Welcome back, everyone. We have CervoMed Inc. they trade on the Nasdaq under the symbol CRBO. It's a clinical-stage company focused on developing neflamapimod, an investigational orally administered small molecule brain penetrant that inhibits p38 MAP kinase alpha. Please welcome Chief Commercial and Business Officer Matt Wenton. Matt, sorry for mispronouncing all of that. I'm going to give the floor to you so you can say all those technical terms instead of me. No problem. Thanks, Anna. I know it's a mouthful. Good morning, everyone. Thank you for your interest in CervoMed and for joining the presentation this morning. We're going to talk about the opportunity of neflamapimod in dementia with Lewy bodies and then spend some time at the end of the talk for questions. These are our forward-looking statements. For further details, I would refer you to our website, CervoMed.com, for our most recent SEC filings. CervoMed is a clinical-stage company that's focused on neurological diseases of aging in Boston. Our lead product, neflamapimod, is about to enter phase three trials for dementia with Lewy bodies. It's a well-documented compound that has been tested preclinically, as well as in phase two studies. We have a broad data set, which I will spend some time walking you through and showing the significant clinical effect that we are seeing in patients with DLB. DLB represents a very large market opportunity and, in particular, pure DLB, which is where our focus is. Those are DLB patients that don't have any other Alzheimer's disease co-pathology. There are currently no other approved therapies. As I mentioned, we are looking forward to start our Phase 3 pivotal studies next year and anticipate hearing back from the FDA later this quarter. What is dementia with Lewy bodies? I will refer to it through the presentation as DLB, but DLB is a chronic neurodegenerative disease that is actually the third most common neurodegenerative disease behind Alzheimer's and Parkinson's disease. It is actually clinically more impactful than Alzheimer's disease. It progresses faster, and patients typically end up being in a nursing home in about two years from diagnosis to progression of disease. It has a greater impact and caregiver burden than we see with other diseases like Alzheimer's disease. It's characterized by the presence of Lewy bodies, which are abnormal clumps of protein alpha-synuclein that occur in the brain. This can be diagnosed clinically through cognitive deficits, as well as having two of the four following symptoms. You can have fluctuating cognition, you get visual hallucinations, you get a unique sleep disorder called rapid eye movement sleep disorder, where you end up acting out your dreams and have very active sleep cycles, as well as movement problems and Parkinsonian symptoms. Through this clinical diagnosis, you can diagnose about 80% accuracy. Neflamapimod is specifically designed to target the underlying neurodegenerative process that causes the dementia in these patients. In DLB, the disease occurs in a specific part of the brain called the basal forebrain. This is different than Alzheimer's disease, which predominantly occurs in the hippocampus, or in Parkinson's disease, where it occurs in the basal ganglia, different parts of the brain. The cause of this disease in DLB is due to synaptic dysfunctions or impaired communication between brain cells, specifically a type of brain cell called cholinergic neurons. Neflamapimod works to reverse the synaptic dysfunction, which is caused by neuroinflammation due to these protein clumps that we talked about of alpha-synuclein, which ultimately leads to tau pathology and disruptions in axonal transport and driving symptom of disease and further progression. DLB can be further segmented into what we refer to as pure DLB or DLB with co-pathology or co-Alzheimer's pathology. About 50% of the DLB population is considered pure DLB that just has cholinergic deficits with limited neurodegeneration in the hippocampus, that part of the brain that really is impacted in the Alzheimer's disease setting. This is the population that we have shown that our drug may be optimally designed for, and we have segmented in our earlier trials, and it's going to be the focus of our phase three trial. This is a highly valuable and untapped commercial market. There are no other therapies available. You can see on the right-hand side of the slide some of the number of patients that we are talking about, somewhere between 150,000- 180,000 in the U.S., 280,000- 420,000 in Europe, and about 100,000- 250,000 in Japan. It is a large-sized market. This segmenting of the population can be done by an easy blood test that's commonly available. You don't need a PET scan or spinal tap or any complicated medical procedures to do so. As mentioned, we have published, along with many scientific leaders and physicians in the field, strong preclinical data showing that we're able to reverse cell loss in the cholinergic neurons in mice models. We're able to improve performance in behavioral tests and show proof of concept scientifically that the pathway that our drug works is being targeted. Our phase 2 clinical data, which has been published in Nature Communications, was a 91-patient study for 16 weeks. Here we saw significant improvement in the key dementia rating scales called CDR-Sum of Boxes or CDR-SB, which I'll go into a little more detail on other slides. We also saw improvement in gait and motor function, as well as improvement in key biomarkers that are representative of the neurodegenerative process. We saw