49 People With Pancreatic Cancer Who Beat the Death Sentence

Fenbendazole, mebendazole, and ivermectin are producing responses across four continents that oncology’s best chemotherapy cannot match

Fenbendazole Can Cure Cancer presents Case Reports of people who have treated their own cancers along with other articles to help understand how fenbendazole works to treat cancer. Previous articles covering other cancers are in the Archives link. This Substack is one of several sources that aggregate Case Reports from those that are self-treating their cancers with repurposed antiparasitics including fenbendazole, mebendazole and ivermectin. This article is the first in a series that will synthesize these Case Reports looking for guiding signals in the data and reports. The sources of these Case Report data are Fenbendazole Can Cure Cancer, OneDayMD, Dr. William Makis, and various Social Media Fenbendazole Groups.

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The Worst Diagnosis in Oncology

Pancreatic ductal adenocarcinoma (PDAC) is what oncologists use when they want to explain hopelessness. Over 90% of cases carry activating mutations in KRAS — the master driver oncogene that no approved targeted therapy has successfully dismantled for the general PDAC population. The disease is almost always diagnosed late. Surgery is possible in fewer than 20% of patients. FOLFIRINOX — the most aggressive chemotherapy regimen in common use — extends median survival by a few months against gemcitabine alone. Five-year survival for Stage 4 disease: approximately 3%.

These are the numbers your oncologist will cite when they tell you to get your affairs in order. What they will not cite are the 49 documented cases — from New Zealand to New York, from Kentucky to Romania — in which patients given weeks to live are alive years later. In which tumors dismissed as untreatable have collapsed under protocols built on antiparasitic drugs that cost less than a daily cup of coffee.

This article is that record. Read it. Share it. And if you are facing this diagnosis, understand that the biological problem is solvable — even if the institutional problem is not.

Key Numbers:

• 49 — Documented pancreatic cancer cases using antiparasitic protocols (2022–2026)

• 93% — Maximum pancreatic tumor shrinkage recorded (Case No. 33)

• 99.9% — CA19-9 drop recorded (Case No. 9: from 44,960 to 21)

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The Mechanism: Why Antiparasitics Hit PDAC Hard

The foundational argument of my book — Cancer Is a Parasite — is that cancer shares deep biological architecture with parasitic organisms. Nowhere is this convergence more therapeutically relevant than in PDAC. The vulnerabilities that parasites share with pancreatic cancer cells are precisely the vulnerabilities that benzimidazoles and ivermectin have been exploiting for decades in veterinary and human medicine.

Fenbendazole (FBZ) and Mebendazole (MBZ) — Eight Anticancer Mechanisms:

1. Microtubule Disruption. FBZ binds β-tubulin with high affinity, depolymerizing the mitotic spindle. Cancer cells in rapid division cannot complete mitosis. Cell death follows.

2. Warburg Effect Blockade. GLUT1 and GLUT4 glucose transporter suppression starves PDAC’s glycolytic dependency. KRAS-driven tumors are extraordinarily glycolytic — cut the glucose, cut the fuel.

3. p53 Reactivation. FBZ stabilizes and upregulates p53 — the tumor suppressor that PDAC has silenced or mutated. Restored p53 function triggers apoptosis in tumor cells.

4. Cancer Stem Cell Elimination. Both FBZ and IVM target cancer stem cells — the self-renewing subpopulation responsible for recurrence and chemoresistance that conventional chemotherapy misses entirely.

5. Multidrug Resistance Reversal. IVM inhibits NF-κB pathway activation and efflux pump overexpression — the primary mechanisms driving PDAC’s notorious resistance to consecutive chemotherapy regimens.

6. CYP24A1 Inhibition. FBZ blocks CYP24A1 — the enzyme tumors upregulate to destroy local vitamin D (Supple, 2026). Restored vitamin D activity re-enables immune surveillance that PDAC has suppressed.

7. VEGF Pathway Suppression. FBZ reduces vascular endothelial growth factor signaling — cutting off tumor angiogenesis and, in several cases, contributing to resolution of malignant ascites.

