Ladies and gentlemen, thank you for standing by. At this time, all participants are on a listen-only mode. After the speaker's presentation, there will be a question-and-answer session. Please be advised that today's event is being recorded. I would now like to turn the call over to Helen Rubinstein, Vice President of Investor Relations and Communications at Neumora. Please go ahead. Good morning, everyone, and thank you for joining us today to discuss top-line data from the Signal-Seeking Study with NMRA-511 and Alzheimer's disease agitation. Before we begin, I'd like to point out that this presentation contains forward-looking statements which are based on our current expectations and beliefs. We have a number of important disclosures on this slide, which we urge you to read. With me today are several members of Neumora's management team, including Co-Founder, Chief Executive Officer, and Chairman Paul Berns, President Josh Pinto, Chief Scientific Officer Nick Brandon, and Chief Operating and Development Officer Bill Aurora. With that, I'll now turn the call over to Paul to begin. Paul? Thanks, Helen, and good morning, everyone. We're pleased to be with you today to review data from our Phase IB Signal-Seeking Study with NMRA-511 and Alzheimer's disease agitation. Now, Neumora was founded with a clear purpose: to tackle the brain disease crisis. And to achieve that goal, we have focused on advancing programs with best-in-class pharmacology and brain-penetrating chemistry, targeting novel mechanisms of action with the potential to improve upon the current standard of care for hundreds of millions of people. The data we're sharing today is an important step forward for our vision in Alzheimer's disease agitation. We're very pleased that the Phase IB study achieved its goal to identify the clinical effect of NMRA-511 in this underserved patient population, demonstrating a compelling effect size that supports further development. Now, before we dig into further detail, I'd like to take a moment to thank the patients, caregivers, and investigators involved in this Signal-Seeking Study for your important contribution to advancing research in this devastating condition. I'll now turn the call over to Josh to talk more about our strategy in Alzheimer's disease agitation. Then Bill and Nick will review the data in more detail. Josh? Thanks, Paul. Agitation in Alzheimer's disease affects over 70% of individuals living with Alzheimer's disease dementia and is among the most disruptive of AD symptoms. Managing behavioral symptoms of the disease, such as agitation, is an important treatment consideration as they're associated with greater caregiver stress, earlier placement in long-term care facilities, and increased morbidity and mortality. Anxiety is thought to be an underlying driver of aggression in AD, and as this population ages, the unmet need will continue to increase for patients, their caregivers, and the healthcare system. It is well established that there is a significant unmet need for patients with agitation related to Alzheimer's disease and their caregivers, and as a result, we believe there's a highly compelling opportunity for a product with a differentiated benefit-risk profile. The currently or soon-to-be-approved products in this space are burdened by tolerability issues and limited efficacy that can be a concerning factor in a vulnerable population, reinforcing the opportunity to improve the benefit-risk profile of drugs for this indication, and that is why we are so encouraged by the NMRA-511 data we're sharing today. We believe that the clinical effect seen in the Phase IB study shows that NMRA-511 has the potential as a next-generation treatment for AD agitation. The goal of the Phase IB study was to understand the effect size of NMRA-511 in AD agitation, and it achieved that goal. In the study, NMRA-511 demonstrated an effect size similar to Auvelity in the total population and an even more pronounced effect size in patients with elevated anxiety at baseline, greater than Rexulti. Notably, these effect sizes were achieved with a more favorable safety and tolerability profile, which leaves room to evaluate higher doses, which could drive greater efficacy. Importantly, we believe this finding is well-aligned with NMRA-511's mechanism of action. Anxiety is often present early in the disease course, so we believe that these findings suggest potential for an important role for NMRA-511. These results suggest the opportunity to optimize or tune the profile of NMRA-511 as we advance further development, enabling us to study higher doses, which we believe will enable us to achieve a differentiated benefit-risk profile. So let's dig into the data in more detail. First, Nick will start by walking through the preclinical evidence for the mechanism. Nick? Thanks, Josh. As shown on this first slide, the link