Good afternoon, everyone, and thank you for joining the 2026 HC Wainwright 28th Annual Global Investment Conference. My name is Dr. Jay Montgomery, an associate research analyst at HC Wainwright, and I'm happy today to introduce our presenter for the next session, Lisa Ricciardi, CEO of Cognition Therapeutics. Lisa? Thank you. Thank you. Thank you all for coming. Appreciate it. Why don't we begin? Public company going back to October of '21. For those of you who are unfamiliar with the company, here's a snapshot. We trade on the NASDAQ. We're located in Westchester. Clinical stage company. So programs are in dementia with Lewy bodies. We anticipate beginning a phase three program. That's what's next for the company. And Alzheimer's disease, we've completed a mild to moderate study and we have a program reading out in early Alzheimer's disease this time next year. We'll be right back on this stage with great results. We hope. Small company, 12 people, well leveraged. With our team, also as you see at the bottom, we've received 170 million dollars in grant funding, believe me when you're a small company, looking at the overhead, that's been extremely valuable for us. Cash to the end of next year, 21 million point 21.6 million. People often ask in this environment, well, what about your grants? Are they safe? Yes, they're safe. And this 21 million is the balance of an 81 million dollar grant that is covered our work in Alzheimer's disease. Here is our lead drug. It's called Zarumicin CT1812. This is the only mechanism, I will explain here, this blue molecule on the top. Oops, I should be pointing up here. Is the drug. It binds to these two proteins, the sigma two receptor, TMM97 PGRMC1. What does that cause? What it causes over here in the oligomer receptor, it causes reduced binding affinity. So amyloid alpha-synuclein might otherwise dock here. But they don't. And oligomers that are bound are released. So people often said to us when we first started, oh, you pull out amyloid. No, we don't. We prevent this binding. We're far earlier in the process. And we believe that's part of what allows our drug to create a great deal of value. Now, what we're going to talk about is reflected down here. We ran a trial called Shimmer. 86% overall results, meaning slowing of disease. Importantly, slowing 89% in psychosis, which is hallucinations and delusions. So we'll come back to this. This conversation is about our data in dementia with Lewy bodies. Let me stop here. Our focus is on neurodegenerative conditions, AD and DLB. We've always had an interest in Parkinson's disease. You may know these things are highly related, both being driven by toxins called alpha-synuclein. On the right, in the market, you see this more and more and more. What some people call the residual symptoms turn out to be gigantic markets. So if it's agitation, in Alzheimer's disease, psychosis in Parkinson's disease, think neoplasm on track for a billion dollars, and so on. So we see this as a shift, not just treating the underlying disease, but these symptoms, which remain unmanaged, create huge opportunities for investors. Our focus on psychosis has evolved. In our Shimmer data, which we'll show you today, showed tremendous data, results, excuse me. In January, we went to the FDA, and the FDA said, well, listen, your data in psychosis happens to be the strongest part of your results. So what you really should do is discuss this with the psych division. And we did in the month of May. So where we are today, it's wait, as you probably know, there are two divisions within neurology, right? The overall neuroscience is neurology and psychiatry. And at the end of our May meeting, what became clear is we would go back to the neurology team and present to them our proposal for how we're going to measure psychosis in DLB patients. Most of the study has been agreed to. But for us as a company, it's been a long process to get there. So in brief, psychosis, if you're familiar with it, it is two things. It is hallucinations and delusions. Most often, patients who have DLB will say, this is the one thing they want to go away. These patients have a lot of problems, but that's what's key to them. It is higher in DLB than in other rates. Take a look over here. Alzheimer's patients also experience psychosis. A lot later in the course of their disease. Same thing with frontotemporal dementia, Parkinson's disease. So it's not uncommon. But this is core. For the diagnosis of DLB. And it's pretty difficult for families to manage. One quick word. If you're unfamiliar with dementia and with Lewy bodies, you can take a look down here. This will help explain why it's difficult to diagnose first. Everything fluctuates with these patients. Cognition fluctuates. So if you try to do a test with patients Tuesday at 10:00, you're unlikely to get the same result. You're going to get it 4:00 in the afternoon. Highly variable, very, very frustrating. Visual also auditory hallucinations. Somebody will say, why is that song still playing all day long, right? It's a series of things. Delusions, false belief, often fixed false belief. Somebody will say to their caregiver, you're an imposter. You're not my husband, wife. This sometimes results in aggressive behavior. This is a Parkinsonian condition, right? These people have alpha-synuclein throughout their brain, which means they have, as you see here, rigidity, postural instability. Big problem here is that they can't, patients with these conditions, cannot safely take antipsychotics. So we want to treat the psychosis in this population, knowing that there is this underlying condition. We believe we have a great way to do it. REM sleep disorder, all the other symptoms. It's complicated, and it certainly takes a long time to diagnose. In brief, there are. Actually, no drugs approved for patients that have dementia with Lewy bodies. So everything over here which we've just described gets treated with something here. These are many of them are older drugs. And they have varying effects. You can see on the side, a number of black box warnings. So physicians have things they can offer patients, symptomatic treatment. Think of opening the medicine