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Table of contents
Summary
Introduction
Part 1: Why are cancer patients shopping at Tractor Supply?
Part 2: Cancer therapy is an outrageous scandal
Part 3: An email from William Supple, PhD
Summary
• Benzimidazole antiparasitic drugs, including fenbendazole and mebendazole, have documented anticancer activity through multiple overlapping mechanisms, including microtubule disruption, glycolytic inhibition, p53 reactivation, angiogenesis inhibition, and cancer stem cell targeting.
• Fenbendazole’s metabolic attack on cancer’s glucose supply through GLUT transporter and hexokinase II suppression gives it advantages over mebendazole against drug-resistant cancers. Mebendazole has more human pharmacokinetic data and crosses the blood-brain barrier. Neither drug has been through proper clinical trials for cancer. Both should be taken with fat.
• Liver enzyme elevations during benzimidazole therapy are transient and, in documented case reports, correlate with active tumor destruction rather than drug toxicity. No chronic liver damage has been reported in cancer patients without pre-existing liver disease.
• Cytotoxic chemotherapy contributes 2.1 to 2.3 percent to 5-year survival across all adult cancers, which is invisible statistically. Radiation contributes 2.7 percent at the population level. Treatment-related mortality is systematically hidden by attributing deaths to cancer rather than treatment.
• Oncology’s buy-and-bill financial model pays physicians more for prescribing more expensive drugs. This arrangement would be a federal crime under the Anti-Kickback Statute (AKS) in any other medical specialty.
• The net survival calculation, subtracting treatment mortality from treatment benefit, has never been published for most cancers. The silence tells you everything about what the answer would be.
Introduction
Pushback arrived after the recent interview with William Supple, but his views on fenbendazole and cancer are more accurate than the criticisms, and his book is definitive. The objections and the rebuttals from his book Cancer Is a Parasite (2026) follow. Supple also wrote an email about these issues that appears in Part 3.
Oncology is a vast industry, and its corrupt toadies have every motivation to destroy the credibility of repurposed drugs like these. That said, better evidence than this sad fact follows.
Supple’s central claims that benzimidazole-based parasite drugs have anticancer activity are supported by dozens of preclinical studies. The mechanisms are known: microtubule disruption, p53 reactivation, Warburg effect interference, angiogenesis inhibition, and cancer stem cell targeting.
Case reports are not proof of a reliable cancer cure, but they are all we have in our age of pharmaceutical study fraud and information suppression. As Paul Marik says, “A thousand case reports are data.” Fifty sequential case reports are substantial evidence. Fenbendazole’s numbers are in the thousands.
The cautious conclusion about fenbendazole is that although it is not universally effective against all cancers, adding it to protocols is wise, and adverse consequences are unlikely. As BCC told me, “When your life is on the line, you throw out all your hand grenades at once.” Pick up a copy of Supple’s book HERE to learn more.
Part 1: Why are cancer patients shopping at Tractor Supply?
People with cancer are buying dog dewormer at farm supply stores because the system designed to help them has failed them. They are doing this not because they are stupid but because they looked at what conventional oncology offers for most cancers, the price, and the survival data, and concluded that a fifty-pound bag of antiparasitic medication for under a dollar a dose was a more rational bet.
Fenbendazole is the best studied drug of its class, but clinical trials have not been done
The benzimidazole anthelmintics include fenbendazole, mebendazole, and albendazole. They share a core structure: a benzene ring fused with an imidazole ring. They all bind beta-tubulin and disrupt microtubule formation. Their anticancer properties overlap, but they are not identical.
Mebendazole is FDA-approved for human use and is available in the United States as a prescription medication (Emverm) and through compounding pharmacies, as well as in veterinary formulations. The WHO includes it on its List of Essential Medicines. It has decades of human pharmacokinetic data, including long-term high-dose studies in patients with echinococcosis at 40 to 50 mg/kg/day for months to years. It crosses the blood-brain barrier, and polymorph C mebendazole reaches therapeutic concentrations in brain tissue in preclinical glioblastoma models. For patients with primary brain tumors or brain metastases, this property is significant.
