Okay, keeping on going here, we have CNS Pharma, John Climaco, CEO, ticker is CNSP. And if you go back to our research, a lot of you have it already, we recently upgraded this stock in early September. I'm sure John remembers. Yes, we do. So the reason for that, our views of their lead drug, Berubicin, had never changed. Over a couple of years, they were in this cycle of as a perpetual financing overhang, very challenging. Biotech sucked, for lack of a better word. It was just made it impossible to have an anthracycline there in glioblastoma. It's like a triple whammy across the board, right? John's done an incredible job, we think, over that time, navigating the company, basically threading needles to keep it financed and keep their pivotal stage trial, or potentially pivotal trial, in glioblastoma going. Over the summer, they're able to raise enough capital through a variety of mechanisms, mostly through the ATM, to get enough cash to get to the end of the trial. So now you have the company in a position it has not been in in quite some time. It's well-funded for the rest of getting through their data, which is coming in 2025. And there's a low bar in glioblastoma, especially when you're going up against Lomustine in recurrent disease. Our view is that there's a pretty good probability they can have success here. So CNS is at... It's not at the bottom, but it's at the best position it's been maybe ever, and I think it's a good time to hear from John. I don't know if I kinda butchered that a little bit, John, but do you wanna give us, like, a synopsis of the company and why people should be excited about it, you know, right now, whereas the last couple of years have been a little bit challenging? Yeah. No, you didn't butcher it at all. In fact, I think you hit it right on the head. You know, we feel internally, despite you know, where the stock price is right now, that we're in the best position that we've been in for probably ever. Primarily because, you know, as you say, we've finally taken care of this epic financing overhang that's been there for years through this challenging, you know, biotech marketplace. I've heard you talk today about this, you know, and how difficult it's been. We have threaded the needle. It's been painful at times, but, you know, the... I've always said the only way that we really create lasting shareholder value is by getting a drug approved. And we are finally financed such that we can complete this trial to what we believe will be pivotal data, foundational to a registration. And, you know, and our trial's fully enrolled with Berubicin, so we're really kind of in a, you know, in a wait-and-see right now, but not waiting for very long. We anticipate that we will, you know, lock the database, sometime, you know, probably this year. And we're, you know, we're looking out into the first quarter again, as when we will be releasing top-line data, and we will see, you know, what the largest GBM study in the world right now, that we're aware of, will tell us about this drug. And, you know, it was designed from the beginning with guidance from FDA to be a pivotal study. And, you know, excuse me, a study that, you know, that focuses on overall survival, that pivotal endpoint that they need for registration. And I think that's what we've done. We've said for a long time, you know, of course, we can't promise what the results will be, but we can absolutely promise a definitive answer on this drug. And we feel extremely confident that the study is powered for that, designed for that, and we will be presenting some really compelling data for a situation that is, you know, abysmal for the patients. As you say, the bar is quite low here, really. There's really nothing effective. You know, I say it many times. We don't even have a one-size-fits-most solution for these patients, let alone a one-size-fits-all. Berubicin is an incredibly exciting drug, you know, coming from the anthracycline class, so very well understood, very well trusted. Oncologists know how to use these drugs. They know their limitations, and they know their effectiveness. Regulators know that as well. What's so special about this drug, of course, is that it, you know, passes the blood-brain barrier, and there are no other anthracyclines that do that. You know, and as I think you note in your report, and we've said many times, you know, this looks like this is a non-cardiotoxic anthracycline as well, which is really a breakthrough. There isn't another drug like that out there right now. There's some potentially in development, but, you know, this one is really close to demonstrating pivotal data in a disease space that really needs it. So we're thrilled right now. We're really excited. You know, we wish the market was recognizing that a little bit, but, you know, we've faced headwinds pretty much since the word go in this disease space. I think everybody assumes that because everyone has failed in GBM, everyone will fail, and we just don't think that's the case. We've taken a very logical approach to this from the beginning. We've got a class of drugs that we know is effective against these type of tumors. Our job was to prove it, and I think we're gonna do that. There's one other in development that has no cardiotoxicity. We know what that is- ... but they're completely different. This is not for the brain- Right ... they're going for, and they're giving big doses, right? Good for them. It's amazing, by the way. It is. It It is. But people hear anthracycline, they're like, "Oh, boy!" Like, you know, they get nervous. Just, just help everybody understand a couple of things. One, your dose