Romero, and I'm one of the senior biotech analysts here at J.P. Morgan. Our next presenting company is Neumora Therapeutics, and presenting on behalf of the company, we have CEO Henry Gosebruch. Henry, over to you. Okay, short and sweet. Thank you, Tess, for that introduction, and yeah, it's great to be here on Monday morning of J.P. Morgan, and I'm certainly excited to tell you all about Neumora and why we believe Neumora is a very compelling investment opportunity. Now, one important element of our story is that we have not one, but two clinical assets in our pipeline, each with a clinically validated mechanism, and each with important data coming in 2024. In addition, we have a rich set of additional clinical catalysts, both in 2024 and 2025, each with the opportunity to drive significant shareholder value. 2024 and 2025 will be exciting years for Neumora. I know we're eager to jump in, but before I can, I have to note that I'll be making forward-looking statements. So I would ask you to please refer to our SEC filings for some additional important disclosures. So why are we at Neumora so passionate about our work? Well, brain diseases really represent one of the greatest unmet medical needs and one of the biggest medical challenges facing us today, and affecting upwards of 1.5 billion patients globally. 1.5 billion patients globally. And it's not even just those patients, it's their families, it's caregivers, it's society at large. Yet despite this enormous medical need, patients are still inadequately served. In most diseases, the prevailing standard of care is an older medicine that either leaves efficacy on the table or comes with an unacceptable side effect profile. We believe patients deserve better, and we believe novel pharmacology is needed to truly meet this brain crisis head-on, and that is what Neumora is all about. So in 2019, when our founders at Arch were thinking about how to address the global brain disease crisis, they came up with a bold vision: Let's redefine the treatment of brain diseases by developing novel pharmacology, and let's pursue this idea at scale. Let's not bank on one asset or one technology, but let's create a company with multiple assets and with the kind of balance sheet to be able to think big. Let's also build a data science and precision medicine capability that would allow to improve upon the industry's probabilities of success. So as I stand here today, just a little over four years later, I'm really delighted to say that we are a long way toward achieving this vision. 2023 was really a pivotal year in that journey. We've assembled an industry-leading pipeline with seven novel assets, all with IP into the 2040s. We've built a precision toolbox that we apply on a fit-for-purpose basis across our pipeline to increase our probabilities of success. Our lead program is all the way to phase 3 and could be FDA approved as early as 2026. navacaprant could actually be the first novel treatment introduced in the monotherapy segment of MDD in decades. I'm really proud of how the team executed. Going back to 2023 in particular, we announced very robust phase 2 data, and we initiated three phase 3 pivotal studies, all by year-end. By the way, that was ahead of our public guidance. In addition, we initiated a phase 1 study for 266, our M4 PAM, late last year as well, again, ahead of our guidance. And of course, we completed an IPO in September and extended our cash runway into 2026. Now, why is cash runway into 2026 important? Well, it's nice to have two years' worth of cash, but it's really more about a number of very important catalysts that we will see over the 2024 and 2025 years. Each of these catalysts has the potential to drive significant shareholder value. So what are these catalysts? For navacaprant, our, our lead pro- program, we'll be able to see top-line phase 3 data in MDD in the second half of this year. KOASTAL-2 and KOASTAL-3, the other phase 3 studies, for navacaprant, will read out in the first half of 2025. In the first half of this year, we'll also be initiating a study in bipolar depression, and we'll see data from that study in 2025. For 266, we will see healthy volunteer data in the middle of this year, and we'll see efficacy data in schizophrenia next year. And for 511, we'll see phase 1b data in Alzheimer’s disease agitation next year. So again, a very rich set of catalysts. So with these catalysts, and obviously, the recent M&A activity in our space, we're really delighted to be really at the forefront of pioneering a new area in neuroscience development and to finally help patients living with brain disease. Now, we're working with urgency because we know patients are waiting. Now, obviously, there's a lot of excitement in the obesity space right now, and rightly so, but the opportunity in CNS could be just as large... and at Neumora, we're poised to launch our first commercial product, navacaprant, in 2026. Now, by the end of the decade, our current pipeline has the potential to address needs that affect upwards of 40 million patients in the U.S. alone. And given our strong IP out into the 2040s, our total addressable market actually expands to 100 million patients in the U.S. alone. So clearly, this is a very big market and a very big opportunity. So here's a look at our pipeline on one page. We're one of the few companies advancing both neurodegenerative and neuropsychiatric indications. Each one of our 7 programs is novel pharmacology. Each one of our programs has strong IP into the 