cabinet. You kind of take one of everything to give to this population. But these drugs have not been developed for patients with Lewy body dementia. And so there are a number of safety considerations. Let's look at these neuropsych symptoms. In particular, so antipsychotics, all right, Haldol, you have no idea how much Haldol is still prescribed. If you think about cuckoo's nest, maybe something you saw many years ago, right? These drugs are still prescribed in this population, and others. And it can cause very significant, even death, in terms of side effects. Now you have the atypicals. We're not another atypical. Pimavancerin is neoplasm. Quetiapine is Seroquel. This is Rexulti, the new drug from Otsuka. So these things are used off label. However, there's a variety of things that have to be managed, whether it's QTc interval effects, et cetera. Of course, we have the benzos. That's one way to get patients not to be agitated. You entirely depress their symptoms, and their mobility. And of course, falling gets worse in cognitive abilities. One thing about this population because of the Parkinsonian condition, these people fall a lot. They're in the emergency room a lot. And believe it or not, they actually cost more to care for when you do aggregate studies than people with Alzheimer's disease. 80 patients live four to seven years. If you had to pick an average, you'd say five. Excuse me. That's Lewy body patients. 80 patients, seven to 10 years. These patients cost more. And a lot of it has to do with this kind of instability. So you're probably not wanting to give them benzos. But doctors do what they have to do because they want to alleviate some of the limitations or some of the problems the patients are having. We have a once daily oral drug, 100 milligram dose is what we agreed with the FDA. We would study in Alzheimer's disease. We've talked about it in Lewy body dementia. If you've looked at any of our data, you often see one line, which is the 100 and the 300 milligram doses. We can tell you the dose profile overlaps. Actually, I have all the data broken out. And the 100 with fewer side effects is as effective as the 300 milligram dose. And the agency did not say to us, oh no, go back and study a lower dose. That's off the table. So we are looking at patients who have psychosis coming into our study. You can see the age group. People have to be in a home setting, not institutionalized. We have a very good safety profile. And you can see here on the bottom what we're looking to measure. Now, where does all that come from? In January of '25, we went to Amsterdam to an international Lewy body dementia conference, read out our results. The results of this trial called Shimmer. So this is the population. You can see the MMSC scores, MRI, 130 patients. This is an international, excuse me, this study was done entirely domestically. Alzheimer's was studied in the US as well as Europe. But these patients all came from the US. Two doses of drug. And as I said here, think about the challenge of running a trial like this. You had to measure everything because these people have everything. So the NPI is a standard instrument for looking at neuropsych symptoms, cognition. You could use a MoCA. You could use CDR, some of boxes. You could use a variety of things. Fluctuations, clinicians fluctuate, assessment of fluctuations. You may be familiar with the UDPRS that comes from Parkinson's disease, a motor skill. And so on. When we looked at all of these things, and you can imagine how pleased we were when at the end of the day, we looked at the results and saw improvements across the board. In all of these conditions. Now, let's start over here. This is at the end of six months. The top are the neuropsych symptoms. We'll break them out for you. This dotted line represents, as you see, the midpoint. Everything to the right of it favors a result of drug. And to the left favors placebo, what we saw in the MoCA was this very wide dispersion in the results. But you can look at this visually and say to yourself, this looks like a drug that could really benefit patients who have dementia with Lewy bodies. So let's start with one of the things we're most excited about, neuropsych symptoms. What does that mean? It actually means all of this. Anxiety, delusions, hallucinations, et cetera. You talk to caregivers, they'll tell you exactly what they're dealing with every day. Patients will say the delusions and the hallucinations are most disturbing to them. That's the one thing of all these things they have. They want to deal with the most. And you can see how well they were treated, again, everything to the right favors a result on drug. You can see the results here at week 26. So the purple line, 100 and 300 milligram doses, basically the same as if I showed you the 100. And placebo is right here, this gray line. So the point is patients not on drug worsened. Patients on drug were effectively slowed in their disease, maybe to the point where they really didn't see further symptoms. Psychosis per se, now this is what we discussed with the FDA earlier this year. These are patients that had background psychosis. Here's the effect of drug, 100 or 300. 109% slowing. What does that mean? These people were a little better at the end of six months than they were at the beginning. Placebo patients obviously got much worse. So this is why we've come to this as a proposed registrational endpoint. The alternative is you look at, oh, REM sleep, cognition, motor function. You'll get all five of those things, and you put it in a blender, and you try to come up with a single result. The agency said, no, this is where you have the most effective response in your patients. Let that be the lead indication to get you through approval. Now, this is an interesting endpoint. It's not something I had encountered elsewhere in my career. This is an assessment of the caregiver, the husband, the wife, the child, whomever. And what we saw at the beginning of the study, they were here. And at the end of the study, they did not worsen in terms of their degree of difficulty caring for these people. Whereas patients on placebo, their caregivers continued to