is extremely low. Cardiotoxicity shouldn't be an issue. It's never even come up, anyway. Two, even if it did, you're talking about glioblastoma, recurrent, and life expectancy here, so you have to weigh the risk-reward. You're worried about a heart failure, you know, two years down the road, or can this person be alive with their family for another six months, or whatever the number's gonna be? Right. Can you talk about those two things, that aspect? Sure. Sure. You know, first of all, Berubicin is. It's a very potent drug, you know, derived from another anthracycline. It's about 10X that potency, so we can afford to give a very low dose and still see treatment effect. We saw that in the phase I, you know, very exciting data that supported the start of this study. So we're pretty confident that, you know, we have an extremely potent and still very effective anthracycline. You know, we've used some extremely sophisticated measurements for cardiotoxicity. We look at troponin levels for all the patients, you know, during the study, and we've just seen nothing. So, you know, obviously we're not making that claim right now, but, you know, the data tells us that this is a beautiful drug in that regard. And you're right, that even if it were not, you know, we're looking at a cost-benefit for these patients who are, you know, whose life expectancy, you know, is very, very short for recurrent and relapsed GBM. And, you know, versus a potential problem, you know, from toxicity that might not manifest for 10 years. So I think the cost-benefit analysis is clear for these patients even if we're not able to achieve that claim. But you know, we believe that we will be able to achieve a claim of non-cardiotoxicity and removing that black box label from the anthracyclines that they all have. What makes that so exciting is, you know, that's really part of our vision for this drug. You know, I talk about a pipeline and a drug, and that's really what we have here. Because as you can imagine, right, if you have a space where you have a non-cardiotoxic low-dose anthracycline that's blood-brain barrier penetrant, suddenly a whole host of opportunities opens up for utilization of a drug like that- ... where, anthracyclines, you know, traditionally just don't go or aren't effective because those patients are gonna hit the lifetime maximum dose before we see any effect. Let alone those patients that have metastatic disease to the brain, who can't use an anthracycline because there aren't any available today that penetrate the brain. So we think on that front, we have, we really have, you know, an amazing drug that was designed to do something very specific and very much needed, but has the ability to open doors to do all kinds of stuff in the future. So we started, you know, with the place where we felt the clinical need was the greatest, and the regulatory bar was the lowest, and that's GBM. I think that we've got a study that's designed and powered effectively to answer that question. When we succeed there, which we're quite optimistic that we will, we intend to take this drug, you know, as far as it will go. Before, I guess, we get to the trial that's going on now, is the name of the company implies, right? CNS, right? So you're doing other things or have ambitions to do other things beyond glioblastoma. Maybe you could talk a little bit about what other indications, including, you know, if this trial is successful, moving to front line, first line glioblastoma, maybe at least in unmethylated patients where temozolomide has... this won't work anyway, starting there. Yep. You know, your thoughts? Yeah, I mean, you've got it, right? So as I said, you know, we don't have a drug today, you know, in the pharmacopoeia that's one size fits most, and it's really those unmethylated patients who are the majority of the patients. 60% of the patients don't have an effective first-line chemotherapy drug. So, you know, if you wanna have another really chilling conversation about GBM, talk to neuro-oncologists in Europe who send their patients to hospice directly from radiotherapy. It's just horrible. So, you know, we have a drug that's not affected by methylation status. Now, you know, this trial is aimed at second line. However, you know, I don't think it's a big leap to say if you have a drug that's not affected by methylation status and is proven safe and effective, that it would, you know, it'd be able, in the clinic, to quickly step up, in utilization to fill that void for those 60% of patients that don't really have an effective drug for them today, first line. I would imagine that, you know, we'll have a lot of support in the neuro-oncology community, in our, you know, community of 45 PIs, you know, here and in Europe, who would love to investigate the ability of this drug to make a difference for those patients. I would imagine we'll see the drug used in that way, potentially even before that happens, simply because the need is so clear and obvious, and there really wouldn't be any, you know, barriers to the utilization of this drug in that way. So we think that there's a great future in GBM, expanding beyond potentially second line, where we're aimed right now, into first line, at least for the unmethylated patients. And then beyond that, you know, the sad case is we've got, you know, a number of cancers, you know, that have very well-known metastatic pathways to the brain. Once those cancers metastasize in that way, you know, those folks have the same treatment problem that the primary, you know, brain cancer patients have, which is that now they've got a tumor growing inside the blood-brain barrier, and