Executive Summary

Chronic lymphocytic leukemia (CLL), chronic myeloid leukemia (CML), acute myelogenous leukemia (AML), and related leukemias often require ongoing targeted therapy or intensive chemo, with resistance as a key challenge. My Cancer is a Parasite book highlights preclinical activity of mebendazole against AML and broad effects of the antiparasitic trio on hematologic malignancies (Supple, 2026, Chapters 2 and 9).

The same OneDayMD series covers 10 leukemia cases, mostly CLL and CML, using similar ivermectin + benzimidazole protocols (OneDayMD, 2026).

Standout Leukemia Cases with Protocols

• Case 8 (2026): 56-year-old North Carolina man, CLL — Ivermectin + fenbendazole for 4 months → normalized blood counts. Follow-up (8 months later): switched to ivermectin + mebendazole → continued normalization of blood work; oncologist extended monitoring interval.

• Case 9 (2026): 56-year-old Illinois man, CML — Ivermectin + fenbendazole.

• Earlier referenced cases include AML patients receiving ivermectin for concurrent parasitic infections while on chemo, with stable outcomes, and a pediatric ALL case with long-term remission after ivermectin for Demodex.

Key Trends and Patterns (with Protocol Details)

• Hematologic Improvement: Rapid blood-count normalization and marker stabilization, often within 4–8 months (e.g., CLL Case 8).

• Indolent Disease Benefit: Particularly effective in early/low-burden CLL with minimal intervention.

• Protocol Commonalities: Ivermectin (1 mg/kg/day) + fenbendazole or mebendazole (typically 444–1,000+ mg/day); some transitions between FBZ and MBZ.

• Safety: Well-tolerated long-term; no reported toxicity in these cases.

Important Caveats

These are self-reported observational data—not controlled trials. Confounders include prior/concomitant therapies and positive-outcome bias. The book and OneDayMD stress physician oversight, regular monitoring (blood work, imaging), and the need for randomized trials (Supple, 2026; OneDayMD, 2026). Early cases have supported peer-reviewed interest.

The case series below provides granular real-world detail, reinforcing Cancer Is a Parasite’s framework that these accessible antiparasitics may offer meaningful options in hematologic malignancies.

Ivermectin, Fenbendazole, and Mebendazole in Leukemia: What the Reports Actually Show

A field summary of documented case reports and patient/clinician testimonials, with a clear line drawn between the two.

Disclaimer: This article is for educational and discussion purposes only. It is not medical advice. Ivermectin, fenbendazole, and mebendazole are not approved or guideline-recommended treatments for lymphoma or leukemia. Anyone considering these agents alongside or instead of standard therapy should do so only under the supervision of a physician who can monitor bloodwork, liver function, and drug interactions. Self-medication without medical oversight carries real risk.

Introduction

Repurposed antiparasitics keep showing up in the cancer conversation, and hematologic malignancies — lymphoma and leukemia — are where some of the loudest reported responses are coming from. Two very different bodies of material feed that conversation, and it matters that readers can tell them apart.

The first is a small handful of actual peer-reviewed case reports and a safety-focused literature review. These exist in indexed journals, have DOIs, and can be checked by anyone.

The second — and far larger — body is testimonial: patients and Canadian oncologist, Dr. William Makis, posting treatment timelines and scan results on X.com. These are real people describing real experiences, but they are uncontrolled, unblinded, self-reported, and in most cases delivered alongside conventional chemotherapy — which makes attributing the outcome to any one agent impossible at present.

Both bodies of material are presented below, in their own sections, so neither gets mistaken for the other.

What’s Actually in the Peer-Reviewed Literature

Ivermectin safety in AML (De Castro et al., 2020). A short report in Leukemia & Lymphoma described continuous high-dose ivermectin (roughly 1 mg/kg/day) as well tolerated in patients with acute myelogenous leukemia, with the authors noting this safety profile could inform repurposing discussions more broadly (de Castro et al., 2020).