8. Chemosensitization. IVM reverses tumor resistance to concurrent chemotherapy. Cases consistently show: modest chemo response alone, then dramatic collapse once IVM is added. The mechanism is real and documented.

This is not one mechanism. It is eight — against a cancer that defeats single-pathway therapies by evolving around them. As explained in Cancer is a Parasite, the multimodal logic of antiparasitic treatment is precisely why the case series below shows responses that oncologists call miraculous. It is not a miracle. It is mechanism operating on multiple axes simultaneously.

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The Cases: A Global Signal

The Chemosensitization Proof-of-Concept

The most scientifically powerful cases are those that isolate the contribution of antiparasitics by providing a direct before-and-after comparison. Case 33 is the archetype.

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Case No. 33 · France · December 2025
54-Year-Old Man — Stage 4 Pancreatic Cancer Metastatic to Liver

Five cycles of FOLFIRINOX produced only a 17% tumor burden reduction — classified as non-significant by RECIST criteria. The patient then added ivermectin (1 mg/kg/day) and mebendazole (1,500 mg/day) to ongoing chemotherapy.

Results over the next five identical chemo cycles:

• Pancreatic primary: 32 mm → 13 mm (93.3% volume reduction)

• Liver Seg 7/8 lesion: 58 mm → 45 mm (53.3% volume reduction)

• Liver Seg 7 lesion: 18 mm → 8 mm (91.2% volume reduction)

• Retroperitoneal lymph node: 11 mm → 7 mm (74.2% volume reduction)

Same chemo. Same patient. The only variable was the antiparasitics. Chemo alone = 17% reduction over 5 cycles. Chemo + IVM + MBZ = up to 93% reduction over 5 cycles. This potentiation effect is consistent across most solid tumor cancers as detailed in Cancer is a Parasite.

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Case No. 40 · Canada · April 2026
56-Year-Old Man — Stage 4 Pancreatic Cancer

Started ivermectin and fenbendazole alongside chemotherapy in September 2025. Six-month results:

• Pancreatic mass: 40×32 mm → 17×23 mm (78% volume reduction)

• Liver lesions: 55% volume reduction

• CA19-9: 2,784 → 37

His oncologist remarked, “Cancer patients almost never see dramatic results like this with chemo alone. This is treatment synergy.”

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Case No. 39 · Romania · March 2026
75-Year-Old Man — Stage 4 Pancreatic Cancer

Triple therapy — ivermectin + fenbendazole + mebendazole — alongside chemotherapy, started November 2025. Five-month results:

• CA19-9: 18,630 → 1,000 (95% drop)

• Pancreatic mass: 45×35 mm → 22×14 mm (92% volume shrinkage)

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No Evidence of Disease — The NED Cases

Several patients achieved complete radiologic clearance — No Evidence of Disease — in a cancer where that outcome is not supposed to exist.

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Case No. 41 · New Zealand · May 2026
70-Year-Old Man — Stage 4 Pancreatic Cancer · Given 2–3 Months to Live

Diagnosed with Stage 4 disease and given a two-to-three-month prognosis. Declined all conventional oncology. In May 2025, began ivermectin, fenbendazole, and hyperbaric oxygen therapy (HBOT).

Twelve months later: No Evidence of Disease. No chemotherapy. No radiation. No traditional oncology treatment of any kind.

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Case No. 35 · Argentina / Quebec · January 2026
43-Year-Old Woman — Unresectable 5 cm Pancreatic Mass

Presented with a 5 cm pancreatic tail mass confirmed non-resectable by surgery in Canada. For 11 months: ivermectin (72 mg/day), fenbendazole (1,500 mg/day), mebendazole (1,500 mg/day in the final month).

CT scan with contrast at 11 months: “Pancreas appears normal with no anomalies.”

Her Argentine oncologist — in contrast to his Canadian colleagues — requested a copy of the protocol to apply to other patients.

