CEO of JTCIR Team, I will be the moderator for today's event. I am very pleased to be joined by John Climaco, Chief Executive Officer of CNS Pharmaceuticals, and Professor Michael Weller of the University Hospital Zurich, Department of Neurology. Before we get started, I just wanna remind our audience that CNS Pharmaceuticals is publicly listed on NASDAQ, and trades under the ticker CNSP. During today's discussion, the company will be making forward-looking statements, and I encourage everyone to view the company's latest SEC filings on their website at cnspharma.com for the latest information. We have great audience participation today, and as normal practice, following my discussion with John and Professor Weller, we will be opening up for a live Q&A, so keep your questions ready. Welcome John and Professor Weller, so happy to have you join us today. Great to be here. Hello. Great. Before we dive into today's discussion, John, I'd like for you and Professor Weller a chance to introduce yourselves to our audience, provide some of your background. John, how about we start with you? Sure. I'm the CEO of CNS Pharma. I've been in this role for over five years, really since we started the company, and have helped bring the company to this point where we have this great trial, and lots of incredible physicians, including Dr. Weller, participating around the world. Yeah, that's me. Great. We'll definitely get into all that you're doing at CNS, specific with your GBM study. Congratulations on all the progress. We see a lot of press releases going out, showing the advancement of that program. Congratulations. How about you, Professor Weller? If you could provide your background, that'd be great. Sure. I guess mostly good morning to all of you, or good afternoon. The light shows you that we have dark night in Switzerland. I apologize for that. I am the chairman of the Department of Neurology since 2008 at the University of Zurich. Special interest is brain tumors. I'm also heading the brain tumor center here, and I work on the board of the European Organisation for Research and Treatment of Cancer, and clinical trials in glioblastoma are my passion. Great. Wonderful. Thank you, Professor Weller. We'll have a lot of questions for you. Before we get into that discussion, John, how about we provide the audience with a high-level overview of CNS Pharmaceuticals? Sure. CNS Pharmaceuticals is a drug development company, and we specialize in oncology and particular CNS oncology, as the name would imply. We have been around for about six years. We were founded by Dr. Waldemar Priebe, who's a professor of medicinal chemistry at The University of Texas MD Anderson Cancer Center. We were founded primarily to advance a program around a drug called Berubicin, which is our lead compound. We'll talk a lot about Berubicin, I'm sure, today. Berubicin is a novel anthracycline. It's the first drug of its kind shown to cross the blood-brain barrier and actually attack GBM tumor cells in human beings. It's quite an exciting drug. We have a great trial going on, as I said, which Professor Weller is participating in as an investigator. You know, I think one of the reasons why we've made as much progress as we have, you know, in this relatively short period of time is because we really are laser-focused as a company in this one area. I have a really strong belief that, you know, the fastest way that you kill little companies, I've said this before, is by trying to do too much with too little. We are a small company. There are just five of us, but we are absolutely dedicated to this mission. As such, I think we've been able to put, you know, all of that effort and expertise into this, as well as bringing in an incredible, you know, network of clinician investigators around the world to help us realize this goal of trying to see this drug approved and provide some hope for these patients. Terrific, John. Thank you. This is the GBM Spotlight event. Glioblastoma multiforme, GBM, is truly a devastating disease that has been a challenge of publicness to the entire oncology community. Professor Weller, can you please give our audience a background on GBM? Sure. I'm gonna maybe give a very short background, and we can discuss certain issues later in the Q&A session. It's a primary brain tumor, which means to indicate that it starts in the brain, it also kills in the brain, it almost never leaves the brain. That's not the way that other cancers cause mortality. It's unclear from which cells the tumor originates. People can be affected at any age groups. Even infants can have it, but the risk steadily increases over time. The general frequency is 3 per 100,000 every year, and that's fairly stable worldwide, which is interesting. Tells you that maybe environmental causes are not so relevant if at the equator and among Eskimos, it's the same risk. Must have other causes. The only causes that are really identified up to date is the wrong parents. There's a certain minor genetic trait, but that's really rare. The other identified reason is irradiation from artificial sources. That's among the only reasons. Patients have not done anything