Hello, and welcome to Virtual Investor Conferences. On behalf of the Life Science Investor Forum and our co-host, Zach Small-Cap Research, we're very pleased you joined us for our quarterly conference. We have a full day of executive presentations, and kicking us off is a live presentation from Cognition Therapeutics. Cognition Therapeutics is a clinical stage biopharma company developing solutions for age-related degenerative disorders of the central nervous system. Please note you may submit questions for the presenter in the box to the left of the slides. You also may view a company's availability for one-on-one meetings by clicking the Book Meeting tab in the top toolbar. At this point, I'm very pleased to welcome Lisa Ricciardi. She's the President and Chief Executive Officer of Cognition Therapeutics, which trades on the NASDAQ under the symbol CGTX. Welcome back, Lisa. Thank you. Thank you, John. Thank you to those of you who are participating this morning. I'm very pleased to update you about our progress at Cognition Therapeutics. The presentation I'm showing you is on our website under the Investor section. For the sake of time, I will not cover every single slide, but everything is available for you online. Please see our forward-looking statements. Let's begin with a very brief overview. The way our drug works that is in clinical trials is we refer to it as oligomer antagonism. That is to say, we block toxic oligomers from binding in synapses, damaging synapses, and killing neurons. We don't remove plaque. We prevent the oligomers from binding with their toxicity. That's the mechanism. What we have seen is consistent efficacy in both Alzheimer's disease and Lewy body dementia. That will be the subject of our conversation this morning. Tolerated safety profile. To be clear, ARIA is not anticipated with our mechanism of action. We are not removing plaque vessels. We have a very modest side effect profile for a once-daily formulation. There is no need for visits to infusion centers or surveillance on an ongoing basis to look for blood brain bleeds. Last, we believe we may be the first drug to market the treatment of Lewy body dementia. I'll take you through that information first. One other clarification. Our lead drug, we refer to as CT1812, we were recently given our generic name. It's called zervimesine. This morning's conversation will be about the proof of concept data we've generated. A reminder, we have fast-track approval for Alzheimer's disease, and we're working on similar regulatory recommendations for our Lewy body dementia program. Now, before we dive into the data, let me show you. We are running a program in Alzheimer's disease. It's the first purple bar. It's called START. This trial is an 18-month trial with 540 patients. You may know that with early-stage disease, it simply takes a long time for patients to degenerate, and that's the reason why you have to follow them. This is an 18-month trial, and it is recruiting well. The second bar, the orange bar, indicates dry age-related macular degeneration. Many of you may have seen that last month we indicated we stopped this program. There were no safety concerns. There was good data. In fact, we had a publication go out about two weeks ago on the underlying science in macular degeneration. We made the choice to put our resources into Lewy body dementia and Alzheimer's disease. We see great interest from potential partners, and as a small company, we had to prioritize. Doing this has allowed us to change our focus, put cash into these programs. Now, let's talk about Lewy body dementia, which is DLB. DLB and LBD are synonymous. I'll be using both those terms. AD is Alzheimer's disease. You may be aware that Alzheimer's disease is always associated with Aβ. That's part of the toxic elements that are in the brain. In Lewy body dementia, patients predominantly have alpha-synuclein oligomers. There are two types of oligomers we address. Importantly, copathology is very common. Lewy body dementia patients, up to 80% of them, have both alpha-synuclein and Aβ oligomers. In Alzheimer's disease, 50% of the patients have both of these toxicities. Why should that matter to you? Because in all of our trials and preclinical work, we have shown a protective function against these toxic elements. We believe our drug is well-suited for both of these patient populations. Let me take you first through results from our dementia and Lewy body trial. We refer to this trial as SHIMMER, and it read out in December. Briefly, on the upper left, you see the second most common cause of dementia. Most people haven't heard of Lewy body dementia, and yet it's the size of Parkinson's disease. You're talking about a million and a half patients versus 6 million in Alzheimer's disease. There is definitely cognitive impairment in this population, which precedes many, many other types of symptoms. Predominantly, the disease is seen in men. These patients decline faster than Alzheimer's disease patients. Sadly, it takes about a year and a half. Patients go to three specialists. They have six or seven visits. It takes a long time to correctly diagnose this patient population. On the right, you'll see the core symptoms. In some cases, it looks like Parkinson's disease. It looks like sleep disorders. It's complicated, and patients don't all present the same way. Our trial design is reflected here. We did a six-month study, two doses of drug, one of placebo, 