These Two Drugs Eliminated Cancer Metastasis | Here's What You Need to Know

0:00 Two cheap decades old drugs just stopped cancer recurrence cold 100% of patients. That sounds amazing, but you need to know the entire picture. Today we're covering another way to prevent cancer recurrence from small metastasis. So if you've been wondering, how do I prevent my cancer from coming back? This video is for you. And in many ways, this one is really exciting, probably applicable to most cancers, if not all. And as usual, there are a couple of important things that make it a very, very bad idea for some folks. So stick around until the end instead of just calling your doctor to start immediately. Hello and welcome to Elevating Cancer Treatment, where we explain the science and debunk myths to help you navigate your health journey. My background is a

0:46 little different. Beyond educating about cancer, I'm actually designing new drugs that are defining the future of oncology. This direct hands-on experience offers me a very different perspective of how these cancer treatments work on the body, interact with the cancer cells, and cause side effects. And these are insights that I'm excited to share with you. If that sounds interesting, make sure to like this video, subscribe to the channel, and hit that notification bell so you never miss an update. And please share it if you find it useful. I'm Dr. J. Chaplan. An important reminder, I'm a PhD, not an MD. The information in this video is education and it's not medical advice. Every cancer is unique and no general information applies to everyone. Please remember that. Always consult with your health care provider for guidance on your specific situation. And two quick things. First, as a thank you

1:32 for being here, I've created a free resource, 10 things to elevate your chemo journey, which you can download from the link below. And second, by signing up, you'll also get updates on that innovative cancer treatment I'm working on. I'm confident it represents a significant advancement in amunotherapy. So, please take a moment, download your free guide, and join us in shaping the future of cancer treatment. So, in October of last year, 2025, a new clinical study came out looking at a strategy to prevent cancer recurrence. And on the surface, the results are honestly jaw-dropping. And this one could be very useful for those of you who cannot take advantage of the lowdose aspirin approach we talked about previously in this video. So today, let's walk through what this study

2:18 found, why it's impressive, and probably applicable to all cancers, which is incredibly unusual for cancer drugs, and where the limitations are, including who this approach may or may not be appropriate for. So the big claim, this is a phase 2 clinical trial in breast cancer. They were primarily trying to find the right dose of the drugs. Efficacy was an add-on. It focused on patients after their primary treatment. So for example, their tumors were already removed. Standard treatment had already been completed. Breast cancer was resolved. But bone marrow samples showed that microscopic tumor cells, small metastases were still present. Single cells that could later come back and seed metastatic disease. So the goal here wasn't shrinking big tumors. The

3:05 goal was preventing recurrence. Kind of like we saw again with the lowd dose aspirin episode. And here's the headline result. At 3 years out, 100% of the patients on this combination therapy had no evidence of cancer recurrence. Zero. None. None of them had recurrence. That's extraordinary. It really is extraordinary. So what was the treatment? The study used a combination of two old drugs. The first is everimmus and the second one is hydroxychloricquin. Now those are not experimental drugs. They're not as old as aspirin, but hydroxychloricquin is getting up there. They are not new. They're widely used and they're both generics. They've been generics for quite a while. So, they're off label access should be easy. They

3:52 should be cheap and all of that matters to you. So, all of this makes sense. Why does the first drug evermus make sense? We've known for a long time that Everelmus is useful against cancer. The first thing you need to know about is mTor, short for mamalian target of rapamy. That's a major metabolic and growth hub inside of every cell in the body. MTOR sits at the center of the wheel for every cell's growth and metabolic controls, including cancer cells. It's sort of like a grand central station for all of these signals. the surface of the cell picks up growth signals, filters them in. MTOR translates the message and then sends it out to be acted on. It's at the center

4:37 of all of this. So, it takes in those signals from all sorts of different systems. Krass, we've talked about a whole bunch of others, Heru, everything. And it controls nutrient uptake, cell growth, metabolism in general, protein production, cell death, all of that. So, how is that relevant to cancer? Cancer lives on uncontrolled growth and replication. So when you inactivate mTor inside of the cancer cell, you shut down more than one of cancer's core engines. And that's why Everly was approved for use in cancer all the way back in 2009. None of this is surprising from a biological standpoint. If you shut down the always on metabolism and growth of a cancer cell, of course, it's going to help cancer. [snorts] The big problem with that is resistance. That's the

5:22 issue. Cancers can become resistant to evermus pretty quickly. And that's where the second drug comes in. Enter the dragon. No, enter hydroxychloricquin. Hydroxychloricquin is an even older drug. It's been around since 1955 and it's best known as an antimmalarial drug and an autoimmune disease drug. At the cellular level, what it does is it disrupts lysosomes and those are basically the stomach of the cell. It's where things get digested inside of a cell. This really matters because it also blocks autophagy or autoagi, however you say it. I say autophagy, you probably say autoagi. And that's something that you've probably heard of in the context of fasting. And we'll do an entirely

