Sumant, a senior biotechnology analyst at Canaccord Genuity, and it's my pleasure to have CervoMed here with us today. CervoMed is developing neflamapimod for dementia with Lewy bodies. Dementia with Lewy bodies has significant unmet need. It's the second largest dementia, and it's unfortunately not addressed as much as Alzheimer's disease. It's a really challenging indication and we're happy that a company like CervoMed is taking on that challenge. For CervoMed, we have CEO John Alam on the podium here, and we have Matt Winton, who's the Chief Business Officer, and also William Elder, who's CFO and General Counsel out in the audience. We do have a mic going around, so please feel free to ask questions. Raise your hand and I'll get the mic across to you. For this, we'll have John go through a few slides and then we'll go into an interactive Q&A. With that, I'll turn it over to you, John. Thank you, Sumant. Somehow this conference ends up being an incredibly fortuitous time every year, and it's always nice to have a conference here in our hometown. We are Boston-based. I do have a few slides because I do want to catch up people a little bit. This year, already to this point, the first half of this year, we have actually for, I think, the size of company that we are, have made as much progress as anyone in this whole sector. We have a phase III-ready drug in dementia with Lewy bodies, which is a major indication, and this is as well having progressed into another significant indication, and with a subtype of frontotemporal dementia. I'm not going to go through all of this, but if you look at this in every aspect in terms of clinical data, in terms of financing, in terms of non-clinical data, regulatory progress, across the board, significant progress in a very short period of time. Everything is really coming together. That's why I say it's a perfect time to be coming and speaking with you, and Sumant has teed up, I think, a great set of questions for us to go about. But I did want to focus on three very specific things that I think many in the investment community have, given all this progress, have yet to fully catch up on. I just want to highlight a few things around that. One is in terms of the biology of dementia with Lewy bodies and why we call this a targeted therapy for dementia with Lewy bodies. In the end, there is a tremendous amount of science that is developed externally that really now defines what is the underlying disease process in dementia with Lewy bodies, which is about neuroinflammation and the interplay between that and alpha-synuclein and how it impacts a very specific part of the brain, the basal forebrain cholinergic system. I am not going to walk you through the science, but it is all referenced down below, mainly last two years set of papers that goes to this is what dementia with Lewy bodies is. Probably an exclamation mark on that is a paper published in Neuron, which is the major neuroscience journal, July 15th this summer, a month ago, that says that the biggest study ever done across neurodegenerative diseases in terms of proteomics, that the key mechanism for dementia with Lewy bodies that leads to symptoms and disease progression is at the end, interleukin-6 and interleukin-1 beta signaling. That is at the heart of, that is the mechanism of attraction of our drug. It is blocking interleukin-1 beta signaling and impacting interleukin-6 production and other cytokines and other downstream effectors. But this is the science meets what is then otherwise what we actually. This is data we presented for the first time at ADPD, in the ADPD conference in April, of we are a very potent blocker of interleukin-1 beta signaling on the left that translates directly into reducing interleukin-6 levels in the spinal fluid. So puts the whole mechanism together towards targeting specific disease mechanism in dementia with Lewy bodies, all vary both from the science standpoint and what we have now understood of what our potency and activity of our drug is, all very recent news that comes together. The second point is around the phase II b clinical trial results, where I think those who have been following the story that much of it in the past year has been comparing two different drug batches, one at higher blood levels versus one that at lower blood levels and the effects during the extension period. Data we presented at ADPD, then at further at Alzheimer's Association International Conference last month, is that within the placebo control period, even with the batch of capsules that had lower blood levels, if we look at what is now the standard cutoff, which is 21 picogram per mil for whether a patient has Alzheimer's disease in addition to DLB and identify the pure DLB population. On here, there is a 0.7 point improvement in CDR Sum of Boxes, which is greater than the 0.5 considered clinically meaningful with that lower blood concentration level Batch A of capsules in the placebo control period. 