2020s and 2040s, and we own worldwide rights to each one of these assets. So let's focus on our clinical pipeline in a little bit more detail. Each of our three clinical assets has either demonstrated or has the potential to demonstrate best and/or first-in-class potential. Each of our assets has composition of matter IP into the 2040s, and each is a multi-billion-dollar revenue opportunity. So going left to right, navacaprant, our lead asset, is a highly differentiated kappa-opioid receptor antagonist. This is a class that has been clinically validated by multiple independent sponsors. We believe we clearly have best-in-class pharmacology with navacaprant, and in terms of timing, we're neck and neck with J&J. Now, J&J is pursuing an adjunctive MDD indication, while we are focused on the much larger monotherapy treatment in MDD, which is roughly two-thirds of the market. NMRA-266 is our M4 PAM asset, where again, we just initiated phase one studies in December. Now, obviously, there's been a lot of excitement in the muscarinic space recently, very strong clinical validation and some strategic activity that clearly indicates that this class has potential way beyond schizophrenia across a number of important indications. We believe the SAD/MAD data that we'll be able to generate by the middle of this year will be a really important value driver for this asset. Should we see a similar profile in that, and should we see some of the same on-target toxicology effect at higher doses that we've seen with emraclidine, it could be a big unlocking of value for this asset, as there's so much validation on efficacy. So getting through the SAD/MAD part could really improve our confidence that we have an efficacious asset at the right, at the right dose. Finally, 511 is our V1a receptor antagonist. Here again, we have best-in-class pharmacology. Now, this is a class that perhaps has not been quite as de-risked as the other two classes, but we've seen some really intriguing Sorry, preclinical data and some anxiety models, and thus, we believe we actually have a really interesting asset on our hands here. We'll be starting efficacy studies in Alzheimer's disease agitation in the first half of this year, and we'll see data from that indication in 2025. Turning now to our preclinical pipelines, again, we have a very exciting set of preclinical assets as well. Four different programs, each with strong biological rationale, each focused on large potential indications: Alzheimer's, Parkinson's, ALS, schizophrenia. All programs are based on novel pharmacology, and several of these programs have strong human genetic validation. We expect this pipeline to generate an attractive flow of INDs over the next several years. So let's turn to navacaprant, our highly differentiated kappa-opioid receptor antagonist. This asset has the potential to be the first novel mechanism introduced for the monotherapy treatment of MDD in decades. We clearly have best-in-class pharmacology here, with roughly 300-fold selectivity for kappa over mu, and that compares to other assets in the class that are roughly 30 to 31-fold selective kappa over mu. We've also been able to show a receptor occupancy of over 90% over a sustained 24-hour period. We believe this profile will give us a key competitive advantage, as it allows us to dose higher without seeing the mu-mediated AEs, such as diarrhea. So let's look at our phase two results in more detail. Data from our robust phase two study support the differentiation hypothesis I just discussed on the prior page. In a pre-specified cut in 100 moderate to severe patients, we saw statistically significant and clinically relevant efficacy on the core symptoms of depression, benefits treating anhedonia, and this is a difficult to treat symptom that is not adequately addressed by the current pharmacology. Yet it exists in about 70% of patients presenting with MDD. So it's a key part of our value proposition. And we saw a very clean safety profile. In fact, when you look at the table here on the right, we present these figures at a greater or equal to 2% cutoff, not the typical 5% you see in these tables, 'cause otherwise there wouldn't be much to show on this table and no side effects to report. This was a robust study in approximately 40 US sites, with over 200 patients ultimately in the study. These robust data and positive feedback from FDA gave us confidence to initiate a comprehensive, robust, well-powered phase 3 program that will enroll over 1,000 patients. We are running three replicate studies, but we'll only need two to be successful for an NDA filing, thus increasing our probability of success. We expect to see top-line phase 3 data from our first one here, the KOASTAL-1 study, in the second half of this year. We expect KOASTAL-2 and KOASTAL-3 to read out in the first half of 2025. Now, there's strong rationale and KOL enthusiasm to interrogate this mechanism far beyond MDD. To that end, we are starting an efficacy study in bipolar depression in the first half of this year, and we expect to see data in 2025. On the far right, you see there's a number of additional indications that we are considering, and I look forward to updating you as we make continued progress on selecting additional indications for this asset. Our KOASTAL program is designed to deliver a very robust package for our NDA in 2025. We'll be studying navacaprant in the moderate to severe population, building on the excellent phase 2 results I just reviewed. We'll be using the