Welcome to CTAD SHINE phase 2 Data Update Conference Call. At this time, all participants are in a listen-only mode. A brief question-and-answer session will follow the formal presentation. If anyone should require operator assistance during the conference, please press star and zero on your telephone keypad. As a reminder, this conference is being recorded. I would now like to turn the call over to Lisa Ricciardi, President and CEO of Cognition Therapeutics. Thank you, and over to you. Great. Thank you, Ziko. Good morning, everyone. Thank you for your patience. We had a few technical difficulties but are now ready to roll. Appreciate you waiting. As said by Ziko, I'm Lisa Ricciardi, the President and CEO of Cognition Therapeutics. Today, we're going to take you through the results of new analyses, which were pre-specified in our SHINE study. Our SHINE study was a study of mild to moderate Alzheimer's disease, which we completed over the summer. These analyses that we're showing you today were presented yesterday here in Madrid at the CTAD, or Clinical Trials on Alzheimer's Disease Conference. Honestly, these results are the most exciting findings we could have hoped for from the SHINE study. Next slide. We will be making forward-looking statements, which are subject to the risks described in slides and in our filings with the SEC, and we encourage you to review this information. Now, let's turn to our mechanism of action. For those of you new to Cognition Therapeutics, our lead asset is referred to as CT1812. Unlike many other therapies tested in Alzheimer's disease, this drug, CT1812, is delivered orally and as a once-daily dose. CT1812 has a mechanism that is different from the monoclonal antibodies you may be familiar with. The binding of CT1812 to its target causes toxic oligomers to be displaced from their binding sites. In their binding sites, they damage synapses, and this ultimately leads to the death of neurons. As a result of this mechanism of action, we characterize our drug, CT1812, as a neuroprotective agent. Our Chief Medical Officer, Dr. Tony Caggiano, will now walk you through the results of our pre-specified analyses in the SHINE study. Tony? Thank you, Lisa. So this SHINE study was completed earlier this year, and top-line data were presented in July at the AAIC meeting, or the Alzheimer's Association International Conference, in Philadelphia. The study enrolled 153 people with mild to moderate Alzheimer's disease. All study participants had a confirmed diagnosis of Alzheimer's disease, and this diagnosis and the amyloid positivity was confirmed using either PET imaging or by biomarker assessment of the cerebrospinal fluid. The study was conducted across more than 30 study sites in the United States, Australia, Spain, Netherlands, and the Czech Republic. Participants were randomized evenly to receive 300 or 100 milligrams daily of CT1812 or a placebo for six months. SHINE was a phase 2 clinical trial, and as with most phase 2 studies, it was designed with several objectives. First, to demonstrate safety and tolerability. Secondly, to identify signals of efficacy that can be used to support larger and typically longer clinical studies. Another objective was to capture biomarker information. Additionally, phase 2 studies often include pre-planned or pre-specified analyses of different patient populations, with the goal to generate information that will identify the optimal patient population and define the study designed for phase 2 and phase 3 program. The SHINE study was designed to evaluate safety and identify efficacy signals. To assess efficacy, we used standard cognitive scales, including ADAS-Cog 11, ADAS-Cog 13, and MMSE. We also used two functional scales, the ADCS-ADL, and CGIC. One of the most important pre-planned analyses in the SHINE study was the grouping of patients based on their baseline plasma p-tau217 levels. Many studies have shown that patients with lower p-tau217 may be more responsive to therapy. To explore the potential of CT1812 treatment on patients with lower and higher p-tau217 levels, we compared patients above and below the median. In our study, we chose to use the median baseline plasma levels as the cutoff, and this turned out to be 1.0 pg/mL. Now, let's turn to the results. There is a growing consensus among the field that plasma p-tau217 is a sensitive marker of overall Alzheimer's disease biology. Plasma p-tau217 has been used to predict responsiveness to therapy. Most recently, in Lilly's TRAILBLAZER 2 study, there was a notable increase in the drug response in people with lower levels of tau. Similar observations were made in Eisai's lecanemab study in participants with low tau burden as well. In the SHINE study, we defined subgroups as below and above the median plasma p-tau217. This