between vasopressin and regulation of anxiety in the brain has been extensively characterized in both preclinical and clinical studies. The left-hand side of this slide talks to the large body of preclinical data, which shows that vasopressin modulates anxiety-related behaviors, with the data at the bottom showing an example of a V1a receptor antagonist modifying anxiety-related behaviors in a classical test of anxiety. There are also a set of human studies which support the translation of this biology and, critically, the impact of V1a antagonists. The graph on the right-hand side shows that in healthy volunteers, administration of intranasal vasopressin increased autonomic responsiveness to threat stimuli and increased anxiety, while the headline titles of the publications on the far right are with a V1a antagonist known as SRX246. One study in healthy volunteers showed suppression of anxiety in a human anxiety model, while the same compound showed reduced aggressive behaviors in a subgroup of patients with Huntington's disease. Together, we believe this data supports the strong link between V1a and anxiety. Our own work with NMRA-511 is consistent with this body of evidence. As part of our preclinical package, we conducted a human threat test in marmosets, which is a test that measures stress and anxiety levels. In the model, marmosets were exposed to an unfamiliar human driving high levels of anxiety. In our study, the marmosets that received NMRA-511 demonstrated reduced anxiety behaviors without reduced locomotor activity. These data were presented previously at the ACNP conference in 2022. This strong connection between anxiety and V1a drove our decision to pre-specify analyses of patients with elevated anxiety in the Phase IB study. This background should set up the data you will now hear Bill talk through from this study. Over to you, Bill. Thank you, Nick, and good morning, everyone. I'll start by reviewing the design of the Phase IB study. This was a two-part Signal-Seeking Study that was not powered to detect statistical significance. Instead, we used this study to evaluate the effect size of 511 to inform additional development in AD agitation. Part A was a two-week randomized double-blind placebo-controlled period that was designed to assess the safety, tolerability, PK, and cardiodynamics in healthy elderly participants. We shared data from Part A at our R&D day in October, and they are available in the appendix of this deck, which is posted on our website. Part B was multi-center randomized double-blind placebo-controlled as well, a parallel group cohort to evaluate the safety, tolerability, and efficacy of 511 among adults with agitation associated with dementia due to Alzheimer's disease. It's an early-phase study. It wasn't powered for statistical significance, but that being said, the primary endpoint for Part B was to change from baseline to week eight in our CMAI total score. We also pre-specified an analysis of patients with elevated anxiety for the reasons Nick mentioned: the underlying biology, the mechanism of action, and the fact that anxiety is highly clinically relevant as a symptom in AD agitation. Anxiety was assessed by the RAID, or the Rating of Anxiety in Dementia Scale. This is a validated 18-item scale, a score of 11 or greater or 12 or greater, or thresholds for clinically significant anxiety. Part B enrolled 80 patients with AD agitation across two arms: 511, 20 mg twice daily, and placebo. On the following slides, I'll review data from Part B of the study. As you can see from this slide, the baseline demographics and characteristics were balanced across 511 and placebo groups, generally speaking. You'll note that the baseline rates of anxiety were slightly elevated in the placebo group, meaning that if we had higher rates of anxiety, one would expect perhaps the active to have an even more profound effect than I'm about to share, which we're really pleased with. On average, the baseline CMAI scores were 68.2 in the 511 group and 68 in the placebo group. On the next two slides, we'll show data for two populations in the study: the modified analysis set, which includes 71 patients, and the pre-specified elevated anxiety population with a RAID of 12 or greater, which includes 36 patients. This slide shows data from the modified analysis set. As you can see on the left, 511 drove a clinically meaningful reduction in CMAI total score, with an absolute reduction of 15.7 points at week eight and a Cohen's d effect size range that ranged from 0.2- 0.23. These findings support that 511 has the potential as a treatment for AD agitation. The right side of the slide shows the CMAI subscore results at week eight. I'll take a moment to highlight the aggression subscore. This measure may be important for both patients and caregivers, as caregiver safety is important when we think about