6:07 separate episode on that. Autoagi is a great thing under some circumstances and bad under others. This autoagi is a recycling process where cells actually will break down part of their own components in order to survive when resources are scarce. That's why fasting activates it. you restrict resources, the cells will cannibalize bits of themselves. Now, cancer cells are very good at this. If they're not getting enough nutrients from the outside to grow, they will cannibalize parts of themselves to keep growing. You might think that this is a good idea, but it actually keeps the cancer cells alive and growing. If you try and restrict nutrients in the blood, individual cancer cells will literally shrink in their own size in order to keep doubling and make progeny cells that are smaller but can rebound quickly.

6:53 Autophagy is one of the ways cancer cells sidestep the growth blockade caused by everimmus. So when you combine ever blocking the growth signaling and hydroxychloricquin which blocks autophagy, you cut off both escape routes. Now even this combination is not new. So let's talk about when this combo has been tested because it has been tested before. It's been tested in cell lines. It's been tested in animal models and it's been tested in humans. We have clinical data. So the most important for me and hopefully for you is the clinical testing because that shows us what actually works in human beings. It was clinically tested in renal cell carcinoma, a form of kidney cancer. In that clinical trial, it was very

7:39 different. The patients had failed somewhere between one and three prior standard treatments. That drug combination was used alone, nothing else because of those multiple treatment failures. The result was an impressive 45% progressionfree survival. So, it didn't necessarily get rid of the cancers, but it at least stopped them from growing. And that's two old cheap drugs. Great. That sounds impressive, but and and this is a significant but, there was no control group of any type. I I don't know why trials are set up this way. So, we don't know if that 45% is better than 40%, better than 30%, better than 5%, better than zero. We have no idea how people would do if they weren't on that. We don't have any comparison. Now, I get it that the study

8:25 designers didn't want to withhold therapy from people, which is admirable. You know, you don't want to hurt people, but they could have at least found historical patient records to create a reference point. There were people before this was tried that they could have used as a comparison and that didn't happen. So that efficacy signal of 45% is really promising but the size of it is incredibly hard to judge. Is it good or spectacular? We don't know. Now the new breast cancer study, let's come back to that again. October 2025. They use the same drug combination but in a very different setting. Again, this was after the primary tumor had been removed, after regular treatment had concluded, and they were focusing on preventing microscopic metastases from

9:10 coming back and receded cancer. So, in many ways, this is similar in spirit to how again the lowd dose aspirin has been explored for metastasis prevention. This is just through a completely different mechanism. So, this was a combined phase 1 and phase 2 trial. It was mostly done to figure out dosing and safety. So patients in the combination group received hydroxychloricquin 600 milligrams twice a day morning and evening they received one daily dose of Everlymus 10 millig that's a pretty high dose so both of them hydroxychloricquin and everimmus they did try higher doses of hydroxychloricquin in earlier phases but those caused high-grade side effects lots of vomiting lots of GI distress and nausea lots of headaches so they reduced

9:57 it and 600 milligrams twice a day is what they used Now, obviously, there are side effects, but no serious side effects. They tailored it right. That was the point of this study. Overall, the regimen was reasonably well tolerated, better than generic chemo, and not without side effects. People had very little trouble completing the 3 years of the trial. So, dosing every day for 3 years. The result, 3 years, absolutely no one in that combination group had a recurrence of breast cancer. Now remember this for later. Each drug alone, Everlymus and hydroxychloricquin also reduced recurrence risk, just not nearly as much. The combination was clearly superior. Once again though, God, I hate it when they do this. There

10:43 was no control group and no historical comparator. We don't know how good this was. Most cancer studies look at a five-year progression free survival, not three. So while this result is very very impressive and it really is, the interpretation is still very difficult and very limited. So here's why this matters beyond breast cancer and where it gets really interesting, at least for me. We now have one clinical trial showing benefit in primary tumor control, kidney cancer. We have one clinical trial showing very significant benefit in metastasis prevention for breast cancer. And both of the drugs in this combination target fundamental features of cancer biology. MTOR dysregulation happens in a huge number

11:28 of cancers. In many ways, it doesn't matter what signaling pathway starts the problem at the beginning on the outside of the cell. Almost all of those signals end up funneling through mTor. Again, it's the hub of the wheel. It's the grand central station. And you saw that in the figure earlier. Because of that, this approach should be broadly applicable to preventing recurrence and metastasis across many different cancer types, probably all cancer types. And that part is incredibly exciting. It means that this is a great option for the same kind of benefit as the lowdose aspirin we talked about last week, but without that risk of bleeding or gout and poor interaction with anti-coagulants or blood thinning medications. Now unfortunately there's