median value, again, was 1.0 pg/mL. The baseline characteristics of the entire modified intent to treat population, or MITT, were reported at AAIC. These data are still available in the presentation on our website under publication. The mean age was approximately 73 years, 60% of participants were female, and the average MMSE was 21.37. Now, looking more carefully at the below median subgroup, here in the middle and identified by the blue box, you will see the basic characteristics in this subgroup are very similar to the entire population, with the expected differences in starting values as predicted by lower overall Alzheimer's brain pathology. Full details of the safety and tolerability profile from this study were also reported at the AAIC meeting, and they can also be found on the company website under publication. Briefly, treatment emergent adverse events, or TEAEs, were well balanced between treatment groups, with 76.5% of CT1812 treated individuals and 78% of placebo-treated individuals experiencing at least one TEAE. TEAEs were mostly mild or moderate. As expected, there were more drug-related adverse events at the highest, or 300 milligram dose, of CT1812. And importantly, there were no discontinuations due to adverse events in the 100 milligram dose group. Thus, in SHINE, we identified a dose range with strong efficacy signals and no troublesome side effects. We'll now turn to the subgroup analysis that was presented here at CTAD just yesterday. So looking now to the data where we see a strong response in the subgroup of patients with plasma p-tau levels below median, or by definition, half of the population. On this slide, you'll see three charts. On the left are the data for all 150 patients measuring cognition using the ADAS-Cog 11 scale over six months. The CT1812 treated participants showed 39% less cognitive loss than placebo, which is in line with current approved therapies and a very nice result from this phase 2 trial. In contrast, and as predicted, the placebo patients continued to worsen. As reported earlier in the year, this treatment effect was observed across all of our cognitive outcome measures. Now, what we find even more exciting is the strong response that we observed in the pre-specified patient group with plasma p-tau217 below the median. On the chart here in the middle, you'll see the results on the same cognitive scale, the ADAS-Cog 11. In this case, participants with below the median level of 1.0 pg/mL experienced essentially no cognitive decline. Said another way, these participants remained effectively at their starting scores throughout the six months of this trial. Additionally, you'll see that the treatment effect continues to widen over the course of the six months. This means the drug is continuing to show benefit. In comparison, on the right, you'll see the charts for the ADAS-Cog 11 scores for participants who were above the median p-tau level. These participants declined similarly, whether they were on drugs or on placebo. The ADAS-Cog 11 results were replicated in the other scales that measure cognition in this study. Looking now at the Mini-Mental State Examination, or MMSE, on the left is the difference between CT1812 treated and placebo-treated participants from the whole study population. This is the data that were reported at AAIC. The CT1812 treated participants declined 70% more slowly than did those on placebo. On the right, you'll see the results for the participants who were below the 1.0 pg/mL cutoff for p-tau217. By the end of the six-month study, the CT1812 treated participants had retained their original cognitive scores. Said another way, these participants had no loss of cognition during this trial period, according to this scale. The placebo group, as predicted, continued to decline. Importantly, the treatment effect is stronger in patients below the median baseline. These patients had very little or no worsening from the start of the study. Also, you'll see that the treatment effect continues to widen as it did with the ADAS-Cog 11 throughout the six months of this study. This means the drug is continuing to show benefit. In the SHINE study, we also included measures of function, namely the Alzheimer's Disease Cooperative Study, Clinical Global Impression of Change, or CGIC, and the Activities of Daily Living, or ADL. While these types of measures generally require larger groups and longer studies to observe change, you can see we are beginning to see clear separation with better function with the CT1812 treatment when we look at the below median p-tau217 subgroup. The data from this subgroup defined by baseline plasma p-tau217 presented today in our podium presentation, or presented last night in our podium presentation at CTAD, represent really a defining moment for