behaviors such as hitting and pushing that can be dangerous. As you can see, 511 drove a 5.3-point reduction in the subscore, a particularly important finding when one considers the treatment goal of prolonging the time to institutionalize care for patients. Turning to patients that had elevated anxiety at baseline, as you can see on the left, 511 demonstrated an unsurpassed effect size in this pre-specified analysis, with a 20.1-point absolute reduction in CMAI total score at week eight and a Cohen's D effect size range from 0.51- 0.64. This represents unsurpassed effect size as it had been demonstrated in AD agitation, and the absolute reduction is similar to the results demonstrated by Rexulti in Phase III. The CMAI subscore for elevated anxiety populations is shown on the right. Here you can see similarly robust results on the CMAI aggression sub-factor score. Additionally, we know from other sponsors that the FDA has been particularly interested in CMAI subscale data, so we're pleased to see similar findings with 511 to those shared by other sponsors. Turning to tolerability and safety data, the profile here is favorable. The data on the left shows the most common adverse events seen in either group. Treatment-emergent adverse events in the study were typically mild to moderate in severity, and importantly, the discontinuation rate due to adverse events in the study was very low at 2.5%. I'll also point out that we did not see sedation or somnolence in the Phase IB study, a finding that has been associated with other treatments for Alzheimer's disease agitation that may be troublesome in this vulnerable population. We believe these tolerability and safety findings support the evaluation of higher doses of 511, which we believe will enable us to achieve a differentiated benefit-risk profile. In summary, there are several key takeaways from the Phase IB study. First, 511 was safe and well tolerated. Second, 511 demonstrated clinically meaningful reductions in CMAI total score in the modified analysis set, with an effect size similar to the current or potentially soon-to-be-approved medications in this indication, and an unsurpassed effect size in patients with elevated anxiety. Third, 511 drove important improvements on the most clinically relevant symptoms of AD agitation, those measured by the CMAI aggression subscale. These symptoms often cause patients to move into long-term care facilities, so managing them is an important treatment goal. Fourth and finally, the results seen in the study are well-aligned with the understood mechanism of action for 511. These data give us confidence to pursue clinical development for 511 as a treatment for AD agitation. With that in mind, there are three next steps for the 511 program. First, we plan to initiate and complete a MAD extension cohort in 2026. We're working expeditiously to design and optimize MAD extension, and we're excited to provide further details when we initiate the study. Next, we plan to transition from the current twice-daily formulation to a once-daily extended-release formulation in 2026. In addition to the once-daily treatment being more favorable for patients and caregivers, we believe the extended-release formulation will expand our IP, adding four years of exclusivity to our current expectations. We expect to be able to exclusively market 511 into 2046 based on the composition of matter or patent. With these steps, and once upon completion, we plan to initiate a Phase II/III study for 511 in AD agitation. In closing, we're really excited about the potential for 511 to make a difference for patients and caregivers who are facing this devastating condition. With that, I'll turn the call over to Helen. Helen, back to you. Thanks, everyone, for your time and participation today. I'll now turn the call back over to our operator, Shannon, to host our Q&A session. Shannon? Thank you. To ask a question, please press star one one on your telephone and wait for your name to be announced. To withdraw your question, please press star one one again. Please stand by while we compile the Q&A roster. Our first question comes from the line of Myles Minter with William Blair. Your line is now open. Hi. Thanks, everyone, and congrats on the data. Two questions for me. One is on the ability of you to go to a higher dose of MRA-511, where you think you can elevate from this 20mg BID dose that we're seeing today. And the second is, in that sort of Phase II/III trial that you're thinking about and as you get more data from this dose expansion, would you formally enrich a patient population for baseline anxiety here as you did on the RAID sub-analysis? Thanks very much. Yep. Hey, Myles. It's Josh here. Happy to answer those questions from you. I think on the higher dose potential, Myles, in terms of the dosing for this study, in our previous MAD, it had dosed to 40 mg