22 December 2025

Three Cancer Cases, One Old Drug: Dr. John Campbell Reviews Fenbendazole

Fenbendazole and Cancer: Dr. John Campbell Reviews a Case Series

In a detailed 20-minute video, Dr. John Campbell examines a recently published paper titled “Fenbendazole as an Anti-Cancer Agent: A Case Series of Self-Administration in Three Patients.” The video asks a deliberately uncomfortable question: are potentially useful cancer treatments being overlooked—not because they don’t work, but because they are old, cheap, and off-patent?

Fenbendazole, Dr. Campbell explains, is a widely used veterinary antiparasitic drug. Its patent expired decades ago, making it inexpensive, generic, and commercially unattractive. That economic reality, Campbell suggests, may help explain why promising signals receive limited follow-up.

The Three Reported Cancer Cases

Case 1: Stage IV Metastatic Breast Cancer

The most striking case involves an 83-year-old woman with widely metastatic stage IV breast cancer, involving the liver, lungs, spine, pelvis, and multiple vertebrae. Imaging and biopsies confirmed extensive disease, and she was placed under hospice care, having declined further chemotherapy.

In November 2021, she began self-administering fenbendazole at ~222 mg daily. Over the following months:

  • Liver enzymes normalized

  • Tumor marker CA 27-29 dropped from 316 to 36.6

  • A PET scan in April 2022 showed no abnormal metabolic activity

  • By June 2022, she was declared in complete remission


All conventional treatments were discontinued. She reported no adverse effects, remained recurrence-free, and continued fenbendazole nearly three years later.

Campbell emphasizes the improbability of such a reversal in terminal, multi-metastatic breast cancer, describing the outcome as something even experienced oncologists would rarely encounter.

Case 2: Metastatic Prostate Cancer

The second case describes a 75-year-old man with metastatic prostate cancer, involving the spine, pelvis, and humeral head. He received a mix of conventional therapies alongside fenbendazole, following a regimen similar to the widely circulated Joe Tippins protocol (fenbendazole taken several days per week).

Over 26 months, imaging showed sustained regression of metastatic lesions, and PSA levels remained undetectable. The patient continued fenbendazole with no reported toxicity and maintained a near-complete response.

Case 3: Metastatic Melanoma

The third case involves a 63-year-old man with metastatic melanoma, with disease in the abdominal cavity, stomach, bowel, muscles, and vertebrae. PET scans initially showed widespread hyper-metabolic lesions. After treatment—including fenbendazole—the patient entered remission and remained recurrence-free for at least 11 months, again with no reported adverse effects.

Across all three cases, the authors reported no significant side effects, a notable point given the severity of disease.
 

The Biological Rationale Behind Fenbendazole’s Anticancer Effects

Dr. Campbell’s discussion centers on whether the clinical outcomes described in these three cases can be reconciled with established cancer biology. From a mechanistic standpoint, fenbendazole belongs to the benzimidazole class of compounds, a group that has been studied for decades for its effects on rapidly dividing cells.

Microtubule Disruption and Mitotic Arrest

Fenbendazole binds to β-tubulin, a core structural protein required for microtubule assembly. Microtubules are essential for mitosis, intracellular transport, and maintenance of cellular integrity. Cancer cells—particularly metastatic and high-burden tumors—depend on continuous microtubule polymerization to sustain uncontrolled proliferation.

By destabilizing microtubules, fenbendazole:

  • interferes with mitotic spindle formation,

  • causes cell-cycle arrest,

  • increases chromosomal instability,

  • and promotes apoptosis in rapidly dividing cells.

This mechanism is not speculative; it is shared by established chemotherapeutic agents such as taxanes and vinca alkaloids, though fenbendazole appears to act with substantially lower systemic toxicity at the doses reported.

Metabolic Stress and Energy Disruption

Beyond structural interference, benzimidazoles have been shown in preclinical studies to impair glucose uptake and utilization in malignant cells. Cancer cells rely disproportionately on altered metabolic pathways—often referred to as the Warburg effect—to meet their energy demands. Disrupting glucose handling places tumors under severe metabolic stress, particularly in late-stage disease where metabolic flexibility is already strained.

