Good afternoon, everyone. I'm Sumanth Kulkarni, a senior biotechnology analyst here at Canaccord Genuity, and thanks to everyone for making it here and also for tuning into the webcast. We have a really interesting company here today, CervoMed, which is also at an extremely interesting point in its evolution because we are looking at a phase II confirmatory trial readout late this year that could redefine the treatment landscape for dementia with Lewy bodies. We have John Alam, the CEO and founder of the company, and also Bill Elder, who's general counsel as well as CFO, here. So with that, I'll turn it over to John to make a few comments and set the stage here before we head into the Q&A. John? Thank you, Sumanth. It's great to be here, and this is our, I think, my fourth CG conference. It's about, just about the last year, a year ago, that we completed the reverse merger that launched, CervoMed. It's been a really productive year. From a business standpoint, we've completed, I think all of our objectives coming out of the reverse merger, we've completed over the last, 12 months. We now have four analysts covering us, including, of course, Sumanth. We raised $50 million. We came out of the reverse merger with a cash runway through to the end of this year, 2024, which covered the phase IIb study results, but we completed a PIPE in March, completed or closed it on April 1, where we raised another $50 million, which extends our cash runway into the end of 2025. There's actually a 100% premium step-up warrant, which with phase IIb results would get triggered and/or would have to be exercised within by mid-2025, which could bring up to another $100 million into the business. So I think from a financial standpoint or a business standpoint, we've achieved all of our objectives, and what that reflects is underlying it, the clinical data, and the program has progressed that much further. We've got three major scientific publications supporting our phase IIa results and where we stand in terms of the potential of our drug neflamapimod in dementia with Lewy bodies. We had, a year ago, just randomized, literally, I think, almost the same day as your meeting, our first patient into the phase IIb trial. We completed enrollment into that trial as planned, in June of this year. And with that, our last patient, last visit for the primary endpoint, efficacy endpoint, will be in October, and data readout, top-line results in December. So it's been a great year. We've built, even within this year, 2024, we've built that much more momentum in the R&D side, on the business side. We're looking forward, going into the end of the year with a lot of strength and going into 2025 with that much more momentum. Thanks for that background. I wanted to see how long we can go without saying neflamapimod. You passed that test. So if you could give us a brief history of the product and what really has changed in the last few years that make this such an almost ideal candidate in the DLB landscape? So the drug is an oral drug, targeting a very specific kinase, p38 alpha kinase. It was licensed out from Vertex Pharmaceuticals by the private company that merged in with a public company to form CervoMed. That was EIP Pharma, the private company, licensed out about almost 10 years ago now. The clinical program initially went into Alzheimer's disease. Vertex had been... This is licensed from Vertex Pharmaceuticals, very different science targeting same mechanism, but acting on the outside of the brain, on the immune system. Because of new science, et cetera, we licensed it out. But the prior Vertex work allowed us to go directly into Alzheimer's disease, where with several different studies, we were able to show blood-brain barrier penetration, target engagement by showing reductions in spinal fluid markers of neurodegeneration and synaptic dysfunction, in AD patients. But as we went through, and we got actually many of our objectives we achieved in AD, but along the way, DLB showed up and, we started a trial, which read out positively. But I think in a broader sense, ultimately, our drug is, and the drug development opportunity in dementia with Lewy Body is actually much greater. We could not have come to that conclusion 10 years ago, and maybe not even 5 years ago, because DLB, as a disease, was less well understood. Our drug and how it acts, we ourselves have progressed that much further, working with some leading neuroscientists. At the end of the day, our mechanism aligns with the underlying pathogenesis and pathophysiology with dementia with Lewy bodies, which is around a very specific part of the brain and the cholinergic neuronal system within the brain. But even more importantly, perhaps from a drug development standpoint, and I would say from an investor standpoint, AD, I think we all know, is just a tough nut to crack. Fundamentally, what the problem is, is that underlying it, by the time a patient has symptoms, even some of the first symptoms, the amount of neuronal death and loss is just too high, particularly in the hippocampus. All you can do is try to slow disease progression, future decline. That takes big trials, long