their chemotherapy options are extremely limited, and all come with, you know, a host of problems associated with them. So we think that, you know, we've got the opportunity to look at some of those other anthracycline-sensitive cancers and, you know, and expand the utility of this drug in that way. We chose, as I said earlier, from a regulatory strategic perspective, to approach that place where the clinical need is the greatest and the bar is the lowest. But there's lots of other places that we can go with this drug, and that's really what I loved about it from the beginning, is that, you know, as I say all the time, this is the hammer in the oncologist's toolkit. We can finally give it to the neuro-oncologists. And this is really... You know, perhaps we haven't emphasized this sufficiently, but, you know, this really is a targeted therapy. It's an organ-targeted therapy. This drug targets the brain. It targets tumor tissue above- Because the brain gets perfused so quickly, but most of the blood goes right to the brain first, and then just takes all the drug out, and then there's really not a lot. That's right. Yeah. That's right. Exactly. So, you know, it's just a really elegant, clean, and simple solution with a 70-year track record in oncology that we're now going to, you know, build upon. Just going back to the phase II, it's fully enrolled. Can you just talk about that? It is comparable to some of the larger GCAR trials. And then what you guys observed in that phase II interim look. Sure. So, so 252 patients in 45 centers in eight countries. It's been fully enrolled since late last year, I think it is. So we did that in, you know, in two and a half years, which we're very proud of, and I think that really speaks not just to the trial design, but to everything that we just discussed about the drug. You know, this is really, you know, I think to a neuro-oncologist, this is the solution that in many ways they've been waiting for, that one-size-fits-all foundational chemotherapy solution. And so, I think they've responded in kind by, you know, by bringing their patients onto this study with confidence. You know, what we saw at the interim look was our DSMB giving the thumbs up for the study to proceed without modification, which, you know, per the trial design and their mandate, that was as good an outcome as we could have. That was really telling us that, you know, the DSMB was charged with a look that we did not see. We were not, you know, unblinded to their look and, but they could see everything. They were charged with looking at both safety and efficacy and in combination, they came back and said, "Proceed." So we were quite pleased with that. We take that to mean that, Seeing enough, right? There's enough separation there. I think there is. There we see there's enough separation. They see signal, they see treatment effect, and they see an excellent safety profile. And all of that sounds a lot like taking a big step toward, you know, an approvable drug. And so- We could try the tea leaves- We charge forward. All right, we like to do that in analysis. So- Right. When did you fully enroll? If I'm remembering correctly, I think- Was it April? Was it March, April? It was April, March or April. Sorry, I- Okay. So, so what's the expectation for the Lomustine? So very important in this trial is that, one, there's no standard of care or best available therapy for recurrent disease. They kinda use whatever they wanna use, but you, you're going with Lomustine, right? So you have a very defined control group. What's the expectation for outcomes in those patients? And are you kind of at that mark where we could say, like, the blinded data is kinda moving past where that benchmark for Lomustine might be? That's certainly what it appears to us. You know, I mean, you know, we've said if we were in the 20-25% improvement range on OS above Lomustine, which is 4-6 months, you know, we're well in range for, you know, for an approval. We think, you know, that the safety profile is outstanding, of course, 'cause this is obviously a question of both safety and efficacy. And, you know, with anthracyclines, that's not necessarily a given. But with this one, I think that we've proved that this is a very safe, very well-tolerated drug. You know, based on what we can see, and you know, reading between the tea leaves without you know, promising anything, you know, it certainly appears you know, in this large data set, which really does you know, compare to any trial that we're aware of, that there's a separation there. One of the things that we did you know, at both before the interim and then again after the interim was you know, we had our biostats team take a look at our stats and the trial powering. You know, my sort of personal nightmare was that, you know, we'd somehow get to the end, and everything would look great, and we'd just fall a little bit short, on the power. And, we were really shooting, you know, high on that, and we feel like, based on, you know, you know, reviewing everything three different times, top to bottom, that this study is very adequately powered, to prove, you know, an improvement in OS. I don't know if you have the answer to this. I'm not expecting you to but- Okay ... but it, let's just say, so the FDA has communicated with you guys that this should, or you designed it to be registrational, potentially serve as register. which is not outrageous, given the indication you're in phase II trials, you know, that that could be sufficient. Right. What happens if you're not successful stat sig on improvement in OS over Lomustine to control Lomustine arm, right? But