Annovis Buntanetap

A company called Anovus Bio has developed a drug called Buntinetap that targets a shared cause of Alzheimer's and Parkinson's diseases, which is impaired axonal transport. This transport system is like the highway system inside brain cells that ensures everything gets where it needs to go. Buntinetap inhibits the production of multiple neurotoxic proteins simultaneously, including amyloid beta, tau, alpha-synuclein, and TDP-43. Clinical trials have shown promising results, particularly for Alzheimer's disease, with the drug improving cognitive function in patients. However, results for Parkinson's disease were mixed, with significant improvements seen in specific subgroups of patients, such as those with longer disease duration, postural instability, and gait difficulty, and impaired cognition. The drug has shown to be safe and well-tolerated with minimal side effects. Future research will focus on understanding why the drug works for certain groups and fine-tuning treatment approaches get ready to really get into it today. Always. We're talking brain science big time. Alzheimer's, Parkinson's, these diseases, they really hit home for a lot of people. Absolutely, yeah. And it feels like we've been trying to crack the code on these diseases forever. Right. What if there's a piece missing though? What if we've been looking in the wrong spot this whole time? Yeah, that's what's so intriguing about what we're going to talk about today, right? We're going to focus on a company called Anovus Bio. Okay. And their approach is super unique. They're suggesting that there's a shared cause underlying both Alzheimer's and Parkinson's impaired axonal transport. Okay. Impaired axonal transport. That sounds complicated. It does. It sounds like a mouthful. Yeah. Break it down for me. What is that? Okay. So think about it this way. Think of your brain cells as like bustling cities, right? And so every city needs these ways to transport goods, essential goods, food supplies, all that. Right. Got to keep things moving. You got to keep things moving. Axonal transport is basically like the highway system inside these brain cells. Okay. That ensures that everything gets where it needs to go. Makes sense. But imagine if those highways get all jammed up, deliveries stop, things pile up, and the whole city, it just can't function. Right. Everything goes haywire. Exactly. So that's what happens in axonal transport disruption. It's like a logistical nightmare for your brain cells. So, okay. I'm with you. Instead of just looking at the symptoms, you know, they're saying maybe the problem is actually with the transport system, like the roads are messed up. Exactly. Yeah. It's a very different way of thinking about it. That's a bold claim. It is a bold claim. So what are they doing about it? So they've developed this drug, it's called Buntinetap, and it's designed to tackle this very issue. So is Buntinetap like our traffic controller then, like getting those highways clear? I love that analogy. That's a great way to put it. Yeah. And what's so cool about Buntinetap is that it's not just focusing on one specific thing. It's like this multi-target wonder drug. So it's inhibiting the production of several different neurotoxic proteins simultaneously. Okay. So it's like a multi-pronged approach. So what are these proteins and how do they play into these diseases? Right. So you've got amyloid beta and tau. Those are the ones that are really notorious in Alzheimer's disease. And then you've got alpha-synuclein. That one's the main culprit in Parkinson's disease. And then you've also got TDP-43, which is something that we often find in ALS. Wow. So many diseases. And you're saying that this one drug might be able to tackle all of them by going after this root cause, this axonal transport disruption. Yeah. It's a really interesting approach. That's huge. It is. So do they have like trials, clinical trials to back this up? They do. They do. And the results are really promising, especially for Alzheimer's disease. They've completed multiple trials, even a phase two, phase three study. And there are some really, really interesting findings. Wow. Okay. I'm seeing some potential here, I've got to be honest. But we need to look at the data. Of course. Yeah. Let's start with Alzheimer's. What were they looking at in these trials and what did they find? So one of the key things they were looking at was cognitive function. And they use something called the ADASCOG, which is a commonly used scale. Basically, it's like a report card for thinking and memory skills. And in these trials, BUNTIN-ATAP consistently helped the patients improve their scores compared to those who got the placebo. Okay. So the people taking BUNTIN-ATAP were actually showing improvement in their thinking, their memory. Yes. That's amazing. How do we know this wasn't just a fluke? How do we know for sure? That's a great question. That's where the design of these studies is so important, right? So