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Case No. 24 · Pennsylvania, USA · October 2025
53-Year-Old Man — Stage 4 Pancreatic Cancer

Started IVM (1.5 mg/kg/day), FBZ (1,500 mg/day), and chemotherapy in late March 2025. Six-month results:

• PET scan: no evidence of metabolically active disease

• Liver metastases: completely resolved

• CA19-9: 154 → 17

His oncology team repeatedly told him the disease “would come back,” characterized his recovery as “no longer a curative discussion,” and attempted to dissuade him from ordering the confirmatory PET/CT that proved his NED status.

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Case No. 17 · Maryland, USA · June 2025
67-Year-Old Woman — Stage 4 After Failed FOLFIRINOX

Three months of neoadjuvant FOLFIRINOX: no improvement, suspected Stage 4 progression with new liver metastases. She started IVM (1.5 mg/kg/day), FBZ (1,000 mg/day), and CBD oil in early March 2025.

CT at 2.5 months:

• Pancreatic head mass: “no longer visualized”

• Liver nodules: absent

• CA19-9: 942 → 9

Complete radiologic clearance in a patient who had already failed FOLFIRINOX entirely.

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The Standout Data Points

Case No. 9 · age 77, male 2025
Stage 4 Pancreatic Cancer Patient

Protocol: Mebendazole 1,000 mg (morning) + Fenbendazole 888 mg (afternoon). No ivermectin. No chemotherapy.

Results:

• CA19-9: 44,960 → 21 (99.9% reduction)

• Large liver lesion: 70% volume reduction

• Second liver lesion: 87% volume reduction

“I do not remember a person with results like this.” — His oncologist, after 35 years in practice. He called the results a miracle.

It was not a miracle. It was fenbendazole and mebendazole operating on a cancer that had no defense against their mechanisms.

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Case No. 20 · Stage 4 pancreatic cancer. The Canadian MAID Case · 2025

A Canadian patient with Stage 4 pancreatic cancer recurrence — with lung metastases — was offered Medical Assistance in Dying (MAID) as the primary clinical recommendation.

He started fenbendazole (444 mg/day, escalating), then added ivermectin.

Result: “The CT scan showed that all signs of cancer were undetectable and essentially resolved.”

His primary oncologist was shocked by the turnaround. The patient avoided Canada’s first clinical offer — euthanasia — through a drug that costs less than a cup of coffee per dose.

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What the Oncologists Said

The tumor responses documented above are extraordinary. But arguably more revealing is the institutional reaction — a pattern that repeats across nearly every case in this series.

Case No. 34 (Kentucky): The oncologist told the patient her tumor would not shrink. It shrank 82%.

Case No. 26 (Florida): A tumor shrank 56% in volume on ivermectin and fenbendazole alone, after the patient abandoned FOLFIRINOX. Official chart notation: “stable disease.”

Case No. 12 (California): When the Stanford oncologist saw the results — 81% CA19-9 drop and 46% reduction in PET metabolic activity — she was reportedly “not happy” that her patient was taking fenbendazole and ivermectin.

Case No. 24 (Pennsylvania): PET-confirmed NED. The oncology team told the patient the disease “would come back” and attempted to prevent him from ordering the confirmatory scan that documented his remission.

Case No. 9: CA19-9 dropped from 44,960 to 21. His oncologist’s response after 35 years in practice: he called it a miracle. The only oncologist in this series honest enough to admit he had no framework for what he was seeing.

Pattern Recognition: Across 49 cases, the institutional response to antiparasitic-driven remission follows a consistent sequence: (1) dismissal of the protocol, (2) minimization of the response (”stable disease”), (3) attribution of any improvement to concurrent chemotherapy, (4) warnings that the disease “will come back,” and (5) in extreme cases, active discouragement of confirmatory imaging. This is not a bug in the oncology system. It is a feature of a system whose financial architecture is incompatible with $1-per-dose treatments.

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Fenbendazole vs. Mebendazole: Which Wins for Pancreatic Cancer?

Both are benzimidazoles. Both share the core mechanism of β-tubulin binding and GLUT transporter suppression. The Italian head-to-head comparison (Florio et al., Cancers 2019) gives fenbendazole a slight edge for pancreatic cancer specifically.