trials. You can never show that in phase II. That's where we ended up, and we had nice biomarker results. We showed effects on neurodegeneration markers. We had nice trends on clinical results, but ultimately, you have to raise the capital to run a big set of phase or potentially two phase III trials to know whether your drug works or not. DLB is very different, particularly in the half or so of the population who are ahead of that tipping point in terms of how much neuronal loss you have. That's the early stage DLB patient population. You can actually make patients better. You can restore function. Our phase IIA data is showing that, if you have the right mechanism, and with our mechanism and targeting very specific pathways within the cholinergic neurons, I think we have perfect alignment there. Again, all of that has come together really within the last even 2-3 years. And though, you know, people talk about AI in these terms of like this gradually then suddenly concept, we've made steady progress over the years, but it's all really come together very nicely in the last couple of years. And I think it just—what we have in front of us right now is really quite good. Got it. Thanks for that kind of walk through history and just fast-forwarding to exactly what's changed. So I'm just gonna make this—this is a bit of an ancillary question, but I think it's important, in the sense that you had a recent, very significant board change. You added an executive chair. What made Josh Boger sign on to being a part of this? Well, so this is Joshua Boger, who is the founder, and for 20 years was the CEO at Vertex Pharmaceuticals, and he was my boss some years, years ago. He was actually an early investor in EIP Pharma, and when it was in LLC. He's followed the story very closely, even his first investment, you know, he read the 20 papers that he asked of me, and I provided, followed it all the way through. And I think it's very much, again, what I said before, of just everything coming together, and as it came together, he, we had a discussion, and he said: "I think there's something very compelling here that needs to be moved forward. Can I help you?" You know, we had the discussion, and it is what he provides is that additional perspective of where we're going to be going beyond the phase IIb trial. He's built a major company, one of the truly major companies in our space. And there's a perspective and background he can provide. He has a network, but it's deeply rooted in who he is. He is a medicinal chemist, he's an R&D guy, he has a vision of, you know, helping as many patients as he can, and we fit that for him. So this is not so much an investor question on what kind of misconceptions might be there with DLB and AD, and things like that, but more of a, I guess, a scientific question in the sense that when you walk the halls of AAIC, which is an Alzheimer's conference, another, like another Alzheimer's conference, like clinical trials in Alzheimer's disease, what is the main thing that people who kind of are in the know like about your approach, and what are the key sources of controversy about the approach? So I think, again, what's come together very nicely in DLB is that DLB is just recognized as the disease of cholinergic deficit, a deficit of the neurons that produce the neurotransmitter acetylcholine. In AD, there is also a perspective that there are groups of people who believe that its cholinergic deficit is a core part of that, particularly early and needs to be addressed, but it's much more controversial. That controversy doesn't exist in DLB, and I think that a little bit of that, again, five years ago, you would not have necessarily gotten that perspective. But now it's very clear there's a set of studies using MRI, also a very specific PET ligand of the cholinergic terminals, that shows that in DLB is a disease of cholinergic neurons and dysfunction and degeneration of those neurons. And that has been, I would say, in the last two years of these meetings, it's just very clear. We get incredible support in that regard, and I think you see it in the in our clinical trial results or in the progress we made in terms of enrollment. There are 22 Lewy body centers of research centers of excellence. 14 of them were in our phase IIb trial. There are, we had the three top centers in the UK, which are, two of them, I would say, are the two of the three top centers in the world. They were in our trial. There's incredible enthusiasm around this drug and mechanism because of the science we have, the preclinical data, and the clinical data as it's coming out. And so I think that I don't see much controversy actually in with neflamapimod in DLB. Cool. So you have a very elegant scientific approach. You're clearly testing this hypothesis with your confirmatory trial here. What do you think, other than simply vagaries of clinical trials, what do you think the key risks are as we approach this readout? I think that we have done as much as anyone has done in our field in terms of the scientific risk. I think as we had discussed last fall at CTAD, I really felt that our primary risk in the phase IIB trial was actually