Cognition Therapeutics. Our data suggests that we can identify a population through a simple blood test that we can reasonably expect will have a robust and durable cognitive benefit from once-daily oral CT1812 treatment. Furthermore, SHINE identified a dose range that is both well tolerated and shows strong trends for efficacy. Let me turn it over to one of our advisors and an expert in the field, Dr. Anton Porsteinsson from the University of Rochester. Anton? Yes. Thanks, Tony. And I want to make a couple of points. First of all, that p-tau217 is becoming the kind of dominant biomarker in Alzheimer's disease as we look at the various biomarkers in terms of their utility in aiding diagnosis. So basically, we've heard over the past year, and we're hearing it again and again here at the meeting, that p-tau217 is having the highest sensitivity of the biomarkers, of the blood biomarkers, for predicting what we would see on an amyloid PET scan or a cerebrospinal fluid test. It measures two things. It measures the level of amyloid burden, so the amyloid dysregulation, and also the level of tau burden. So the higher p-tau217 values that you have, the higher the degree of pathological damage from the hallmarks of Alzheimer's disease. And consistent with that, you actually have triggered multiple other cascades, like neuroinflammation and oxidative stress, leading to kind of more rapid neurodegeneration and more rapid clinical decline. So when you have a drug like CT1812 that has a very specific mechanism of action, it impedes the synaptic effect of toxic beta amyloid. It makes a lot of sense that this drug is going to be more effective in the earlier stage of the disease. And by that, I'm talking about pathology. It's actually interesting that it's not only within people that have mild cognitive impairment or even mild Alzheimer's disease, there can be quite a range of p-tau217 values. So it doesn't translate completely into the clinical setting. And you actually can have people with a little more kind of late mild to early moderate disease that also have relatively lowish p-tau217 levels. So there is actually the possibility that a fairly wide range of patients kind of selected by what is likely to become the most common blood biomarker in Alzheimer's disease may be specifically helped or may specifically benefit from CT1812. So that was the most exciting takeaway for me from this presentation. Anton, thank you. Tony, any other comments, or shall I jump in? No. Thanks, Anton. Lisa, please proceed. Okay. Slide 13. Here we go. Summary and conclusions. So let me say, from our perspective, you heard these sentiments echoed by Anton. We think these findings are very important. Participants with plasma p-tau less than the median taking CT1812 did not lose cognitive function over the six months of the study. This was measured in multiple ways, different scales. We believe this efficacy signal is profound. I'd go so far as to say we think results like these are the goal of every Alzheimer's drug developer. Now, the logical question you may be asking is, how does this shape our plans for CT1812? Going forward, we'll be working on a registrational path for our drug that involves developing protocols for phase 3 trials, holding an end-of-phase 2 meeting with the FDA, and of course, getting their guidance and support for our program. Slide 14. Let's just take one brief look at Cognition as a company. Let me remind you, investors, of additional studies we're running in multiple indications. As discussed today, we've successfully completed our Phase 2 study in mild to moderate Alzheimer's disease, the SHINE trial. By year-end, we anticipate that another clinical trial will read out. This is our Phase 2 study in patients that have dementia with Lewy bodies. We refer to this as our SHIMMER trial. Not mentioned on this slide is our START trial, which is a study of 540 patients who have early to mild disease. And last on the far right is a study we're recruiting right now. We're studying geographic atrophy secondary to dry AMD. This is also a Phase 2 study, which we refer to as MAGNIFY. We're recruiting over 240 patients for this study. Reminder, this is an oral drug treating a retinal or back-of-the-eye condition. Let me turn to the last slide, 15, the promise of CT1812. We believe that in CT1812, we have a first-in-class drug which displaces toxic oligomers. In multiple studies, we've shown the positive results in Alzheimer's disease patients. Our mechanism of action, importantly, is not associated with ARIA as a side effect. As a well-tolerated oral drug, CT1812 holds the promise in treating Alzheimer's disease, and it may be the first oral drug for the treatment of Lewy body dementia and dry AMD. We're going to continue to advance our clinical programs with