decline. And one of the most important things to look at is when you see here on the right, anxiety, delusions, hallucinations, aggression. Same symptoms that the patients reported. And we felt like that internal consistency was pretty important. Moving on, fluctuations. These are patients who wake up and from day to day and moment to moment, this is cognitive, this is physical movement. It's very disturbing for them. They'll go into a doctor's office, and the doctor will talk to the patient. And it's often called showtiming. Patients like this is what's going on. Did you see that latest movie? Whatever it is. And the wife, we've heard these anecdotes. The wife is like, are you kidding me? You can barely function on a day-to-day basis. You show up in front of the doctor, and I look like a fool. It's a simple analogy but the point is the degree of variability is tremendous. Whoops, let me go back to that. Going the wrong way here. So the fluctuations were markedly reduced by a 91% slowing. ADL activities of daily living. Tony, Chief Medical Officer right here, will often say the FDA might say, excuse me, I keep hitting this, and I'm sorry. The FDA might say, well, if you have too fewer fluctuations, actually how does that change your life? It's really hard to know the answer. On the other hand, if you can get up, bathe yourself, get dressed, make a meal, make a mental list or a written list of what you have to do, leave your house and get home, that shows a real impact of drug. So you may be aware that the FDA and these kinds of conditions is quite interested in understanding what is the impact on patients in terms of their ability to function in their daily life. Now, take a look at this. 52% slowing. Tony will often explain this to people in the following manner. And I think it's important to understand. We told you these patients are diagnosed and have dementia with Lewy bodies anyway for four to seven years. Honestly, by year five, most of these patients increasingly have passed away. So you say to yourself, huh, if I can give a patient back 50% of their time that means out of four years, two years, maybe they can function better. Another way to think about it is however long it would take them to get worse, I've doubled the amount of time until they get worse. I'm trying to find language that helps you appreciate what this means for patient. Motor function, we talked earlier. Patients that have underlying problems with Parkinsonian symptoms typically can't take antipsychotics. There are a variety of important and severe side effects, including rigidity, death, for example. And so the fact that you can treat these patients and not harm them we consider really excuse me, really important. Briefly, CDR. This is not the CDR sum of boxes. This is a cognitive battery of tests. So it is looking at cognition. The CDR sum of boxes is typically, in Alzheimer's disease. And so you saw a positive impact here. In terms of not worsening, it's noisy for the reason we said. You bring a patient in and now it's Tuesday at quarter of three, Wednesday at three o'clock, whatever it is. And at five o'clock, you get a totally different result. These patients are very hard to test for this reason. It's part of the reason why, as we consider studying psychosis, we want to take a one-month look back, six weeks, whatever it is, so that you get an adequate window of time to really understand what the patient has experienced. So when we sat down, I said, we're pretty excited about what we want to do. And that is go from our phase two results into a registrational program. We've agreed with the agency that we will study hallucinations and delusions. That's formally known as psychosis. We're going to go back. We did this already. I need to update this slide. We have another FDA meeting coming up where we intend to finalize this. We have a 100 milligram dose, a nine-month study, and we believe the proper endpoint is the NPI2, that neuropsych2. I showed you 12 results. You can pick the two that are hallucinations and delusions. So that's a matter of discussion. With the agency. So based on the results we've seen and the experience, patients who are still on drug have we are more than enthusiastic about getting to this trial. Now, I'll spend just a moment on this. This, as you see, Alzheimer's disease. We read out a study in 2024. It was referred to as SHINE. And in the SHINE study, we looked at patients who had low PTAU. PTAU is a measurable protein. You can go to lab or lab core quest and take a look at what your PTAU level is. Everyone in this study has Alzheimer's disease. This is not low PTAU like some of us might have sitting here. And when we looked at those patients, at the end of the study, these patients here, again, 100 and 300 combined, look where they were at the end of the study. This is their cognitive decline, which is to say you were able to freeze for six months. Those cognitive capabilities in this particular population and people who were on placebo, as you saw, had a dramatic worsening in their results. So this is similar to ACI and Lily. In fact, that's why Tony wanted to do this study. This was a pre-specified endpoint, not post-hoc analysis. And so what's running right now, that trial was in mild to moderate patients. Mild cognitive impairment through mild. Think of us as moving back in time to patients with less severe Alzheimer's disease. This is a 500 patient, 545 patient study. 50 sites in the US, all grant funded. We'd love to say to investors, do you know you get this trial for free? Paid for by the NIH. You're going to find these results. If you invest in our DLB results, along the way, this study will read out. We anticipate this reading out next year at this time. Now, some important things about this study. I don't see it readily on the slide. Tony and the others agreed with the steering committee if you're going to do a real-world study, you know how long it takes to get these things off the ground. Well, by then, lecanemab and Casumla had been approved. And so we said to physicians, you can bring patients who are stable on lecanemab or Casumla into this study. And that gives us an opportunity to understand