EXPERIMENTAL PROTOCOL • 2025-2026

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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Core Drugs
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Priority Supplements
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Cancer Types
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⚠️ Critical Disclaimer

Protocol Overview

The Makis Protocol represents 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. Dr. Makis has authored over 100 peer-reviewed publications throughout his career and has become a prominent voice in discussions around repurposed drugs for cancer.

It is important to note that 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. All dosing information below is derived from Dr. Makis' recommendations and anecdotal protocols—not from established oncological guidelines.

Ivermectin

Macrocyclic Lactone • Broad Spectrum
Low/Mild 0.2–0.5 mg/kg, 3×/week
Moderate 0.5–1 mg/kg daily
Aggressive 1–2.5 mg/kg daily

Cycles: 3 weeks on / 1 week off • Take with fatty meal for absorption

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

Benzimidazole • Preferred for Advanced/Metastatic
Standard Daily 444–1776 mg/day
Pulsed Protocol 888–1000 mg, 3–6 days/week

Take with fatty meal • Cycle periodically • Monitor liver function

Proposed Mechanisms
  • Microtubule disruption → mitotic arrest
  • GLUT4 glucose transporter downregulation
  • p53 tumor suppressor reactivation
  • Mitochondrial dysfunction induction

Key study: Dogra et al. 2018, Scientific Reports — PMID: 30254312

Mebendazole

Benzimidazole • Preferred for Brain Cancers
Typical Daily 1000–1500 mg/day

FDA-approved for human use (antiparasitic) • Superior blood-brain barrier penetration

Proposed Mechanisms
  • Microtubule disruption similar to fenbendazole
  • Anti-angiogenic properties
  • Enhanced CNS penetration for brain tumors
  • 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 where blood-brain barrier penetration becomes critical.

Cancer Type Preferred Drug Rationale
Brain Cancers / Glioblastoma Mebendazole Superior BBB penetration
Ovarian Cancer Mebendazole Clinical trial precedent
Prostate Cancer Fenbendazole Preclinical data support
Pancreatic Cancer Fenbendazole Anecdotal response reports
Breast Cancer Fenbendazole Preclinical cell line data
Lung Cancer Fenbendazole Joe Tippens case anecdote
Colorectal Cancer Mebendazole Recent protocol preference
Lymphoma Fenbendazole Systemic distribution
Melanoma / Sarcoma Fenbendazole Preclinical efficacy
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.

1

Vitamin D3 + K2 + Magnesium

5,000–10,000+ IU/day

Target serum level ≥80 ng/mL (200 nmol/L). K2 and magnesium support proper utilization and prevent hypercalcemia.

2

Curcumin (with Piperine)

600mg+ daily

NF-κB and TNF-α suppression. Piperine increases bioavailability by up to 2000%.

3

Berberine

500–600mg 2× daily

AMPK activation, glucose metabolism control. May enhance metabolic stress on cancer cells.

4

Milk Thistle (Silymarin)

250–350mg/day

Liver protection during benzimidazole use. Critical for hepatotoxicity prevention.

5

Zinc

Target 80–120 μg/dL serum

Immune function and mitochondrial support. Monitor levels to avoid excess.

Optional Additions

Black seed oil, lactoferrin, turkey tail mushroom, melatonin (10–40mg), 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 every 1–3 months to detect potential adverse effects early.

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Liver Function

ALT/AST, bilirubin, ALP — hepatotoxicity risk with benzimidazoles

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Kidney Function

Creatinine, BUN — assess renal clearance

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Complete Blood Count

Monitor for anemia and neutropenia

Comprehensive Metabolic Panel

Electrolytes, glucose levels

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Tumor Markers

Cancer-specific markers (PSA, CA-125, CEA, etc.)

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Vitamin D & Zinc

25(OH)D and serum zinc levels

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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.

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 — starves cancer cells
  • Reactivates p53 tumor suppressor in some cancer types
  • Induces mitochondrial dysfunction and oxidative stress

Mebendazole — CNS-Penetrant Benzimidazole

  • Similar microtubule disruption mechanism to fenbendazole
  • Superior blood-brain barrier penetration — critical for CNS malignancies
  • 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

PMID: 30254312

Tang et al. 2021

"Ivermectin, a potential anticancer drug derived from an antiparasitic drug" — Pharmacological Research

PMC7505114

Gallia et al. 2021

"Mebendazole and temozolomide in patients with newly diagnosed high-grade gliomas" — Neuro-Oncology Advances (Johns Hopkins Phase 1)

PMID: 33506200

Pharmaceuticals 2025

"Ivermectin as an Alternative Anticancer Agent: Molecular Mechanisms and Clinical Evidence" — Review Article

PMC12566834

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
  • All three drugs have established safety profiles for their original antiparasitic indications
  • Anecdotal reports describe dramatic tumor marker reductions in some cases

⚠️ What We Don't Know

  • No large-scale RCTs exist for cancer use of any of these drugs
  • Optimal dosing for cancer is extrapolated from animal/anecdotal data only
  • 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

If you choose to follow this supplement protocol, here are quality options available on Amazon:

Research-Grade Compounds

Swiss Chems carries ivermectin and fenbendazole for research purposes.

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Related Resources

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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. All dosing information is derived from anecdotal reports and preclinical research, not established medical guidelines.

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.

MeetPeptide and its contributors assume no liability for any actions taken based on the information provided herein.