QD. We elected 20 mg BID in this study just to maintain more AUC coverage and not hit C-MAX. We believe that we can dose higher with this product given the clean safety profile. And we actually think in these neuropsych conditions, dosing to an MTD could be important to just drive the maximal amount of drug in. With NMRA-511, we had done modeling work on receptor occupancy that suggested that these doses would be above the 90% threshold. But unfortunately, for V1a, there is not a receptor occupancy ligand, so all the work is just based on modeling. So I think for this one, Myles, our goal is just going to be to push higher. And we think with the pre-clinical margins we have and the safety and tolerability, we'll be able to go much higher. At this point, we haven't outlined exactly where the doses are yet, though. And then, Bill, maybe do you want to answer the question on the Phase II, Phase II formal enrichment? Sure, Myles. With respect to the data that we've seen in the Phase IB, we're pleased with the overall population results we've seen, although we have seen a more pronounced and an unsurpassed efficacy signal in the patients with elevated baseline anxiety. So we are in a position where we could enrich, but we don't feel that that's critically necessary to be able to reap the full benefits here that we've seen. So more to come on the details of the design and the population that we'll pull into the study. Yeah, and I would just add, Myles, that if you look at just the prevalence of anxiety within AD, it's about 70%, so it's an equivalent large population, and there's significant overlap in terms of AD anxiety and AD agitation, so we actually think this is a large market opportunity. Whether we formally enrich or not, we think that the market here is large, so in the end, we will be capturing the broad potential of the AD agitation patient population. Thank you. Our next question comes from the line of Douglas Tsao with H.C. Wainwright. Your line is now open. Hi. Good morning. Thanks for taking the questions and congrats on the progress. So just to understand, when we think about this sort of Phase II, Phase III study, it sounds like your initial inclination is not to necessarily enrich for the anxiety levels. But will that necessarily be a pre-specified subpopulation so that in theory, it could be confirmatory evidence down the road if you see that signal? Yeah. Doug, this is Josh here. I think one important thing to remind folks of is if you look at the Auvelity pivotal studies, so the ADVANCE studies, as well as study six and seven from Rexulti, those programs actually did enrich in their studies. They not only had a CMAI cutoff, but they had an NPI cutoff as well to enrich for patients with an NPI agitation score above four. So we think there's precedent out there, Doug, for these subtle enrichments that just help to hone in on the patient population. So as we move forward, we are going to think about what is the optimized patient population. But we think with this data, we absolutely have a path forward to look for a broad opportunity in terms of treating patients with AD agitation. But if we can improve the baseline anxiety scores, we think that there's an even elevated opportunity. And one thing I would note, if you look at our baseline demographics, the baseline RAID score is the one area where there was slight imbalance between placebo and active. The placebo actually had a higher baseline RAID score of 14.3 than active 511 at 11.8. And so we actually believe if those groups are balanced in the total population, you might even see a larger treatment response. And so we're actually feeling, Doug, fairly confident in terms of how we move forward, whether we're thinking about the full broad population or whether we think about slight enrichment for anxiety, as we know there's precedent with both the other sponsors that have enriched in their pivotal studies. And then just, again, as a follow-up, just given the tolerability that we've seen, as well as magnitude of the signal, how are you thinking about going into broader indications where sort of agitation and anxiety are prevalent? Yes. And so, Doug, with this mechanism, we've seen other sponsors that have studied V1a receptor antagonists in a range of indications. Autism, PTSD have been some of the historical ones. We're now seeing folks moving into social anxiety and GAD. Our focus right now is AD agitation. It is a very large kind of patient population, significant unmet need. And we're first going to look forward to moving there. But we see an opportunity here broadly across a range of other anxiety potential populations. We'll look to explore those further down the road. And just a final quick one. Timing on completion of the MAD studies? Doug, we're planning to initiate the MAD extension study that tests higher doses of NMRA-511 this year. We