Good afternoon, and welcome to the Jefferies Global Healthcare Conference in New York. My name is Ella Rosenblatt with the Jefferies Healthcare team, and it is my great pleasure to introduce Lisa Ricciardi, CEO of Cognition Therapeutics. Thank you, Ella.

First, our thanks to the Jefferies team for including us in the conference. We appreciate the chance to be here. So, I'm the CEO of Cognition Therapeutics. What I'd like to do today is take you through our future program, our next program, which is a registrational program in Lewy body dementia psychosis. We completed a public offering in the fall of 21, so please see our forward-looking statements. For those of you unfamiliar with the company, here's a high-level background. As we indicate here, we're a clinical stage company. We are a drug development company focused, as you can see, on CNS. Our lead programs are in Lewy body dementia, as well as in Alzheimer's disease. Our cash runway takes us through June of next year, and our grant funding, $25 million, takes us through the end of our clinical program. We get lots of questions, and we've had no issues with regard to funding of our clinical trials vis-a-vis grants. Now, if you're thinking about cognition therapeutics, there are several reasons why this is a very worthwhile investment consideration. First, let's begin with the unmet need on the left. People often say Lewy body dementia, and then they try to remember, is that what Bruce Willis has? Is that what Robin Williams had? Okay, this is a condition the size of Parkinson's disease. It's a million and a half patients, and there are no treatments, straight up no treatments. So the first thing to tell you is we're working in an area where there's and a clear objective need. Second, we're data-driven, not hypothesis-driven. With regard to clinical results, we've read out multiple phase two trials. We'll take you through some of that here today. We have an oral profile. Why is that important? All the health equity talk we hear about patients having access to infusion centers and imaging centers. This does not pertain to us at all. Our small molecule is readily scaled up from easily accessed materials we believe will be able to distribute this drug around the world. Now, for me personally, the focus strategy here is the most crucial. When you talk about psychosis, you're talking about a set of indications that are precedented. The endpoints are clear. We're talking, frankly, partnering with the FDA to identify how we will run our trial, what we will measure. Furthermore, as it says here, there are multiple commercial drugs, large drugs in this category. So we believe investors will appreciate the value of that. Last to the right, we have an AD catalyst, a program in Alzheimer's disease, and we'll touch on that in the end. Let's begin by talking about what is dementia with Lewy bodies. People understand it's a neurodegenerative condition, and you're not alone in understanding it. This is something that is under-recognized because it's under studied, leading to it being underdiagnosed. It's a vicious due loop. You can't say that about Parkinson's disease. If you go on clinicaltrials.gov, you'll see 30 programs, and yet this is a very similar size and, in fact, overlapping population. So on the left-hand side of this slide, we'll touch briefly on what the symptoms are. It's the second most common form of dementia. Everybody can say, oh my gosh, Alzheimer's disease, six million Americans and growing, and that's correct. This is a million and a half. This is not rare and orphan. The issue with Lewy body dementia is that it impacts a lot of things at once. Cognition, movement, sleep, and neuropsychiatric symptoms are particularly challenging. In fact, 80% of these patients experience psychosis, psychosis being defined as hallucinations and delusions. And this is one of the most crucial reasons why patients get institutionalized. The burden on the family is very difficult. The burden on the person with DLB is horrendous. By way of background, patients with DLB live four to seven years after diagnosis. Now think about it. It takes a year and a half on balance to get diagnosed. If you're tripping and falling first because the muscular symptoms show up first, you spend six months trying to get to see a movement disorders doctor, by the time you circle all the physicians that are needed to help you understand what you have, you are way into the course of the disease. So it's particularly challenging. Now, why did we pick psychosis per se? Well, as it says here, this is high prevalence. It's an important condition. It's high prevalence within DLB. And there are no approved treatments. Seventy-five, eighty percent of patients will experience delusions and hallucinations. Zero, right in the middle, that's how many drugs are approved. We're pretty excited about being potentially the first to market for these patients. And as I indicated, the number one says that's the reasons why people move out of their homes. If you look on the lower right, the healthcare system, it's hard to believe that something could be more costly than Alzheimer's disease. But as I indicated, these patients are frequently falling and they're in the emergency room because they have a