Fenbendazole monotherapy in Diffuse Large B-cell Lymphoma DLBCL (Abughanimeh et al., 2020). An 83-year-old man presented with a duodenal ulcer that biopsied as diffuse large B-cell lymphoma, GCB subtype, staged IVa with hypermetabolic disease in the gastric antrum, duodenum, a peri-aortic lymph node, and the lungs. He declined chemotherapy and began self-directed fenbendazole at roughly 1 g/day. Follow-up CT and PET/CT scans over the following months showed smaller lymph nodes and improved lymphadenopathy with no new lesions, while he gradually tapered the dose to three pills weekly due to peripheral neuropathy (Abughanimeh et al., 2020). The authors were careful to note that disease regression was observed but causation could not be established — and that further study was needed.

Ivermectin and incidental parasitic/dermatologic infections in cancer patients (Lai et al., 2025). A 2025 systematic review in Acta Poloniae Pharmaceutica catalogued published reports of ivermectin use in cancer patients who had concurrent parasitic infections — most of these were treating the infection itself, not the cancer. Within that catalogue:

• A patient with adult T-cell leukemia/lymphoma and HTLV-1 infection was stabilized and discharged on a combination of ivermectin and chemotherapy; the authors stated ivermectin may have contributed but drew no firm conclusion.

• Several stem-cell-transplant and leukemia patients treated with ivermectin for Demodex or other parasitic skin infections saw those skin symptoms resolve, with no claim of anticancer effect.

• An 80-year-old woman with AML and crusted scabies cleared her skin lesions on ivermectin plus topical permethrin — again, a parasitic infection, not the leukemia, was being treated.

That is the entirety of what we could find published and indexed on ivermectin/fenbendazole/mebendazole specifically in lymphoma and leukemia patients as of this writing. There are no phase II or III trials, no randomized data, and no published series showing these drugs driving remission as primary anticancer agents in blood cancer. As such, the following may be the best available evidence to date.

Patient and Clinician Testimonials (X.com)

The volume of reported lymphoma and leukemia responses comes almost entirely from testimonials directly from patients or family members. None of these are peer-reviewed; none have been independently verified; nearly all occurred alongside conventional chemotherapy, immunotherapy, or radiation, which makes isolating the antiparasitic’s contribution impossible.

Patterns across the leukemia testimonials (roughly a dozen reports, 2025–2026): Reports spanned AML, CLL, and CML. Several CLL cases described gradual normalization of white blood cell and lymphocyte counts over months on ivermectin with or without fenbendazole or mebendazole, without concurrent chemotherapy in some cases (patients on “watch and wait”). One CML case reported reaching major molecular response on conventional follow-up testing after starting ivermectin and fenbendazole alongside standard monitoring. Reported responses were not universal — Dr. Makis’s own commentary on the CLL cases notes that “some... respond amazingly and obviously... while others don’t seem to,” which is an honest acknowledgment that these are not uniform results. Any reference to “I” refers to Dr. Makis.

(Full case-by-case detail, including specific patient narratives and dates, is preserved in the original OneDayMD compilation linked at the end of this piece for readers who want the unabridged testimonial record.)

Discussion

Why hematologic cancers, mechanistically. Both drugs have plausible reasons to intersect with blood cancer biology. Fenbendazole and mebendazole destabilize microtubules in a manner mechanistically related to vincristine, a backbone drug in many lymphoma regimens, and preclinical work has pointed to apoptosis induction, anti-angiogenic activity, and Hedgehog pathway inhibition. In fact, at least one prominent oncology group has recommended replace the standard of care drug vincristine with more effective and safer mebendazole (DeWitt, et al., 2017). Ivermectin’s proposed anticancer mechanisms include WNT/β-catenin inhibition, PAK1 modulation, and induction of mitochondrial dysfunction. Blood cancers — circulating, immune-modulated, and often microtubule-drug-sensitive — are a reasonable place to look for that kind of activity, at least on paper.