wrong. They always ask us, "What could I have done differently?" With all the modern treatments. When I talk about the median survival. Median survival ... level is still only 12 months, even in high-tech countries like the U.S. and Switzerland. Very helpful, Professor Weller. Can you go into more detail of the unmet needs for GBM, and why it's been such a challenge for doctors and clinicians to overcome? Sure. There are several reasons. Maybe I start with the question, why can you not simply remove it, right? We have great neurosurgeons that are capable of doing all kinds of things. The problem is that this tumor grows in a very infiltrative manner, even behind the so-called blood-brain barrier. It's not a circumscribed disease. It's not growing like a lump in the brain where you see clearly the borders. That's limiting surgery. The tumor cells are really very fit in terms of survival, even under circumstances where there are few nutrients, hypoxia, they can really survive multiple attacks. The brain location has also an issue because our immune system is not very active in the brain, for good reasons, because probably evolution didn't want to have too much inflammation ongoing. A tumor can really grow relatively unrecognized in the brain. That's also why immunotherapy has failed. Finally, there are, as many of you may know, tumors these days that are really driven by a single molecular pathway in lung cancer or melanoma. Targeted therapy has changed the fate of patients. glioblastoma does not have such a single pathway that can be targeted. That has made all these efforts at targeted therapy relatively futile. That's where we stand. Very, very helpful. If you could then now discuss the journey for patients from the time of diagnosis and the current standard of care. Most patients that are diagnosed with a glioblastoma have been completely unaware of their disease until a very few weeks ago, so it's really a major change in their life. History is short, often starts with an epileptic seizure or some neurological abnormality, depending on where the tumor is growing. That triggers MRI imaging, and then if you're experienced, you're almost never wrong, and you can assume what the diagnosis is. Surgery is absolutely important because the extent of tumor that you can remove is prognostic. Also these days, we of course have to submit tumors to molecular profiling to see whether the tumor has any vulnerabilities. As I said, in glioblastoma, that's not so often the case, the molecular workup is important. When patients recover from surgery, which is very quickly, they have to be confronted with the truth, which is really challenging. Of course, you would assume that you should always say all the truth upfront, but this is simply very, very difficult, so we usually do that in fractionated manners, wait for patients and relatives to ask the essential questions. You cannot bring the bad news in a few minutes. It takes a lot of time, because many of these patients are young. There is a standard of care, which includes radiation to the tumor field with a safety margin, plus chemotherapy. The chemotherapy benefits roughly a third of the patients defined by a molecular marker, and then starts the best time for the patients, because patients always think they are different. They may be the ones that are long-term survivors, but within a few months to rarely a few years, recurrence is diagnosed. It's inevitable. The standards of care are very poorly defined. Our joint agreement worldwide is that treatment with lomustine, a relatively old compound, is the standard of care. That's also part of the clinical trial. This is a relatively inefficacious standard of care, and at some point, it is wise to really involve palliative care specialists to see that the journey is going into the right direction, and that patients and caregivers know what they have to expect. Thank you, Professor Weller. It's extremely helpful. I think we'll shift our focus now to CNS Pharmaceuticals lead program for Berubicin, which you mentioned, John. It's currently being evaluated in a potentially pivotal phase II program for the treatment of GBM. John, if you could give us a update on the clinical development of Berubicin. Sure. Well, you know, I mean, first of all, let me say thank you to Dr. Weller for that, you know, very clear explanation, and also just what I would call a very sober look at this disease. You know, the, and it's really, if you think about everything that was said, you know, I think you'll find our motivation as a company and why we've designed this trial the way we have, and why we are so aggressively promoting this. It's simply because, you know, to me, You know, I mean, I take a strong interest in new medical technology, and it is a place where I can, you know, as a non-clinician myself, make a difference here. This standard of care, you know, at this point in history, when, as Dr. Weller, you know, points out, so many other cancers have seen the benefit, really incredible benefit of targeted therapy, and here is this devastating almost, you know, formerly fatal cancer where the standard of care is more or less sitting