haven't provided any specifics yet on exactly when we'll initiate it. The current plan is to complete that by the end of the year, which would support moving into a Phase II or three study thereafter. Great. Thank you. Thank you. Our next question comes from the line of Yatin Suneja with Guggenheim. Your line is now open. Hey, guys. Thank you for taking my question. Just a couple for me. Just first on the data, could you just comment? I know these are just fresh data you're still analyzing, just consistency of data across other endpoints that you might be looking at. So that's one. And the second question is on the other update that you provided on the navacaprant, you are increasing the size of the study by 25%. Just talk a little bit about that. What is leading you to increase the size and then how the disclosure is going to happen for the navacaprant program? Thank you. Yep. Hey, Yatin. This is Josh. Maybe I'll answer your second question on the navacaprant update this morning, then I'll turn it over to Bill to really focus on the consistency of the other data in the 511 study. And so in terms of the release this morning, I think what we highlighted is that we are going to look to maximize the potential patient population within KOASTAL-2 and 3 studies. We previously disclosed our protocol allows for up to 25% increase in enrollment. I think the reason we're doing this is since we paused the studies at about this time last year, we implemented SAFER and VCT to provide additional control measures to get a high-quality patient population. We believe that we're seeing what we want out of those measures in terms of higher screen fail rates. And our team feels like we're getting a higher quality of patient population into the KOASTAL-2 and KOASTAL-3 studies. And so we want to maximize the potential patient population. So what you'll see from the readout in the second quarter is a combined readout of both KOASTAL-2 and KOASTAL-3. We'll be able to provide top-line results on KOASTAL-2, top-line results on KOASTAL-3. We'll also be able to provide some data on the post-pause pooled population, which should be north of 400 patients to give a true read of does the improvements in patient selection truly work for navacaprant. And so we're really looking forward to it. And we're thrilled that we've been able to kind of get what we believe is a more optimized patient population in the KOASTAL-2 and KOASTAL-3. Bill, maybe over to you on the consistency of the data. Sure. Thanks, Yatin, for the question. We are, as you mentioned, just with the data in hand, fresh, hot off the press, going through the additional information. Thus far, with what I've seen, the data look consistent and concordant with what we've gone through, and so we're pleased with overall the data that we have seen from what we've presented today and consistent with the findings for the data that come from other rating scales as well. Thank you. Our next question comes from the line of Brian Abrahams with RBC Capital Markets. Your line is now open. Hey, guys. Good morning. Thanks for taking my questions. Two for me. I guess first, just as you're thinking about dose escalation, I'm curious if you saw any relationship between exposure and effect size in this initial study there and the degree to which that might support further dose escalation? And then secondarily, it looks like the strongest signal that you're seeing is around aggressive behaviors. And so I'm wondering if there might be ways, as you kind of continue the program going forward, to further enrich for that signal in Phase II, III and/or pivotal work? What's the regulatory amenability like around these types of CMAI sub-scores? Thanks. Yeah. So Brian, this is Josh here. On the exposure effect side, I think what we did see in the MAD studies, Brian, was dose-proportional PK and response. In this study, we only really looked at 20 mg BID. So the exposure response or the exposure curve is not very broad. That is why we want to look at exploring higher doses. And we're in a proper dose-ranging study next, Brian, is to get this exposure effect size curve. But I think with where we are, we're quite pleased with the effect size we've seen with the 511 thus far. And then in terms of the strongest signal around aggressive behaviors, I would just remind you that Rexulti and Auvelity in their pivotal studies did enrich, as I mentioned before, for more agitation using the NPI agitation index, requiring a score above four. And so I do think we have seen other sponsors enrich. But Bill, maybe I'll turn it over to you and see if you want to comment any more on the strong signal we found in the aggressive behaviors. Actually, I think you covered it really nicely. Nothing more to add at the moment. I guess I was thinking more in terms of enriching for the endpoint itself rather than the population. Is that a possible