130 patients, all done in the U.S. Under assessments, you can see the measurements that we use to assess patients' improvement in symptoms. These are all standard measures for the various conditions. Principally, a Phase II study is a safety and tolerability study. I will show you safety first. Let's look at the bottom of the page. You can see that adverse events, serious AEs, and even deaths are not dissimilar between drug and placebo. In fact, serious AEs are somewhat less in this population. The deaths you see here were all determined to be unrelated to drug. The one thing we follow is in the center of your screen, discontinuations related to liver function tests. What we know is patients with elevated liver function tests return to normal and have no underlying impairment in disease. So overall, you see our safety profile here. I will tell you it was very consistent with our results in Alzheimer's disease as well. Now, in this trial, I want you to understand the complexity of studying these patients. Under behavior, there are a series of conditions: anxiety, delusions, aggressions. There are 12 elements that are studied, and it's captured in the neuropsych inventory. Cognitive abilities are impaired patient function, and we're talking about activities of daily living, bathing, dressing, being able to leave the home and find your way back, as well as movement, gait, posture, tremors. All of these things are impaired. Let's look at how our drug impacted the symptoms in this study. As you can see from the headline, 91% slowing of disease progression across all of these factors. It is a non-trivial thing to design a clinical trial that can capture all of this information, but we were able to do so with our PI, Dr. Jim Galvin. We'll turn to these things one at a time. I'll cover them briefly. 86% reduction in neuropsych measures. What are those neuropsych measures? You can see them on the right: anxiety, delusions, hallucinations, aggressions, and so on. To be clear, these are the behaviors that cause patients to have to be moved into some type of care facility. We often hear about an 85-year-old woman taking care of an 85-year-old husband, and she can no longer handle a person demonstrating these kinds of behaviors. It's extremely challenging. Let me show you the results. On the left-hand side of the screen, the gray line is placebo. Patients on placebo continued to deteriorate over the 26 weeks of the trial. Going down is worsening. The two purple lines show patients on 100 or 300 milligrams of drug, and you can see their deterioration was almost unchanged, 86% slowing over the six months, which is a very, very good result. Now, let's talk about something else: caregivers. There is a tool for the caregivers of these patients. On the upper left-hand corner, it says NPI Distress. This is an index for the caregiver of the patient. The gray line shows if a person was taking care of someone on placebo, that person did pretty terribly by the end of the study. However, people with participants on drug, which are the two purple lines, you can see 114% slowing in their level of distress over the course of the study. You see as well on the right-hand side, when you look at the individual elements, they're very much corroborated, the patient as well as the caregiver's impact of disease. That is a big one for treating this patient population. Cognition is impacted in Lewy body dementia. There are many components of cognition. I will cover this briefly. On the left, the CDR. This is not the CDR used in Alzheimer's. This is a computerized drug battery. There are many elements of cognition. This captures episodic memory, and you can see an 85% slowing in the loss of memory. The MoCA in the middle showed a 60% slowing, and on the right, importantly, fluctuations, a 91% slowing. Gray line is placebo. The two doses of drug you can see from beginning to end, pretty much unchanged. Why is that important? In dementia with Lewy bodies in particular, patients vary so significantly from being on. This is referred to as showtiming. Often, people would say, "You didn't know the person had an illness," and yet, in a matter of hours or days later, there is no affect. They are not responsive, and you can't move them in and out of this. These fluctuations occur a great deal. It's one of the hallmarks of the disease. Importantly, we wanted to understand how do patients do when they're on drug. By do, I mean, are they able to bathe and dress and shower and feed themselves? The characteristics you see identified on the right answer is yes. There was a 51% slowing of disease, progression of deterioration, if you will, for patients on either dose of drug. Last, movement, you see here, if you're familiar with Parkinson's disease, the UPDRS is a score from Parkinson's disease that measures movement, and patients had a 62% slowing of their disease progression. Importantly, you can treat patients with our drug, whereas often antipsychotics can't be given to patients with Lewy body dementia because it makes their condition worse. In sum, the trial met and exceeded our expectations. Let me turn to Alzheimer's disease. The SHINE study read out over the summer, two doses of drug, one of placebo, 153 patients treated around the world. You can see here, using standard measures of cognition, 39% slowing, 70% slowing, 39, 50% slowing. Four measures of cognition were looked at. All of these were very much on par with what you see