Parkinsonian-like condition. So it's an enormous burden on the healthcare system and for the caregiver. Last vis-a-vis the person with Lewy body dementia, I will tell you that we can all think of people that have Alzheimer's disease, my uncle, my whatever, my grandfather, and they don't remember that they've told you the same story all the time, right? Once Alzheimer's patients get to a certain place, they are blessedly unaware. Patients with Lewy body dementia tend to be on the younger side. You have people who are actively in their careers, 50, 60 years old, experiencing hallucinations, delusions, and all the other neuropsych symptoms without a clear indication of what it is. So it's a very different type of condition. What do doctors do about this? Well, as the headline says, this is a condition associated with a patchwork of off-label drugs. We're not going to go through this. I can merely tell you that of all the symptoms identified on the left-hand column, they're being treated with drugs that were developed for something else, and it has frequently untoward implications for the people with DLB. Now, we've chosen to focus on psychosis, so let's take a look at the drugs available for neuropsychiatric conditions. The existing options are inadequate. Many of these drugs are actually harmful to patients that have Lewy body dementia. When you talk to physicians, and we've done research, they have some degree of awareness about this, but they don't have many choices. And so the bottom line is no approved therapies. Doctors will judiciously use what they can, but there are concerns for patients taking any of these kinds of drugs. Let's talk about our drug. We refer to our lead program, our drug, as zervimicine. CT1812 is what you'll see in the literature. We've published a great deal over the years. This is an oral small molecule drug. We believe that we'll be using a 100 milligram dose, as we have consistently done in many of our trials. It's a once-daily oral drug. Safety profile, very good. You do not expect or anticipate aria based on the mechanism of our drug. Side effect profile was excellent in studies. As for the target patient profile, we will study the groups that we have studied, starting as young as 50 up to 85 years old. Importantly, community neurology setting. If you're on the East Coast and the West Coast, you typically believe you can find any doctor you need when you need them. And then in what the politicians call flyover states, which is where most of Americans live, it's really hard to find doctors and specialists. So we believe being able to develop a drug that community physicians, neurologists can administer will be very important for patients. Then last on symptom focus, as we indicate on the lower right, we're going to be studying hallucinations and delusions. We do have data, however, on how our drug works across all the other types of symptoms in Lewy body dementia, and I will take you through that. A word in brief about the mechanism of the drug and how it works. We affectionately like to say, you know, 20 years of research in about 30 seconds, so let me boil it down for you. On the far left side, we're talking about toxic proteins. Everyone is familiar with A-beta as a toxic protein. Alpha-synuclein is principally the toxic protein here. It's associated with Parkinson's disease and other conditions like Lewy body dementia. These proteins accumulate in the brain. They sit, the oligomers, the proteins accumulate into oligomers. The oligomers sit in a docking station, if you visualize that, which is the synapse. Ultimately, the synapse and the neurons are damaged. We believe that our drug on the far right corner acts on the underlying disease biology. When CT1812 is taken by a patient, that binding of the toxin in the synapse pocket, the affinity is reduced. That is, the toxin is relieved, if you will, from the synapse, and it's cleared through the CSF, and no other toxins bind. So it's a very simple and elegant mechanism, if you will. And what's key is that that happens on the front end of the disease. If you look at amyloid and Alzheimer's disease and all those years of trying to peel out plaque at the end stage of a process, this is the opposite. This is the front end of where toxicity is doing damage. That's where we see our drug working. So we indicate on the lower left, servimicine is different because, well, first, there is no dopamine action. If you're familiar with patients taking dopaminergic agents, it has a very adverse effect on these patients, sometimes causing paralysis, hospitalization, so you need to avoid that. As I said, we act on the early disease biology, and we believe that in, unlike typical or atypical antipsychotics, which in six weeks can have an acute impact on hallucinations or delusions, what we are doing is affecting the underlying disease. This is a fundamental change for the patient, if you will, providing protection, if I may say that. Now, in the middle here, we talk about 86% slowing of neuropsych symptoms. I'll show you that data. But in particular, on the far right-hand corner, 89% slowing of the symptoms of hallucinations and delusions relative to placebo. This is where we had our most important discussions with the FDA. They looked at that