45, 46, 48 number of patients gets you to a P value of 0.054, which is consistent with this is actually the magnitude effect we were looking for in the study to begin with. We were powered for a significant effect with 80 patients per arm. We come up there, but there's a clear signal. More importantly, perhaps, there is a significant effect if you look at the upper half, that in terms of blood concentrations and above the median, there's flat. Again, the drug effect that we were looking for all in the placebo control period goes to then you should really be looking at then at higher blood concentrations, and that's when then the Batch B results all makes sense. Indeed, when you have higher blood concentration, higher drug effect. This is then in the end, what one I'm sorry. Let me go back. Should on the right-hand side effect in our phase III trial, lowest cutoff level with Batch B blood concentrations, flat in terms of drug effect, and a big difference to placebo, more than a one-point improvement. Again, all data that we presented more recently and puts the whole story together. Batch A does work, lower blood concentrations, but you do even better when you go to the Batch B. This is then showing you what the full potential of the drug is in dementia with Lewy bodies. Then the other one, which is, again, I would say that people haven't fully caught up to is really what is, in my mind, really very remarkable data in terms of MRI within the study, the phase IIb study. On the left-hand side, this was only a sub-study. Only patients in the U.K. and the Netherlands received MRIs in the study. So it's a small number, but it's very compelling data. Neflamapimod, this is placebo control period. Eight patients +3.5%, actually a small increase in the volume. The more, the better. You actually have a clear structural effect, while placebo goes down as it does in every clinical trial or longitudinal study in dementia with Lewy. It's this progressive loss of volume in the basal forebrain that is the disease of pure dementia with Lewy bodies. With 16 weeks of treatment, you get full stabilization, if not a slight improvement. Significant P value with only 18 patients because of the magnitude of the drug effect. Then that's further supported, and I think it becomes even more interesting. Those placebo patients who are going down here, and you can see them here, here. When they go onto neflamapimod at week 16, when they go into the extension, they actually turn. Stabilization, stabilization, and these three actually improve. Really direct pharmacology and biology in terms of the drug effect. Then it is where all of this data that I just talked about is actually what we put into what's called the ILAP process, Innovative Licensing and Access Pathway. This is the first time, in particular, the placebo-controlled data with Batch A, that a regulatory agency has seen that data because we didn't have that analysis until very recently. We submitted that in April, and it's part of the reason why, in my view, why we received that designation, which is a regulatory agency validation of the data that we have in DLB to this point. I'm going to stop there. I know that was probably a little bit longer than you wanted me to go, and I apologize for that. It really has been a terrific first half of the year. Everything has come together very nicely. The last point maybe to make is, this was in our announcement yesterday. Maybe go back to I'll actually just go to here. Finish with this one. This is just the overall DLB. I think we have a very uniquely positioned drug in a major disease indication. I would ask you to. All around this is about there is history to this company. I know many of you followed it. We've had our ups and downs. I acknowledge it. The ask is look at us now with what all the data that's come together. I think it's a very compelling story in DLB. What is also added to that is the non-fluent variant primary progressive aphasia. 15,000 patients in the U.S. Significant rare neurologic disorder. It's a subtype of frontotemporal dementia. It is what Bruce Willis and Wendy Williams have. Bad disease. No treatments available. We have great scientific rationale. Validation of that. Despite the numbers, we actually over-enrolled and enrolled much more rapidly than we thought. We enrolled 25 patients into what is the first therapeutic trial, scientifically mechanism-based targeted trial in this disease indication. In our press release, in our quarterly release yesterday, it's part of my quote We have the initial biomarker data, as we had said, in the first eight patients, so it's at eight out of 25. It's very preliminary data, but definitely encouraging, and we've shown it to the primary investigators and our advisors. Seems to be headed in the right direction. We didn't want to put out the specifics because it's only eight patients. The main message is that we will be presenting 12-week data at the International Society of Frontotemporal Dementias in October, and then we should have most of the 24-week data at the time of Clinical Trials on Alzheimer's Disease meeting in November. The message is that I think we have a real shot in this context, and neurofilament light chain disease in these rare diseases is a very meaningful result. Again, look at us today. It's been about DLB, but we also do have, I think, a real good second shot on goal in non-fluent variant PPA. Great. Thanks for that. You took out several of my questions there