with the antibodies, 25-30% slowing in their trials. We did a pre-specified analysis. We got the data last. This is the last data we got. And we looked at a particular set of patients, patients that have lower levels of p-tau or phosphorylated tau. We wanted to look at this because p-tau is both a predictive marker of response to therapy, as well as it tells you about an overall amyloid and tau burden. This analysis and type of analysis was used by the drug companies AC Immune and Lilly. We knew, because they came before us, that this would be a valuable thing to do. On the left, the overall 150 patients. On the right, the patients who had lower levels of tau. We literally took 150 patients, drew a line in the middle based on a simple blood test, and took the patients with a lower level of tau. You can see 95% slowing of the progression of Alzheimer's disease. On the left, mild patients, 129% slowing of progression, 91% slowing of progression. We have learned, importantly, as we look to Phase III, this patient population will be a readily identifiable target for us and that they have shown a tremendous response to drug treatment. Our SHINE safety and tolerability studies are very similar to what I showed you for SHIMR. It is all available on our website. We would say, in conclusion, the drug is safe and well tolerated. All cognitive and functional measures trended in favor of drug in both trials. Our goal is now to go to the FDA and to plan our Phase III programs. Last, I talked about our START trial. These are early patients, three dose groups, two of placebo, two of drug, one of placebo. As I said, this trial is recruiting well. This will give us the opportunity to have information about early, mild, and moderate disease patients. Fantastic for us as we contemplate going forward. In conclusion, consistent efficacy across two diseases, no ARIA seen in these trials, none anticipated, once-a-day administration, and again, potentially the first drug to get to market to treat Lewy body dementia. Now, last September, when we filed our Q, we had $22 million of cash, which was anticipated to take us to the beginning of the second quarter of 2025 or to the second quarter. We will update this on March 20th. We'll be filing our 10-K. We'll have an updated cash and runway. All of our financials will be updated at that time, as well as our grant balance, which here is reflected as $53 million. What I'd like to do is turn to questions at this time. Let's see. First question, how long, oh, I'm sorry. How long will current cash balances enable you to function without outside financing? As I said, in two weeks, March 20th, we will have an updated cash position reflected in our 10-K. Our runway will be there as well. How will the company go about funding Phase III? Excellent question. We are looking at all the options available to us for funding a Phase III study or studies, Alzheimer's, Lewy body dementia. To be clear, the ideal scenario is to find a partner and to work with a partner on the clinical trial, on the regulatory work, on the CMC around the world, and in that process, to obtain non-dilutive or cash funding. That is the ideal scenario. Now, we're very much in discussions with a number of companies. There's nothing I can confirm today. I have no guarantee. We're going to have a deal signed. I'm confident we will find a path forward with funding. This would be the most important thing that we're focused on right now. Next question, how will you respond to the NASDAQ listing requirement? Great question. Many of you may have seen on our investor page press release this morning indicating we have been granted the second of two six-month periods of time to come back into compliance with NASDAQ. This means our stock has to trade above a dollar for 10 days consecutively. We went into the out-of-compliance in September. We had till March, and now we know we have another six months to rectify that situation. We are very confident that we will, in fact, do that, be in compliance. We have coming up end of Phase II meetings with the FDA for Alzheimer's disease, end of Phase II meetings for all Lewy body dementia, and then, of course, any updates on potential partnering or obtaining sources of funding. I am very confident that in the coming six months, the kinds of things you will see from Cognition will create value that takes us out of the position we're in, which is not in compliance. In the START trial, have any participants been dosed? Yes, the trial has been running for close to a year and a half, and it is recruiting very well. Let's see. I see some other questions here. Do you still have an ATM in place? How often are you using it? The answer is yes, we do have an ATM in place. In our quarterly filings, we provide an update on how much money we have raised off the ATM. You will see that reflected in the March filing. Another question, you did not include the CDR sum of boxes in SHIMMER. CDR sum of boxes is a scale typically used for early-stage patients in Alzheimer's disease trials. When I showed you the CDR in the SHIMMER trial, that's a computerized drug battery. It's a different measurement, even though it is a little bit confusing. Another question, some companies in the space seem to have stability issues with their drug candidates. Are you concerned about the same? No, we are absolutely not concerned about the same. We routinely test for the potency of the drug that we have in our drug supply