improvement of those. All this together has led us to run a larger phase 2b study, as you can see the design here of 159 patients using that specific cutoff from the blood test, looking at phospho tau or p-tau 181. Based on design cutoffs, we are able to enroll this population, this pure DLB population into this trial and examine them for 32 weeks. Now, as mentioned, our primary endpoint in the phase 2a, as well as in the phase 2b, and it will be our proposed primary endpoint for our phase 3 study is the CDR-Sum of Boxes. This is the gold standard for evaluating severity and progression of dementia. It's been established and has been shown to be effective in many phase 3 trials, especially in the Alzheimer's disease space. There have been several publications. A recent one looked at 500 patients with DLB to show that this scale evaluates the treatment effects in DLB and is an appropriate scale to use. You can see on the right the different domains that it measures from cognitive domains of memory, judgment, orientation, and reasoning to more functional domains of home and hobbies, personal care, and community affairs. This broad-ranging domains makes it useful for a disease like DLB that not only affects cognition but can have motor and psychological presentations of disease as well. While we were designing the study and while it was being enrolled, there were two interesting things that were identified that were strong insights for us. First, there was a large study that was published of 1,300 individuals that looked at this blood test, the p-tau 181 blood test, to look at where the cutoff should be for DLB. Based on this new data, we actually went with a more stringent cutoff than what we initially thought. This more stringent cutoff allows us to better enrich the patient population that we think is going to be most effective on our drug, but at the same time, it doesn't change the total population that's addressable. It's still about 50% of the overall DLB population. This really allows us to get more specific without affecting the number of patients that can be treated. The other thing that we saw in a walkthrough in the discussion today is one of the batches of drug that we use did not achieve target plasma concentration. It was an older batch that unfortunately was not absorbed as well as previous batches. You can see on the graph below, on the right side of that graph, we need about 5 ng/mL on average of drug in each patient to be effective. On the right side, you can see the batch A or the old batch, which showed just over 4 on average ng/mL of drug in the blood speculum of these patients, which was not clinically effective. This allowed us to do a couple of things in the study. As some patients, you can see in group one here, were on batch A or the clinically ineffective batch throughout the whole study, both the placebo-controlled portion that was 16 weeks, as well as the open-label extension trial. While other patients received both a mix of A and B, and some patients received only B. This allows us to do a series of comparisons that allow us to compare batch B to batch A, so batch B, which we know is clinically active, to a batch which is not clinically active or under-dosed, as well as patients that were on placebo. Patients that were on batch B that were clinically effective. Now I'm going to walk you through some of that data. This is looking at the CDR-Sum of Boxes scale. As you can see, when we look at all participants, as expected, using batch A, which is the batch that did not achieve active plasma levels of drug, we see no effect. No significant differences are observed. Even when we do the cutoff to focus only on pure DLB patients or those with low likelihood of AD co-pathology, we started to see a little bit of a trend, but still not significant improvements in the CDR-Sum of Boxes scale. However, when you look at batch B versus batch A, batch B being green, batch A being blue in the extension phase, in either all patients or in the patients that are pure DLB, you start to see a significant effect on clinical progression here. We actually received a 52% reduction in the mean change in CDR-Sum of Boxes scale. That change increases when you go from the total population to our enriched or optimal population, which is up to 82% reduction. When we break it down to an individual patient effect on the CDR-Sum of Boxes scale, you can see these patients here were on placebo for the first 16 weeks of the study, and then they switched to batch A, which we know was not clinically effective. You can see a lot of noise. They continue to get worse. Going up on the scale is getting worse. There's really no effect of this drug. When you look at batch B, which we know was active in these patients, you can see as they were on placebo, they continue to get worse, and you get a complete shift in the slope of all the patients. The data results tighten, and you get a clinically significant effect of 0.005 in patients in showing improvement, leading to a mean difference of 1.12 in the CDR-Sum of Boxes. To put that in perspective, 0.5 in CDR-Sum of Boxes is typically the rule of thumb for something that's clinically meaningful. We see a very robust effect here. This is a Kaplan-Meier curve looking at progression of patients who increase on the CDR-Sum of Boxes, who get worse by 1.5 points in the scale. You can see the placebo is the blue, and by about six months, about 50% of these patients have progressed more than 1.5 points, which is really clinically meaningful. Batch A, the batch that was under-dosed, didn't achieve active plasma