still. There's good reason for that, you know, you know, as we heard. Our approach was I think one informed by all of those difficulties, and interestingly enough maybe, I would say sort of, counterintuitively it pointed us in the direction of a traditional chemotherapy approach. You know, as we've heard, this cancer does not really succumb to targeted therapies for different biological reasons, and we felt that perhaps a really truly efficacious, let's say colloquially one-size-fits-all chemotherapy foundation in the pharmacopoeia or treatment paradigm might be missing here, and maybe we had something that would provide that promise. As I said, you know, this is an anthracycline. You know, it's a very commonly used class of chemotherapy drugs. They've been around for 6 decades, so, you know, I often say there's probably not an oncologist practicing anywhere in the world that didn't train on these drugs along with their toxicity and side effect profiles. I think that gives physicians, clinicians, a lot of confidence in this drug and in the use of this drug in an experimental clinical trial setting where, as you've heard, you know, these patients have few options, and their time is very, very limited. That I think is a key sort of component of why we've had such a strong enrollment and strong participation by clinician investigators around the world. We have now over 100 patients on this study, which is really a remarkably large sample size, for a program like this at its stage. You know, we are going head to head against lomustine, which is part of, you know, the current standard of care even though it's not approved for this indication. Really our goal, our first goal, coming up soon in the third quarter of this year will be to perform our preplanned futility analysis, when we will look at a subset of the data that we've collected so far really with an eye toward determining, you know, whether or not there is a reason to continue the trial. It's formally called a futility analysis, so we really will be looking to see, are we at least as good as lomustine. You know, our hope and belief based on the phase I data is that the answer will be a resounding yes, and we will continue on. I think that will give, you know, clinicians, patients, and investors, a lot to be excited about in this space because there really isn't a whole lot else going on here. I think the exciting thing about the drug is that we're really taking a well-known class of drugs with a very well-understood mechanism of action, and because of a modification in the molecule, you know, in the lab of our Founder when he was developing this drug, we're able to deliver that drug in a way that other drugs like it have not been able to be delivered to the brain, where this cancer lives and grows through its entire cycle. I think there's a rational, approach to this. I think the clinical need here is well understood. I think the trial is a really excellent design. I think that's supported by the fact that the sample size now, of over 100 patients, you know, approaching kind of halfway in of our planned enrollment, has been as strong as it has. You know, ultimately that's again, that's really what we're all about at CNS is this drug right now in this trial and trying to, you know, trying to change the game here a little bit in GBM and provide another tool in the neuro-oncologist's toolbox. Very, very helpful, John. Professor Weller, I'm interested to hear your thoughts on the design of the Berubicin phase II potentially pivotal trial and how it differentiates from other ongoing clinical trials for GBM? Maybe my first comment to that question is that I think most of the other drugs have not failed because of poor trial design but simply because they didn't work. I think that the company has learned to early on go into a randomized fashion. The trial size at the moment, the way I see it, is 210 patients, which I think is a fair compromise. You want to have really enough patients on trial to see whether you have a signal or not and whether it's worth the effort. There's also the interim analysis, which from an ethical point of view is also a strength because you don't want to expose patients to drugs that don't work. Having said that, we do that a lot because, as indicated, lomustine is also not a super strong standard of care. Coming back to the patient journey, I think you all out there have to understand how difficult it is if patients come with their first recurrence to tell them, "Look, we have no evidence-based medicine anymore." That's why I think patients are really open to go on clinical trials. It's very important. The design of the trial of putting two-thirds of the patients on the experimental arm of course makes it more attractive to patients because patients can get the lomustine everywhere. That's a fact. Patients like trials in this situation. Excellent. Okay. Professor Weller, another question. Having seen the demonstrated data from CNS Pharmaceuticals' phase I trial in Berubicin, if it were to be approved for the treatment of glioblastoma, how do you see its role in the current treatment paradigm? Well, that's a very hypothetical