• Mebendazole is FDA-approved for human use — easier to obtain via prescription

• Fenbendazole is lower cost (~$1/dose) and available OTC for veterinary use

• Both are fully interchangeable when one is unavailable

• Case No. 9 (CA19-9: 44,960 → 21) used mebendazole + fenbendazole, no ivermectin

• Case No. 27 (Michigan, 50% tumor shrinkage) used mebendazole alone

Bottom line: Get whichever you can access. Both work. The combination is stronger than either alone. For pancreatic cancer specifically, the published comparative data favors fenbendazole — but mebendazole has produced landmark results on its own.

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Protocol Overview from the Case Series

The following is a report of observed dosing ranges across 49 documented cases, presented for informational purposes only.

Fenbendazole
Range: 444 mg/day (low-dose responders) to 2,000 mg/day (aggressive Stage 4)
High-dose range for PDAC: 1,000–1,776 mg/day
Administration: with a fatty meal to maximize bioavailability; 6–7 days/week

Mebendazole
Range: 1,000–1,500 mg/day across all documented cases
FDA-approved for human use; fully substitutable for FBZ when unavailable

Ivermectin
Range: 12 mg/day (low-dose, still effective in Case 6) to 2 mg/kg/day
Most common range for Stage 4 PDAC: 1.0–1.5 mg/kg/day
Critical role: chemosensitizer, MDR reversal, cancer stem cell targeting

CBD Oil
100 mg/day — noted in multiple high-response cases (Cases 30, 31, 23, 16)
Anti-inflammatory and anti-proliferative synergy with benzimidazoles

Adjuncts (documented across the case series)
Modified citrus pectin 15 g/day · Vitamin D3, 2,000 - 10,000 IU/day · Curcumin 600 mg ×2 · Quercetin 500 mg · Berberine 600 mg 2–3× · Turkey tail mushroom · Zinc 50 mg · Serrapeptase.

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The Signal Is Too Large to Dismiss

Forty-nine cases. Fourteen countries. Ages 33 to 78. Stages 2 through 4. Chemo-naive patients, multiple chemo-refractory patients, post-Whipple recurrences, patients given two months to live. The responses are not scattered noise — they cluster around a consistent biological signal: benzimidazoles and ivermectin are active against PDAC, and their activity is amplified by chemotherapy synergy.

The methodological caveats are real: these are anecdotal cases, subject to reporting bias and confounding from concurrent therapies. These are also the identical caveats used to suppress every important medical advance before randomized trial evidence catches up to clinical reality.

The question is not whether these 49 cases constitute proof in the RCT sense. They do not. The question is whether 49 globally distributed cases — producing biologically coherent, mechanistically explicable responses across diverse patient populations — constitute sufficient signal to demand clinical investigation. They do. Unambiguously.

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What To Do With This Information

You have options your oncologist will likely not present. Not because they are dangerous — benzimidazoles have a 50-year mass drug administration safety record — but because they fall outside the institutional training and incentive structure of modern oncology.

Pancreatic cancer patients can not wait for Phase III evidence. With a median Stage 4 survival of three to six months, you do not have the time that randomized trials require. The cases reviewed here are the evidence available now. Waiting for clinical trials to prove that a $1/dose drug is effective for pancreatic cancer is a fool’s errand.

Document everything. CA19-9 levels, imaging reports, protocol details, timeline. These case reports exist because patients and families documented what they did. Case No. 50 and beyond should be yours.

Invoke Right to Try. US legislation exists precisely for this situation. There are physicians around the world that operate telehealth practices offering integrative oncology consultation for patients seeking antiparasitic protocols, search under holistic, functional or integrative medicine specialities. (Maybe it is a good idea to start a database of these physicians for your quick access😉). There appears to be no reason against most of those suffering with pancreatic cancer to add antiparasitic therapy to their treatment protocol; either under the guidance of their doctor or as a self-treatment effort.

Read the science. Cancer is a Parasite: Kill It with the Safe, Over-the-Counter Antiparasitic Fenbendazole (Skyhorse/MAHA Books, 2026). The material in the book and the reference list there will arm you for every conversation you may, or may not choose to have with your oncologist.