Fenbendazole is approved for veterinary use and lacks formal human pharmacokinetic studies. It is available over the counter at farm supply stores and online for pennies per dose. This accessibility drove its adoption by the cancer patient community. The standard dose of 222 mg was entered into human use by accident, as the dose for a ten-pound dog, and stuck because it worked.
The Kory clinic and others favor mebendazole based on cell-line potency comparisons. IC50 (the concentration required to inhibit 50 percent of cell growth) is lower for mebendazole in melanoma cells: 0.30 to 0.32 micromolar versus 1.2 to 1.4 micromolar for fenbendazole. A lower IC50 means less drug is needed to kill the cancer cells.
Supple and Nguyen et al. (2024) make a different argument. Fenbendazole hits a metabolic axis that mebendazole does not attack as aggressively. Fenbendazole simultaneously destabilizes tubulin, causes mitochondrial translocation of p53, inhibits glucose uptake, downregulates GLUT transporters, and suppresses hexokinase II, a key glycolytic enzyme that most cancer cells depend on. The Nguyen review in Anticancer Research states that fenbendazole “surpasses albendazole and mebendazole in treating drug-resistant cells” and attributes this superiority to its glycolytic inhibition.
This distinction is medically important. Patients who have exhausted standard chemotherapy are, by definition, dealing with drug-resistant cancer cells. Fenbendazole’s metabolic attack on glycolysis targets a vulnerability that microtubule disruption alone does not. As Supple writes in Cancer Is a Parasite: “By blocking glucose and slashing lactate production, fenbendazole dismantles a key engine of tumor growth and drug resistance. This potent metabolic attack offers a powerful way to kill cancer cells that have become resistant to traditional chemotherapy drugs.”
The case reports support this. Many of the documented fenbendazole responders, including the 362 cases compiled by OneDayMD and the 22 detailed in Supple’s book, were patients discharged to hospice after exhausting standard treatment. They were in the throes of drug-resistant disease. That fenbendazole worked where conventional drugs had failed is consistent with its glycolytic mechanism.
No clinical trials comparing fenbendazole to mebendazole for cancer exist. The IC50 data favor mebendazole in some cell lines. The metabolic mechanism data favor fenbendazole against drug-resistant cells. Cancer at one month is different from the same cancer at one year, and the effectiveness of different agents varies over time. Patients and physicians should know both drugs, understand their respective advantages, and recognize that the definitive comparison has not been done. Taking either drug, or both, alongside other interventions, is the strongest position available with current evidence.
The peer-reviewed Baghli, Martinez, and Marik protocol published in September 2024 recommends mebendazole at 200 mg per day for low-grade cancers, 400 mg per day for intermediate-grade, and 1,500 mg per day for high-grade cancers. For fenbendazole, the protocol specifies 1,000 mg three times per week for high-grade cancers, with 222 mg daily as the baseline dose supported by the largest number of case reports. Both drugs should be taken with fatty food.
The liver risk
A paper warning about fenbendazole and liver damage by Yamaguchi et al. (2021) appears first on most search results for this topic. Search ranking at that scale does not happen by accident when money is at stake.
Supple reviews this paper in his book and identifies a serious confound: the patient was also taking pembrolizumab (Keytruda), an immunotherapy drug that lists hepatic damage as a major side effect. She had been on pembrolizumab for months before trying fenbendazole for one month. Whether the accumulated immunotherapy caused the liver enzyme changes, an interaction between the two drugs occurred, or fenbendazole-induced tumor lysis produced the transient elevations is unknown. The Yamaguchi paper does not resolve this question.
Supple tracked his mother-in-law’s ALT (alanine aminotransferase) and AST (aspartate aminotransferase) alongside her tumor markers throughout treatment. When she started fenbendazole, her liver enzymes were normal. As her tumor markers dropped over the first two months, her enzymes rose to around 150 (the normal ceiling is roughly 30). Then, while she continued on fenbendazole without interruption, they returned to normal and stayed there.
If fenbendazole were hepatotoxic, the enzymes would have stayed elevated for as long as she took it. They did not. The transient spike coincided with the active cancer-killing phase and resolved without stopping the drug. The explanation Supple offers: as fenbendazole destroyed billions of cancer cells, the cellular debris flooded the bloodstream and passed through the liver for processing. The liver was working hard. It was not being poisoned.