In-vitro potency does not guarantee that achievable human plasma concentrations matter clinically, and almost every reported “success” above happened with chemotherapy running in parallel, which is itself capable of producing the same scans. There is no controlled comparison anywhere in this material — no arm without the antiparasitic to tell us whether it added anything. But that doesn’t mean we should throw the baby out with the bathwater. In an era of high-stakes financial oncology treatments to protect we may never see randomized controlled trials of inexpensive, safe, off patent medicines like the oncological antiparasitics. Therefore, a more rational approach may be to adopt a Best Available Evidence standard of causality in this perverted pharmacological environment. The evidence that fenbendazole, mebendazole and ivermectin possess therapeutic effectiveness in treatment of some leukemias, either as mono therapies or synergistically with standard of care treatments, warrants further study.

References

Abughanimeh, O., Evans, T., & Kallam, A. (2020). Fenbendazole as a treatment for diffuse large B-cell lymphoma. Annals of Hematology & Oncology, 7(2), 1284.

Damian, D., & Rogers, M. (2003). Demodex infestation in a child with leukaemia: Treatment with ivermectin and permethrin. International Journal of Dermatology, 42(9), 724–726. https://doi.org/10.1046/j.1365-4362.2003.01916.x

de Castro, C. G., Jr., Gregianin, L. J., & Burger, J. A. (2020). Continuous high-dose ivermectin appears to be safe in patients with acute myelogenous leukemia and could inform clinical repurposing for COVID-19 infection. Leukemia & Lymphoma, 61(10), 2536–2537. https://doi.org/10.1080/10428194.2020.1786559

De Witt, M., Gamble, A., Hanson, D., Markowitz, D., Powell, C., Al Dimassi, S., Atlas, M., Boockvar, J., Ruggieri, R., & Symons, M. (2017). Repurposing Mebendazole as a Replacement for Vincristine for the Treatment of Brain Tumors. Molecular medicine (Cambridge, Mass.), 23, 50–56. https://doi.org/10.2119/molmed.2017.00011

Lai, Y., Guan, X., Chen, X., Chen, J., Zhang, X., & Lu, M. (2025). A review of ivermectin use in cancer patients: Is it time to repurpose ivermectin in cancer treatment? Acta Poloniae Pharmaceutica – Drug Research, 81(6), 913–929. https://doi.org/10.32383/appdr/200570

OneDayMD. (2026). Ivermectin and Mebendazole in Lymphoma and Leukemia: 35 Case Reports (May 2026 Update). https://www.onedaymd.com/2026/02/ivermectin-mebendazole-lymphoma-leukemia.html

Supple, W. F., Jr. (2026). Cancer is a parasite: Kill it with the safe, over-the-counter antiparasitic fenbendazole. MAHA Books/Skyhorse Publishing. (Print ISBN: 978-1-5107-8513-7)

Summary of Individual Testimonial Sources

Ivermectin and mebendazole in lymphoma and leukemia: 40 case reports (June 2026 update).https://www.onedaymd.com/2026/02/ivermectin-mebendazole-lymphoma-leukemia.html and https://fenbendazole.substack.com

Drug repurposing sits at the intersection of curiosity and caution. Ivermectin and mebendazole — long-used antiparasitic medications — have accumulated a growing body of laboratory evidence suggesting anticancer activity across multiple pathways. Meanwhile, a series of reported cases involving lymphoma and leukemia patients describe tumor regression, remission, or hematologic normalization after incorporating these agents into their regimens. The central question is not whether these reports “prove” efficacy, it is whether they, together, send a signal that these antiparasitic drugs are viable anticancer agents.

Leukemia (Acute Myelogenous Leukemia (AML) and Chronic Lymphocytic Leukemia (CLL) (14 Cases)

Case 14: 45 year old woman with AML (Acute Myeloid Leukemia)Dr William Makis posted on X.com in June 2026: IVERMECTIN and FENBENDAZOLE Testimonial - 45 year old ROMANIAN woman with AML Acute Myeloid Leukemia reports after 6 months...blasts decrease 36% to 16% to 8%.
Summary: 45 year old woman with AML Acute Myeloid LeukemiaIn September 2025 she started taking Ivermectin and Fenbendazole on a regular basis. Ivermectin 1.5mg/kg/day Fenbendazole 1000mg/day. RESULTS:36% blasts in July 2025 16% blasts in December 2025 8% blasts in February 2026.