References

Epidemiology, Prognosis & Clinical Context

Conroy, T., Desseigne, F., Ychou, M., Bouché, O., Guimbaud, R., Bécouarn, Y., Adenis, A., Raoul, J.-L., Gourgou-Bourgade, S., de la Fouchardière, C., Bennouna, J., Bachet, J.-B., Khemissa-Akouz, F., Péré-Vergé, D., Delbaldo, C., Assenat, E., Chauffert, B., Michel, P., Montoto-Grillot, C., & Ducreux, M. (2011). FOLFIRINOX versus gemcitabine for metastatic pancreatic cancer. New England Journal of Medicine, 364(19), 1817–1825. https://doi.org/10.1056/NEJMoa1011923 [FOLFIRINOX median OS 11.1 months vs gemcitabine 6.8 months]

Conroy, T., Hammel, P., Hebbar, M., Ben Abdelghani, M., Wei, A. C., Raoul, J.-L., Choné, L., Francois, E., Artru, P., Biagi, J. J., Lecomte, T., Assenat, E., Faroux, R., Ychou, M., Bauguion, L., Bellera, C., Bonastre, J., Ducreux, M., & PRODIGE 24/CCTG PA.6 Trial investigators. (2018). FOLFIRINOX or gemcitabine as adjuvant therapy for pancreatic cancer. New England Journal of Medicine, 379(25), 2395–2406. https://doi.org/10.1056/NEJMoa1809775 [Modified FOLFIRINOX adjuvant; extended DFS over gemcitabine]

National Cancer Institute, Surveillance, Epidemiology, and End Results Program. (2024). Cancer stat facts: Pancreatic cancer. SEER Cancer Statistics. [https://seer.cancer.gov/statfacts/html/pancreas.html — Stage IV 5-year survival 3%]

Rawla, P., Sunkara, T., & Gaduputi, V. (2019). Epidemiology of pancreatic cancer: Global trends, etiology and risk factors. World Journal of Oncology, 10(1), 10–27. https://doi.org/10.14740/wjon1166 [PDAC epidemiology; late-stage diagnosis; surgical eligibility <20%]

Vyas, M., Larson, A. C., Gopalakrishnan, V., & Bhatt, A. P. (2024). The clinical implications of KRAS mutations and variant allele frequencies in pancreatic ductal adenocarcinoma. Journal of Clinical Medicine, 13(7), 2103.https://doi.org/10.3390/jcm13072103 [KRAS mutated in >90% of PDAC; surgical eligibility <20%]

Williamson, T., de Abreu, M. C., Trembath, D. G., Brayton, C., Kang, B., Mendes, T. B., de Assumpção, P. P., Cerutti, J. M., & Riggins, G. J. (2021). Mebendazole disrupts stromal desmoplasia and tumorigenesis in two models of pancreatic cancer. Oncotarget, 12(14), 1326–1338. https://doi.org/10.18632/oncotarget.28014 [5-year survival metastatic PDAC 3%; MBZ in KPC/KC mouse models]

Fenbendazole: Anticancer Mechanisms

Dogra, N., Kumar, A., & Mukhopadhyay, T. (2018). Fenbendazole acts as a moderate microtubule destabilizing agent and causes cancer cell death by modulating multiple cellular pathways. Scientific Reports, 8(1), 11926. https://doi.org/10.1038/s41598-018-30158-6[β-tubulin binding; GLUT4/HKII downregulation; p53 activation; GLUT1 suppression]

Kim, S.-I., Kim, H.-J., Lee, H.-J., Lee, K., Hong, D., Lim, H., & Kim, S. (2023). Anti-cancer effect of fenbendazole-incorporated PLGA nanoparticles in ovarian cancer. Journal of Gynecologic Oncology, 34(5), e58. https://doi.org/10.3802/jgo.2023.34.e58 [FBZ VEGF downregulation; peritoneal tumor growth and ascites inhibition]