This pattern is consistent across Supple’s 22 detailed case reports. None showed chronic elevations in liver enzymes from fenbendazole. In one case (RGR), transient ALT/AST elevation coincided with fulvestrant administration, whereas fenbendazole alone produced no fluctuations in liver enzymes over 8 months of continuous use. Another case (BK) showed no detectable hepatotoxicity despite concurrent use of multiple agents.
Separate case reports in the gastroenterology literature document more severe liver injury in patients who self-administered fenbendazole without monitoring, in one case at doses 10 times the standard amount, and in 2 cases involving patients with pre-existing liver disease or concurrent immunotherapy. These cases are overdosing, drug interactions, or compromised livers rather than a class effect of fenbendazole at the standard 222 mg dose.
Monitor liver enzymes at baseline, at 4 weeks, at 8 weeks, and monthly thereafter during cancer treatment. A transient rise is expected and indicates activity, not damage. Persistent elevation, jaundice, or coagulopathy are signals to stop. Patients with pre-existing liver disease or those taking other hepatotoxic drugs should exercise extra caution. Do not take fenbendazole with acetaminophen (Tylenol), which depletes the liver’s glutathione defense. Pregnant women should avoid it.
These drugs are not monotherapy and not replacements for conventional treatment
Every credible source working with repurposed antiparasitics for cancer agrees on this, including Supple. Pierre Kory and Paul Marik classify benzimidazoles as Tier One repurposed drugs but use them alongside ivermectin, metabolic interventions, and conventional treatment in supervised multi-drug protocols with cycling to prevent resistance. Three case reports from Stanford showing the benefits of fenbendazole involved patients who received it alongside androgen deprivation therapy, radiation, and multi-agent chemotherapy. The original Joe Tippens case, which launched the entire movement, has a confound: Tippens was concurrently receiving pembrolizumab (Keytruda) in a clinical trial. His remission could have resulted from the immunotherapy.
Supple is careful to recommend taking fenbendazole alongside conventional therapy rather than as a substitute. He stresses that every situation is unique, that all options should be considered, and that no one should interpret his work as an argument for abandoning other treatments.
Part 2: Cancer therapy is an outrageous scandal
Patients with cancer are desperate because the system that is supposed to help them is a mess. The evidence for this is a peer-reviewed paper published in Clinical Oncology in 2004, and nobody has refuted it in 22 years.
The 2.1 percent
In 2004, Morgan, Ward, and Barton published “The Contribution of Cytotoxic Chemotherapy to 5-Year Survival in Adult Malignancies” in Clinical Oncology. They examined 22 major adult cancers using randomized controlled trial data and cancer registry data from Australia and the United States. They calculated the absolute contribution of cytotoxic chemotherapy to 5-year survival for each cancer type, then summed the results.
The overall contribution of curative and adjuvant cytotoxic chemotherapy to 5-year survival in adults was 2.3 percent in Australia and 2.1 percent in the United States.
The 5-year survival rate for cancer in Australia at the time was over 60 percent. Chemotherapy contributed 2.3 percent of that. Surgery, early detection, and the natural history of indolent cancers accounted for almost everything else.
The cancers where chemotherapy produces meaningful survival benefit are Hodgkin’s lymphoma, testicular cancer, some non-Hodgkin lymphomas, childhood acute lymphoblastic leukemia (ALL), and small adjuvant benefits in breast, colon, and ovarian cancer. Five to 6 diseases. Since 2004, targeted therapies have added a few more: imatinib transformed chronic myeloid leukemia (CML), and immunotherapy checkpoint inhibitors have produced durable responses in melanoma, some lung cancers, and renal cell carcinoma. Call it 8 to 10 entities total. For the remaining majority of adult cancers, cytotoxic chemotherapy does not extend life.
In lung cancer, median survival increased by only 2 months over 20 years of new drug development. The Morgan paper concluded that a rigorous evaluation of the cost-effectiveness of cytotoxic chemotherapy was urgently required.
The medical oncology community responded with outrage but no data. Twenty-two years later, no one has published a definitive counter-analysis. That silence is not an accident.