MADRS, and the MADRS is particularly well suited to our pharmacology, as it will capture the efficacy benefits of our pharmacology. The primary endpoint will be the change in MADRS at week 6. A key secondary endpoint will be the change in SHAPS score, also at week 6. Again, that is to see the impact of navacaprant on anhedonia, this difficult-to-treat symptom that is not currently addressed or well addressed by current medications. Now, importantly, we've also introduced in this study a number of design elements that really should minimize the placebo response that's seen in other trials. To that end, we've been very careful on site selection. Again, we had a robust phase 2 study with 40 sites, so we had a good universe of sites to start with, but we're very carefully curating additional sites for these studies. We've invested in internal monitoring and in central raters to ensure consistency across all the sites and to ensure that the right patients are enrolled in our studies. We've minimized the number of touch points, both from staff as well as the assessments that in other studies have shown to drive placebo response. So with the robust phase 2 data we generated, these execution steps in running 3 studies when only 2 are required to be successful, we have high confidence that our phase 3 program will succeed. Enrollment is off to a great start, and we look forward to seeing the data in the second half of this year. Now, navacaprant would enter a very large commercial market, a market that is really looking forward to novel pharmacology and new treatments, especially for the monotherapy setting, which again, is about two-thirds of the market. So last year, we partnered with L.E.K. to assess this market and perform some market research. And we were really pleased to see that prescribers had a preference for navacaprant over existing treatments. That was due to the novel mechanism of action, the convenient once-daily dosing without titration, the excellent tolerability and safety profile I described, and the strong efficacy, not just on depressive symptoms, but also on treating anhedonia, which makes our mechanism unique. Now, it's important to remember that MDD affects a primarily younger patient population, so this is actually an indication that's relatively insulated from pressures based on the Inflation Reduction Act. Turning now to 266, our potential best-in-class M4 PAM asset for the treatment of schizophrenia. We've demonstrated its potency and selectivity comparable to emraclidine, the other M4 PAM being studied. This is a class that has been clinically validated, and of course, recent M&A has further built the excitement of the potential for this class across a number of indications, so this could go far beyond schizophrenia. We're very pleased to have started our phase 1 studies, and we look forward to seeing results from our SAD/MAD study in around the middle of this year. An attractive profile from that study would give us high confidence that we have an active agent with similar efficacy potential as emraclidine, and thus, the SADMAD readout in the middle of this year will be a key catalyst for this program and a key catalyst for Neumora. Turning now to 511, our V1a receptor antagonist. We've demonstrated best-in-class pharmacology with this asset based on its potency and selectivity. And again, while this class may not have been as clinically de-risked as the other two classes I reviewed, we've seen some really interesting preclinical data here, and we plan to initiate an efficacy study in Alzheimer's disease agitation in the first half of this year, and we'll see data from that study in 2025. Now, agitation related to Alzheimer's disease is a big commercial opportunity. In fact, there's only one approved agent, but that agent carries a Black Box Warning, so attractive commercial opportunity. So pulling it all together here, 2024 and 2025 are very catalyst-rich years for Neumora. We'll be seeing top-line phase III data from navacaprant in the second half of this year, and more phase III data from the other two studies in the first half of next year. We'll be initiating a phase II study in bipolar depression in the first half of this year, and we'll see results from that study in 2025. We'll see results from our healthy volunteer study of 266, the middle of this year, and we'll see efficacy results in 2025. And for 511, we'll initiate an Alzheimer's disease agitation study in the first half of this year, and again, we'll see data from that study in 2025. So these catalysts provide multiple levers for us to drive significant shareholder value. So I hope I've demonstrated to you why Neumora is a compelling investment opportunity. With our current pipeline, we have the opportunity to reach more than 100 million patients in the U.S. alone, and we will reach those patients with novel pharmacology. We have two clinically validated programs, both advancing very rapidly. We have strong preclinical programs enabling a steady flow of INDs. All of our programs are focused on novel pharmacology with IP protection out in the 2040s. We are leveraging our precision toolbox to increase the probability of success across our programs. We have a strong balance sheet with cash runway into 2026, which will enable us to see a number of high-value catalysts. We've been able to recruit an experienced management team, a team that's not just experienced in neuroscience development, but has a proven track record of shareholder value creation. And we've already