Park, Y. H., Choi, J. W., Lim, H. Y., Park, J. H., Kim, J. Y., Lee, J. H., & Kim, S.-T. (2024). Oral fenbendazole for cancer therapy in humans and animals. Anticancer Research, 44(9), 3725–3737. https://doi.org/10.21873/anticanres.17167 [FBZ mechanism review: microtubule, GLUT1, p53, anti-angiogenesis; safety record]

Song, B., Park, E.-Y., Kim, K. J., & Ki, S. H. (2022). Repurposing of benzimidazole anthelmintic drugs as cancer therapeutics. Cancers, 14(19), 4601. https://doi.org/10.3390/cancers14194601 [Benzimidazole class comprehensive review: FBZ, MBZ mechanisms across cancer types]

Mebendazole: Anticancer Mechanisms and PDAC Activity

Florio, R., Veschi, S., di Giacomo, V., Pagotto, S., Carradori, S., Verginelli, F., Cirilli, R., Casulli, A., Grassadonia, A., Tinari, N., & Cama, A. (2019). The benzimidazole-based anthelmintic parbendazole: A repurposed drug candidate that synergizes with gemcitabine in pancreatic cancer. Cancers, 11(12), 2042. https://doi.org/10.3390/cancers11122042 [Comparative benzimidazole screening in PDAC cell lines; FBZ and MBZ antiproliferative activity]

Limbu, K. R., Chhetri, R. B., Oh, Y.-S., Baek, D.-J., & Park, E.-Y. (2022). Mebendazole impedes the proliferation and migration of pancreatic cancer cells through SK1 inhibition dependent pathway. Molecules, 27(23), 8127.https://doi.org/10.3390/molecules27238127 [MBZ inhibition of PDAC cell proliferation and migration]

Rottenberg, S., Disler, C., & Arriola, P. (2021). The rediscovery of mebendazole as a targeted therapy. Trends in Cancer, 7(6), 527–540.https://doi.org/10.1016/j.trecan.2020.12.010 [MBZ mechanism; microtubule; p53; CSC; repurposing rationale]

Williamson, T., de Abreu, M. C., Trembath, D. G., Brayton, C., Kang, B., Mendes, T. B., de Assumpção, P. P., Cerutti, J. M., & Riggins, G. J. (2021). Mebendazole disrupts stromal desmoplasia and tumorigenesis in two models of pancreatic cancer. Oncotarget, 12(14), 1326–1338. https://doi.org/10.18632/oncotarget.28014 [MBZ reduces PanIN formation, desmoplasia, liver metastasis in KRAS-driven PDAC mouse models]

Ivermectin: Anticancer Mechanisms

Dominguez-Gomez, G., Chavez-Blanco, A., Medina-Franco, J. L., Saldivar-Gonzalez, F., Flores-Torrontegui, Y., Juarez, M., Díaz-Chávez, J., Gonzalez-Fierro, A., & Duenas-Gonzalez, A. (2018). Ivermectin as an inhibitor of cancer stem-like cells. Molecular Medicine Reports, 17(2), 3397–3403. https://doi.org/10.3892/mmr.2017.8231 [IVM preferentially inhibits CD44+/CD24− cancer stem cell subpopulation]

Dou, Q., Chen, H.-N., Wang, K., Yuan, K., Lei, Y., Li, K., Lan, J., Chen, Y., Huang, Z., Xie, N., Zhang, L., Xiang, R., Nice, E. C., Wei, Y., & Huang, C. (2016). Ivermectin induces cytostatic autophagy by blocking the PAK1/Akt axis in breast cancer. Cancer Research, 76(15), 4457–4469. https://doi.org/10.1158/0008-5472.CAN-15-2887 [PAK1 ubiquitination-mediated degradation; Akt/mTOR blockade; in vivo tumor suppression]

Jiang, L., Wang, P., Sun, Y.-J., & Wu, Y.-J. (2019). Ivermectin reverses the drug resistance in cancer cells through EGFR/ERK/Akt/NF-κB pathway. Journal of Experimental & Clinical Cancer Research, 38(1), 265. https://doi.org/10.1186/s13046-019-1251-7 [IVM reversal of multidrug resistance; NF-κB pathway inhibition; chemosensitization]