with that, so you did save some time on those. Now, just to help us move beyond the old versus new debate. Yeah. You have presented some really interesting MRI basal forebrain volume data. To your knowledge, is there any way placebo can affect the basal forebrain volume? No. We have the data there, right? Right. We have a placebo control. You do not see that. What is important in that, it is an increase. It is not a slowing and decrease, and those kind of results are always more complicated because you do not know, especially with the numbers we are talking about, of what is the true placebo rate or progression rate. This is a true increase, and the reason it is an increase, why you can have an increase, is that this is very good published data certainly in animals, but there is reason to believe that it is true going to be in humans as well. The atrophy that you see on MRI, which is a decrease in the volume, is not just loss and death of neurons, but it is actually individual cell shrinkage. They are still there, and if you treat the underlying disease, they can actually increase. That's exactly what we see in the animal models, where you see there's some loss, but there is also neurons that are shrunken. When you treat for a month with neflamapimod, they plump back up. So there's a biological reason why you should perhaps see an increase, that's exactly what we're seeing. Again, I think the second part of that are following the placebo patients again, that they go down then they go back up, is that much more evidence of a true drug effect. Got it. Just stepping back, bigger picture question, dementia with Lewy bodies as an indication, why do you think there hasn't been as much attention to that indication as Alzheimer's? I think it's a very straightforward answer, is that everything I showed you just now is within the last two to three years. There's been this huge focus on Alzheimer's disease over time, but it has come fully around. The advantage that DLB has, all the technologies that have been developed, whether it's biomarkers, MRI techniques, you can just leverage it off the shelf now, you're just seeing it. Five years ago, if you went into PubMed, couple papers every best week, maybe every month on DLB. Now I make it a point that I'll go into PubMed minimum once a week just say, "Dementia with Lewy bodies," up pops another five to 10 papers. It's just moving at a breathtaking pace, which it's just worked well to our advantage. We were a little bit ahead of our time, but the backfill out of the science just explains, in my mind, everything, it's working to our favor. You said moving at a breathtaking pace, so I am going to use a Formula One analogy here. You are in pole position with your product in dementia with Lewy bodies. We know that you are phase III-ready. It looks like that phase III is contingent upon two things, not necessarily both, but funding and/or potential for a partnership to move things along. Given your position within the DLB competitive landscape, what is the key thing that needs to happen to get a partnership signed here? I think it is process at this point right now. It is having the discussions, and again, things have been moving very quickly. On some of this, we have been playing catch up. I think we are in that spot now where we have that full understanding. We can have those types of discussions, and it is really summarized here. This is the value proposition for a pharmaceutical company, I think in particular, this is very specific, very differentiated science that is specific to, and works in, dementia with Lewy bodies. It is substantially clinically de-risked, and it is a great commercial opportunity. We are having discussions. We are moving forward. We have not given a timeline, and part of the reason is that we are, in terms of what a strategic partnership looks like, we are actually quite agnostic. There is a variety of different models that can work, and each one has its own timing, and we may come to a certain point of, yes, we have a deal on the table, but we have another ongoing discussion that, from a business and structure standpoint, could work better, and may be better for us to wait another two months than doing something at a certain point in time. I think that setting a timeline today just sets us up for forcing us to do a deal that may not be the best for either the drug or the business, and we have to solve for both. Got it. So neflamapimod more recently received an Innovation Passport designation from the U.K. What makes the U.K. appreciate this product more than the FDA seems to be doing right now? I think part of it is what I said before. What we put down in front of them is inherently the best foot forward in a sense. In being able to get the process going in April, there is a lot more information than we had at any point in the past. I would not say that they are necessarily more than what the FDA does not see. We went in last fall, and the FDA, what we presented to them, the question we asked them is agreement on primary endpoint, CDR Sum of Boxes, phase III trial design, single phase III trial. All of that agreement between the U.K. and the FDA is the same. They are very much in the same spot. For