these were what we call double blind placebo controlled trials, which is like the gold standard in medical research. So neither the patients nor the researchers actually knew who was getting the real drug versus the placebo. And so that really helps to eliminate any bias and increase the confidence that we have in the results. Okay. So some really promising signs of Alzheimer's. Yes. What about Parkinson's disease, though? Did they see the same promising results there? So this is where it gets kind of interesting. The initial results from the phase three Parkinson's trial, they were kind of mixed, actually. Yeah. Across the board, across the whole patient group, they didn't see the same statistically significant effects. Okay. So not as cut and dry as the Alzheimer's results then. Right. Exactly. Okay. Does that mean it just straight up doesn't work for Parkinson's? What's going on? Not necessarily. Not necessarily. This is where these subgroups come in. So while it didn't work for everyone, Bunten-ATAP did show some really remarkable improvements, but only in specific groups of Parkinson's patients. Okay. I'm intrigued now. Tell me more about these subgroups. What were they? Sure. Yeah. So first they looked at patients who had been living with Parkinson's for more than three years. So they were further along in their disease progression. Exactly. Exactly. Okay. And did Bunten-ATAP make a difference for them? It seemed to. So to measure improvement, they used something called the MDS-UPDRS, which I know is kind of a mouthful. It's a mouthful, yeah, but help me understand it. Yeah. So think of it like it's basically a ruler for Parkinson's symptoms. Okay. It measures things like tremors, stiffness, and how well people can do everyday tasks like buttoning a shirt or like writing a text. Okay. So like a higher score on that ruler would mean more severe symptoms. Exactly. Exactly. And so in this trial, the people who had been living with Parkinson's for longer and who took Bunten-ATAP, they saw their scores improve significantly compared to those taking a placebo. Wow. Okay. So they were actually moving better, functioning better. It seems like it. Yeah. They were experiencing a better quality of life, which is huge. That's really something. Okay. So that was one subgroup. What about the others? The second group that really stood out was patients with postural instability and gait difficulty or PIGD. PIGD. That sounds not great. It does. Yeah. Very descriptive. What is it? Imagine struggling to walk, always feeling off balance, like you're going to topple over. Yeah. No, thank you. Yeah. Right. So that's the reality for folks with PIGD. It's a very common symptom of Parkinson's, unfortunately, and it can be really debilitating. So did Bunten-ATAP offer any relief for those people, those with PIGD? So just like with the group that had the longer disease duration, Bunten-ATAP, again, it led to really significant improvements in those MBS UPDRS scores. So for PIGD patients, that meant they were steadier on their feet. They had better balance. That's huge for someone who's struggling with those things every day. Okay. So we're seeing a little bit of a pattern here, I think. It seems like this Bunten-ATAP, it might be especially helpful for folks with more advanced Parkinson's or a more aggressive form of the disease. Am I reading that right? Yeah. No, I think that's a really, really astute observation and definitely something that researchers are going to be looking into more. Now, the third subgroup is really interesting, I think, and that's patients with impaired cognition. Okay. So now this is kind of looping back to our Alzheimer's conversation. Right. Because you mentioned that cognitive decline is a feature of both of these diseases. Absolutely. Yeah. And so in this trial, they found that for the people on the placebo, their cognitive function actually declined over the six months. Oh, wow. But for the people taking Bunten-ATAP, they either stayed the same or they actually improved. So not only is it maybe helping with these movement-related symptoms, but it could also be protecting against that cognitive decline. Right. And this ties back into that idea of axonal transport that we were talking about earlier, right? So if this drug is improving that flow of information and resources within those brain cells, then it could be having a protective effect across these different cell populations, these different brain regions. Interesting. And so it ends up impacting both their motor function and their cognitive function. Okay. Well, this is all incredibly promising, I got to say. But before we get too far ahead of ourselves, we do have to talk about the safety. Of course. Especially with a new drug. So what did they see in the Parkinson's trial in terms of side effects? So the good news is that just like the Alzheimer's trials, Bunten-ATAP seemed to be safe and well-tolerated in the Parkinson's trial. They really didn't see a lot of serious