the goal of providing patients a simple, convenient, well-tolerated drug for multiple serious conditions. Now, before we turn to Q&A, we'd like to acknowledge the people that made this study possible. Our thanks go to, first and foremost, the SHINE study participants and their partners. Without their courage and their commitment, nobody's research would advance. Our clinical investigators around the world, U.S. and international clinical research partners, our own clinical operations staff, and of course, we have to thank our many funding partners, including our investors, the NIA, and the ADDF. Now we'd like to take questions from this morning's call. Thank you. Ladies and gentlemen, we will now be conducting a question-and-answer session. If you would like to ask a question, please press star and one on a telephone keypad. A confirmation tone will indicate your line is in the question queue. You may press star and two if you would like to remove your question from the queue. For participants using speaker equipment, it may be necessary to pick up your handset before pressing the star keys. Ladies and gentlemen, we will wait for a moment while we poll for questions. The first question is from Jay Olsen with Oppenheimer. Please go ahead. Jay, may we request you to unmute your line from your side and go ahead with your question, please? Jay, may we request you to unmute your line from your side, please? Oh, hi. Sorry about that. Congrats on the presentation, and thank you so much for taking our questions. We had a couple of them. I guess maybe to start off, I guess, can you just talk about read across from SHINE and anything that we should expect from START, especially since you're studying the 200-milligram dose in START, which may have important differences from the 100 and 300 milligrams that you studied in SHINE? Tony? Sure. Yeah, so we believe that CT1812 has great potential across a wide range of disease severities. In this study, we looked at mild to moderate. And as you mentioned in the START study, we're looking at early and mild. Based on the mechanism, we believe there is potential across indications. Now, the read-through, again, we think there's a great positive. This is a positive factor, particularly the fact that we can identify the lower p-tau group as highly responsive. While this, by definition, represents half of the mild to moderate population, we should actually increase the numbers that are included as we move more into the more mild populations, so that's very good. And then, as you asked about the 200-milligram dose, indeed, we think one of the great things that came out of the SHINE study was that we were able to identify a dose at 100 milligrams that had nearly the full effect as the 300-milligram dose group, but really did not have any issues with safety and tolerability. As we said, we had no discontinuations due to AEs. We had no elevation of liver enzymes in the 100-milligram dose group. So it really defines for us a range where we can see good tolerability and really nice trends for strong efficacy. Great. Thank you so much. We're looking forward to that. And then maybe a bigger picture question is, as you look ahead to future studies of CT1812, can you just talk about how lecanemab and donanemab may factor into your clinical study plans, especially as the use of those drugs increases over time? And also, any thoughts you have on increasing the geographic range and diversity of your clinical study population? Thank you. Thank you. The next question? Yes. Tony? Yeah. Sorry. Tony, can you answer Jay's question? Yeah. Thanks. Sorry, Ziko. Yeah. Absolutely. So Jay, in the START trial, which is the early and mild Alzheimer's, we're allowing individuals to have been on a course of lecanemab or donanemab. Now, there's some restrictions as far as how long they've been on and reduction in signal and so forth. But we're allowing that for several reasons. One, we believe that there's potential for CT1812 as a monotherapy as well as in combination with other drugs. But also, we want to make sure that we're able to generate good tolerability data when used in conjunction. And we didn't want individuals having to choose between the first approved meaningful disease-modifying drugs in our study. So we've allowed that. Now, I don't think any of us know how many individuals will be treated with the new monoclonal antibodies. We'll see what happens in the market. And certainly, as we plan phase 3, we'll need to plan that, whether we require folks. We have much like START where they can have been on, or we do studies completely independently, remembering that in our range, we have a large number of individuals who are not really good candidates for those antibodies as well. So those plans are being made right now. Tony, it's