question of course. I mean, we I think both Dr. McKwain and I, we both indicated that lomustine as a standard of care is a compromise because it's really important that we compromise worldwide, because otherwise we couldn't do such a trial in different countries. We have to agree on something. I think we would also all agree that in principle, if a drug is really active, it should be able to beat lomustine because it's not a strong standard of care. Since no treatment at recurrence has ever shown efficacy, if the trial was clearly positive, it would be very difficult not to establish this as a standard of care. We have to see what the data looks like, right? I think in the end, of course, the company knows that it depends on the magnitude of the signal. If the signal is very, very clear, there will be no doubt a few months later this will be in the guidelines. If it is not clear, maybe more trials or more considerations are appropriate. We have to see. I think that's exactly right. That's, you know, I think that's really what's informed our design and our thinking about this all along is, I mean, obviously we all wanna see a strong signal. There are, you know, in the design process, there's ways to favor the opportunity to see a strong signal and a clear signal one way or the other, because what we don't want is ambiguity at the end. You know, we really do want a strong signal. I think we took the chance to enroll more patients, you know, overall, as a plan, than we might have otherwise in a more cautious approach. We felt strongly based on the phase I data, and we felt strongly that this trial design, if powered sufficiently, would be demonstrative of efficacy for this drug. Thank you, John. Professor Weller, given the depth of complexity, GBM brings to patients and the medical community, many companies have experienced shortcomings in their drug development for this disease. Can you speak to why you think Berubicin has such promising mechanism of action, and how it differentiates from other drugs both previously and currently under development? I think we both briefly covered that targeted therapy is unlikely to work for the vast majority of glioblastoma patients. Immunotherapy probably has had the challenge of raising the immune response in the brain, and targeting the brain is also the issue for many pharmaceutical agents because they do not cross the blood-brain barrier. Let me quickly comment on that. I mean, in the center of the tumor, this barrier usually doesn't exist. That's why we see these lightening scans with contrast enhancement. What we need to target is also the infiltrating tumor cells. I think the novelty of Berubicin is not the mode of action. We know that this mode of action kills glioma cells. There is no doubt. We know that for decades. The question has always been to get the drug where it belongs, and I think that is the potential chance, and that's the novelty about this compound, that it's supposed to reach the tumor cells hiding behind that barrier. Because I'm so skeptical about the targeted drugs, in my lectures I always talk about dirty drugs. John, forgive me for that, but I think we need drugs that have a certain broad range of activity that are also not prone to develop or cause acquired resistance. I think this is a mechanism now. After years of targeted therapy, we need drugs with a broad spectrum of activity. I think the advantage is it's not too targeted, it's not too ambitious, it's not super fancy. It's an old mechanism that works. It's just maybe better delivery, but it will be nice for patients if it works. Brilliant. Um. You know, maybe you should go on the road for us instead. I know. Yeah. That was excellent. That was fantastic. Really, I mean, you know, we get this conversation oftentimes with investors about, well, you know, why? Why an old mechanism of action? Why chemotherapy? Couldn't it be something sexier? The answer is, as Professor Michael Weller said, the data doesn't really support these sexy approaches right now. The data supports the need for something more broad. Here we have a very clear biochemical hypothesis. We have a very clear understanding of how this drug works. I think we have a quite a clear understanding of how it passes the blood-brain barrier as well, and therein really is the secret sauce. I've said this, you know, many times that we should think about this. You could refer to it as a dirty drug. You could refer to it, I suppose, as a, as a sledgehammer, you know, or a carpet bombing approach. It's not a laser-guided missile, although interestingly enough, its mechanism does really target a specific type of cell in the brain that's overexpressing topoisomerase II, which is really only gonna be these rapidly dividing tumor cells. Yeah in terms of its functionality to get where it needs to go and how it works overall, you know, it is an old class of drugs. It's a very well-understood class of drugs, and I think that actually plays to our benefit, particularly at this stage, where, you know, I've said this many times as I've talked about this situation, you know, and I think, you know, Professor Weller really put a very