go-forward endpoint? Yeah. So Brian, we could talk to the agency about it. Bill, I think as you commented, what we know from agency commentary on the Rexulti label, Brian, is that they put a lot of weight not only into the total CMAI score, but how the factors moved. And if you look at the Rexulti label and how their factors moved, they moved almost identically to how 511 moved them, where you saw the largest response on the aggressive behaviors and a more smaller response on the other factors. And so I don't know at this point, Brian, if we'd formally enrich for another measure. But I do think as you look forward, there is commentary out there where the agency absolutely puts weight not only in the total score, but in the factor sub-scales as well. That's super helpful. Thanks again. Thank you. Our next question comes from the line of Graig Suvannavejh with Mizuho. Your line is now open. Hey, good morning. Thanks for taking my question. Congrats on the data. Maybe just a big-picture question on the AD agitation opportunity for 511. Can you provide maybe your assessment of how Rexulti has performed in this indication? Any sense of market share penetration for the asset? And also your thoughts on Axsome's AXS-05 in AD agitation and its potential there? Any pluses and minuses that you see? And And then positioning of 511 in the context of those two assets. Thanks. Yeah. Absolutely, Graig, and so I think in terms of how we see 511 positioned relative to the two programs out there, so Rexulti, which is obviously approved, and Auvelity, which is potentially soon to be approved. It's clear with Rexulti that it's really the side effect profile and the black box warning for mortality and elderly is some of the challenge there as it relates to bringing that program forward, and so as we've said for about the last year, we think that in this population, which is a vulnerable elderly population, we need to be focused on bringing new therapies to market that have a much better benefit-risk profile so that can drive much more tolerability while still giving comparable efficacy or is driving much more significant levels of efficacy. And so as we look at the landscape here, what we believe we've demonstrated from 511 is that we absolutely have a favorable safety and tolerability profile. And as we compare against that relative to data that other sponsors put out, feel pretty good. We don't see any of the challenges that Rexulti has seen. We don't have sedation or somnolence in our study. And so we think that there are absolute tolerability advantages. As you look at the effect size, we feel like we've got the opportunity to tune. And that's what we're going to be really focused on as we move forward this year. We've got a very compelling effect size comparable to what Axsome's generated for Auvelity in the total population. As I mentioned there, I actually think that that score could be slightly higher if we had balanced on the RAID score at baseline between active and placebo. And then we see when we enrich for elevated anxiety, which Nick highlighted today is absolutely linked with the mechanism of 511, we see unprecedented and unsurpassed clinical effects. And so we believe that within this range and this patient population with a drug that is safe, our ability to dose higher and really push an opportunity is quite compelling. And so, Graig, we think that there's quite a big opportunity in this space. It's a large market opportunity. Almost all the patients with Alzheimer's experience some form of agitation or anxiety. And we think that a product like 511 that is very safe and well tolerated with a strong effect size should have a great opportunity within the treatment paradigm. Okay, Graig, just a quick follow-up on your other strategic priorities that were announced this year. Just on 215, the NLRP3 inhibitor for obesity, I think slight changes in timelines, but still data this year in 2026. Can you give us a sense of kind of how you're viewing that opportunity against the ever-changing competitive landscape, more broadly speaking, in obesity, especially from a small molecule perspective? Yeah. Absolutely. And Graig, just to update, so I think that the update we provided on 215 this morning was just a slight change. We've moved our guidance from clinical initiation in the first quarter to first half of this year, but still anticipate delivering proof of concept top-line data by year-end. In terms of the program, where we really view the potential for this opportunity is in the emerging oral landscape. As we think about the weight loss space, the incretin-based injectable therapies such as the GLP-1s have driven great weight loss, but the GI tolerability issues are a challenge. And as we're seeing the market move towards more cash pay, we think that an oral small molecule can offer a couple of commercial advantages. One, the