Radiation therapy has the least support
Barton et al. published a systematic review in 2017 estimating the population-level benefit of evidence-based radiotherapy. Radiotherapy provides a 5-year overall survival benefit in 2.4 percent of all cancer patients. Adding concurrent chemoradiation provides an additional 0.3 percent. The total: 2.7 percent, for a specialty that treats nearly half of all cancer patients.
Radiation has a supposed survival benefit in cervical cancer, head and neck cancers, certain lung cancers, some rectal cancers, and prostate cancer. For breast cancer, post-mastectomy radiation improves cancer-specific survival but simultaneously decreases non-breast cancer survival through cardiovascular toxicity. The net effect on overall survival is roughly a draw.
Comment: If you are even half awake, you understand that benefits in the low single digits like this are meaningless, but the story gets worse:
The “surrogate endpoint” fraud
Tumor shrinkage does not mean patients live longer. Response rate, progression-free survival, and disease-free survival are the metrics oncology uses to evaluate drugs. These are “surrogate endpoints,” not overall survival. A tumor that shrinks 30 percent and then recurs 3 months later as a resistant clone is a treatment failure, but it gets recorded as a response. The FDA has approved drugs based on response rate that have never demonstrated a survival benefit. Oncology has built an entire regulatory and commercial apparatus on metrics that do not answer the only question patients give a rat’s ass about: Will I live longer?
This is not an oversight. It is a design choice. Overall survival trials take longer, cost more, and produce results that are harder to manipulate. Surrogate endpoints accelerate approval, expand indications, and generate revenue faster. The people who designed this system understood what they were doing.
The deaths that disappear
Treatment-related mortality from chemotherapy and radiation is systematically undercounted. When a patient with advanced cancer receives toxic chemotherapy that suppresses the immune system and damages the organs, and then dies 2 weeks later, the default coding is “died of cancer.” The treatment’s contribution to hastening that death is invisible in the data.
A Royal Marsden Hospital audit found 161 deaths within 30 days of chemotherapy in a 6-month period. Of these, 77 percent were classified as unrelated to chemotherapy and attributed to disease progression. A British National Confidential Enquiry into Patient Outcome and Death investigated over 600 deaths within 30 days of chemotherapy and found the treatment caused or hastened death in 27 percent of cases. Forty-three percent of patients suffered significant treatment-related toxicity. For acute myeloid leukemia, the 4-week mortality rate after standard induction chemotherapy was 15 percent in academic centers and 29 percent in community hospitals.
These numbers count only the deaths within 30 days. Deaths at 60 or 90 days from cumulative organ damage, immune suppression leading to infection, or cardiac toxicity fall outside that window. Secondary cancers caused by chemotherapy and radiation appear years to decades later and are never counted against the original treatment. Anthracycline cardiomyopathy kills breast cancer survivors 5 to 15 years after “successful” treatment. Those deaths show up as heart disease, not as chemotherapy complications.
The net survival calculation, subtracting treatment-related mortality from treatment-related benefit, has never been published for most cancers. Where chemotherapy’s survival contribution is near zero, the net is negative: the treatment kills more patients than it saves. The calculation that would settle the question is the calculation that never gets funded. So now you understand why discerning patients are shopping at Tractor Supply.
Follow the money
Cancer drug spending in the United States exceeds $200 billion per year. Individual treatments exceed $100,000 to over $1 million per year, with immunotherapy and CAR-T cell therapies leading the way. Oncology is the most expensive medical specialty, and oncologist compensation reflects this, with median pay exceeding $500,000 and many practitioners earning substantially more.
The engine of this system is the buy-and-bill model. Unlike most of medicine, oncologists purchase chemotherapy drugs directly and administer them in their offices. Under Medicare, they receive the Average Sales Price (ASP) of the drug plus a 6 percent markup. Six percent of a $10,000 monthly drug is $600. Six percent of a $100,000 annual immunotherapy regimen is $6,000. Before the 2005 Medicare Modernization Act, margins of 20 to 80 percent were documented under the old Average Wholesale Price system. The “reform” to ASP plus 6 percent was a Pharma compromise that preserved the fundamental incentive structure while trimming the most visible excesses.