sharp, clear point on it that, you know, this is an incredibly challenging conversation for clinicians to have with their patients because it's very rapid, it's a lot of really bad news all at once. There's no time to waste in determining the treatment path forward. There may be this sort of honeymoon after the initial therapy, but again, those conversations are gonna return. At that moment in time when sort of the, maybe the penultimate reality of the situation has hit for everyone, that's where we're asking clinicians to have a conversation about our trial with their, with their patients. I think that that conversation is tremendously facilitated by this very well-understood class of drugs. You know, there's nothing that neuro-oncologists, oncologists in general don't know about how anthracyclines behave or what their toxicity is like or what their side effects and what needs to be done to manage those. We have worked with all of our clinician investigators, certainly at one point to amend our protocol to make sure that managing some of those side effects was as easy as possible going forward and would produce the best results. I think all of that has helped us get to this point. You know, as Professor Michael Weller said, I think there's a great, you know, there's a clinical and a biological rationale for this approach. Now the good news is, I think, for investors is that, you know, we are not going to be waiting for years and years to see how this all pans out. We will get our first real look in the third quarter of this year, how things are looking. You know, we expect based on everything that we know about this drug from the past, that we will have a clear rationale to proceed as aggressively to the end as we can. Appreciate that, John. Professor Weller, you're so important for this discussion, so appreciate all your insight, and all that you are willing to share with us. I'm gonna switch before we open to Q&A now to you, John. In your opening remarks, you mentioned your small team, but you have so much conviction and so much passion about what you're doing. I think help our audience understand and speak to the expertise of the team that you have around the CNS table. Sure. you know, it started with our founder who's a, you know, fantastic medicinal chemist, you know, who really solved a very tricky problem that's much beyond my, you know, chemistry understanding, and that is, you know, how does one create a lipophilic anthracycline? he did that, and that was the basis of, you know, the excitement around the drug initially. We then, you know, had a trial that was, you know, in part conducted by some of our scientific advisors that produced some very interesting efficacy data into phase I, which really gave us sort of the rationale to start the company and move forward. speaking from inception going forward from there, we had, you know, a very small team, but we really do have some critical players. I would start with Sandra Silberman, our Chief Medical Officer. She designed this trial. She's been a very strong advocate for GBM. She has incredible drug development experience, both in small and very large organizations, and has put some blockbuster drugs on the market. Gleevec probably being the most well known of those. Sandra is a terrific asset to us. Our colleague, Dr. Don Picker, who is our Chief Scientific Officer, Don is an incredible medicinal chemist himself, and this is a very challenging molecule to manufacture. It's highly cytotoxic, so there aren't that many places in the world where you can do it. When it was manufactured for the phase I, it used a process that is no longer acceptable to regulators. We had some process and manufacturing challenges to overcome to make sure that this drug, if it proved efficacious, could actually be manufactured at scale. We have solved those problems, and that's really thanks to Don's efforts, so we are, you know, well in a position to manufacture this drug at commercial scale, should we have the opportunity. Our worldwide Vice President of Clinical Operations, Zena Muzyczenko, she is really kind of the unsung hero, I would say, of this program, totally dedicated and really is responsible for the nuts and bolts of building this trial out and is the person that, you know, all of Dr. Weller's colleagues around the world interface with in terms of bringing sites online and getting patients into the study and collecting data and all of those things. I think, you know, we again, we have a very small team, but, you know, what we lack in numbers, we more than make up for in passion and focus and skill set. I think we have, you know, we have what we need, and the proof is in the pudding, as I often say. You know, you don't enroll as strongly as we've enrolled if you don't have a great and well-designed and run trial. A great drug, of course. Absolutely. Well, appreciate that. Like we talked about, you've had a lot of key accomplishments with respect to the Berubicin phase II potentially pivotal study. Now we're here, you know, in April of 2023. Can you talk to us, you had mentioned the interim analysis and so forth. Let's talk about more broadly. For