Case 13: 60 year old man with CLL (Chronic Lymphocytic Leukemia) Dr William Makis posted on X.com in April 2026: IVERMECTIN ONLY Testimonial - 60s year old Canadian man with CLL Leukemia reports after 6 months: in Remission! Can you use Ivermectin as the only repurposed drug? Yes!
Summary: 60 year old man with CLL Leukemia. He had beaten CLL prior to COVID but after taking two COVID-19 Vaccines, it came back with a vengeance in 2023. By 2025 he was failing Acalabrutinib. In August 2025 he started Ivermectin. Oncology: Venclexta and Rituximab. He did not take Fenbendazole. In remission after 6 months. Interestingly, many lymphomas and leukemias seem to be very responsive to ivermectin and preclinical research (as well as published human cases) have shown this as well.

Case 12: 56 year old man with Chronic Myeloid Leukemia (CML) Dr William Makis posted on X.com in January 2026: IVERMECTIN and FENBENDAZOLE Testimonial - 56 year old Illinois man with Chronic Myeloid Leukemia (CML) shares his success story! Sometimes Cancer patients send me their success stories full of enthusiasm and optimism.
Summary: 56 year old man with Chronic Myeloid Leukemia (CML)Started Ivermectin and Fenbendazole in July and saw his WBC count drop 78.6 to 7.99 within 2 months October 2025: “The very first thing the doctor said was: “someone told me you had leukemia but I can’t find it. Dr. seems very happy and a little surprised at how well he is doing!” Jan.2026: “I reached major molecular response below 0.1%...which is considered remission! This is usually achieved after 18 months...WBC 4.27”

Case 11: 56 year old man with Chronic Lymphocytic Leukemia (CLL) (Part 2)Dr William Makis updated on X/Twitter in January 2026: IVERMECTIN and MEBENDAZOLE Testimonial - 56 year old North Carolina man with CLL Leukemia reports after 8 months - normalization of blood work, Oncologist changes follow-up from 3 to 6 months. Leukemia success stories are amazing because mainstream Oncology claims NOTHING helps outside chemo.
Summary: 56 year old North Carolina man with CLL LeukemiaIn May 2025 he started: Ivermectin 1mg/kg/day Mebendazole 1000mg/day CBD Oil 100mg/day Results over 8 months:WBC 13.3 to 12 to 10.7 to 10.0 Lymphocytes: 10.11 to 6.24 to 4.39.
KEY POINTS:Leukemias are tricky cancers. Some CLL cases respond amazingly and obviously to repurposed drugs, while others don’t seem to. What an easy solution this case was! No chemo!

Case 10: 56 year old North Carolina man with Chronic Lymphocytic Leukemia (CLL) (Part 1) Dr William Makis posted (X/Twitter) in October 2025: IVERMECTIN and FENBENDAZOLE Testimonial - 56 year old North Carolina man with Stage 0 Chronic Lymphocytic Leukemia (CLL) normalizes blood counts after 4 months. I’m always happy to see Leukemia success stories, because Leukemia is not easy!
Summary: 56 year old North Carolina man with Chronic Lymphocytic Leukemia (CLL) Stage 0. He had NO COVID-19 Vaccines. He had NO chemo. He had NO conventional Oncology treatment. On May 16, 2025 he started: Ivermectin 1mg/kg/day Fenbendazole 1000mg/day. Oncologist had him on “watch and wait”, meaning you watch until your Leukemia gets worse. Results after 4 months: Lymphocytes 10.11 to 4.39 WBC 13.3 to 10.7 There is no mistaking the results. Once again… He had no CHEMO. He had no Oncology Treatment of any kind. According to mainstream Oncology, this is impossible and this patient shouldn’t exist. Yet he does and he’s quite happy with the results.

Cases 8 - 9: Acute Myelogenous Leukemia (AML) patient and Chronic Lymphocytic Leukemia (CLL) patient. 2 Case testimonials from Dr William Makis (X/Twitter) in January 2025: IVERMECTIN and FENBENDAZOLE Testimonial - Two blood Cancer Cases: Acute Myelogenous Leukemia (AML) patient becomes “cancer free” and Chronic Lymphocytic Leukemia (CLL) patient improves 1st time in 2 years!

