Controversial Cancer Treatments Fenbendazole, Mebendazole and Ivermectin Explained

What if something simple like a dewormer drug that costs less than a cup of coffee could disrupt the same pathways that some chemotherapy drugs do? These types of repurposed drugs are becoming more popular. And what should you know about fenbendazole, menbendazole and ivermectin? So let's get into the detail and out of the hype. We'll look at some of the published papers, but we're going to really focus on clinical care because it's nice to have published papers that give us excitement. But at the end of the day, how do we use this in patient care? Many well meaning integrative doctors like to give these drugs without really understanding how they work, the mapping and basically thinking, well they're cheap enough, so let's give you access and we hope that they work. But there are actual targets that will show you whether these or other medications or whatever combinations you're using will help you. But you have to get the right targets to get the right outcomes. And that's the key in the architecture of repurposed drugs. I'm Dr. Dino Prado, founder of Envita Medical Center. For the last 25 years, my team and I have worked with thousands of late stage cancer patients that have failed the top cancer hospitals across the country. And we've helped them. And one of the key ways we've done that is using repurposed drugs. We learned years ago the best way to do this is with the right targets. Deep molecular mapping and making sure people get the right medicines, not the ones that are just popular on the Internet, but the right ones for you. And that's why you should always have clinical care, giving the guidance with real testing. We're talking about the repurposed drugs like menbendazole, fenbendazole, ivermectin. How do they actually work? What are their mechanisms and where is the early clinical signals come from on whether it's working or not and how, most importantly can we administer these medications to patients? Patients, not blindly, but with targets. See this is what most people don't understand is that no matter whether you're using a conventional drug that's already approved, or a repurposed drug called an off label medication, or a natural phytotherapeutic intravenously, or a cancer cell vaccine, a cellular biologics or whatever combination, are they the right fit for you? So instead we're going to talk about when they're the right fit. This is going to be like a master class in understanding repurposed drugs for patients. So you don't have to worry about whether it works or not. Instead we're going to use biomarke heat map signatures that tell us which medications are the best combinations. This also can include diet and lifestyle changes which are going to accelerate your care. So unfortunately most of these medications are prescribed blindly. Patient decides to get them from an integrative doctor, order them online and hope for the best. And because they're fairly inexpensive and thank goodness many of them do not have too many toxicities, so they figure let's do that. However, they may not be getting the result that they want. And that's the real goal here because oftentimes we get calls from patients after they've tried everything. Integrative care, standard of care, top hospitals, and then they've even tried benbendazole, menbendazole, you name it. I can go through a whole list of repurposed drugs, Ivermectin, methylene blue, ozone therapy, all these great integrative cares, but it is not working for them. So let's understand how they work so you can get out of guesswork and into precision. So when we decide to use a repurposed drug in cancer, it's because it works in combination with either what you're doing or with the mechanisms that are going to shut your cancer down. So we're not guessing. We're using precision targeting. We're looking at specific patterns, pathways that are over active, genes that are upregulated tumor microenvironments which are telling us whether the tumor is hot or cold, basically whether your immune system can see the cancer or not. And then we look at the metabolic pathways that are feeding the cancer. We find these by running what we call deep mapping. And this deep mapping is multi omics next generation sequencing. These are the DNA. We'll be looking at hundreds of markers in this area, full transcriptomics rna, thousands of markers when you combine these. And then here's one of the most important ones, immune spatial biology, where we're looking at the body's own ability to fight cancer through the immune system. So we look at these things, we look at the tumor microenvironment and the heat maps and the algorithms and the bioinformatics that we've developed over the years gives us the tools of what patients need. So let's identify these. Let's say there's an issue with microtubule vulnerabilities. There's a drug resistant pumps or metastatic signaling loops pro cancer immune modulation factors that impact glycolysis for the cancer. Well then there could be repurposed drugs that are logical for these patients and the treatments can well align with their current care. This is where we can get a 1 plus 1 equaling 11 a significant benefit for the patient using the repurposed drug agents in a way that is safe and in correct combination with their care, which is very different than the way you're seeing it used right now. That's why oftentimes it doesn't work for everybody is because it's not being targeted. Now one of the nice things about repurposed drugs are they're first of all cost effective and they've been around a long time. So we have a lot of safety