demonstrated that we can either meet or exceed our timelines. So with all this solid progress, we have the potential to truly reshape neuroscience, drug development, and finally help patients living with brain diseases. So with that, I'll invite my colleagues, Bill Aurora, Rob Lenz, and Josh Pinto, on stage for the Q&A. Thank you. I'll stand. I'll stand. Thank you, Henry, for that presentation. I thought I would start us off here talking a little bit in more detail about KOASTAL-1, and how we should think about a clinically meaningful change on the primary endpoint of the MADRS, and how does the prior data inform what you might see in KOASTAL-1 and KOASTAL-2 and KOASTAL-3 as well? Okay. So, Bill, do you want to tackle that, or Rob? Sure. Maybe, Bill, do you want to start with just reviewing and contextualizing the data that we saw on the phase II, and then I can share on phase III how we're translating that through? Sure. So in phase II, we were really delighted with the results we saw. In the moderate to severe depressed population, we saw robust efficacy across a range of measures, including anhedonia, which we know has historically been difficult to treat, but recalcitrant to the existing agents that are approved, while seeing a favorable tolerability profile with no adverse event reported at a rate of 5% or greater. We also did not see weight gain or sexual dysfunction, which we know can often be a limiting factor for patients in their twenties, thirties, forties, the demographic that often has MDD, initiating therapy, and certainly can be impediments to staying on therapy. So we took many of the elements that we saw with the efficacy data across a range of MDD symptoms, including anhedonia, and have contemplated those with the phase III program. Thanks, Tess. Mike? So, you know, you asked sort of how do we contemplate the overall profile of the medicine? And how clinicians and regulatory authorities view that is, it's the entirety of the risk-benefit profile, right? That can't be captured in a single outcome measure or a single adverse event, but it's the totality of that data, and that's exactly how we're thinking about it. Bill highlighted a couple interesting highlights that we think are differentiating pharmacology that are clinically meaningful with navacaprant, in particular, the effects on not just the improvements in mood, depressed mood, but also the improvements in anhedonia, as was robustly captured in an outcome measure that we call the SHAPS. As you alluded to in the phase III study, we're moving for the primary outcome measure to be with a scale called the MADRS, and the reason for that was related to the profile that we saw in phase II, as Bill mentioned. In particular, the MADRS better captures the totality of the benefit that we believe is conferred by navacaprant. In particular, the improvements on anhedonia are better captured with the MADRS scale than with the HAM-D17, which was used in phase II. And in terms of what constitutes, you know, clinical meaningfulness specifically on that scale, so there's decent literature that shows that benefits of, you know, about two points or more are really viewed as clinical meaningful. If you look at historical regulatory precedents for approved medicines, they are on that order of magnitude, on the MADRS scale. ... And so what have you noted publicly about the powering assumptions around these studies? Or is there any additional detail you can provide us in terms of how well-powered you think you are? Sure. So when we think about the powering, that to me is sort of the, a broader question around the variety of steps and measures we're taking to increase the overall probability of success of, you know, seeing a positive outcome in the individual trials as well as the program. So at the highest level, from a programmatic perspective, you know, as Henry mentioned, we're conducting three replicate, essentially identical phase 3 studies, with the expectation of only requiring two for successful filing and approval. That's the programmatic level. And then if you go down to the study level, there's a number of measures that we're taking from a design perspective, as you're alluding to on the powering, but also on the implementation or operationalization of it. So just focusing first on the design aspects, we're focusing on that population of moderate to severe, which is exactly the population in whom we saw the greater treatment effect in phase II. Regarding the powering, you know, as I mentioned, we're moving toward the MADRS that more fully captures the benefit of the pharmacology than the HAM-D. And then we're strongly powered to see a statistically significant benefit, not only in the primary outcome measure of the MADRS, but also in the key secondary outcome measure of the MADRS, which again, we really view as a potential meaningful clinical differentiation for this profile. And then the outcome measure, we're also incorporating that into a 6-week as the primary outcome measure versus 8-week, and that was intended to help minimize the placebo effect that tends to get bigger the longer that the trials go on. I would maybe just add to that, despite the comments we made about the MADRS scale being, being the better scale from a pharmacology perspective, so we might actually see an increase in phase III as opposed to a decrease in phase III. We've actually powered the phase IIIs to detect statistical significance, even if there's a discount to the treatment effect out of the phase II. So