operational. We were the first to actually target an early-stage population and enroll them. There was some sentiment out there of, you know, what, how feasible was that? And that I fundamentally felt was our biggest risk, and I think that we have shown that we could address that. And the reason that turns out we could address it, it actually turned out to be less of a risk than perhaps even we had thought. Because it turns out that most patients in the mild dementia stage actually still are in the early stages. They don't have elevated markers of neurodegeneration being more advanced in terms of the neuronal loss in the hippocampus. So, which I think actually bodes well for commercially as well as we look out long term. It is truly that DLB, you know, the bias in AD is that you need to go to an early stage so early that you have two problems: one, you can't find them, and two, even when you find them, they don't have enough deficit to be able to get a clinical signal. That's not true in DLB. It is, of the diagnosed patients, at least a half of them are still in the early stages, but these are diagnosed patients with dementia with Lewy bodies, so there is a clinical deficit, so you can actually treat them. Again, that I fundamentally believe, though, was our main risk, and we've overcome that. And then, otherwise, in the business, I think during... it's always financial risk, which we have, again, with the PIPE, with the warrants that are at a 100% premium, I think we have addressed to a great extent, and but it's always there. And then, as we look into 2025, it's going to be continuing operational risk in terms of just we have to scale at that point. Bringing in people, recruiting, integrating them, and in real time, as we're progressing the clinical program as well. But if you look at our phase IIA data, which I know you have in great detail, you know, we have positive in the overall ITT analysis. We were able to use the blood biomarker, p-tau181, to identify the more advanced patients, and when you look into the data set, that the results in the overall ITT analysis is really driven by the half or so who are in the early stage. And therefore, fundamentally, the result there, the magnitude is double. We're doing everything that people are asking for is, that, you know, in clinical trials, they said, "How do you get the maximum efficacy signal?" And that's what we're doing there. We have biomarker results, with GFAP, glial fibrillary acidic protein, which is a really sensitive marker of neurodegeneration, where we saw an effect there. We have an effect on EEG. Collectively, very consistent data, multiple endpoints, biomarker, EEG. You know, I think we've done as much as one can do, and... But it is all going towards getting rid of the black box that I think a lot of CNS drug development has been in, where you just blindly go into a broad population and see what happens. Which to some extent, we did in phase IIA, but we've been able to use all the tools available to us now to really, optimize the outcome, for, for the phase IIB trial. So it's always difficult to answer a question on behalf of others, but I'm gonna try to draw up on your pharmaceutical experience here to answer this one. Now that we have more of an evolution of understanding around how DLB works, what you might need to actually target it, why have we not seen more efforts from biopharma to target this? Is it because of distraction with Alzheimer's, which, which is a much larger indication? 'Cause DLB is not a small indication by any means. So it's primarily that, I think distinction with Alzheimer's disease. But it's also everything that I've said again about DLB. So for people who are not familiar with the company, we had a nice KOL event about three weeks ago. That's on our website. It's worth listening to. We had a leading neuroscientist as well as a clinical translational person, John-Paul Taylor from the U.K., that talks about all of this, and but you can look at what they presented and where they had their references. Many of them are from the last two years. So this is. It's really developing very rapidly, and R&D programs that get laid out years in advance. What you're seeing in the clinic is often 5, 6, 7 years ago. I think people are going to get there, but they do have to come back to the cholinergic system. The bias... Because of Alzheimer's, the bias in some ways is still towards thinking about the aggregated protein, which we are downstream of, but I think it is more important to think about the downstream consequences. The other part is, much of the pharmaceutical industry has gone towards proteins and antibodies for all sorts of different business and reasons, and not necessarily because of technical. In the brain, and for a lot of what they're talking about, you have to get into the brain, and you have to get inside the cell, inside the neuron, and I think that's primarily a small molecule problem. Got it. So I'll get Bill involved here. Now, we have this molecule that's been around for some time. It is going to be a new chemical entity ex when it's approved, but how are you thinking about the patent landscape here and