On commercial insurance, the numbers are staggering. A 2024 study in The Oncologist found that the median markup negotiated with commercial payers at major hospitals ranged from 118 percent to 634 percent above ASP for some cancer drugs. For a single bevacizumab infusion, a hospital keeps a $277 markup at Medicare rates versus $7,490 at the median commercial rate. The same study confirmed that commercially insured patients were more likely to receive high-priced treatments, consistent with physicians responding to these financial incentives. A commercially insured cancer patient is not a person to be healed. He is a revenue event.
Here is what makes this arrangement extraordinary. The federal Anti-Kickback Statute makes it a crime to pay or receive remuneration to induce referrals for services covered by federal healthcare programs. Penalties include fines up to $25,000 per violation, imprisonment, and exclusion from Medicare and Medicaid. In every other field of medicine, a physician who profits from prescribing a specific drug is violating federal law. If a cardiologist received a 6 percent commission on every statin prescription, he would go to prison. Oncology operates under an exception to this. The buy-and-bill system allows oncologists to profit directly from the drugs they prescribe. The more expensive the drug, the higher the dose, and the longer the treatment, the more money flows to the prescribing physician. This arrangement was engineered by Pharma to create a permanent financial incentive for overtreatment, and it operates in plain sight.
The incentive runs in exactly one direction: toward the most expensive drug, the highest dose, and the longest treatment duration. Every financial pressure in the system pushes toward administering rather than observing, treating rather than referring to hospice, adding another line of chemotherapy rather than having an honest conversation about dying. Published research confirms that oncologists’ drug choices are responsive to profit margins.
Comment: Drug representatives pressure oncologists to “make their quota” at the end of every month by telling them how much extra money they will both get if they increase their prescribing. This translates into increasing the dosing of some toxic garbage that doesn’t work for each hapless, helpless, suffering patient.
A Dana-Farber study found that 56 percent of terminally ill cancer patients received palliative chemotherapy in their final months. Those patients were more likely to die in an ICU (11 percent versus 2 percent for untreated patients), less likely to die where they wished, and more likely to undergo CPR and mechanical ventilation in their last week of life. Palliative chemotherapy in this context does not extend life. It generates revenue, accelerates the medicalization of death, and the resulting deaths are coded as cancer deaths, never treatment deaths.
Ignorance of the evidence is no excuse
Oncologists complete a decade of postgraduate training. They read the journals. They know the Morgan paper exists. They understand what surrogate endpoints are. They see the buy-and-bill statements. At a certain level of education and intelligence, the failure to synthesize publicly available information into an honest assessment of your own practice is not ignorance. It is a choice. Whether that choice is conscious or unconscious is irrelevant to patients who die from it.
The parallel to psychiatry is exact. Robert Whitaker’s work in Anatomy of an Epidemic documented that long-term outcomes for schizophrenia patients are worse on antipsychotics than off them. Antidepressant trials used inert placebos that could not mimic side effects and therefore could not maintain blinding. The entire evidence base for maintenance psychiatric medication rests on withdrawal studies that confuse discontinuation syndrome with relapse. Psychiatry never funded the long-term randomized discontinuation trial with proper active placebos that would settle the question, because the answer would destroy the business model. Oncology never funded the net survival calculation that would subtract treatment mortality from treatment benefit for the same reason. In both fields, the study that would prove them right is the study that never gets done. The silence tells you everything.
Most oncologists believe they are helping people. But good intentions do not undo the consequences of actions taken inside a corrupt system. The information architecture of oncology was designed to make treatments look effective. Surrogate endpoints, hidden treatment mortality, financial incentives aligned with overtreatment, and regulatory capture by Pharma created an environment where well-meaning physicians dispense treatments that, for the majority of cancers, do not extend life and shorten it. The oncologist who never examines the structural incentives of his own field is like the citizen who never examines the laws he lives under. Ignorance of the evidence is no excuse when the evidence is freely available, and your patients are dying.
What to do
If you have one of the 8 to 10 cancers where conventional treatment has demonstrated an overall survival benefit, take the treatment. Hodgkin’s lymphoma, testicular cancer, childhood ALL, CML, some non-Hodgkin lymphomas, and the immunotherapy-responsive cancers (advanced melanoma, some lung and renal cancers) have data behind them. If you are in one of those categories, conventional treatment saves lives.
