a moderate microtubule destabilizing agent and causes cancer cell death" — Scientific Reports
Tang et al. 2021
"Ivermectin, a potential anticancer drug derived from an antiparasitic drug" — Pharmacological Research
Gallia et al. 2021
"Mebendazole and temozolomide in patients with newly diagnosed high-grade gliomas" — Neuro-Oncology Advances (Johns Hopkins Phase 1)
Pharmaceuticals 2025
"Ivermectin as an Alternative Anticancer Agent: Molecular Mechanisms and Clinical Evidence" — Review Article
Key Takeaways
✅ What We Know
- Preclinical studies demonstrate anticancer activity across multiple cell lines
- Mebendazole has Phase 1 clinical trial data from Johns Hopkins
- Ivermectin modulates multiple signaling pathways relevant to cancer biology
- Mebendazole is FDA-approved as a human antiparasitic; fenbendazole is a veterinary anthelmintic with no approved human indication, so it has no established human safety profile
⚠️ What We Don't Know
- No large-scale RCTs exist for cancer use of any of these drugs
- Optimal dosing for cancer is not established — the only human dose-finding trial cited here is an early-phase mebendazole study in glioma
- Long-term safety at high doses used in these protocols is unknown
- Whether anecdotal outcomes are reproducible or survivorship bias
- Drug interactions with standard chemotherapy regimens
- Whether these work as well without concurrent conventional treatment
Recommended Supplements
The five priority supplements from the protocol, plus tools for the lifestyle section (low-carb tracking, organizing a multi-supplement routine) and background reading:
Related Resources
Explore more research and guides on HighPeptides:
Educational Disclaimer
The information presented on this page is for educational and informational purposes only. It is not intended as medical advice and should not be used to diagnose, treat, cure, or prevent any disease or medical condition.
The Makis Protocol is experimental and has not been validated through large-scale clinical trials. Doses circulated for this protocol derive from anecdotal reports and preclinical research, not established medical guidelines, and are not listed here.
Always consult with a qualified healthcare provider, preferably a licensed oncologist, before making any decisions about cancer treatment. Do not discontinue or modify any prescribed treatments without professional medical guidance.
HighPeptides and its contributors assume no liability for any actions taken based on the information provided herein.