levels, pretty much mirrors that placebo group. However, if you look at batch B, that was active drug, you can see this treatment effect resulted in a substantial improvement and reduced the risk of progression between 67%- 75%. This is not only clinically meaningful, but this is really important to both patients and caregivers to show a lack of progression of disease, stabilization of disease, and is really when you talk to patient and caregivers, what they're looking for in a new treatment. We also looked at some other endpoints, some other scales, whereas the CDR-Sum of Boxes is more patient-driven. The ADCS GIC or the Global Impression of Change score is done when a physician will score the patient on if they are getting better or getting worse and give them a score. In this case, you can see these are batch B compared to placebo. You can see a significant difference across all patients, and that disease difference, that improvement is enhanced when you look at the subset of patients that are pure DLB and that have low levels or low likelihood of co-AD pathology, suggesting that we are able to identify specific patients where we may see enhanced activity of our drug. We also confirmed that using a biomarker critical to neurodegeneration in the brain, something called GFAP or glial fibrillary acidic protein. Here you can see, looking at batch B versus placebo, you see a dramatic decrease in expression of this biomarker that we know is elevated when there is neurodegeneration going on in the brain, statistically significant. I think most impressively, this decrease in biomarker also correlates with the clinical effects that we are seeing in the CDR-Sum of Boxes scale. Both the underlying pathology and the biology that you see in the biomarker data is nicely correlating with the clinical data that we are seeing in the clinical scales that I showed you before. Taken all together, this gives us a lot of confidence that we have proof in concept of a drug that has activity, that we're able to identify the right population to treat, that we've shown improvement in critical well-established endpoints that we are going to use for our phase three trial, and that ultimately we have a potential new treatment for DLB. Safety across all studies to date has been favorable, pretty unremarkable. Actually, we've not had any discontinuations due to severe adverse events. That's been very low. The typical adverse events that you see with P38 kinases has been elevation of liver enzyme. Because this enzyme is really designed to be brain penetrant, and you get a higher concentration within the brain than you do within the rest of the body, we do not see a lot of elevated liver enzyme, and there was no difference observed between batch A, batch B, or the placebo in our studies. As mentioned, we are in the midst of talking with the FDA around our phase 3 trial design, as shown here. It's designed to be a 24-week placebo-controlled randomized study in patients with pure DLB. I think that's the one thing that's important to highlight. Because the disease progresses much faster than Alzheimer's disease or other neurodegenerative diseases, we are able to run a shorter trial in 24 weeks. We estimate around about 300 patients, so it's more efficient than some large trials that you see in other indications, and are looking to start this trial in the third quarter of 2026. In conclusion, we believe we have clinical proof of concept in an untapped multi-billion dollar indication that is ready for phase 3. We are proud of our strong scientific and preclinical results and believe that sets the stage for a successful phase 3 study, and the high unmet need and large market potential, as well as our fast-track designation with the FDA, sets us well for success in executing on that trial. Lastly, although I focused today's presentation on DLB, which is our furthest along asset moving into phase 3, we have two other areas that we are in the clinic with. Recovery after stroke, which is currently in phase 2, as well as frontotemporal dementia, specifically primary progressive aphasia form of this disease, which we received orphan drug designation last year, which is also in the clinic in phase 2. We also have some other 2.0 versions of our drug, which we are working on to move quickly into the clinic for some other diseases as well. Thank you all for your time and attention. With that, I'll turn it back over to Anna and open it up for some questions. Okay, perfect. Thank you, Matt. I know you recently joined CervoMed, so I'm curious as to what was it about the company that attracted you to join? Yeah, thanks, Anna. I came over, I'm three weeks in, so hopefully I know enough just to be dangerous, and it's been a fast and fun and furious three weeks. I came from a rare disease company that was successfully acquired in July. The broader goal was to take some time off and maybe enjoy the rest of the year. I got connected with John Alam, the CEO here of CervoMed, and started having discussions with him. He was kind enough to put me under CDA and gave me access to the whole company and the board to do some due diligence. The more I started digging into the data, the more I started talking to people, the more I got excited about the data, about the opportunity that we have here, and the point where the company is right now, delivering strong data in phase 2 and thinking about going into pivotal studies in phase 3. Just in terms of some background, my background is in neurology and in neurodegeneration. I spent 10 years running large neurology franchises at Biogen and