me, what the ILAP is telling you is the way a regulatory agency looks at it, and a pharmaceutical industry, in my mind, perhaps in distinction to some investors, I will not say all investors, but perhaps the way they look at are much more closely, which is they are looking out to approval and beyond. In particular, the ILAP process, which is licensing and access, because there is a nice component, actually, an NHS component built into this. They are looking at the full value proposition of the drug, and going out both what the potential for value proposition is. That is how a pharmaceutical industry company is going to look at it as well. That is why I think an ILAP designation as a marker to what is perhaps probability of what kind of partnership, why would a pharma company be interested? I think it informs on that. Otherwise, the U.K. is, it was actually in my quote in the MHRA's press release, they are a leader in the DLB field. They just are. The academic community, they are less focused on Alzheimer's in certain respects for a variety of different reasons. They understand also mechanisms that go beyond amyloid and tau, partly because of that as well. But in DLB, their academic clinical community, they are the leaders that feeds into the MHRA. So that certainly helped. Got it. No, that is important context you brought up on the FDA. I guess the FDA is nice, but not the U.K. nice. It is different. No, the FDA, that's not their role to think. Sure. I think the European and the U.K. regulators inherently are always thinking about access as well. Do you have any examples of products that have received the Innovation Passport and then went on to form partnerships with major biopharma? Not yet, because the process as it exists now is only since January of 2025. Before that, they were actually handing out ILAPs left and right, and they gave out too many, so they shut the process down, reinvented themselves. Since January of 2025, they've granted now five out of, I think it's actually 21 applications. So it is a high hurdle to receive it. This is not like Fast Track where you just have to say unmet need and serious disease. This is actually you have to have demonstrated potential to be transformative. The way they define it should be potential to be a step up, not just marginal treatment effects that they're looking for in their evaluation. Got it. In the last couple of minutes, we know CervoMed is not just DLB. You mentioned non-fluent variant primary progressive aphasia, where you have some data that you will present at CTAD here in Boston, actually later this year. What exactly do you expect to present, and what are the most relevant biomarkers in that context? You also have the product included in EXPERTS-ALS, which is amyotrophic lateral sclerosis, your product there. The product has been included in that trial. Again, the U.K. has stepped in to fund that trial. Could you expand on that as well? In PPA, the biomarker that is relevant is neurofilament light chain. It is more profoundly elevated. It is the primary driver. It is very well correlated with disease and disease progression. We will present, again, week 12 data on neurofilament light chain in October at the International Society for Frontotemporal Dementias, ISFTD, and then most of the 24-week data at CTAD in October. I think this has potential to be a substantive catalyst. NFL is certainly in ALS established as a surrogate endpoint. It has similar kind of potential in our view, in PPA. Again, the data that we have seen to this point says that we have a shot here. There are always questions whether you can move NFL, but there are examples in various diseases now, and it looks like PPA may be one of those contexts as well. We are actually quite optimistic and hopeful in that context. On ALS, we are working closely with the U.K. group. Mac, people can come up and ask him questions. He is our main point person there. It is actually going very well. We are going to go with the 50 milligram TID dose that we have otherwise would use in phase III. We have made that decision. That gets us to, I think, the optimal dose and concentration to have drug effect. That is progress in the ALS context. I did not highlight it as much because the next milestone is study start by the end of the year, data late next year, by the end of next year. But as things go along, I think you will hear more about that. The science there is really very good. I think it is the only mechanism that has shown, that has been validated in all three major genetic subtypes of ALS, as well as the only one in many respects that has good scientific rationale and data to support in sporadic ALS. The problem in ALS has been scientifically what has been validated has been for the individual genetic subtypes, and no real reason why they would work in sporadic ALS. I think this is the only mechanism, the combination of all three genetics, as well as a generic mechanistic rationale around axonal transport, why I think there are reasons to believe that there should be a good shot at sporadic ALS. Got it. Thanks. I think we're all out of time. Thank you, everyone, for attending, and we hope you can move the chains, and that's not an NFL analogy. Okay.