the remainder of the year, what can investors expect to see from CNS Pharmaceuticals? Sure. I mean, I think you can expect to see more news about the progress of the trial. You know, we are planning for a future where we, you know, where we go through our interim analysis. We report back to the street, how that looks, we continue on aggressively enrolling. We would like very much to complete enrollment this year if possible. That will really depend on, you know, a number of factors as it always does. That's really our goal. That's really what we're doing. I think, you know, again, more news about the trial, more news about enrollment, hopefully more, you know, news about the success of this drug. Excellent. Okay. We are now going to open up this event for the live Q&A portion of the discussion. To our participants, if you'd like to ask a question, please click on the Q&A button at the bottom of your screen and type in your question, and we will get to as many as time allows. We do have a question. Now that we are approximately 50% enrollment, has data collection begun for the planned futility analysis to be reported in the third quarter? Is this futility analysis the same as the interim analysis that has been talked about during past investor presentations? The answer to both questions is yes. The data collection is an ongoing process from day one, you know, these patients are as well characterized as they could possibly be. You know, I really didn't wanna see any data that might be relevant to this process left on the cutting room floor, so to speak. We're collecting a massive amount of data about our enrollees from the initial... you know, even before they're dosed and in the trial. Yes, it is exactly the same. It's always been a futility analysis. The terms, we use them interchangeably, futility analysis or interim analysis. The result really will be the same. What we're looking at is, you know, are we at least as good as lomustine? Okay. Next question: Can you explain the mechanism by which you're able to cross the blood-brain barrier? Sure. Well, I mean, I can do that, maybe Professor Weller would be the better person. Perfect. Yeah. Let's let Professor Weller explain that. No, this was a joke, you know. I think that you are more entitled to just explain what's available to the public domain. I've only seen the data suggesting it does, but other than it is lipophilic, I mean, maybe that's the explanation, right? It really is the... That really is the explanation. I mean, essentially, what doctor Dr. Priebe did was he, as I said earlier, he created a highly lipophilic anthracycline. So he started with a doxorubicin molecule, and he attached a benzyl group to one of the glycone rings at the center of that molecule. From what I understand, you know, that process right there that I just described, both the attachment process as well as the precise location of attachment, is critical to the outcome, which is creating this molecule that's lipophilic or has a strong affinity to fat. Our brain being the most lipid-rich, fat-rich environment in our body, this molecule has such a strong affinity to that environment that it will bypass the ATP-binding cassette transporter pumps. There's a couple of them there, and you can feel free, Professor Weller, to just go right over me if you want. These are the active components. These are the pumping mechanisms that push out harmful substances, and basically, traditionally, all anthracyclines are substrates of these pumps. They don't go into the brain faster than. They're pumped out basically faster than the heart can pump them in. Berubicin is different in that way because it's so lipophilic. It does bypass these pumping mechanisms, and then once it's in the brain, and this is really my favorite part, that's kind of the, I would say, the critical component of it, but perhaps where it sort of makes a transition from just a very broad spectrum to something of a targeted molecule. In this particular environment, there really aren't many cells that are going to be overexpressing topoisomerase II in the adult brain because we don't have a lot of, you know, rapidly dividing cells in a healthy brain. The only ones that are going to be there are the glioma cells that are rapidly dividing as that tumor is growing. Berubicin is going to have a higher affinity for those cells and a selective uptake in those cells as opposed to healthy brain tissue. That's really kind of how it, you know, how it works from a layman's perspective. Well, I think that was very well done, John, so thank you. Yes. We have a lot of great questions here, so I'll keep them coming. What does success look like from your interim analysis readout, and what data do you expect to see? Well, success for us at that point just means that we are at least as good as lomustine. You know, as Professor Weller has said, lomustine is not a great drug. If it were a great drug, one presumes it might be approved, but it is not. It is what's there and available. I think, you know, for our purposes, if we are at least as good as lomustine, we will count that as a major victory. I really should emphasize that because, you