Case 8: AML Patient diagnosed in October 2024. Immediately started 72mg Ivermectin and 1000mg Fenbendazole 3 days on 4 days off. Also did 2 rounds of chemo in November and December, and in December added oral chemo pill Venclexta.

Results after 2 months of Ivermectin & Fenbendazole:”His bone marrow biopsy from December 24th came back clear! His blood work is looking good.”

Case 9: 63 age, male, CLL patient with a high WBC count in Sep.2022, on “watch and see”I didn’t go aggressive here, started: 70mg Ivermectin and 500mg Mebendazole: Results: WBC 16.1 (Oct.2) → 15.6 (Dec.6) —> 14.1 (Jan.15) Lymphocytes 13.0 (Oct.2) —> 12.5 (Dec.6) —> 11.3 (Jan.15) On Dec.11 I made a few minor adjustments: increased from 500mg to 1000mg/day Mebendazole and added 1000mg/day Lactoferrin. After 2 years of being abnormal, the WBC and Lymphocytes are trending towards normal range (almost there)!” It is definitely trending down since beginning the protocol”

Case 7: Adult T-cell Leukemia/Lymphoma (ATL)A patient with ATL and HTLV-1 infection was successfully stabilized and discharged after a combination of ivermectin and chemotherapy. The authors note that ivermectin may have contributed to disease control, but no firm conclusions can be drawn. (Lai Yuwen et al 2025)

Case series 4 (2025): Several patients with Blood cancer (Leukemia, Lymphoma) and parasitic infections. Several patients receiving hematopoietic stem cell transplants or undergoing treatment for leukemia were treated with ivermectin for Demodex or other parasitic infections. In these cases, skin symptoms resolved rapidly, and patients remained stable over the short-to-intermediate term, though direct anticancer effects were not confirmed. (Lai Yuwen et al 2025)

Case 5: 80 yr-old female with Acute Myeloid Leukemia (AML). A female patient diagnosed with crusted scabies showed improvement after treatment with 9 mg ivermectin (days 1, 2, 8, 9, and 15) and systemic 5% permethrin cream for seven days. Two weeks later, all the skin lesions in the patient were repaired. (Lai Yuwen et al 2025) Case Series (N=3) (2020): Continuous high-dose ivermectin appears to be safe in patients with acute myelogenous leukemia (AML).In the case series by De Castro et al. (2020), a daily dose of 1 mg/kg. This regimen was found to be well tolerated, with no major side effects reported throughout the treatment period. Notably, the authors also observed clinical benefits associated with this dosing protocol.

The AML Data: Physicians shared an anecdotal, compassionate-use experience involving three pediatric patients with refractory acute myeloid leukemia (AML). Based on separate preclinical cancer data, these patients were given continuous, high doses of ivermectin (1 mg/kg/day for up to 15 days). [Leukemia & Lymphoma]

Safety Results: The authors reported that these higher, prolonged doses did not result in major toxic side effects in these patients. [Leukemia & Lymphoma]

Case 1: 6-year-old male with Acute Lymphoblastic Leukemia (ALL) and Demodex folliculorum infestation. A 6-year-old male with ALL remained well and in long-term remission after ivermectin treatment for Demodex folliculorum infestation. 200 μg/kg ivermectin and 5% permethrin cream were administered, and the treatment was repeated after seven days; the rash did not recur. No relapse or progression noted at follow-up. (Int J Dermatol 2003)

Biological Plausibility: A Foundation Worth ExaminingMebendazole

Mebendazole disrupts microtubules, similar in principle to vincristine — a core drug in many lymphoma regimens. Preclinical studies have also suggested: Induction of apoptosis in leukemia cell lines. Anti-angiogenic effects Hedgehog pathway inhibition. Potential synergy with chemotherapy. Importantly, hematologic malignancies are particularly sensitive to microtubule dynamics, making mechanistic overlap notable.

IvermectinIvermectin’s proposed anticancer mechanisms include:WNT/β-catenin pathway inhibition. PAK1 modulation. Mitochondrial dysfunction induction. Immune signaling modulation. Some leukemia models demonstrate selective cytotoxicity at higher concentrations.

