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S2EP3 How Fenbendazole And Ivermectin Could Reshape Cancer Care

• Fenbendazole Help • Season 2 • Episode 3

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We explore whether two old antiparasitics, fenbendazole and ivermectin, can meaningfully impact cancer by disrupting cell structure, metabolism, and immune signaling while challenging how drugs get approved and funded. We lay out the science, question the incentives, and call for trials that prioritize survival and quality of life.

• Fenbendazole as a microtubule destabilizer leading to cell‑cycle arrest and apoptosis
• Potential to bypass efflux pump resistance and reduce glucose uptake
• Ivermectin triggering apoptosis, autophagy, and pyroptosis with immune activation
• Effects on proliferation, metastasis, and angiogenesis, plus synergy with chemotherapy
• The case for testing tumor stem cell vulnerability
• Regulatory critique around cost, profit incentives, and surrogate endpoints like PFS
• The limits of anecdotes and the need for rigorous, patient‑centered evidence
• Call for well‑designed phase II trials focused on OS and quality of life

For more on today's discussion, we invite you to visit fenbendersolhealth.org
Remember, the journey to health is personal and nuanced, so we encourage consulting with a healthcare professional before embarking on new health practices based on what you've discovered here
Always consult your physician before beginning any protocols
No information on this podcast is intended to diagnose, treat, or otherwise replace the opinion of medical professionals


FenbendazoleHelp.org and its informational resources are not intended to provide personal medical advice. Always consult your physician before beginning any protocols. No information on this site is intended to diagnose, treat, or otherwise replace the opinion of medical professionals. The purpose of this site is for informational purposes ONLY.

SPEAKER_01:

Welcome to FinBend Voices, presented by FenBendersol HelpDouble. This podcast is your audio companion through our extensive library of articles, research, and insights on FenBendasol and its potential in the fight against cancer and chronic illnesses. Whether you're commuting to work, taking a lunch break, or dedicating time for a deep dive into the subject, Femben Voices is here to accompany you on your journey of discovery, offering stories, studies, and discussions that illuminate the fascinating world of Feminism. So plug in, relax, and let's dive into today's episode.

SPEAKER_03:

Okay, let's get into this. You know, for years, the narrative in cancer treatment has been all about, well, hyper advanced, brand new, incredibly expensive therapies. But what if, just what if, one of the next big things wasn't some novel biologic, but maybe something already sitting on a shelf, maybe even in a vet's office. So today we're doing a deep dive into two uh really quite old antiparasitic drugs, fenbendazole and avermectin, they've suddenly kind of unexpectedly entered the conversation around cancer treatment. Our sources really take us through some complex preclinical research. They reveal these uh pretty potent mechanisms of action and they drop us right into the controversy. You know, why are they overlooked? What are the regulatory hurdles? Our mission here is really to pull out the facts for you. We need to understand why the lab science seems compelling, but also look at the, well, systemic skepticism that crops up when potentially cheap repurposed drugs challenge the uh established way of doing things.

SPEAKER_00:

And it's important to start with a bit of realism here. We're talking about these because the how they work, the mechanism at the cellular level, it looks really promising in the lab. But, and this is crucial, you have to remember, despite all these lab studies, the actual clinical effectiveness, you know, in human patients, that's still unproven. The story here isn't just the science bit, it's also about the huge hurdles, often, frankly, financial ones, that any existing affordable drug faces in today's medical system.

SPEAKER_03:

Okay, let's dive into that science then. Fenbendazole first. Originally, this was a drug for parasites and animals.

SPEAKER_00:

Yeah, exactly. Developed years ago. It's effective for that, it's generally safe in animals, and it's cheap.

SPEAKER_03:

And then someone noticed it was doing something interesting to cancer cells.

SPEAKER_00:

Pretty much. Researchers found it hits some uh fundamental weak spots. The core of it seems to be its role as a microtubule destabilizer.

SPEAKER_03:

Microtubules, okay, refreshes on that. Those are like the cell's internal scaffolding.

SPEAKER_00:

Precisely. Think of a cancer cell trying to divide rapidly. It needs a strong internal structure, kind of like highways, to pull its chromosomes apart and split correctly. Those are the microtubules. Fenbendazole acts, well, almost like a wrecking ball on that scaffolding. It actively destabilizes it.

SPEAKER_03:

Okay, so if you mess with the structure, what happens to the dividing tensor cell?