data and said, wow, focusing here is one thing, but if you shift here to hallucinations and delusions, you're likely to have the biggest impact. How do we know this? Well, a year ago in January, we read out, as you see in the upper right-hand corner, are our SHIMR trial. This is a phase two study, 135 patients. It was done all domestically. Two doses of drug, one of placebo. Take a look at the assessments. Can you imagine running a clinical trial where you have all the endpoints, all the cognitive endpoints associated with Alzheimer's disease, motor endpoints? You might see that in a Parkinson's trial, UDPRS, activities of daily living biomarkers. This was a large effort to appropriately capture results of our drug on all these symptoms category that patients with Lewy body dementia have. And I'll show you the results here. On the left, I like to think of this as the grand slam or whatever the thing is in golf. I married a big golfer, and when you win all those tournaments, that's what we got out of CT1812 because we had a very important impact on every one of those categories. Let me take a look on the right-hand side of this slide and talk about how you read this. So what we were measuring was at six months, placebo patients declined precipitously. How did patients on drug do? And it didn't matter if we had pooled scores, the 100 milligram scores were identical to this. So on the top line, let me go to the second one, the NPI-12, neuropsych symptoms. I told you we're in the area of hallucinations and delusions. Neuropsych symptoms were measured as a basket. Anxiety, delusions, hallucinations, depression, sleep disorders, irritability, euphoria, apathy, shall I go on? There were a dozen measured, and they were measured for both the duration and intensity of the impact on the patient. And you can see that everything to the right of the dotted line was to the benefit of patients. So that was an extremely important result. The NPI2, right underneath that, is the result when we look just at delusions and hallucinations. Going down, CAF stands for fluctuations. These are people whose motor and cognitive functions vary day to day and hour to hour. You see both memory and mocha, things that you will know from other cognitive trials, such as Alzheimer's disease. UDPRS is the movement scale. Activities of Daily Living, second from the bottom, and the very last thing, CGIC, C-G-I-C, Clinician's Global Assessment of Change. In a word, everything we studied in this trial was much better for patients than anybody on placebo. And yes, we did have nominal p-values in here as well. We were extremely pleased with the results. And as I indicated, on the left-hand side, we understood that we were having an important and profound impact for patients on the underlying course of their disease, all parts of their disease. From there, we've now moved to a registrational program. This is all in the planning stages. What we're looking at is, as I said, the indication being psychosis. We're working with the psych division of the FDA. We met with them a week and a half ago. We anticipate a one-to-one randomization for 100 milligrams of placebo. We're considering a nine-month trial. The endpoint will be the NPI-2 or something like that, and then an open-label extension, of course, to follow these patients over time. So we're in the planning stages. Is this a domestic trial? Is it an international trial? Are there two registrational studies? Is there one single one? All of these very important questions are things we're considering now with our team as we wait for the FDA meeting minutes, which we anticipate having in several weeks. I've talked a lot about the FDA. We've had a very strong partnership with the agency. If we move down this slide, the first box indicates we have an expanded access program. These are patients being able to stay on the drug longer, funded by patients, administered by us. That's an indication of patient preference to be staying on this drug. In January of this year, we had a type C meeting where we talked to the agency in March. We said, all right, our focus will be psychosis, not all the symptoms. It's really hard to measure everything from cognition, memory, activities of daily living, all the neuropsych symptoms. You can't boil the universe. So what we then did was to take a look at psychosis per se. We just met with the FDA in March. Right now, as I said, we're finalizing our registrational plan and preparing to talk to the European authorities. As I said, we're looking at a U.S. trial, an international trial, so we need input on all of that. What I'd like to do is take a moment and step back to show you our Alzheimer's data results. We have a very large trial running now. We chose not to start another Alzheimer's trial because we believed that it made sense to get the readout on that data first, hence our pursuit of Lewy body dementia. This slide I'm showing you on the upper right-hand corner, you see it refers to the SHINE trial. This is a study we read out in 24, 155 patients. This was done internationally, two doses of drug, a six-month study. Our results were somewhat better than the monoclonal antibodies. The antibodies showed 25%, 35% reduction in disease progression, and perhaps people