you're numerically better, you're even non-inferior, you're a safe drug. Is there a pathway where, hey, you're gonna give neuro-oncologists another option with this drug? It still has legs. It's not done. In recurrent, it's impossible. I mean, you know, it's so hard. It's very hard. Is there still something there where they say, like: "Okay, maybe you get an accelerated approval, and maybe move to another line of therapy"? Is that anything you guys have thought about? We have thought about that, and, you know, without going into it too much, let me just say that we have thought about various fallback positions that can move this drug forward if we fall short. Now, I mean, I wanna be really clear, again, based on, you know, what we can see which is really, you know, far from everything. We're not too worried about falling short, but if we did, for example, you know, we've got two very distinct patient populations that we have in our study, the unmethylated and the methylated. The unmethylated, you know, not only have a different response, you know, to some of these drugs, but their clinical need is totally different. And I think that in discussions, you know, with regulators, that may very well play into, you know, how this drug proceeds forward if we don't make our primary endpoint, which I think that we will. But if we didn't, we do have to remember that, you know, if this drug is even comparable, you know, to Lomustine, there's definitely an option here for those, you know, those patients first line who have nothing. They're- Yeah. Those patients, of course, you know, second line is academic for those patients 'cause they're not really getting anything effective today. And Lomustine, I think it's really important to note, I've said this before, It's nasty stuff that- It's really nasty stuff, and it's kinda nasty stuff for not a whole lot of benefit. And not only that, you know, I know you guys know this, but you know, Dr. Weller in Zurich, who wrote the, you know, the paper supporting Lomustine, he's one of our investigators. And the interesting thing about that data is that, you know, his studies back in 2018, I think 2017 and 2018, included astrocytoma patients because what we now call those patients astrocytoma patients, but at that point, they were still classified as GBM patients. Well, that's an easier-to-treat disease that's gonna respond more favorably to Lomustine treatment. So those studies, which still didn't rise to the level of approval, were obviously unintentionally seeded with easier-to-treat patients. But we've taken all those patients out. These are only GBM patients today. So our expectation is that, you know, when we sift through all this, we don't even think Lomustine is going to perform at the level that the literature would suggest that it has in the past. While Berubicin, of course, we have tremendous confidence in its performance. So, this is a different animal for Lomustine. This is really the first time that Lomustine has been tested in what we would call GBM patients today, as opposed to what we called them, you know, five years ago, six years ago. So we actually think that Lomustine has a harder, you know, hill to climb, if you will, which of course tees up Berubicin to look even better. Because those astrocytoma are there, though, in that study, six to eight month median overall survival might be skewed lower, right? If you take them out, maybe it's four to six, three to five, something- That's right. Unfortunately worse, but, you know, maybe beneficial to Berubicin in this trial. That's right. And what's- Are you powered to what on the Lomustine arm, over? I think both are 85%, so- Six months - I mean, one month. Oh, on a month? You know, what are we looking at? I think I gotta get back to you on that. Yeah. Yeah, don't say if you're not sure- Yeah ... at the moment. Yeah. Okay, Chad, you were, you had a question. Yeah, just quickly, I was wondering, you know, with the other GBM asset you guys brought on, TPI-287, in July, how does that complement Berubicin, and what's the clinical development plan there? Yeah. So, so TPI-287, we're really excited about. You know, look, I'm a super big believer in sticking to your knitting and doing what you do best- ... better than anybody else. And we're really good, I think, at developing, and clinically testing cytotoxic chemotherapy for neurooncology. It kinda limits the scope of what's actually exciting that might make sense for us to get our, you know, our hands on. And, we looked at a ton of different compounds. And, you know, the bar was pretty high 'cause Berubicin had great data coming into our work, and so we were looking for something that looked at least that good, and the field gets pretty small, pretty fast. So we were looking for something that would be complementary. We were looking for something with a different mechanism of action. We were looking for something with great, you know, data, and we found it, you know, in this novel abeotaxane. So totally different, you know, mechanism of action, you know, microtubule dynamics inhibitor. We think that the fact that it has a different mechanism of action separates it, of course, from Berubicin, makes it complementary. There's no reason that, you know, one would impact the other. We've always said, I think all the leading lights in the field have said, you know, there's not going to be a single silver bullet in this space, and as good as Berubicin is, you know, it's not gonna be a silver bullet. We're gonna need to fire multiple shots at these tumors to extend survival, you know, and maintain quality of life as long as possible. So we have another