For everything else, demand that your oncologist show you overall survival data, not response rate, not progression-free survival, for your specific cancer at your specific stage. If overall survival benefit has not been demonstrated, you are being offered treatment based on metrics that do not predict whether you will live longer. You deserve to know that before you consent.
Look this up yourself, for artificial intelligence has made medical knowledge accessible to everyone. Keep your entire medical history inside a Claude AI project, and use it to evaluate every treatment decision you face. Claude analyzes lab results, searches the current literature, compares survival data for your specific cancer and stage, and gives you an assessment of what the evidence shows.
Comment: A Claude subscription costs $20 a month, and the return on that investment is beyond anything I have seen in 40 years of medicine. For a fraction of the co-pay on a single chemotherapy session, you get access to the same literature your oncologist reads and the ability to ask questions he would never volunteer the answers to. I would gladly pay $100 a month for what this tool provides, and I recommend it to everyone.
The bottom line
The alternative community discovered a class of cheap, available drugs with anticancer activity that was being ignored by the cancer doctors.
The larger scandal is about an oncological establishment that spends hundreds of billions of dollars annually on treatments that, outside of a handful of diseases, have never been shown to extend life. It is about a system that measures success by tumor shrinkage instead of survival, hides treatment mortality by attributing it to cancer, and pays its practitioners more when they give more drugs through a financial arrangement that would be a federal crime in any other medical specialty. It is about a calculation that could determine whether the whole enterprise saves more patients than it kills, and the fact that in 22 years, nobody has done it.
This is why people are buying dog dewormer at Tractor Supply.
Part 3: An email from William Supple, PhD
Supple sent the following after reviewing the criticisms that arrived in response to Part I. His email is reprinted with permission and lightly edited for clarity.
Robert:
The Nguyen et al., “Oral Fenbendazole for Cancer Therapy in Humans and Animals,” Anticancer Research44(9):3725–3735, 2024, states that fenbendazole “surpasses albendazole and mebendazole in treating drug-resistant cells.” It attributes this superiority to fenbendazole’s glycolytic inhibition, a mechanism the other benzimidazoles lack.
The strongest argument regarding fenbendazole’s superiority is that it simultaneously destabilizes tubulin, causes mitochondrial translocation of p53, inhibits glucose uptake, downregulates GLUT transporters, and suppresses hexokinase II, a key glycolytic enzyme that most cancer cells depend on. Mebendazole does not robustly hit the metabolic axis the way fenbendazole does.
The case reports on Substack, in the book, and on OneDayMD (362 fenbendazole case reports) are proof of concept in humans. Many of the case reports in the book had exhausted standard of care treatments and were released to hospice. Then they tried fenbendazole. These people were in the throes of drug-resistant disease as described above, and fenbendazole was the best choice available to them at the time.
As I detail in the book, fenbendazole is a veterinary dewormer that humans are using to self-treat cancers, while mebendazole is a human version of a similar drug. Fenbendazole is used because it is readily available, inexpensive, and over the counter, while mebendazole is not.
One issue that should be addressed is how the passage of time affects cancer evolution and treatment. One fundamental tenet of the Cancer as Parasite theory is that since cancer at one month is different from that same cancer at one year, we should not be surprised to see different agents’ effectiveness vary over time. I suggest that some of the conflicting results regarding fenbendazole versus mebendazole are related to this dimension.
I never intended the Substack or my book to be the final word on benzimidazole antiparasitics and cancer. My intent was to start the conversation among those who should have been discussing these issues all along: MDs, oncological researchers, parasitologists, and epidemiologists. It appears I have achieved that objective.
Let me know if you have questions.
Thanks,
Bill
PS: I discussed my mother-in-law’s liver enzyme time course in detail. The lack of chronic liver enzyme elevations in any of my case reports is consistent with her experience. What is inconsistent with contemporary human data is the studies claiming hepatic damage from fenbendazole. I review the Yamaguchi study in my book.
Comment: Supple’s book, his case compilation, and the Nguyen review are the three documents to read if you want the full picture of where this science stands. The conventional oncology establishment has not engaged with any of them. That tells you more about the establishment than about the evidence.
Editing credit: Jim Arnold of Liar’s World Substack. He told me that when he learned that the educational system was purposefully not teaching reading properly, it broke his heart, changed his life forever, and he wrote “Fun with Dick and Jane”.