Anton. Hello. Can I make one comment in connection with Jay's question? And that was about basically expanding the range of historically underrepresented people. And I want to point out that the START study is done kind of in collaboration with federal funding and the Alzheimer's Disease Clinical Trials Consortium. And there is tremendous effort there on reaching out to historically underrepresented groups. We just completed recruitment for another study where we actually had a very, very commendable recruitment of minoritized populations. And the focus is the same here. With this being a federally funded study, there's great emphasis that we will expand our reach, and I'm pretty optimistic that we'll see that. So let me conclude with that. Thanks. Great. Thanks, Anton. Thank you, Anton. Jay, one reminder. Superb. Half our patients from the SHINE trial came from Europe. So it was half, half U.S., ex-U.S. So that does not necessarily give you the underrepresented populations that Anton was referring to. But myself, from where I sit, I'm really pleased that a small company could orchestrate a trial in important places around the globe. So I believe as we go forward, we will look to find those populations in broader geographies. Great. That's super helpful. Thanks so much for taking all the questions. Thank you. The next question is from the line of Mayank Mamtani with B. Riley Securities. Please go ahead. Yes. Good morning, team. Thanks for taking our questions. And good to see this helpful pre-specified subgroup analysis. A couple of questions from us. Could you comment on how the median p-tau level you saw here compares to what has been observed in other amyloid antibody trials? And is there some sort of a cut-off-based sensitivity analysis you may have done to further corroborate those results? I understand that would be more on a post-hoc basis, but just want to understand this one peak, this level that you're using to define low and high, how that is looked at from other studies. If Dr. Porsteinsson have any perspective on that. And then I have a follow-up. Sure. Yeah. So this median was simply. We measured p-tau in our participant population, which was MMSE of 18 to 26. And then we used the median as a cutoff to run this comparison with equal groups on either side of the cutoff. That cutoff, as we showed here, ended up being 1.0 picograms per mL. By definition, it was the middle or halfway, included half on either side within our population. Now, as you're asking, compared to other study populations, obviously, there's a lot of different assays out there. You'll see different reports of the levels. However, the lab that ran this assay has normative data from a wide range of studies. Our median level and our mean level is nearly identical to theirs in the mild to moderate population. One thing to clarify is, by definition, these are not low tau. So these are all folks who had confirmed amyloid pathology and through their CSF had confirmed amyloid ratio and an elevated phospho-tau to total tau ratio. So these are not extremely low tau. These are just the bottom half of the population here. And looking at the sensitivity analyses, that's exactly what we're doing right now. So stepping through our data set, looking at levels just above and just below this median to see if there's a particular point that we may use for future studies as a cutoff. But that has not been completed yet. Got it. Thank you. And I guess the related question is on the target population and maybe the treatment duration that you are looking for in the next study. And if you have already planned end of phase two meeting or submitted a request for that, any input on that would be helpful too. Yeah. Sure. Are you going to the summer? Oh, go ahead. You answer, Tony. Okay. Yeah. So absolutely. So we're working on that right now. These data give us really good confidence that we could do both six-month studies as well as the longer 18-month studies, which obviously have different benefits moving forward. You've probably seen announcements from other companies and have seen current companies that are doing studies that are of different lengths, including six months, 12 months, 18 months. So we're putting together those plans now. And then, obviously, we'll not proceed to phase three without agreement from FDA that the plans are reasonable. Okay. And lastly, on the DLB update coming up, I know you presented the baseline patient information also at CTAD. And it looks like, from a quick review, that you have enrolled a slightly earlier stage patient cohort there. Anything to glean from there? And also, obviously, broadly from the SHINE study that informs your confidence for SHIMMER? Thanks again for taking our questions. Yeah. So you're right. So we presented the baseline