Fenbendazole has also been implicated in:

  • increased reactive oxygen species (ROS) generation,

  • impaired mitochondrial function,

  • and disruption of substrate-level phosphorylation.

These effects selectively burden cancer cells, which operate near the limits of metabolic tolerance, while sparing most normal tissue.

Relevance to the Three Cancer Types Observed

The cancers described in the case series share biological features that make them plausible targets for fenbendazole’s mechanisms:

  • Metastatic breast cancer often exhibits high microtubule turnover and metabolic fragility, particularly in liver and bone metastases.

  • Prostate cancer, especially when bone-metastatic, depends heavily on cytoskeletal integrity and mitochondrial signaling, making sustained metabolic pressure particularly damaging.

  • Melanoma is among the most metabolically aggressive cancers, with high oxidative stress and mitochondrial reliance, which may explain its sensitivity to agents that disrupt cellular energetics.
     

The fact that three biologically distinct cancers—breast, prostate, and melanoma—showed regression under similar dosing conditions strengthens the argument that fenbendazole may be acting on shared vulnerabilities of malignant cells, rather than cancer-specific mutations.

Dosage Patterns and Treatment Regimens

Dr. Campbell is careful to distinguish reported usage from recommendations. The paper documents dosing patterns rather than prescribing them.

1. Continuous Daily Dosing

In the most detailed case (stage IV breast cancer), fenbendazole was taken at approximately 222 mg daily, continuously, for several months.

At this dosage:

  • liver enzymes normalized rather than worsened,

  • no hematologic or systemic toxicity was reported,

  • and treatment was tolerated long-term.
     

2. Intermittent (“Pulsed”) Dosing

Campbell also references the commonly discussed Joe Tippins protocol, which involves:

  • ~222 mg fenbendazole

  • taken three days per week,

  • followed by four days off.
     

From a pharmacologic perspective, intermittent dosing can:

  • reduce adaptive resistance,

  • limit cumulative toxicity,

  • and exploit delayed apoptotic signaling in cancer cells.

This pulsed approach is consistent with broader oncology strategies, where treatment cycling often yields better outcomes than constant exposure.

Safety Signal and Risk–Benefit Considerations

Across all three cases:

  • no significant adverse effects were reported,

  • liver and metabolic markers improved rather than deteriorated,

  • and patients tolerated fenbendazole for extended periods.


While absence of reported toxicity in a small case series does not establish safety conclusively, it does suggest a favorable risk–benefit profile, particularly in patients with terminal or refractory disease.
 

Summary of Case Findings and Mechanistic Context

The video reviewed by Dr. John Campbell analyzes a published medical case series documenting the self-administration of fenbendazole in three patients with advanced cancers: metastatic breast cancer, metastatic prostate cancer, and metastatic melanoma. In all three cases, fenbendazole use coincided with measurable tumor regression, normalization or suppression of disease-specific biomarkers (including CA 27-29 and PSA), and imaging results showing absence of metabolically active disease on PET scans over extended follow-up periods.

The reported dosing patterns involved approximately 220–222 mg of fenbendazole, administered either daily over several months or intermittently several days per week, consistent with regimens commonly referenced in existing case reports and informal protocols. Across the three cases described in the paper, no significant adverse effects were reported during prolonged use.

From a biological standpoint, fenbendazole’s known mechanisms—specifically β-tubulin binding, microtubule disruption, interference with mitosis, and induction of metabolic stress—are consistent with processes critical to the survival and proliferation of malignant cells. These mechanisms are not cancer-type–specific and apply broadly to rapidly dividing and metabolically dysregulated cells, which provides a mechanistic basis for observing effects across different tumor types.

The information presented in the video and summarized in this article establishes the following factual points:

  • fenbendazole is an off-patent benzimidazole compound with established cellular effects;

  • measurable clinical regression was observed in three advanced cancer cases during fenbendazole administration;

  • biomarker and imaging data were used to document disease status;

  • dosing and duration were sufficient to observe sustained effects without reported toxicity;

  • the observations span multiple cancer types with distinct tissue origins.


Taken together, the material reviewed documents observational clinical outcomes, associated dosing practices, and biologically plausible mechanisms that align with known cancer cell vulnerabilities. No claims of causation or generalized efficacy are established within the case series itself; the