Liu, J., Zhang, K., Cheng, L., Zhu, H., & Xu, T. (2020). Progress in understanding the molecular mechanisms underlying the antitumour effects of ivermectin. Drug Design, Development and Therapy, 14, 285–296. https://doi.org/10.2147/DDDT.S237393 [IVM: PAK1, WNT-TCF, Hippo, Akt/mTOR, CSC inhibition, MDR reversal — mechanism review]

Tang, M., Hu, X., Wang, Y., Yao, X., Zhang, W., Yu, C., Cheng, F., Li, J., & Fang, Q. (2021). Ivermectin, a potential anticancer drug derived from an antiparasitic drug. Pharmacological Research, 163, 105207. https://doi.org/10.1016/j.phrs.2020.105207[Comprehensive IVM anticancer review: PAK1, WNT/β-catenin, apoptosis, CSC, MDR reversal]

Wang, K., Gao, W., Dou, Q., Chen, H., Li, Q., Nice, E. C., & Huang, C. (2016). Ivermectin induces PAK1-mediated cytostatic autophagy in breast cancer. Autophagy, 12(12), 2498–2499. https://doi.org/10.1080/15548627.2016.1231494 [Companion to Dou et al. 2016; PAK1-AKT-MTOR axis mechanistic detail]

CYP24A1 Inhibition and Vitamin D Biology

Christakos, S., Dhawan, P., Verstuyf, A., Verlinden, L., & Carmeliet, G. (2016). Vitamin D: Metabolism, molecular mechanism of action, and pleiotropic effects. Physiological Reviews, 96(1), 365–408. https://doi.org/10.1152/physrev.00014.2015 [Vitamin D catabolism; CYP24A1 as primary degrading enzyme; anti-tumor functions of 1,25D3]

Luo, W., Karpf, A. R., Deeb, K. K., Muindi, J. R., Morrison, C. D., Johnson, C. S., & Trump, D. L. (2010). Epigenetic regulation of vitamin D 24-hydroxylase/CYP24A1 in human prostate cancer. Cancer Research, 70(14), 5953–5962. https://doi.org/10.1158/0008-5472.CAN-10-0617 [CYP24A1 upregulation in tumors; suppression of vitamin D signaling in cancer]

Schuster, I. (2011). Cytochromes P450 are essential players in the vitamin D signaling system. Biochimica et Biophysica Acta, 1814(1), 186–199. https://doi.org/10.1016/j.bbapap.2010.06.022 [CYP24A1 biology; azole class inhibition of CYP24A1 heme iron coordination]

Supple, W. F. (2026). Cancer Is a Parasite: Kill It with the Safe, Over-the-Counter Antiparasitic Fenbendazole (Skyhorse/MAHA Books)

Supple, W. F. (2026). Fenbendazole-mediated CYP24A1 inhibition as a universal potentiator of vitamin D signalling: The first in a new class of vitamin D protector drugs, submitted.

Chai, J.-Y. (2013). Albendazole and mebendazole as anti-parasitic and anti-cancer agents: An update. Korean Journal of Parasitology, 51(4), 355–364. https://doi.org/10.3347/kjp.2013.51.4.355 [Benzimidazole safety profile; decades of human use; antiparasitic and emerging anticancer data]

Deluao, J. C., Winstanley, J., Petrova, R. M., McIlvenna, L., Bhatt, A., & Sobinoff, A. (2024). Serious adverse events reported with benzimidazole derivatives: A disproportionality analysis from the World Health Organization’s pharmacovigilance database. PLOS Neglected Tropical Diseases, 18(11), e0012634. https://doi.org/10.1371/journal.pntd.0012634 [WHO pharmacovigilance data; generally favorable benzimidazole safety profile in mass use]

Ndjonka, D., Rapado, L. N., Silber, A. M., Liebau, E., & Wrenger, C. (2013). Natural products as a source for treating neglected parasitic diseases. International Journal of Molecular Sciences, 14(2), 3395–3439. https://doi.org/10.3390/ijms14023395 [Benzimidazoles in mass drug administration since 1960s; safety in hundreds of millions of doses]

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Cancer is a Parasite Book Notes

Cancer is a Parasite is the #1 book in many Amazon categories like breast, lung and prostate cancer! If you buy it on Amazon, please post your reactions and review on Amazon - a few words is all it takes. I think you can post comments on Amazon even if you obtained the book elsewhere. I would also ask that you comment here as well and as always, ask any questions that arise.