know, the reason we have a standard of care such that we do today involving lomustine is because we don't have anything else that is even as good as that drug. To achieve, you know, parity, or, you know, approximate parity with that drug at this point is a major step toward approval. You know, one would imagine that if we are, you know, better than this drug as we develop more data and go forward from there, you know, as again, as Professor Weller noted, it would be, I think, a very big challenge for regulators around the world to ignore this drug. It would also be very rational step to see it quickly become the standard of care. In order to get there, obviously, to eventually prove, you know, that we are in fact, a better drug, we certainly initially have to show, from an ethical basis for the patients as well as for our really first look, to show that we're at least as good as. That's really what we will be talking about, and I think that, you know, if we achieve that as we expect that we will, that will be something that, you know, every constituent, clinicians and patients and investors, as well as our whole team, should and will celebrate because it is a major advancement for this disease. Sure. A lot of people keeping an eye out for that data. Here's our next question. I think it's a great question. If the interim data is successful, is it possible to go to the FDA to seek approval? Yeah, that's a great question. The answer is, I would say it is a qualified yes. We have a Fast Track Designation with this drug, which gives us a very open line of communication with the FDA, which is great. We have utilized that in the past. Frankly, we utilized it on designing, you know, and choosing the primary endpoint for this study, which I think was very important. FDA gave us very clear guidance on that, which is one of the reasons why we have such a strong conviction that we are, you know, we are on the right track. We can't and, you know, we can't predict the biology, but we know that we are aiming for the target that matters, and that is overall survival. That's sort of the first piece there. In terms of what would we do with this data, well, I think it in part depends on what the data is. Clearly, if we see, not only that we are, you know, at least as good as, but if there's an indication that we may be superior, definitely we will be having that conversation. I think that even if it is just dead heat between the two arms of this trial, we will still be having that conversation with the FDA because as I said, just, you know, to achieve, you know, parity with lomustine would be an achievement at that stage, and it would warrant a conversation with FDA about the second half of the trial. What else do they want to see? Where would the bar actually be for approval? you know, could we, could we be approved at parity? Yes, you know, in answer to the question, we would definitely be seeking a discussion with the FDA at that point. Okay. Our next question, we do have a time for a couple more questions. What age group of patients are you currently enrolling in this study, and are you exploring childhood GBM? Sure. This is a study for adults. We're, we're not, you know, enrolling pediatric cases, but it's definitely, you know, a patient population that we have interest in. You know, there's no reason why this drug couldn't be of use in a pediatric population, so it's not something that we're studying right now. I don't know, maybe Professor Weller, do you want to talk about the, you know, pediatric cases at all and sort of what, you know, what's there or what might be needed? Well, I think, first of all, there is no reason to believe that depending on a certain age cutoff, it's a completely different disease, right? That's not very logical. It's really challenging from the clinical point of view to randomize children, so that's why children are usually taken onto trials at a later step. I think from a regulatory point of view, agencies in the U.S. and Europe will want to see some data on the pediatric population. I think if the signal was clear in the adults, probably a non-randomized smaller series of patients could suffice. I think investigators would support that if there was a clear signal in the adult population. Thank you. Time for just a couple more questions. It seems that Berubicin is an innovative drug with great potential. Does the company plan to evaluate Berubicin for other opportunities? Yes, absolutely. We do. You know, it's one of the advantages of having a broad tool like this. You know, it certainly could have applicability in metastatic disease. You know, there's obviously lots of cancers that are sensitive to anthracycline therapy. We think that there are as a whole host of opportunities going forward for this drug. This would not be, you know, we achieve our initial goal, and that's the end of it. I think actually that would be sort of just the opposite. We really, you know, it probably bears mentioning here that, you know, people have asked, "Well, why, you know, why did you target the toughest of the tough cancer?" There's a lot of reasons that we did that, one of them certainly