data on them. But the reason we won't see people using these in high quantities is because pharmaceutical companies cannot make money on repurposed drugs or intravenous phytotherapeutic natural plants or oxygen therapies or cellular biologics. Unless they're approved. You just won't see them. These therapies will always be lagging. And what you'll mainly see is what big pharma brings to market because they can profit from them. So that's why you may wonder why haven't I been prescribed this by my doctor? Well because it's not covered by insurance and it's not standard of care. It's off label. But there's a place for off label drugs. So let me start with the first one and we'll walk our way through these three. Menbendazole. It is a microtubule disruptor and so think of it this way. Menbendazole was FDA approved and it has a C safety profile as an anti parasitic. So some people may have parasites but that's not why we mainly use it in cancer. The crucial question is whether the mechanism of action aligns with your specific targets. Cancer cells rely on microtubules. These tiny structural tracks to divide. Menbendazole interferes with these tracks similar to drugs like taxanes that have been around for a long time. Vinca alkaloid drugs. These are old time chemotherapy drugs that work on microtubule depolymerization and stopping this way that cancer cells divide and spread. What's really nice about the alkal and the vinca drugs as chemotherapy, when they're correct matches, they actually kill cancer cells. Most of the chemotherapy that's out there is cytostatic, slows the cancer down, not cytotoxic, killing the cancer. What's nice about these is they actually kill the cancer. So we don't just want to stop the cancer cells from growing like we see in a lot of cancer drugs. A lot of the new drugs that come to market slow things down. These can actually kill the cancer if the targets are correct. And they achieve that by targeting the microtubules, particularly in rapidly dividing cancer cells. The types that are mo. Here's a little background. The cytotoxic mechanism of the taxanes. These drugs stabilize microtubules, preventing them from breaking down, which in turn blocks cell division and leads to cell death. For the cancer cell, that's fabulous. The vinca alkaloids. These drugs destabilize the microtubules, preventing them from forming properly, which also stops the cell division and triggers cell death. This is also a cytotoxic drug by nature. Because both classes of drugs interfere with the process of cell division. They're considered cytoto, fast growing cancer cells. Their action is not limited to cancer cells, and they can damage healthy cells. That's why when you're treating patients that have these targets, you want to use them in micro dose and not high dose, because that way you can interfere with the cancer cell and protect their healthy cells. And these drugs deal with mitosis, this area of cell division. While their primary effect is on mitosis, these drugs can also induce apoptosis, also known as programmed cell death. Other phases of the cell cycle further contributing to cytotoxic or the dying of cancer ce Very interesting part of the story. Menbendazole shares a similar primary mechanism with the vinca alkaloids and the taxanes by targeting the microtubules. Isn't that interesting. But it's better tolerated and acts as a potent agent in specific cancer contexts, exhibiting both a cytotoxic and cytostatic properties. Meaning the menbendazole can kill the cancer cells and it can also slow them down if you have the right targets. In addition, it has a very important property. It can pass the blood brain barrier. So this can become huge for people have glioblastoma brain cancers or their cancers metastasized to the brain. If this is the right target. I want to say that because you need the right target, you just don't want to give it blindly and prescribe it. You know, you'll look at old studies where in some patients they'll say, well, we lived longer, responded better because we used the drug. But it has multiple targets. Menbendazole also inhibits new blood supply to tumors called angiogenesis. It reduces the VEGFR2 marker. So if you have that, this will slow down the spread. Think of it almost like Avastin anti angiogenic drugs, even something like high dose virus, vitamin C intravenously. In the high doses, it can slow blood supply to the tumor, it can induce apoptosis. That's the killing of the cancer cell on its own, its mechanism to die off, it'll downregulate and modulate glycolytic genes that are involved in the cancer eating glucose. So it works on the metabolic pathway and it can penetrate the blood brain barrier, which I said was one of the big keys up front. And I want to emphasize that by saying that again because that's why menbendazole can be a good combination and it can help people achieve better care, better therapeutic targeting. When used correct correctly, this means menbendazole can be considered when supervised correctly for brain metastases, glioblastoma, cancers that have spread, or just where microtubule signatures and angiogenesis signatures are the strongest in the heat map. So how do we know that? How do we define that? It's not basic tests. When you run transcriptomics, I'm going beyond just looking at a VEGF marker. When you look at transcriptomics for menbendazole, you'll see something called atuba overexpressions of the microtubule genes. You'll see GLUT1, SLC2, A1, HK1 or LDHA upregulation. These are all genes that are telling us if these heatmaps are strong and in combination. And the algorithm with other medicines you're doing, this