characteristics. And we had announced early in the year that we had completed enrollment. There's six months of treatment. And obviously, those will be rolling out. And we'll be reporting data soon. As far as the read from this study, it's very encouraging that we have a molecule that can displace oligomers, and we see positive effects in Alzheimer's disease. To me, that has to be encouraging as far as the potential in DLB. Now, again, we'll wait and we'll see the data, which we'll be reporting out soon. But I think it's encouraging. As far as the characteristics, they're more or less as we expected. We define a range of cognitive impairment. Unlike Alzheimer's disease, there aren't definitive biomarkers for defining brain pathology. But overall, very much as we had expected. Thank you. The next question is from the line of Elemer Piros with Rodman & Renshaw. Please go ahead. Yes. Good morning, Lisa. Hello, Tony. Good morning. Yes. What I observed that you had to exclude 12 patients from the p-tau217 measurements. Is it because you didn't have samples for those 12? Yeah. Exactly. Those are just individuals where there are insufficient CSF samples to complete all of the assays. That's exactly correct. Yes. And so when we look at the, I think, Tony, you characterized it as not low tau but medium tau population and the ones above the cutoff, their baseline MMSE scores were somewhat overlapping 14-29 and 13-28. So is there a correspondence between the lower tau population and what we would call a mild Alzheimer's disease? Yeah. And I think Anton had tried to explain some of that as well. There certainly is some correlation. So those with the much higher tau burden, you would expect to have a somewhat worse clinical picture. And you can see that in the baseline characteristics where their starting MMSE scores were a little bit worse in the high tau compared to the low tau. Now, as we were also trying to explain, there isn't a very steep relationship here. And that when people presenting with mild, moderate, or severe clinical symptomatology will have a wide range of low to high tau burden. So whether we are treating the most severe or the most mild, there will be individuals with lower and higher tau. Yes. And lastly, Tony, would you have expected a lowering of p-tau217 levels due to the drug administration over this six-month period? It's hard to say. I believe that as we look in larger and particularly longer trials, the signals of protecting and slowing neurodegeneration will become much more obvious. At the AAIC meeting from the full SHINE population, we reported the reduction in the neurofilament light chain in the CT1812 treated individuals. I think we'll begin to see other signals as we do larger and longer trials. But you haven't looked at tau level changes over this six-month period yet? We have not reported that and looked real carefully at that yet. Obviously, as we have all this blood and CSF biomarkers, we'll be putting out much more careful reports around the changes and the comparison between the blood and the CSF, hopefully very soon. Thank you. Thank you very much. Absolutely. Thank you. The next question is from the line of Aydin Huseynov with Ladenburg Thalmann. Please go ahead. Good morning, everyone. Thank you for additional analysis. I got a couple of questions. So I just want to go back to p-tau217 questions. So could you share if you have the absolute numbers of p-tau217? I know you talk about median, but would be curious to know what are the absolute numbers. And also, if you could, what was the name of the test and what is the regulatory status of that test that you used? Yeah. Sure. So maybe you can clarify what you mean by the absolute numbers. So the 1.0 picograms per mL is the absolute number. You're looking for the range or? Yeah. And what is the name of the test that was used? It's not commercially available yet, right? Yes. Yeah. So this is an assay that we ran with our partners out of Amsterdam. And it's the, I'm blanking on the name of it. I apologize. The ALZpath assay. And it is commercially available. Now, like all assays, it's dependent upon lab and so forth. And so you run them in batches. But this ALZpath p-tau217, it's run on the Simoa platform. It is commercially available. And it's generally pretty widely used. Yeah. Tony, if you let me just pipe in, it's Anton. That'd be great. Yeah. It was the ALZpath Simoa. And widely used. We saw actually a couple of presentations here this morning about p-tau217 from Sweden, study done in Sweden, study done for another pharmaceutical company using exactly this technology. So it is in wide use. And one of the attractiveness to it is that it's quite scalable. It doesn't require quite as much complicated machinery like, for example, the mass spec measures. Okay. Thank