drug there with a different mechanism of action that has an excellent safety profile, extremely solid, recently published data on its phase I where there were just excellent overall response rates and overall OS data. So in terms of clinical development, you know, we are still working on the initial program and what we're gonna do there and our approach to FDA. But I would say that, you know, investors could look at what we have done with Berubicin and the clinical network that we have built, and the efficiency with which we've run this trial and the speed that we've run it, starting from, you know, a standing start with no investigators, no facilities, none of that stuff. We have all of those things now here and in Europe. So I expect that the program will be accelerated by virtue of our ability to repurpose all of that clinical work that we have done. You know, we're gonna be having a sort of all-hands, several-day, you know, team meeting next month on our Berubicin efforts, what we've learned, what we did right, what we could do better, and how we're gonna go forward with, you know, with TPI-287 in the clinic. And I expect that we will have, you know, some events before the end of the year, where we can talk with more, you know, specifics about what that program is gonna look like. But in general, I would say this, you know, I, I was biased from the beginning toward an aggressive approach with Berubicin. I've said it many, many times, you know, colloquially speaking, we knew going into this program that Berubicin worked. We know that this drug has positive impact on these tumors because we can see it in the phase one. We know what these drugs do on the bench. The trick is getting them across the blood-brain barrier, and we know that Berubicin does that. We know a lot of the same things already about TPI-287, so I am inclined to take a similar approach, that being an aggressive, you know, large trial, like what we've done with Berubicin, and push TPI-287 as fast as possible toward registration. I think that in this disease, you know, one of the few things that we have going for us in studying this disease and these drugs is that GBM just doesn't resolve spontaneously. There's no mystery or gray area about whether you're having an impact or not. It's really just a question of magnitude of impact. If you see people living longer, it's probably some degree of treatment effect. Because otherwise, the sad fact is they're going to expire. And so, we've seen all that with TPI. Now the question is: can we prove it, and prove it to the level that will allow for registration? I think the path to doing that, both in time and money, that's most efficient, is the kind of trial that we've conducted with Berubicin, and you know, we know how to do that really, really well. So I think that's probably what we'll be doing. But you know, I always default to Dr. Silberman and Dr. Picker on that. They are really you know, the experts in doing this, and so... but I think investors can look forward before the end of the year to a lot more clarity and detail about you know, our approach with that drug. Don't go to sleep on CNS. We're out of time, John, but, you know, it's. You know, we're hopeful that the trial works. One of the best CEOs I ever met in biotech, when he redesigned a trial or just whatever it was, I'm like: "Well, is it gonna work?" And he said, "I have no effing idea." That's verbatim. And he's like. And it was the most honest answer I ever got. He's like, "I think we did everything that we could do to give it the best chance for success, and I'll just leave it there." You know, as analysts, we can try to be predictive, and if you go back and you look, April was the last patient, right? And if the lomustine arm is really six-to-seven months, you know, it'd probably be less than that if you take out the astrocytoma patients from that data. Be conservative and say six months. That last patient, that's right now, October. We're at six months, but you can't even start counting from there. That's just the last patient. You have to go back further to really- That's right ... see that, where that overall survival number really is. It's reading tea leaves, and in biotech, it's who the heck knows, but I think everything is as good as it could possibly be for CNS right now, heading into its data, you know, over the next six months or whenever it's gonna be, so take a look at CNSP. John, thanks for coming on, and we'll have you back- ... hopefully talking about that trial outcome. So- Yeah, we're looking forward to it, too. Really appreciate, you know, all the good questions and the great report. You know, look, we're in the same boat. You know, ultimately, it'll come down to the statistics, and we don't know what that'll be, but I think we've done everything we can to tee this thing up for success. So we're, you know, we're anxiously awaiting turning the card here. Thank you so much. We'll catch up with you soon. Thanks, Chad. Sounds good. Thanks, guys. See ya. Okay, bye. Hey, welcome back to our last panel of the day. I'm Chad Yahn, Senior Biotech Associate, joined by my colleague, Joanne Lee. We're pleased to have with us Immuron. We have joining us, Steve Lydeamore, CEO, and Jerry Kanellos, CSO. Immuron is focused on developing and commercializing orally targeted antibodies for the treatment of infectious disease. We don't currently cover the company, but they are not here by accident. There's been a lot of really interesting things going on, even just in the past few days, with the company. And we think it's something worth taking a look at. So with that, I will turn it over to Steve.