is where you can get a 1 plus 1 equaling 11. You can have a VEGFA or a VEGFR2 or these angiogenesis markers that are specific. And if the immune system is cold, meaning it's hiding from your immune system and resistant. And we see that in spatial biology with a whole other set of algorithms. Now putting that all together, menbendazole becomes a good idea to add in combination. Now it's not a one hit wonder, but it's in combination we can get better responses. So it makes sense to use it as a target, not blindly. This is what I want to emphasize today as I'm going through these. You are going to become very knowledgeable in these three drugs. I'm giving you some specific ideas in targeting not hey, this is the cure to cancer. Just take these drugs, you're fine. Yes, it will help some people, but not all of them. There are other Drugs that we can do that are off label, many, many others. These just happen to be the popular ones everybody wants to talk about. But there are many others based on your RNA transcriptomics and your genomic targets that us the response rate with these treatments. So you can see how important precision oncology is because this is what I'm talking about. It works to find the correct targets, not just with off label repurposed drugs like these, but also what are the right chemotherapies, what are the right immunotherapies, what are the right natural agents, what are the right combinations of these things to help you go into remission and give you the best chance of responding. Remember, this is only one repurposed drug we're talking about here. We're going to go over a few more, but there are many, many others. And based on this testing, we can find the right targets for each patient, which gives us huge advantage. All right, let's move right along to fenbendazole. This is the veterinarian drug with intriguing case signals. So listen to this. Obviously it's not approved in the United States for humans, but patients still order them from pharmacies and they get them. It's a veterinarian drug and in recent years it's gained so much attention because of its microtubule destabilization. It also works on HK2 like Menbendazole. It suppresses that, it helps with the glycolysis pathways. So this is all good on the metabolic side of cancer. But let's talk about how it's a little bit different. Has some exciting pathways. Pathways. On the microtubule side, it works with beta tubulin, blocking the microtubule formation in cell division. So again it's slowing the cancer cell down from dividing. It also works on the metabolic side, downregulating these glucose pathways. So stops feeding the cancer, reduces glycolysis, which is really good. It can also trigger pyratosis, a forming of inflammatory cell death involving gsdme. This pytosis mechanism is particularly interesting because it releases danger signals. These signals can help the immune system go from being col hot. So it can be an immunotherapy in certain cases where the targets match, then bendazole, which is not recommended without supervision. I want to say that make sure you're under the care of a doctor, but you're running all these targets and most doctors don't do that. That's my problem. They just will give a medication because, well, it might help, it can't hurt. And that's Not a bad approach, but that's not precision. How does that combine with your current care, your current targeting? So when you run the transcript nomics on fenbendazole, what you're going to see is a heat map for, for HK2, these high glycolytic paths, GLUT1 what we call all the glycolytic signatures. When you're talking about the metabolic cause of cancer, you'll see those. This will downregulate that. Now you'll say all cancers have that. Yes, but not to the same level. That's why I'm saying there's not a one size fits all. When you do the testing you can see what's important for the patient. The microtubule genes. Again very similar to menbendazole. You'll have certain microtubule genes to see if you're a candidate with combination. So when these things all work in your favor and you have the spatial biology which shows you the similar mechanism of fenbendazole, now you know when to give it. So you're not just giving it randomly. Now let's move on to ivermectin. I know I'm going into some details and markers but I want to show you there's a science behind what we can do and we don't have to just guess blindly. There are multiple pathways that are exciting within ivermectin. You know it can affect cancer stem cells. There's all kinds of data. You'll hear people talk about pre clinical studies of anti cancer. It'll stop pathways. But what are the signal pathways, what are the genetic pathways? IVM modulators like PIK3, AKT, MTOR. So you see that some of those work really with other drugs. One of the most common ones you'll hear is like MTOR and using metformin in low dose. Right, because or berberine because it down regulates those pathways. These are off label repurposed drugs to help with what might be feeding the cancer or growing the cancer stat 3 or NF Kappa beta or a series of other pathways that are involved in tumor growth. I'm not going to go through them all here but you can also look at drug resistance and metastasis pathways that are important for the use of ivermectin. So if we're targeting with ivermectin we're looking at cancer stem cells and how prevalent is that in cancer? It increases chemosensitivity. So depending on the type of chemotherapy you're using, it can make it work better and Again, with micro dosing, you can get a 1 plus 1 equaling 11 here. So if you have the right combinations, you have an advantage. Slow