is from a regulatory perspective. Ironically, this is one of the lowest regulatory bars that you can have because there isn't anything approved anywhere for secondary cases of GBM. One would presume that regulators have a significant incentive to move drugs forward that have promise. I think that explains our very quick Fast Track approval and the attention that FDA has given this program. I would say that, you know, we have taken advantage of that by designing an entire program around this space which is very difficult clinically. We think it's one for which we have a very rational hypothesis to proceed. If we are successful here, it will be in part because of that lower regulatory bar, and that will give us, I think, some speed, to, you know, deliver this drug to the broader clinic that we might not have had elsewhere. The goal has always been from the beginning, see Berubicin approved. We chose this indication for a whole host of reasons. One of them was a regulatory position. We felt like we had something here that could be achieved, in this indication and because of the regulatory environment. Then beyond that, I think things actually get a little easier for us, even if, you know, we're at kind of the hardest place biologically. If that makes sense. Does make sense. Very helpful. For our last question, I've had several people asking sort of a similar question, so I'm gonna combine it to one and try to get everyone covered. First, are you going to commercialize Berubicin if successful on your own? Are you speaking with pharma partners? Are you planning to talk to potential big pharma companies at the time of your interim results? That was kind of a combination of. Sure a few questions. Sure. I mean, I think that, you know, ultimately the decision as to how we do this will be what is in the best interest of our shareholders and patients. You know, how do we bring this drug to the most, you know, the widest use the fastest, and do the best by our shareholders, of course. I think that probably argues for those kinds of conversations, which we have already had several. You know, I don't think you run a trial like this with the data behind it without drawing some attention in our space. You know, yes, we have those conversations regularly, and we intend to continue them. I'm a really big proponent of doing what you can do, you know, better than anybody else, and I think we can do what we're doing right now, which is develop this drug and drugs like it better than anybody else, very efficiently and in a very targeted manner. You know, I don't think necessarily that that includes, you know, commercializing at a, at a, at a broad, you know, scale. That's a whole different animal, there's lots of firms that do that very, very well, and I think would be eager to have an asset like this, you know, in their bag at the appropriate time. you know, there's no necessary need to reinvent the wheel of how you cover neuro-oncology worldwide with a drug like this if we can find a partner where we, you know, our incentives are aligned and our feelings about the program and patients and all of those things are aligned carefully. I have a fair amount of experience doing that. I think that, you know, one of the things we will do at the appropriate time is try to seek, you know, if it's possible for us, the right partner to help us carry this, you know, out to clinical use around the world as quickly as possible. Appreciate that, John. That is all the time we have for Q&A. Just want to thank you both for all the work that you're doing. You're providing so much hope with your work to patients, their caregivers, to clinicians, and ultimately to investors, everyone associated with this. Thank you for all that you're doing. John, before we conclude, I'd like to ask you if you have any closing remarks. You know, well, thanks everybody for, you know, for tuning in and the interest and support of the company. Thank you, Professor Weller, for everything that you're, you know, that you're doing. I really appreciate you taking the evening time in Zurich to join us today, but also just, you know, as a great, you know, as an incredible key opinion leading, you know, oncologist in helping us champion Berubicin and execute this trial. We just couldn't do it without you or without your colleagues. We really, really appreciated it. It is how we do what we do. Thank you. Thanks very much. Wonderful. Thank you. I'd like to echo that, but also thank you both to John and Professor Weller. This has been an amazing discussion. You've given a lot of great insight and information to our audience. I'd like to thank our audience for joining in, asking amazing questions, and your participation today. With that, as a reminder, CNS Pharma trades on NASDAQ under the ticker CNSP. I'd like to thank everyone today. Just as a reminder, if you'd like to check out a replay of this discussion today, you can go to virtualinvestorco.com, as well as see any other events that the company or that the firm will be hosting. Wonderful. Thank you everyone, and a special thanks to John and Professor Weller. Have a great afternoon. Thank you. Thank you. Bye-bye.