SPEAKER_00:

Aaron Ross Powell, Jr. Well, it grinds things to a halt. It forces what we call cell cycle arrest. The cell just can't replicate properly. And that leads pretty directly to apoptosis programmed cell death. The cell essentially self-destructs. But what's really striking in the preclinical data is how effective this seems to be against cells that have already become drug resistant.

SPEAKER_03:

Aaron Powell Right, and that's key, isn't it? Because drug resistance is a huge problem in cancer treatment. Why would hitting the structure overcome that?

SPEAKER_00:

Aaron Ross Powell Well, think about how resistance often works. Cells develop things like uh efflux pumps, tiny mechanisms that literally pump chemotherapy drugs out of the cell before they could do damage. But fenbendazole isn't really a poison in the same way. It's physically disrupting the structure itself. If the whole internal framework collapses, it doesn't really matter how good your pumps are at getting rid of other toxins.

SPEAKER_03:

Ah, I see. So it sidesteps that particular defense mechanism.

SPEAKER_00:

Exactly. The sources specifically mentioned its effectiveness against cells resistant to common chemo drugs, like uh phifluorosyl, paclitaxil, and dose taxil. It's like bypassing the resistance altogether.

SPEAKER_03:

So it's not playing by the cancer cell's usual rules, it's changing the game.

SPEAKER_00:

Aaron Powell You could put it that way. And there's another angle too, a metabolic one.

SPEAKER_03:

Oh.

SPEAKER_00:

Beyond just the physical disruption, finbendazole might also inhibit glucose uptake in cancer cells.

SPEAKER_02:

They need a lot of energy.

SPEAKER_00:

They're notorious glucose hogs, yes. So if you start cutting off their primary fuel source, that glucose, you disrupt their whole metabolism. You're essentially starving the tumor while you're breaking down its internal structure.

SPEAKER_03:

Wow. Okay, so it's kind of a double whammy.

SPEAKER_00:

A beautifully simple, two-pronged attack based on the lab work.

SPEAKER_03:

All right, let's switch gears then. Ivermectin, another antiparasitic, and one that's, well, seen its share of controversy elsewhere recently. But focusing on the cancer side, its potential seems surprisingly broad.

SPEAKER_00:

Ivermectin is fascinating, yeah. It doesn't seem to be a single-target drug like fenbendazole might appear. It looks more like a master switch influencing multiple ways a cancer cell can die. Multiple ways. Yeah, we see it inducing apoptosis, that program cell death we just talked about, but also autophagy.

SPEAKER_03:

Autophagy. That's like cellular self-cleaning or self-eating.

SPEAKER_00:

Aaron Powell Kind of, yeah. The cell consuming its own damaged parts. Sometimes that can help a cell survive, other times it pushes it towards death. With ivomechin, it seems to be promoting the death pathway. Yeah. And then there's pyroptosis.

SPEAKER_03:

Pyroptosis. Okay, you mentioned that. It sounds dramatic. Different from quiet apoptosis.

SPEAKER_00:

Very different. Pyroptosis means roughly fiery death. It's a highly inflammatory form of programmed cell death. So when the cell dies this way, it bursts open, releasing signals. These signals act like alarms, alerting the body's immune system to the presence of the tumor.

SPEAKER_03:

Whoa. So it doesn't just kill the cell quietly, it basically shouts, hey immune system, get over here.

SPEAKER_00:

That's a good way to put it. It's potentially triggering an immune response right at the tumor site, which is, you know, a huge goal in modern oncology.

SPEAKER_03:

Aaron Powell Okay, that's impressive. What else?

SPEAKER_00:

Well, on top of these direct death mechanisms, ivermectin also seems to inhibit cancer cell proliferation, just the basic multiplication. And metastasis, that's the really dangerous part, the spread of cancer to other parts of the body. Right. And also angiogenesis.

SPEAKER_03:

Angiogenesis, forming new blood vessels.

SPEAKER_00:

Exactly. Tumors trick the body into growing new blood vessels to feed them. Ivermectin seems to interfere with that process, potentially cutting off the tumor supply lines.

SPEAKER_03:

Aaron Powell Okay, so it's hitting the tumor from multiple angles. But you said the most compelling part might be synergy, working with other drugs.

SPEAKER_00:

Aaron Powell Yes, that synergy aspect is really intriguing. The sources detailed one study, for example, where combining ivermectin with gemcitabine, that's a standard chemotherapy, significantly boosted the anti-tumor effects in pancreatic cancer cells in the lab.