these are, again, as I said, well-powered, robust studies. We know that there are a number of other players in the broader industry that are contemplating the same or similar mechanism to you guys. How do you compare and contrast navacaprant to other KOR antagonists in development, including J&J's aticaprant and Cerevel's CVL-354? What could the advantages be of greater affinity towards KOR than MOR? I think another important point is that you are moving forward in the monotherapy, not adjunctive setting. What could those implications be in terms of your the outcome or the output of these trials? Sure. Let me highlight some of the differences between the agents. First off, I would categorize them as differences in pharmacology, and secondly, differences in development programs. I'll talk a bit about how that translated in our view in the phase II data that have been observed with the various programs. So first off, we believe we have best-in-class pharmacology with navacaprant, with greater than 300-fold selectivity, greater selectivity for kappa over mu opioid receptors, in contrast to the other agents that are in development that are closer to 30 times more selective for kappa over mu. So what that means is we've been able to push the dose, and at the 80 milligram dose, we're able to attain 90% receptor occupancy over a 24-hour time period and avoid mu-mediated adverse events that have been observed with the other agents that include GI side effects, such as diarrhea. When we think about the development programs, they too are different. Ours is a monotherapy program versus the J&J program being in the adjunctive setting. The Cerevel program's at a much earlier stage. So when we think about the development programs, the J&J programs I mentioned, adjunctive in nature, added to patients that have attained a partial response to an SSRI or an SNRI. Ours is a monotherapy program in which we've been able to capture benefits on anhedonia as measured by SHAPS. Those were not benefits that aticaprant was able to capture in their phase II. So clearly, an opportunity for clinical differentiation and a commercial opportunity that really coincides with that. And so in that context, those are some of the differences that I would highlight. Yeah. Maybe, Josh, you want to add a little bit on the commercial opportunity? Yeah, absolutely. And so, Tess, if you think about monotherapy versus adjunctive, it's well published in the literature that across lines of therapy, you know, the majority of patients, upwards of two-thirds or more, are treated with a monotherapy approach. And so we feel like this strategy from a development perspective, will open up the largest opportunity for us as we progress navacaprant towards the commercial market. We've also received feedback, you know, from KOLs, that if a product is shown to have an improvement in the monotherapy setting, they'd be comfortable using it in the adjunctive space. The converse isn't necessarily true, and so we feel like our development strategy will open up the biggest commercial opportunity and ultimately help get navacaprant into, you know, the hands of as many, you know, potential patients suffering from MDD as possible. I should have said, are there any questions from the audience? Please wave your hand if you do have one. I'd love to talk a little bit about the efforts in bipolar depression for navacaprant. What would you like to see here, and how do you think about designing a trial? Sure. I can start.... You know, we always start with the unmet need, and the unmet need in bipolar disease is tremendous, right? These are patients who have dramatically increased suicide risk. Upwards of 60% of patients attempt a suicide and upwards of 20% complete. So it's a travesty in the healthcare community, massive unmet need. And then in terms of what are those core symptoms that are driving that, the depression components within bipolar, it's depressed mood and anhedonia, right? We know the anhedonia is clearly correlated with quality of life in patients with bipolar disease. So if you think about, you know, the ideal therapeutic would be something that would address both the depressed mood as well as the anhedonia, and that's exactly what we've seen in the phase II profile with, with navacaprant. So we think it makes tremendous clinical sense to advance that program, that molecule into bipolar. You know, the details of this study are still being hashed out, but suffice it to say, we'll have an obvious focus on the depressive symptoms and the anhedonia in patients with bipolar depression. And as Henry shared, we look forward to starting that study in the first half of this year. Henry talked a little bit about the NMRA-266 program and schizophrenia in his comments as well. How should we be thinking about the type of PK/PD profile you might wanna see in healthy volunteers to move this program forward, which I think you've guided to as a mid-2024 update? Sure. So let me start by restating the enthusiasm that we have for the muscarinic class, as Henry laid out, massive. I mean, I view this as the largest advancement in the treatment of schizophrenia in over three decades. As we think about, you know, our strategy has been to focus on partial or the positive allosteric modulation. That's to, you know, to avoid the sort of systemic agonism that you see with agonists. I think that's important. And the other is to have selectivity in M4, and I think the emraclidine gave us definitive clinical validation that agonism