down metastases. So if your metastases pathways are up and markers are up, great, your chemotherapy is failing. Sometimes they'll just throw ivermectin in, but you have to know that your medication is on the right targets. These metastatic effects are really important to reduce the migration of the cells, the invasion of the cells from spreading. And so if all those markers are upreg, which there are ways we can see that when we're doing circulating tumor cell separation, we can see the aggregate of macrophages and we can see the aggregate of immune cells. And that actually gives us a metastasis score amongst other markers that we look for within transcriptomics, we can look for IVM, we can look for WNT pathways stat 3 CSC markers like CD44 and SOC2ABCB1. So all of these pathways, whether they're drug resistant or pathways like PGP pump pathways, we can then say, oh, ivermectin has a place here as a chemosensit, as a primer, as an immune modulator, not as a standalone therapy, but as an adjuvant along with many other things that'll come into play with your algorithm. That's the key of precision oncology. We're removing the guesswork and again here we're talking about just one drug. There are so many great repurposed drugs and when they're typed for you, this is where you get the one plus one equaling 11. And unfortunately, way too often we're seeing integrative doctors or functional medicine doctors, just prescribe them, you know, because maybe they don't have too bad of a side effect profile open, see that they work and I understand that. But when you have precision and you're able to combine everything, the on label, off label, repurposed, the integrative, the phytotherapeutic, the cellular biologics. Now you're dealing with so much more information with the proper deep mapping and precision oncology that is matched to you. So here's the real secret. Repurposed drugs don't work because they're repurposed and cheap. That's a nice feature. And we have safety data, which is also a nice feature. But they work only when they match to your tumor's biological wiring, where the heat maps are strong in these areas. And many cancers have these variations. This is why we use the RNA sequencing heat maps, the transcriptomics, the next Generation, sequencing, the immunospatial biology so we can get the pathways correct and we can get out of guesswork and get into precision. And the reason this becomes really important is because instead of just taking an off label drug and it works for a little bit and then stops working, if you can align everything, the immunotherapy, if you needed the micro dose chemotherapy, the integrative agents and the repurposed drugs like these combined, you have an extreme advantage because now everything's working in concert to bring you to healing. So this is where I believe we need to go with all of oncology, not just repurposed drugs, using targeting, getting out of dogma, getting into data and getting precision care. We must look at these things as not on off label or immunotherapies. We need to look at them of what's the right target for the patient? N of 1, what is customly needed for you, the patient, what works for you. Whether we have to build a cancer cell vaccine, immunotherapy, or use phytotherapeutics, nanoparticle IV or we need to go direct to tumor, whatever the method is, whatever the targets are, they're all combined for your specific heat maps. So ivermectin sense here when you need it and then bendazole fits the signature, you can take it. Or fenbendazole could be helpful to modulate the pathway when it's needed. And, and it's just so important to understand that, that these drugs, they don't automatically match everybody's biology and you need to know which ones are right for you and are going to work in your best interest in the right combinations. Repurposed drugs must never be used alone. They must be adjuvants with other targeted therapies. I don't even like to say standard therapies because those aren't targeted either. They're following NCCNN guidelines. It's a one size F double blind placebo clinical trial model of chemotherapy. Instead, we need to find the right targets for you so we can get that on board and then the repurposed on board and then the immunotherapy on board. And now you have the advantages. This is the matching of care. The more you match the care, the more your targets are matched. Far better clinical outcomes you're going to have. That's what I've seen with our experience. And this requires testing and custom drug building so that either in early or late stage cancers you have a huge advantage. This is the key to cancer understanding what you need at the right, right doses for your body. This is the essence of precision oncology. And then putting them all together so they work, their mechanisms match up to giving you a huge advantage. I hope this episode gave you some more clarity, more of like a tutorial of understanding how these drugs should be selected with the right markers instead of a just let's try this or try that and hope it works. Because even if it does work, you won't know why it's working and it may only work for a short period of time and you want a long term response. That's why precision oncology is important because when you align everything, all the treatment custom built for you, you will have the advantage of long term responses which is the goal of what we're doing. So I want you to get out of the hype and into the data that's needed to help balance your treatment so you have precision helping you get well and stay well. I hope this was helpful and may the Lord bless you on your journey to heal.