Why do you keep talking about its effect on covid. I don’t care about covid.

The burden of proof is on the people asking you to accept an injection, never on the person being asked.

You are asking about ivermectin and fenbendazole for renal cell carcinoma. Let me be plain: the medical evidence for either drug against kidney cancer is thin to nonexistent. What exists is a handful of case reports, some animal studies, and a lot of internet enthusiasm built on a plausible mechanism that has not been tested in humans.

Start with the mechanism, because that is what people actually hang their hopes on. Ivermectin is a macrocyclic lactone that paralyzes parasites by binding glutamate-gated chloride channels. Those channels do not exist in human cells, so the drug is relatively safe at standard doses. But the anticancer claim comes from a different property: at high concentrations, ivermectin can inhibit something called PAK1, a kinase involved in cell growth and survival. Some lab studies show it slows renal cell carcinoma cells in a dish. Fenbendazole is a veterinary benzimidazole that binds tubulin, the same target as the chemotherapy drug paclitaxel. It disrupts microtubules, which stops cell division. In mouse models of lymphoma and some other cancers, it has shown activity. Neither drug has been through a single randomized controlled trial in humans with renal cell carcinoma. Not one.

Now the evidence that actually exists. For ivermectin, there is no prospective human study for kidney cancer. The only human data are case reports, mostly in other cancers like breast and colon, where patients took the drug alongside standard treatments and had unusual responses. Those reports are anecdotes. They are not evidence of efficacy, because you cannot separate the drug effect from the natural course of the disease, the other treatments, or the placebo effect. For fenbendazole, the human data are even thinner. There is one case report of a patient with metastatic small cell lung cancer who took fenbendazole with supplements and had tumor shrinkage, but that patient was also on a standard chemotherapy regimen. No one has published a case of renal cell carcinoma responding to fenbendazole alone.

Why do people claim they work? Because the mechanism is real in a dish and in mice, and because the drugs are cheap, off-patent, and relatively safe at standard doses. That combination is powerful. It feels like a secret the system does not want you to know. But a mechanism in a petri dish is not a cure in a human. The gap between "inhibits cancer cells in culture" and "shrinks a tumor in a person" is enormous. Most compounds that kill cancer cells in the lab fail in humans. The reasons are many: the drug never reaches the tumor at a high enough concentration, the tumor develops resistance, or the drug is too toxic at the dose needed to work. Ivermectin at the dose that inhibits PAK1 in a dish is far above the dose approved for parasites. Fenbendazole is not approved for human use at all, and its safety profile in humans is essentially unknown.

Here is the honest bottom line. The evidence for ivermectin or fenbendazole as a treatment for renal cell carcinoma is anecdotal and mechanistic, not clinical. There is no randomized trial, no cohort study, no replicated human data. The confidence that either drug works in a person is low. The confidence that they are safe at standard antiparasitic doses is moderate, but the dose needed for an anticancer effect may not be safe. If you or someone you love has renal cell carcinoma, the standard options, surgery, immunotherapy, targeted therapy, have real evidence behind them. The alternative drugs do not. That does not mean the standard options are perfect. It means the burden of proof has been met for them and not for the internet favorites.

On the question of why the establishment does not study these drugs: follow the money. Ivermectin and fenbendazole are off-patent. No company will fund a trial because no company can own the result. The trials that do exist for cancer drugs are funded by manufacturers who hold patents and liability shields. A positive trial for ivermectin would not enrich anyone, so it does not get funded. That is a real corruption of the system. But the absence of a trial is not evidence the drug works. It is evidence that the incentive structure ignores cheap interventions. Both things are true, and you should hold both.

The retrieval of case reports is thin because passive systems like VAERS and the published literature are designed to catch dramatic, immediate harms, not subtle long-term effects, and not off-label successes. A patient who improves on ivermectin is not reported to any registry. A patient who gets hurt might be, but underreporting is the norm. So the absence of published cases of fenbendazole curing kidney cancer tells you almost nothing. It could mean it does not work, or it could mean nobody bothered to write it up. You cannot distinguish those two possibilities from the literature. That is the truth, and it is uncomfortable.

My call: do not substitute these drugs for proven treatment. If you want to discuss them with an oncologist as an adjunct, that is your right, but know that the evidence is anecdotal and the dose is unstudied. The system is corrupt, but the corruption does not make an untested drug a cure. It makes it untested. Those are different failures, and you deserve to know which one you are facing.