you. This is helpful. Another question I have is, I know that you presented the full analysis of 100 and 300 milligrams. But could you also comment on the sort of low p-tau217 levels for each specific group, 100 and 300 milligrams, if you had that analysis? Sure. And as you said, that's not shown here for simplicity. And because our first analysis plan were the combined groups, we chose just to show that. So much like we showed at the AAIC meeting with the full MITT population, there wasn't an obvious difference between the 100 and 300 milligram dose groups. They both saw the benefit of effect in the low tau group. In some measures, the 100 was a little better. In some measures, the 300 was a little better. So again, for us, it's encouraging that we're at a level that is presumably effective. Obviously, we'll need larger and longer trials. But also, with that 100 milligram dose, we don't have issues of side effects causing discontinuations or other safety issues. So when we publish this data, we'll be sure to obviously include the 100 and 300 as well as the combined groups. Okay. Thank you. And the last one I have is, it seems like ADAS-Cog is sort of more sensitive to this p-tau analysis compared to ADL and CGIC. And maybe this is just an impression. Could you comment on that? How each of these three different endpoints are actually sensitive to p-tau analysis? Yeah. I mean, certainly, the ADAS-Cog scale, and we didn't show it here, but the ADAS-Cog 13 as well, they showed a very nice robust response. If you look at the curves, we really saw a very similar thing with MMSE as we saw with the ADAS-Cog 11, where before, it wasn't very obvious that they were continuing to widen. Whereas now, with the below median p-tau group, it's very obvious across the outcome measures that the treatment effect is continuing to get greater throughout the course of the study, which obviously makes us very excited to see the true potential as we do larger and longer trials. I don't think that we have enough individuals or just not have studied this enough to say that one is particularly more responsive than the other. So Tony, let me also chime in something here. So the difference between these is that one is a cognitive scale that is pretty dynamic. The other are functional scales. And you expect to lose, for example, daily function a little slower. So the six-month time frame may have an impact here. The other thing is that if you think about how CT1812 is supposed to work, especially in a shorter-term study in terms of improving synaptic function in particular, it would have face validity to me. I'm actually glad to see that it's the cognitive measure, which kind of shows the more kind of dynamic synaptic function or reflects that better, maybe shows a larger separation than some of the other scales. Pure speculation in some degree, but still kind of what makes sense to me if I was to speculate. Got it. Thank you. Thanks so much. Very helpful. Appreciate the analysis. Thank you. The next question is from the line of Daniil Gataulin with Chardan. Please go ahead. Yeah. Good morning, guys. Thank you for taking the question. I have one on the correlation between p-tau217 and the NfL biomarker. So earlier, you reported a significant reduction in the high-dose group, but wanted to ask if you see any correlation between the below median p-tau217 and the effect on the NfL. Yeah, so we haven't really reported the subgroup analyses related to differences in biomarker responses. I can tell you that myself and Michael Grundman and our other advisors took a look through to make sure that there's nothing that would give us any worry, but we haven't done that full analysis, and it'll be coming out hopefully in poster form and then paper form sometime soon after. All right. Thank you. Thank you. Ladies and gentlemen, that was the last question for today. I would now like to hand the conference over to Lisa Ricciardi for closing remarks. Terrific. Thank you, Ziko. Results from this study showed profound slowing of cognitive decline in patients with lower levels of p-tau, an important marker of Alzheimer's disease pathology. These participants maintained their cognitive function throughout the study. And on multiple measures, these patients experienced almost no decline. And the benefit continued to widen over time. Findings from this and other trials will guide the development of our clinical protocols. And we look forward to meeting with the FDA to determine how we best progress with our phase three program. Thank you for your interest in our program. Thank you for your questions. Tony, Anton, thank you. And operator, we're done. Thank you. This concludes today's study conference. You may disconnect your lines at this time. Thank you for your participation. Goodbye.