Translational Issues

A recurring issue in repurposing research is pharmacokinetics. In vitro concentrations do not always translate to achievable human plasma levels. However, tissue accumulation, tumor microenvironment effects, and immune modulation are variables not fully captured in cell culture models. Thus, the mechanistic plausibility is neither trivial nor definitive.

What these cases suggest — Across the reported lymphoma and leukemia cases, several patterns emerge: Many patients used ivermectin and/or mebendazole alongside standard chemotherapy. Some reported rapid tumor regression within months. PET-confirmed remission was described in select lymphoma cases. Minimal toxicity was reported in anecdotal accounts. In certain early-stage or indolent leukemia cases, hematologic markers reportedly normalized.These are observational patterns — not controlled outcomes. Yet they raise several research-relevant questions: Could these drugs act as chemosensitizers? Might there be subtype-specific responsiveness? Are certain metabolic or molecular profiles more susceptible?Is immune modulation contributing indirectly?

The Evidence Gap: Where We Stand Clinically

Currently, the published clinical literature shows:

• No phase III trials in lymphoma or leukemia

• No randomized controlled trials establishing benefit

• Limited early-phase exploration in oncology overall

• No survival endpoint data in hematologic malignancies

In evidence hierarchy terms, this places the field at the hypothesis-generating stage. However, absence of high-level evidence does not equal evidence of absence. It indicates an untested space. again, what does the best available evidence indicate?.

Safety Profile: A Key Variable

One reason these drugs attract attention is their established safety record in antiparasitic use. That said: Oncology dosing duration differs from short antiparasitic courses. Drug–drug interactions with chemotherapy are under-studied. Long-term hepatic or hematologic effects require structured monitoring. The safety advantage hypothesis remains plausible but unproven in cancer contexts.

A Research Roadmap

If these case patterns are to be meaningfully evaluated, the next logical steps would include:

• Pharmacokinetic studies confirming tumor-relevant concentrations.

• In vitro synergy testing with R-CHOP components.

• Phase I dose-finding safety trials in relapsed lymphoma.

• Biomarker stratification (e.g., MYC, WNT activity, metabolic signatures).

• Phase II objective response rate trials.

• Randomized adjunct studies measuring progression-free survival.

Without this progression, the conversation remains anecdotal.

Where This Leaves Clinicians and Patients

At present: Ivermectin and mebendazole remain investigational in lymphoma and leukemia. They are not guideline-recommended therapies. Standard-of-care treatments remain the evidence-backed foundation. Clinical trial enrollment remains the safest pathway for exploration. For researchers, however, these reports represent something different: A cluster of biological plausibility intersecting with real-world experimentation. That intersection is often where translational oncology begins.

The 40 reported cases neither confirm nor refute the anticancer potential of ivermectin and mebendazole in hematologic malignancies. They represent a signal — faint, uncontrolled, and methodologically limited — but not biologically implausible. The appropriate scientific response is not adoption or rejection. It is investigation. Whether this signal fades under scrutiny or strengthens through structured trials will determine its place in oncology. Until then, it remains an open question — and an area worthy of careful, disciplined research. The best available evidence is certainly encouraging and worth a serious look.

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.

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.

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)

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.

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.

—

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.

—

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.”

—

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)

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.

—

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.

—

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.

—

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.

—

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.

The Standout Data Points

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.

—

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.

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.

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.

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.

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]

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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: This publication is educational and informational in nature. Nothing published here — including articles, case reports, reader comments, or author responses — constitutes medical advice, a diagnosis, or a treatment recommendation. Dosing figures and administration methods discussed here reflect information from published scientific literature or the personal experiences of individual readers; they are not prescriptions and are not tailored to any individual’s health situation. Always consult a qualified physician or licensed health professional before making any change to your medical care or beginning any self-treatment. The case reports presented reflect the personal experiences of individual contributors and may not be representative of others. We make no claim that any outcome described here is typical or predictable. Statements have not been evaluated by the Food and Drug Administration. Do your own research.