side effects, and very few were actually linked back to the drug itself. That's reassuring. Yeah. So where does ANOVUS go from here? What are the next steps? What are some of the big questions that scientists are asking? Well, I think one of the biggest questions is why it seems to work really well for some groups and not for others. It's like we found a couple of pieces to a puzzle, but we got to figure out how they all fit together to see the full picture. So are we back to the drawing board stage, or is it more like fine-tuning is needed? It's probably more like fine-tuning at this point. They'll likely design new trials, but specifically for those groups that saw the really big improvements. Okay. So we're talking about the folks who had a longer disease duration, the PIGD, the cognitive impairment. It's about making sure that the right treatment is getting to the right people. Absolutely. Yeah, that makes a lot of sense. Yeah. Okay. So I'm wondering now with all of this, what does this mean for other brain diseases? Yeah. Is there potential for Bunten-ATAP beyond just Alzheimer's and Parkinson's? Right. That is the big question, isn't it? Yeah. And that's what's so exciting about this. So remember, Inovus Bio, they're looking at axonal transport as this potential cause for a lot of these diseases. Right. So if they're right, then Bunten-ATAP or other drugs that are similar to it, they could be game changers for all sorts of conditions where, frankly, right now we don't have a lot of options. Yeah, for sure. So what other diseases are we talking about here? Well, one that immediately comes to mind is ALS. Right, Lou Gehrig's disease. Right. And it's a really, really tough disease. It robs people of their ability to move, to speak, even to breathe. Yeah. Absolutely devastating. And the treatments right now are very limited. So how could targeting axonal transport actually make a difference in a disease as serious as ALS? Well, so if you think back to those brain cells, like cities, with ALS, what's happening is the highways, in this case, in the motor neurons, the cells that control our muscles, they're breaking down. Okay. And that disrupts the transport of all the essential stuff. Right. Eventually, those neurons, they die. So if Bunten-ATAP can keep those highways clear, keep those cells functioning, could it actually slow down or even stop ALS from progressing? That's the hope. It's definitely still early, but I think the potential is really huge. And it's not just ALS. They're also looking at frontotemporal dementia, FTD. It's another type of dementia that affects personality, behavior, language. And again, we're seeing that potential link to axonal transport disruption. It's really incredible when you think about it. It's like all these diseases have been locked behind these different doors. Right. And I know this bio might have found like the master key, this axonal transport idea that could unlock treatments for all of them. Yeah. I love that analogy. That's a great way to put it. But as with any exciting new discovery, we need to be cautiously optimistic here. Of course. This is still early research. And while these findings are, they're really promising, we don't want to get ahead of ourselves. Right. Keep those expectations high, but your attachments low. Exactly. Science can move slow. It can. We need a lot more research, larger studies to really confirm these findings and explore the full potential of this whole idea, targeting axonal transport. Well said. Okay. So for our listeners who are like ready to, I don't know, geek out on this, learn more about Inova's bio, follow along with their progress. Where can they go? Their corporate website is a really great resource. They've got updates on all their clinical trials, publications, all that good stuff. Perfect. We'll link to that in the show notes. And for anyone listening who's dealing with any of these diseases personally, whether it's you, a loved one, a friend, I think it's really important to remember that even just a glimmer of hope can make a huge difference. Huge. Absolutely. Yeah. And the dedication of all these researchers, the clinicians, especially the patients and the families participating in these trials, it's really inspiring that hope and that resilience. Absolutely. Okay. So as we wrap up this deep dive, what is one just like thought provoking question that we can leave our listeners with today? Okay. How about this? What if, and this is a big what if, what if targeting axonal transport is as successful as it seems right now? Could it actually change how we treat not just these diseases, but other things that affect the nervous system, traumatic brain injury, even stroke? Wow. I mean, the possibilities are, they're really kind of mind blowing when you think about it. That is something to think about. And that is a wrap on this deep dive into Inova's bio and their mission to hopefully outsmart neurodegeneration. Until next time everyone, stay curious.