to ensure consistency with stability protocols. In fact, you might enjoy seeing a paper just published. It is on our website. The first author is Steven Weissman, who heads our CMC. It talks about how we are scaling to Phase III using a new, very interesting photo flow technology. Take a look at that. Why have you not started Phase III trials yet? Such a great question. To be clear, the way you get to Phase III is by finishing Phase I. What that means is you take 5,000 patients of data from our SHINE trial. You prepare it in a briefing book. You send it to the FDA. You ask for a meeting. They have a long period of time to grant you a meeting. You sit down and talk to them about what is our Phase III protocol going to be. Rinse, wash, and repeat. You do that with Lewy body dementia as well. These are important regulatory steps. They take time. We're in the process of doing them. That will be when we start Phase II, when we have clearance or alignment with the FDA. At the same time, we need to be looking for potential partners, identifying sources of funding, identifying CRO partners, clinical research partners with whom we will execute these trials. There is a great deal of work going on at Cognition and much ahead of us as we prepare for these trials. I think this might be the end of the questions. If there are others, I'll wait. Otherwise, yeah, similar, there's a theme here. I'm amazed by your results. Thank you. We appreciate that. I want to know specifics, how you get to the finish line. As I've indicated, we are actively talking to drug companies, to partners. We're looking at all the options available to us to fund these clinical trials. We too are very excited about the data that we have generated and are looking to secure funding and make that visible to our investors. I see one other question. Are you going to conduct programs for both indications? Are you prioritizing one over another? Great question. Because the SHINE trial finished first in July, that information has been with our team. As I said, there's about 5,000 pages of information. That project is further advanced than DLB, where we just completed the trial in December. We will first prepare for discussions in Alzheimer's disease and then discussions in Lewy body dementia. To be clear, it may be the case that we decide to work with a potential partner who says our interest is in one disease condition over another. The truth is, I don't know which one we'll start with. We are preparing for both. I believe that takes us to one last question. I saw a question about orphan drug. No, these conditions are far too large to get orphan drug status. That is typically reserved for very small patient populations. As you're aware, Alzheimer's disease is about 6 million people just in the U.S., and Lewy body dementia, another 1.5 million. We may have other benefits from a regulatory perspective, but not orphan drug designation. A question here, your Phase II to that of CervoMed. We do not comment on other people's work. I can tell you CervoMed studied a different patient population. If you read their press releases, you will see they went for very early patients that had absolutely no Alzheimer's disease. As I indicated to you, in our population, we saw patients who had mild to moderate Lewy body dementia and thus Alzheimer's disease symptoms as well. Our programs were different. I have commented on our stability testing as well. Are you putting dry macular degeneration on hold? The answer is yes. We actually stopped the trial, stopped enrollment. We will be looking at all that data. Excellent science in that program. Look on our website. A paper just came out recently about the findings we had working with a European researcher. If you ask me, with all the money in the world, I'd go back and start that program. We have made the decision to prioritize resources, both people and dollars, to get our neurodegeneration trials into Phase III. Has the company approached organizations in Europe and Asia regarding grant funding? Grant funding has come strictly from the NIH and within that, the NIA, the National Institute on Aging. Our grant funding has been entirely domestic. Do we have programs that would allow the drug to be approved in regions before the U.S.? These are all excellent questions. That strategy, which is being alluded to here, is all contemplated as we get into Phase III and look at where we execute the trials and then think about, from a strategy regulatory perspective, where would we want to file first? Great questions and all very much before us. I think that's it. I want to say thank you for these excellent questions. Thank you for joining in this morning. Before concluding, two things. Please go on to the Book a Meeting tab. If you wish to have a one-on-one meeting, we would be pleased to talk to you. Second, I want to make sure that I give a round of thanks, first to the participants in their trials and their caregivers. It's a big commitment to do this work. We would not know the benefit of our drug were it not for that commitment. We want to thank the NIA, our clinical trial partners, and you, our investors. Without investor support, we would not be able to sit here today looking at Phase III programs and do somewhat intractable conditions with a once-a-day oral drug. We believe we have something that will change the lives for patients and for caregivers. We thank you for your support in allowing us to do this work.