We are truly at a moment in time where a legitimate cure for cancer is about to enter the mainstream. The stars are aligned and the time is ripe for a real cure like fenbendazole. The ball is now in the court of the revamped Health and Human Services public health infrastructure. It is my hope that the shackles impeding progress from entrenched interests have been loosened enough to find the political will and courage to act in humanity’s best interests. It is truly a great time to be alive!

Items Included in All Posts

Fenbendazole vs. Mebendazole vs. Albendazole vs. Flubendazole: The benzimidazoles are very similar chemically and they have very similar mechanisms of action with respect to disrupting microtubule function, specifically defined as binding to the colchicine-sensitive site of the beta subunit of helminithic (parasite) tubulin thereby disrupting binding of that beta unit with the alpha unit of tubulin which blocks intracellular transport and glucose absorption (Guerini et al., 2019). If someone asks you how fenbendazole kills the cancer cells, the answer is in italics in the previous sentence.

The class of drugs known as benzimidazoles includes fenbendazole, mebendazole, albendazole and flubendazole. Mebendazole is the form that is approved for human use while fenbendazole is approved for veterinary use. The main difference is the cost. Mebendazole is expensive ~$555 per 100 mg pill, while fenbendazole is inexpensive ~48 cents per 222 mg free powder dose (Williams, 2019). As you may recall, albendazole is the form used to treat intestinal parasites in India and these cost 2 cents per pill. FYI, to illustrate how Americans are screwed by Big Pharma, two pills of mebendazole cost just $4 in the UK, 27 cents per 100 mg pill in India and $555 per 100 mg pill in the US.

While most of the pre-clinical research uses mebendazole, probably because it is the FDA-approved-for-humans form of fenbendazole, virtually all of the self-treating clinical reports involve the use of fenbendazole. Because the pre-clinical cancer studies use mebendazole (ironically the human form of fenbendazole) and humans self-treat their cancers with fenbendazole (the animal form of mebendazole) it is very reasonable to assume that mebendazole and fenbendazole are functional equivalents with respect to cancer. It would be helpful if future pre-clinical and clinical investigations simply used fenbendazole as a practical matter. For the purposes of this Substack, fenbendazole, mebendazole and albendazole are used interchangably.

Where to get fenbendazole
In our experience and the experiences of those that write in, it appears that the three readily available brands of fenbendazole (Panacur-C, FenBen Labs, Happy Healing Labs) are equally effective. Panacur-C can be obtained locally in pet stores, while they all can be obtained from Amazon. The article on Questions & Answers discusses the brands of fenbendazole in detail and shows photos of the various brands referenced.

If you would like to report your experiences with fenbendazole you can do so privately by email myfenbendazole@proton.me or more publicly in the Comments section in any of the articles. Also, if you know of people who’ve tried fenbendazole, and it didn’t work, we’d be especially interested in hearing from you now. Understanding the conditions and factors that enhance or impede the success of fenbendazole in treating cancer are valuable.

Disclaimer:
Statements on this website have not been evaluated by the Food and Drug Administration. The contents of this website is for educational and informational purposes only and is not intended to be a substitute for professional medical advice, diagnosis or treatment. This website does not provide any kind of health or medical advice of any kind. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. The case reports presented reflect the real-life experiences and opinions of other readers or users of the website. The experiences of those readers or users are personal to those particular readers/users and may not necessarily be representative of all readers/users. We do not claim, and you should not assume, that all other readers/users will have the same experiences. Do you own research, consult with relevant medical professionals before attempting to self-treat for any condition.