spent several years prior in consulting really focused on neurology. I have a PhD in nerve regeneration and a postdoctoral fellowship in nerve degeneration. Seeing what these results have and being able to dive into the data, it was too good of an opportunity to pass up. My time off was a week and a half and right back to the grind, but really excited to be here and what the future holds. Perfect. Talk a little bit more about your discussions with FDA around the phase three trial and the design of neflamapimod in dementia with Lewy bodies. What exactly should we expect with that trial? Sure. Yeah, no, it's a great question. This is a type C meeting. This is not our end of phase 2 meeting. We've actually met with the FDA prior at the end of our phase 2a, some of those results that I showed. We've already had a lot of discussion with the FDA on what a potential phase 3 trial could look like in DLB. During our initial discussions with them, we had a very similar design in the clinical trial. We had a different primary endpoint. Initially, we were thinking more of a cognitive test, but since there's been a lot of literature and the field is moving to the CDR-Sum of Boxes scale, which the data I showed here, we want to use that as our primary endpoint, and that's part of the discussion we'll be having with the FDA, as well as we are just going to confirm the length of the trial, the number of patients that are needed in the trial, and overall our monitoring and operational approach to managing the protocol. We're not expecting any surprises or any curveballs based on our last discussion. We're eager to get all this feedback, and once we have it, we'll announce that publicly, and that allows us to start set up and moving forward to that phase 3 trial in Q3 next year. We know there are a lot of patients and physicians who are excited to get going on that. We're looking forward to moving quickly once we get the feedback. Can you talk a little bit about how dementia with Lewy bodies is different from Alzheimer's disease? Yeah, no, it's a good question because most people, when they hear dementia, they focus on Alzheimer's disease, and rightfully so, on some levels, it is the largest dementia that's out there. I think we're estimating around 5 million- 6 million people in the US have dementia, and the lion's share of that is Alzheimer's disease. The statistic we like to use is about 5% of those living with dementia have DLB. Really, the difference with DLB and Alzheimer's disease is both where it initially starts, what regions in the brain are affected, as well as Alzheimer's disease causes a lot more cell death or neurodegeneration, which is harder to reverse. Once the cells die, it's hard or impossible to bring them back. Treatment with Alzheimer's disease is very difficult. Also, symptoms in Alzheimer's disease usually present once you have a lot of cell death already. In the case of DLB, symptoms occur much earlier, even prior to cell death of these cholinergic neurons. These symptoms really occur in the reversible phase of this disease. That's why we feel it's really an optimal disease to treat because it does allow us to intervene before that critical point of cell death and to allow to reverse some of the symptoms and prevent progression where it's still earlier on in the progression and development of the disease. Also, since it is a fast-moving disease, I think it allows it to be tested in shorter trials, get quicker outputs, and also understand how your drug is working using different endpoints and biomarkers. I think that's really accelerated the development of this program and allowed us to be ready for phase 3. Perfect. Thank you for that. With the time we have remaining, a few questions. Joseph asks, "Had the briefing document been submitted to the FDA to start the 70-day process for a meeting? Great question, Joseph. Everything that I've presented today, the FDA has it, and they have all of our data and all of the briefing materials, designs of our trials, protocols, and they're in review of that information. Perfect. David asks, "Are all the pure DLB patients newly diagnosed that will progress to having co-pathologies? If so, how long do patients stay in the pure DLB category? Yeah, it's a great question. I think progression in the disease is heterogeneous, and not every patient progresses around the same. Not all are newly diagnosed. Some are currently living with it. I think that's why we think the numbers that we've put forward in terms of this market potential are somewhat conservative because you will have new diagnosed patients that obviously you can treat that are in this pure DLB stage. If we can slow that progression from pure DLB to more complex DLB or more heterogeneous DLB that involves co-pathology of other diseases like Alzheimer's, if they stay in that pure DLB stage, not only do we hopefully have a reduction of symptoms, but that patient will be on treatment for a longer period of time and hopefully not even progress into other forms of the disease. I think our drug we're hoping for can target both existing patients, can target newly diagnosed patients, and then over time, I think more work is still to be done on the effect our drug can have on DLB patients with co-pathology and other neurodegenerative diseases. More to come there. Perfect. We have more questions for you, but we're out of time, so we'll send them to you so you can answer on your own. Thank you so much for joining us on this conference, and we look forward to speaking with you again soon, Matt. Perfect. Really appreciate it, Anna. Thank you.