Overview of the Makis Protocol Framework

The cancer treatment strategies discussed by William Makis center on repurposed medications—primarily antiparasitic agents—combined with metabolic therapies and nutritional supplements. This approach is frequently conceptualized within a framework known as the Mitochondrial-Stem Cell Connection (MSCC) protocol.

The underlying premise of this framework is that cancer stem cells develop due to chronic oxidative phosphorylation (OxPhos) insufficiency. Therefore, the protocol aims to combine agents that theoretically enhance mitochondrial function while disrupting the alternative energy pathways (such as glucose and glutamine fermentation) that cancer cells rely on.

Core Components of the Protocol

The protocol utilizes a combination of veterinary and human antiparasitic drugs along with orthomolecular supplements:

• Fenbendazole (FBZ): A veterinary benzimidazole anthelmintic drug. In preclinical models, it has been studied for its potential to disrupt microtubule polymerization, arrest the cell cycle at the G2/M phase, and interfere with glucose metabolism.
• Ivermectin: An antiparasitic drug approved for human and animal use. It is utilized in these experimental protocols based on laboratory literature suggesting it may influence specific cell signaling pathways and mitochondrial dynamics.
• Orthomolecular Supplements: A suite of vitamins and compounds intended to support metabolic health and induce synergistic cellular stress on malignant cells. These typically include:
  • High-dose Vitamin D3 (often paired with Vitamin K2 and Magnesium)
  • Intravenous Vitamin C
  • Melatonin (typically at higher-than-standard sleep dosages, ranging from 10 to 40 mg)
  • Zinc
  • Natural compounds like Berberine, Curcumin, and Artemisinin
  • Cimetidine (an H2 blocker historically studied for potential anti-metastatic properties in certain colorectal and gastric cancers)

Proposed Biochemical Mechanisms

According to the published literature and case observations associated with this approach, the combination targets several cancer cell mechanisms simultaneously:

1. Microtubule Disruption: Benzimidazoles like fenbendazole bind to tubulin, preventing the structural assembly necessary for cancer cell division.
2. Metabolic Starvation: The protocol attempts to block glycolysis and glutaminolysis, cutting off the primary fuels used by cancer cells that have undergone the Warburg effect.
3. Apoptosis Induction: Promoting programmed cell death through increased cellular oxidative stress, often driven by the combination of high-dose antioxidants (like Vitamin C) and metabolic stressors.

Documented Research and Case Data

In 2025, a case report co-authored by Makis, titled “Fenbendazole as an Anticancer Agent? A Case Series of Self-Administration in Three Patients,” tracked outcomes for individuals utilizing these methods:

• Case 1 (Stage IV Breast Cancer): A patient who utilized daily fenbendazole (222 mg) alongside fulvestrant, radiation, and supplements, resulting in documented remission over a three-year observation period.
• Case 2 (Stage IV Prostate Cancer): A patient with bone metastases who added fenbendazole (222–444 mg/day) and a broad suite of supplements to standard androgen deprivation therapy (ADT), achieving a near-complete response.
• Case 3 (Stage IV Melanoma): A patient who utilized surgery, fenbendazole, and nutritional supplements, achieving remission sustained over 11 months.

Note on Publication Status: This specific case series paper was published in the journal Case Reports in Oncology but was subsequently retracted by the publisher due to administrative and conflict-of-interest disclosure guidelines regarding the authors’ corporate affiliations.

The protocol remains classified as experimental, as wide-scale, placebo-controlled human randomized clinical trials evaluating the safety and efficacy of fenbendazole or ivermectin as primary or stand-alone cancer treatments have not yet been completed.

This video on Fenbendazole Cancer and Hard Science provides an in-depth discussion detailing the proposed biochemical mechanisms and preclinical research behind using benzimidazoles in oncology.

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