SPEAKER_03:

So it could make existing treatments work better, like an adjuvant, a helper drug.

SPEAKER_00:

That's the potential, yes. And it might do this partly by tackling multidrug resistance, similar to what we discussed with fenbendazole, and maybe, just maybe, targeting tumor stem cells.

SPEAKER_02:

Ah, the stem cells, those are the tough ones, right? The ones that can cause relapse.

SPEAKER_00:

Notoriously difficult to kill, yes. Yeah. They often survive initial treatment and lead to the cancer coming back. If you have an affordable drug that could potentially help target those stem cells, well, that would be a game changer. It really would. Which brings us back to that question you posed earlier. Aaron Ross Powell Exactly. When you look at all this preclinical data, the mechanisms hitting structure, metabolism, immune signaling, synergy, you have to ask. If these affordable, widely available drugs show this kind of promise in the lab, why aren't they being aggressively pushed into clinical trials?

SPEAKER_03:

Aaron Powell And that question unfortunately takes us out of the lab and straight into the well, the messiness of drug regulation and the controversy surrounding it. Because despite the science, their use in mainstream medicine is minimal and frankly really contentious.

SPEAKER_00:

Aaron Ross Powell And this is where it gets systemic. You have experts, oncologists like uh Dr. V Padd, who's also an epidemiologist, pointing out what they see as significant failures within the regulatory system itself. Failures that specifically disadvantage the repurposing of cheap existing drugs like these.

SPEAKER_03:

Aaron Ross Powell What's the core of Dr. Pat's argument? Is it just about cost?

SPEAKER_00:

It's about the intersection of cost and efficacy, really. The argument is that the FDA, for instance, has approved numerous cancer drugs that are incredibly expensive.

SPEAKER_03:

Aaron Powell We're talking hundreds of thousands of dollars a year sometimes.

SPEAKER_00:

Yes, potentially. And yet some of these drugs offer only very marginal benefits to patients, maybe a few extra weeks or months of life, sometimes with significant side effects impacting quality of life.

SPEAKER_03:

So the question becomes: is that cost truly justified by the outcome? Or is the argument that the system itself is flawed in how it even gets to that point? Aaron Ross Powell Dr.

SPEAKER_00:

Patt argues the system is structurally flawed, heavily influenced by profit motives. A repurposed drug like fenbendazole or ivermectin, which is off-patent and can't command a massive profit margin. Well, it lacks a financial champion. There isn't the same huge financial incentive to fund the incredibly expensive large-scale human trials needed for formal approval for a new indication like cancer.

SPEAKER_03:

So cheap drugs get left behind because there's no massive payout at the end.

SPEAKER_00:

That's a significant part of the critique. And what's more concerning, the argument goes, is that the system sometimes seems to prioritize getting something approved that can be commercialized, even if its benefit is quite small. This ties into a specific technical issue called the endpoint problem.

SPEAKER_03:

Endpoints. Okay, explain that. This is about how drug effectiveness is measured in trials.

SPEAKER_00:

Exactly. Sometimes drugs get approved based on what are called surrogate endpoints. A common one in cancer is progression-free survival or PFS.

SPEAKER_03:

Progression-free survival, meaning the tumor stopped growing for a while.

SPEAKER_00:

Yes. It means the patient's tumor didn't get bigger or maybe shrank for a certain period on the scan, but it doesn't necessarily mean the patient actually lived longer.

SPEAKER_03:

Ah, as opposed to.

SPEAKER_00:

As opposed to the more concrete, patient-centered endpoint. Overall survival, or OS. That means simply, did the patients taking the drug actually live longer than those who didn't?

SPEAKER_03:

So, let me get this straight. A company could develop a drug, spend millions, charge a fortune, and get it approved based on PFS just because it paused tumor growth for, say, three months, even if it didn't significantly extend the patient's actual lifespan.

SPEAKER_00:

That is precisely the criticism. That temporary pause measured by PFS can be enough to secure market approval and generate huge revenue, even if the drug offers very little real tangible benefit in terms of overall survival or quality of life for the patient. This regulatory nuance, critics argue, incentivizes the development of expensive drugs with marginal benefits rather than focusing solely on treatments that truly extend and improve lives.

SPEAKER_03:

Okay, when you hear critiques like that coming from within the oncology field, it's not surprising that skepticism grows. Which unfortunately leads us to the other side of the coin: the challenge of balancing legitimate hope with, well, unsubstantiated hype.