or positive allosteric modulation of M4 is driving meaningful but clinical benefit. In terms of what, you know, we need to see in the phase I, as Henry alluded to, you know, there's evidence that with, with M4 PAMs, you see transient increases in both blood pressure and heart rate. They're transient. We know that they tachyphylaxis over time. So one would expect to see similar findings in, in the NMRA-266 phase I study. If we did see that, it would give us a lot of conviction that we're having meaningful target engagement, particularly in the central, in, in the brain, where a lot of these effects are, are believed to be mediated, and it really helps us gain that confidence to move quickly into a, a proof of concept study in acute schizophrenia, later in the year. Any questions? This room's a little too quiet. So let's talk a little bit about NMRA-511. You've been in, I believe, healthy volunteer studies for quite some time. Maybe it makes sense to recap what you've learned so far about the therapeutic candidate, and maybe that's the first question. And then I'd love to talk a little bit about how you see 511 fitting in to the Alzheimer's disease agitation landscape. Yeah. I mean, what we've seen so far gives us confidence to do what I talked about, which is to start the efficacy study in the first half of this year. And keep in mind also what I mentioned, that the current approved agent in this class is a Black Box Warning. So, a nice profile coming out of the healthy volunteer study, and again, our confidence, our efficacy study could tell you where we might be thinking about things here. Yeah, and just sort of your question around agitation and Alzheimer's disease. Again, starting with the unmet need, there's a massive unmet need in patients with later-stage Alzheimer's disease because of behavioral symptoms. It is the agitation and aggressivity that compels families to institutionalize those patients. It's really not the cognitive deficits, and as Henry alluded to, and that's a massive healthcare burden on the system and as well as, you know, terribly psychologically for the families of the patients. And as Henry alluded to, there's a single drug that's been approved to date, an atypical antipsychotic that, you know, carries increased mortality risk in exactly this patient population, an elderly patient population, so clear unmet need in this space. In terms of the relevance of the vasopressin 1a receptor, you know, there's clearly now established the relevance of that pharmacology and the pathways in terms of fear and aggressivity. We know that if you actually give, you know, normal, healthy individuals vasopressin intranasally, it actually induces fear. And that's believed to be mediated through agonism through the vasopressin 1a receptor. And so we have a very selective molecule that selectively inhibits that V1a receptor. And so, you know, well-positioned to advance that. As Henry said, we're advancing well through the phase I program, anticipate being able to move that into the agitation and Alzheimer's program this year. First half. First half. ... you all went public just a couple of months ago and made everyone aware of initiatives and platforms and assets beyond even the three that we talked about in detail today. I was wondering if you could give us your latest view on how you think about allocating capital here and what interests you might have as it relates to business development? Yeah, I'll start. So we're very happy with our current pipeline. I mean, we have seven fantastic programs. So as we should be doing, of course, we're looking at things that are out there, but the hurdle for us to bringing another asset is very, very high. The hurdle to beat one of our seven programs is going to be difficult. So I would say we're again, we're out there, we're out there looking, but we have a strong balance sheet, and we absolutely wanna make sure that we have the type of financing that lets us see all the catalysts we talked about. So again, high hurdle for additional BD. I also sort of meant your view, also view maybe the other way around, just on the partnering side, to move- Ah. some of the programs that are potentially at earlier stages forward in maybe other fashions than Well, we're funded to move all of them forward, Tess, so... And we like our programs, so that's not really a focus either, I have to say. Again, that's the reason we did the IPO, and that's the reason we're so excited about the pipeline we have and funding it fully to see a good flow of INDs out of that, out of that set of assets. Tess, on the back of the IPO, we ended the third quarter of 2023 with about $520 million on the balance sheet, and so we have cash runway into 2026. That allows us to enable the progress across the entire portfolio, and in particular, achieve the range of catalysts that we've highlighted here for the clinical stage programs, but also advance each of the 4 earlier stage programs. You know, as Henry and the rest of the team have alluded to, you know, we're really excited about the earlier stage programs and look forward to those programs maturing over the next 12 and 24 months, and we'll be excited to talk more about those as they get closer to the clinic. I think that might be a very good place to leave it. Thank you to the entire Neumora team for being here with us. This was great. And also, thank you for all the audience members for taking the time to listen in. I hope everyone has a great rest of the conference. Thank you. Thank you.