anticipated more, but those were the results. We actually had higher results with an oral drug in mild to moderate patients. Now, the data I'm showing you here, as you can see in this orange bar, says in the median low P-tau population, we knew from Lilly and we knew from ASI that patients with Alzheimer's disease all have elevated P-tau. But when you focus on those with the lower part of P-tau, you see dramatic results. And that's what I'm showing you here. We had a pre-specified analysis. We took the 155 patients, cut it in half, and said, how did those patients do with below-median P-Tau? And what you can see, the orange line on the right shows you a 95% slowing of disease progression over six months. And I always say to investors, think about your mother, father, husband, wife, whoever it is you care about with Alzheimer's disease. What if you could freeze them so that they actually didn't progress in their disease? You can see placebo in gray widening, getting further away. So we think we haven't really seen the full benefit of our drug yet. This was a six-month study. This is a mild to moderate population, as I said. So this was a very important finding for cognition. Now, after Shine read out, Shimmer read out, but in the background, we were running this trial. This trial is called START. Yes, we know there are 25 other letters of the alphabet to name our trials. These are all the S's. The START trial is looking at a slightly different population, more like what you see from Lilly and ASI and Biogen, so mild cognitive impairment early patients. This is an 18-month study. Why 18 months? Because earlier patients take longer to fail. Two doses of drug. One of the most exciting things here, let me clarify. This trial was fully enrolled in December of last year, and as an 18-month study, we anticipate right at this time next year, the last patient will complete the trial, and after two months or so to clean the data, we'll have the results of this study. So we've demonstrated results in mild to moderate Alzheimer's patients. This will fill in the early to mild patient population. An important part about this study, there's an option for concomitant use. We strongly believe, Tony, my chief medical officer, works with the advisory committee, and the thought is, what is standard of care? Well, it changed the minute you had Likimbi and Kisunla get to the market, and we believe that physicians are going to want to know, if I have a patient on an antibody, what do I do with an oral drug, et cetera. In our talks with physicians, they all use the analogy to oncology, and they say, there aren't great drugs for these conditions, so we will mix and match as we see appropriate. If you fast forward in oncology, things are so much more protocol-driven, but that's 20 years of data. We don't have that yet in neurodegenerative diseases. So we have two monoclonal antibodies. We anticipate we'll have more data soon from our drug, and then doctors will better know how might they administer an oral once a day with antibodies when our drug goes through and gets approved. So that is the background on our work in Alzheimer's disease with this very important trial to come next year, the results of the trial. So let me wrap up where I started, talking about cognition as an investment case. We have a lot of external validation I'd like you to consider. So on the upper right hand, NIH, NIA, as a small company, we have received over $170 million of grant funding. That is very meaningful from the NIA, and we consider them true partners in the work that we have done. In addition, at the very bottom, you'll see industry validation, Michael J. Fox, we've worked with, the Alzheimer's Drug Discovery Foundation. It's my firm belief that we would not be working with these organizations if they didn't see high quality, rigorous, scientifically compelling, and clinical results. So that's the first thing I'll say. We're covered by a number of analysts on the street. We have a very strong cadre of opinion leaders that we work with. And I alluded to this earlier with regard to patient demand, the fourth element down there. Our expanded access program started when patients who had been on the Lewy body trial, literally, a wife called me one weekend in the summer and said, oh my god, I'm terrified my husband's getting off this drug what can we do we didn't have the ability to fund it but we've since gotten two different families to provide the funding so that patients could stay on drugs so a different form of validation in the work that we're doing I would conclude by saying we're a data driven company not a hypothesis driven company we're focused on patient convenience getting a drug to patients that have none and a very large commercial category and we intend to get there by working side by side with the FDA as we have done looking at approved precedented endpoints in particular in categories where there are very large commercial products we find that extremely compelling and we hope you do as well so thank you Ella thank you we're done I couldn't tell from the gentleman in the back if we're still recording or if we're good. Great. Are there any questions? If not, I thank you for attending. We appreciate your interest. Thank you. And thank you.