the defensibility of that landscape? We're very confident. As John mentioned, the drug was licensed out from Vertex in 2014. The composition of matter patent has expired. It had at this point expired, but over the years, we've developed a suite of formulation and method of use patents to cover sort of just cognitive function in general, working down to DLB specifically. So we feel very confident in the portfolio that we have, that we'll be able to protect the asset at the commercial stage. We're continuing. We have applications pending right now, so we're continuing to expand that portfolio. All of the IP that is currently active is wholly owned by the company, so we think it's a strong position. Got it. Particularly, given the lack of other drugs you mentioned are being developed in this space, feel we have a very strong ring fence. Going back to your clinical trial strategy and biomarkers, you've had biomarkers even for patient enrollment, like p-tau181, things like that. How important do you think biomarkers will be in an eventual strategy to get this product approved? I think that... So it depends on the claim. So the main claim of our drug in DLB is going to be around our primary endpoint, the CDR Sum of Boxes, which is a global measure of dementia or specifically cognitive function. I think that will be the main driver of effect in terms of biomarkers, and this is GFAP and maybe MRI and looking at the size and volume and functional connectivity of this part of the brain that we're targeting, the basal forebrain. These are all things that can more solidify your position in terms of disease modification and long-term outcomes, which may be more important ultimately towards market access and positioning as much as necessarily approval. If we came to some potential aspect around an accelerated approval, then a biomarker would become more important. But in terms of the main strategy, it's really the primary endpoint in the phase IIB trial, and of course, it would be supportive to have biomarker data in that regard. Got it. That moves us to the primary endpoint here, CDR Sum of Boxes. It is a dementia rating scale. It's not Alzheimer's, right? It's dementia rating. Absolutely. How well suited do you think it is specifically within the DLB context? I think it actually. So there is a—this is another place where all the Alzheimer's work has kind of created a certain kind of perspective, which is that, yes, what you're implying is there are—you will hear sometimes CDR Sum of Boxes is an AD scale, and the reason for that is because so many more trials have been run in AD, and it has become established as one of the endpoints there. We're one of the first trials that have actually used CDR Sum of Boxes as an endpoint in DLB, and certainly, the phase IIB we're running is the first one where it's a primary endpoint. But the data we have says that it's an endpoint that works fantastically well in DLB, and there's some data that's been recently published that would argue that it's actually better in DLB than in AD. For a mild dementia population, the scores on the CDR Sum of Boxes are actually higher, which is worse than in AD, and particularly on the functional endpoints. DLB is a disease. The nature of the dementia, the cognitive deficits, has more direct impact on socialization, so community affairs within the CDR Sum of Boxes, personal care, the things that matter on quality of life and functioning and day-to-day functioning, and that actually shows up in the CDR Sum of Boxes. So in my mind, the CDR Sum of Boxes may actually be better suited for DLB than it is for AD. And our trial data is showing that. But there's also, just very recently, a publication came out on long-term progression. This is the NACC longitudinal database, where CDR Sum of Boxes actually was their main tool for following progression over time, and actually did that very, very well. We have a few seconds, so I'll end with the hot-off-the-press kind of thing. You recently filed your 10-Q. You had a disclosure on that about a trial that you initiated in Strasbourg, France, with the 80 mg BID dosing paradigm. How is that gonna help you in your future plans? So, it's serving two purposes. One is that actually it's our first trial in France, which actually opens up certain opportunities down the line if you have positive phase IIb data in terms of, they have an approach to be able to get early access to patients where you can actually commercially sell the drug. Mm-hmm. But then 80 milligram BID is just in. We don't think that. So there's a potential for a BID regimen in that, which could be helpful in the DLB patient population. The dose we have right now, we think is an optimal dose. TID is. There's really no issues with that in the DLB patient population. It's given with food, so just given every meal. But there may be some patients that may want a BID option. We think that 80 milligram BID can get there, but it has to reach a certain C-trough level, and we have no PK data. Right With that regimen, and this is an approach to be able to get that data. And then it sets us up otherwise for additional indications where BID may be more suitable.