12:15 another significant caveat. It won't be the last one. This was a very small trial. There were three groups. Two single drug groups. Everimmus with 15 patients and hydroxychloricquin only with 15 patients. And then the combination group with 21 patients. That's pretty small. Phase 2 trials almost always aim for 30 to 40, sometimes up to 50 patients per group. So these groups were about half the size at least, maybe even smaller than usual, which means that the study is probably underpowered. And what does that mean? That means that 100% recurrence-free result could still theoretically be statistical luck, especially since the two drugs did really well individually. That makes the risk of a false positive

13:01 on the combination higher. So, you might be wondering why I'm still supportive of these studies and showing them to you even though they're underpowered and they don't have proper controls. People use good controls. It's easy. So, still, even with those problems, what we're looking at is a strong biological logic and prior data. It's really hard to ignore. All of the pieces line up together. It isn't just some random study. It is one piece of a puzzle that fits with everything else we already know about each of those two drugs individually, about how they impact cancer, how they impact basic cell biology and metabolism and how they work together. Everything fits perfectly. This is not strange. Now, I'm not trying to raid on anyone's parade, and I like

13:48 my viewers and clients to have the whole story so that they can discuss it with their care team and make the best informed decisions. So, here is the most important part about this story. This is the one that I really, really, really want you to hear because it isn't being communicated with all the glowing recommendations on Facebook and other social media and you might not know it unless you're very familiar with these drugs like I am. Both of the drugs Everly and hydroxychloricquin by themselves are immunosuppressive. As a matter of fact, Everlyus was originally developed and approved and used as an immunosuppressant to prevent transplant rejection. That's what it was made for. Hydroxychloricquin was developed as an

14:34 antimmalarial, but because of the way it works, it blocks immune cells from processing debris. And in doing that, it reduces immune system reactivation against tumor cells. That's why it's used in autoimmunity. it'll dampen the immune response and together they're much more immunosuppressive than either drug by itself and this has some implications for you. So we'll get to what you can combine it with but what you can't combine it with is any kind of amunotherapy. If you're on checkpoint inhibitor treatment like optivo or kitruda or ratlamab or any of those others you can't do it. If you're on maintenance amunotherapy or even if you're using non-drug approaches to increase immune function again like that

15:19 lowd dose aspirin or that hyperothermia hot tub thing that I mentioned before this combination is going to blunt or completely undercut the effectiveness of anything meant to increase immune function. There's no question about it. I mean the everolimus dose alone is five times what is used as an imunosuppressant after organ transplant. That's important to know. This combination may also make you more susceptible to viral infections. So, being careful about hygiene, washing your hands frequently, and minimizing contact with very large groups of strangers is a wise idea. Additionally, and this isn't mentioned either, while hydroxychloricquin is much much better in this regard than its parent drug chloricquin, both of those are still

16:05 hard on the retina of the eyes and especially so with long-term dosing. So if you already have issues with macular degeneration, you might want to bring that interaction up with your doctor before starting it. So those are the things to watch out for. What it does stack well with, whatever and hydroxychloricquin do stack well with is pretty much everything else. Targeted therapies, antibbody drug conjugates, traditional chemotherapy, radiation, hormone blockers, just not amunotherapy. And that distinction is critical. Everything else are good. imunotherapy no go. So final takeaway here, this is a very promising strategy. It makes total sense. There's decent data behind it. I wish the studies were bigger. I wish they were better controlled, but everything makes sense. It's a very

16:50 promising approach, especially after primary treatment for preventing recurrence and metastasis. And again, these drugs are old. They're very wellstied. They're very available, easy to find. They're mechanistically sound for most, if not all, cancers. And be aware the trials were small. There's no control comparisons, not even historical ones. And the imunosuppression risk is real with a possible additional concern for those of you with macular degeneration issues. Okay, this is still exciting science. I'm excited. It's going to be good for a lot of people. And as usual, it needs careful application and attention to your details. As I always say, talk to your oncology team before considering anything like this. And of course, I am

17:37 always here to consult with as well and help you make those sorts of risk benefit calculations for yourself. Thank you for watching and stay curious. Beyond these videos, if you need more personalized guidance or a deeper dive into specific treatments to have your treatment be as effective as possible, I offer one-on-one sessions and medical advocacy. You can find information on our website, which is linked down below. Again, if you found this video informative, please give it a thumbs up, click the notification bell, and subscribe to our channel for more sciencebased cancer insights.