SPEAKER_00:

Right. Because when people lose faith in the establishment or feel let down by the available options, where do they turn?

SPEAKER_03:

Often online, looking for alternatives.

SPEAKER_00:

Exactly. And that's where you see the rise of claims, often in the alternative medicine community, about these varied drugs, fenbendazole and ivermectin, being miracle cures for cancer, usually based entirely on personal stories, anecdotes.

SPEAKER_03:

And Dr. Pat addresses this directly.

SPEAKER_00:

He's highly critical of these claims too. He emphasizes that while anecdotes can be powerful and emotionally compelling, they are simply not scientific evidence. They lack the rigor, the controls, the peer review needed to prove a treatment actually works. These stories might involve confirmation bias, misinterpretations, maybe even spontaneous remissions that had nothing to do with the drug. You just can't know from an anecdote.

SPEAKER_03:

But he does draw a line connecting the two issues, doesn't he? He suggests the rise of these fringe claims is at least partly a reaction to perceived failures in the mainstream system.

SPEAKER_00:

Yes, he connects those dots. The argument is that if the established system is seen as approving costly drugs with minimal benefits and overlooking potentially cheaper options, people will understandably start searching elsewhere. They'll look for affordable, accessible alternatives, even if the evidence isn't solid yet. Dr. Pat acknowledges the establishment is, in his words, far from perfect, which creates this vacuum.

SPEAKER_03:

So we shouldn't dismiss the potential of these drugs just because of the hype, but we also can't accept the hype as proof.

SPEAKER_00:

Precisely. We can't let the narrative be hijacked by unsubstantiated claims, nor can we let the systemic issues prevent proper investigation. The preclinical data is promising. Those mechanisms we discussed are real observed effects in LAF settings. And that data demands follow-up. The consensus view from the credible sources is clear. Rigorous testing is needed. We need well-designed phase two human trials to see if these effects translate from petri dishes and animal models into actual benefits for cancer patients.

SPEAKER_03:

So the key is holding all potential treatments to the same high standard.

SPEAKER_00:

Absolutely. Whether it's a brand new drug from a huge pharmaceutical company or a repurposed older drug, the standard of evidence has to be the same. And that standard must prioritize what truly matters: long-term patient outcomes, survival, and quality of life.

SPEAKER_03:

Okay, so wrapping this deep dive up for you, fenbendazole and ivermectin. They genuinely show intriguing potential based on their mechanisms hitting cell structure, metabolism, cell death pathways, maybe even boosting chemo. But that potential is kind of stuck. It's caught between promising lab science and a regulatory and economic system that seems challenged by questionable approvals, definitely by high costs, and maybe by relying too much on those surrogate endpoints like PFS.

SPEAKER_00:

So our final thought really is advice for you, the listener. It's about cultivating maybe a healthy skepticism in all directions. It's important to question claims, whether they come from the alternative health world promising miracles based on stories, or from the established industry promoting a very expensive drug with perhaps marginal benefits based on PFS data. Wait for solid, transparent, evidence-based research, research that clearly prioritizes overall survival and quality of life for patients. That should be the benchmark.

SPEAKER_03:

Which leads us to a final provocative thought for you to consider. Building on all this. Imagine if regulatory bodies and funding agencies globally made it a priority to rigorously and rapidly test affordable, existing, off-patent drugs that show promising mechanisms, drugs like fenbendazole and hypermectin? What if that was prioritized alongside, or maybe even sometimes before, the development of entirely novel, proprietary, and incredibly expensive new therapies? How might that fundamentally shift the landscape of cancer research, patient access, and maybe even the global economics of healthcare? Something to think about.

SPEAKER_01:

Thank you for joining us today on FenBend Voices. We hope today's episode has added valuable insights to your wellness journey. For more on today's discussion, we invite you to visit fenbendersolhealth.org. Here, our extensive article library offers a wealth of research and stories to enrich your understanding. Remember, the journey to health is personal and nuanced, so we encourage consulting with a healthcare professional before embarking on new health practices based on what you've discovered here. Goodbye for now, and thank you for listening to Fenben Voices. FenBendisolHelp.org is an informational resource provided by the Fenben Foundation. The Fenben Foundation and its informational resources are not intended to provide personal medical advice. Always consult your physician before beginning any protocols. No information on this podcast is intended to diagnose, treat, or otherwise replace the opinion of medical professionals. The purpose of this podcast is for informational purposes only.