cost of goods for a small molecule should be lower than the injectables, and they do not require cold chain storage for global distribution. And so what we've seen with 511 is the first oral therapeutic with a novel mechanism that can deliver incretin-like weight loss, but with what we believe should be a tolerability profile that avoids the GI side effects in an oral formulation. And so, Doug, we're actually, sorry, Graig, we're really actually really excited for bringing 215 forward into the clinic because we think that this could be really the next wave of innovation with NLRP3 inhibitors coming up as the next big oral opportunity within weight loss. And so we'll be moving 215 into the clinic in the first half of this year, and I'll look forward to generating 12-week weight loss data before the end of the year. Okay. Thanks. Thank you. Our next question comes from the line of Paul Matteis with Stifel. Your line is now open. Hey there. This is Julian. Thanks so much for taking our questions. I guess just more broadly, really interesting result in the elevated anxiety subgroup. I guess just given historically neuropsych trials moving from early exploratory phase one, Phase II studies to Phase II, Phase III, there's some aggression and effect size. And this data is based on 16 patients. I guess what just gives you confidence that you're going to be able to replicate the signal there? And then I guess just more broadly as well, do you plan on sharing the overall effect size for the more fulsome patient population at any time, i.e., not the modified analysis, but the ITT analysis? Thank you. Yeah. And Julian, maybe I'll hit the second question first, and I'll turn it over to Bill to really hit on what gives us confidence we can replicate the effect size and really focuses around some operational pieces. But in terms of the more fulsome population, really there were two patients that were excluded from placebo due to rater changes that drove outlier data sets that was greater than three standard deviations from the mean. Julian, we've run the analysis. When we include those, we still see a very strong effect size in the elevated anxiety population that is equivalent to or still greater than Rexulti. And so we've run some of these sensitivities, and the data still looks fairly strong on that side. But Bill, I'll turn it over to you, and maybe you can hit what gives us confidence we can maintain this effect size moving from Phase II to Phase III. Sure, Josh, and thanks, Julian, for your question. As you know, this was a Signal-Seeking Study. We did not put into place a number of things that we will as we move ahead. Those things include things like ensuring patient compliance and adherence with medication, things like AiCure, which have been utilized in other programs to ensure consistency with medication being taken, to a variety of other operational factors that might include enriching for agitation, as other sponsors have certainly done. These are things we could do operationally as we move ahead, so this is intended to be one study where we move forward to seek the signal and can certainly put into place a lot of the things that other sponsors have and that we ourselves have done in the MDD space as well. Great. Thank you. Thank you. I'm sure no further questions at this time. I'd now like to hand the call back over to Paul Berns for closing remarks. Thank you, operator. And thank you all this morning for joining us today to discuss the top-line data from this Phase IB Signal-Seeking Study with NMRA-511 and Alzheimer's disease agitation. As always, your questions were well thought out, and we do appreciate the input. As you can tell, we're really quite pleased with regards to the demonstrated unsurpassed clinical effect size on the CMAI total score in the patients overall, and in particular in those patients with the prespecified elevated anxiety. And I think that's key. We clearly understand the power of those data. And as Bill has noted and Josh noted today, there are various avenues we could take, precedent set by other sponsors already in working with the FDA, for which there was always natural enrichment that they took in their programs. We're really quite excited with regards to what this data very clearly specifically tells us and how we can look to index into a population that improves our risk. We believe that can improve our risk-adjusted probable success as we move into a dose-ranging MAD extension, as well as we think about further Phase II/three work. It's quite exciting. We believe the drug has the potential to demonstrate an unsurpassed tolerability, safety, and efficacy profile as we move forward in this area of high-impact medical need. With that, I wish you all a happy New Year and have a good day. This concludes today's conference. Thank you for your participation. You may now disconnect.