Ladies and gentlemen, thank you for standing by. This is Arji, your conference operator today. At this time, all participants are in a listen-only mode. After the speaker's presentation, there will be a question-and-answer session. Please be advised that today's conference is being recorded. I would like now to turn the conference over to Helen Rubinstein, Vice President of Investor Relations and Communications. Please go ahead. Good afternoon, and thank you for joining Neumora Therapeutics' Second Quarter 2025 Financial Results Conference Call. Before we begin, I encourage everyone to go to the Investors and Media section of our website at neumoratx.com, where you can find the press release related to today's call. With me today from Neumora are Chief Executive Officer Paul Berns, President Josh Pinto, Chief Operating and Development Officer Bill Aurora, Chief Scientific Officer Nick Brandon, and Chief Financial Officer Mike Milligan. I'd like to point out that we will be making forward-looking statements, which are based on our current expectations and beliefs. These statements are subject to certain risks and uncertainties, and our actual results may differ materially. Please review the risk factors discussed in today's press release and in our SEC filings for additional detail. With that, I'll now turn the call over to Paul. Thanks, Helen. Good afternoon, everyone, and thank you for joining us. At Neumora Therapeutics, we are on a mission to address the largest population health challenges of our generation and to do so at scale. To achieve that goal, we know that we need to generate better medicines, therapies that enable better outcomes, that meaningfully improve the treatment of prevalent diseases, and ultimately that positively impact quality of life for patients and their families. With that aim in mind, we built an industry-leading pipeline targeting some of the most prevalent and burdensome brain diseases. Our approach is centered on advancing programs with best-in-class pharmacology, targeting novel mechanisms of action with the potential to improve upon the current standard of care for hundreds of millions of people. We are proud to be making important progress toward that goal. Today, we announced that we prioritized obesity as the lead indication for NMRA-215, our highly brain-penetrant NLRP3 inhibitor. An increasing body of evidence supports the need for the role of centrally acting drugs to drive weight loss and obesity, and NLRP3 inhibition in particular has shown promise across multiple studies. Importantly, recent data suggests that molecules with high CNS penetration and activity are required for efficacy with this target. Currently, obesity and overweight affect more than 2.5 billion people globally, and by 2035, that number is expected to increase to up to 4 billion people. The need here is immense. Obesity is associated with significant negative outcomes and lower quality of life, and there is room to improve upon the efficacy and tolerability of the current generation of incretin therapies. In fact, up to a third of patients are non-responders to current therapies and do not experience clinically meaningful weight loss. Additionally, patients experience numerous on-target GI adverse effects, and weight regain is common after patients stop taking these drugs. These challenges are highlighted by the real-world use data on GLP-1 therapies. A recent real-world study found that 68% of people taking a GLP-1 for obesity discontinued use of their medication within one year, and research from the Blue Cross Blue Shield Association found that 58% of patients discontinued use before reaching a clinically meaningful health benefit. We believe that NLRP3 inhibition may offer an efficacious, well-tolerated treatment option for obesity, potentially as a monotherapy, in combination with GLP-1 medications, or as a maintenance treatment option. Our deep expertise in neuroscience, and specifically in developing highly brain-penetrating chemistry, makes Neumora Therapeutics uniquely positioned to bring a potential new mechanism to this large and growing public health challenge. The breadth of our pipeline and its potential impact is immense, and we are in a strong position to translate that science into real-world therapeutic breakthroughs. We expect to have up to six clinical data readouts in patients over the next 18 months, and I'm excited to continue to build on this momentum. I will now turn the call over to Josh Pinto, President of Neumora Therapeutics, to review our pipeline updates. Josh? Thanks, Paul. We continue to make important progress across our pipeline, which is a direct reflection of our highly productive team, differentiated approach to neuroscience drug development, and rigorous prioritization of our pipeline. With the initiation of our phase I study of NMRA-861, we now have three clinical stage assets advancing through development, each with near-term catalysts on the horizon, including data from our phase I-B study of NMRA-511 in Alzheimer's disease agitation, which is expected around year-end, top-line data from the optimized phase III K OASTAL program with navacaprant in major depressive disorder, with the first top-line data expected in the first quarter of 2026, and phase I SAD/MAD data for our recently announced M4 PAM, NMRA-861, which is anticipated in the first quarter of 2026. Additionally, we expect to bring another M4 PAM, NMRA-898, into the clinic in 2025, and we are currently running a preclinical diet-induced obesity, or DIO, model with NMRA-215 in mind, a model that we believe is highly translatable to the clinical setting. We are excited to provide more detail on the DIO data this fall, which we believe has the potential to be highly compelling. Looking forward, we expect to initiate clinical studies with NMRA-215 in the first quarter of 2026. As we continue to prioritize our pipeline, we are focused on allocating resources to the programs we believe will make the biggest difference for patients. Given that focus, we will not be advancing our NMDA program this year. As you've heard, we have a wealth of opportunities at Neumora and are entering a catalyst-rich period. With that in mind, we plan to host an R&D event in the fourth quarter of this year to discuss our program in more detail. Each of our programs targets a substantial unmet need and represents a meaningful market opportunity. Our development strategy has multiple pathways for success and the potential to deliver multiple breakthrough and blockbuster therapies to patients in need of better treatment options, and we look forward to sharing more detail later this year. With that overview, I will now turn the call over to Bill to provide an overview of our clinical programs. Bill? Thanks, Josh. We designed our clinical programs to target mechanisms of action that we believe have the potential to fundamentally change how diseases are treated. Our approach is grounded in strong scientific rationale and a commitment to improving patient outcomes. This is clearly seen in our newly initiated phase I study of NMRA-861. NMRA-861 is a highly potent and selective M4 positive allosteric modulator, or PAM, which we believe offers best-in-class pharmacology. Schizophrenia is a complex disorder, and the effectiveness of current treatments is often limited by suboptimal efficacy, side effects, and high rates of nonadherence. We believe M4 PAMs represent a promising new class with the potential to deliver a more favorable therapeutic profile, including efficacy, improved tolerability, and once-daily dosing. NMRA-861 demonstrated robust activity in preclinical efficacy models and was also well tolerated in preclinical safety studies with no convulsions observed in rabbits, dogs, or rats. NMRA-861 is currently being evaluated in a phase I single ascending dose and multiple ascending dose study in healthy adult participants and adults with stable schizophrenia. We look forward to reporting data from that study, including safety and tolerability, human pharmacokinetic data confirming the potential for once-daily dosing and central nervous system penetration in the first quarter of 2026. Additionally, we expect to bring another PAM into the clinic this year as we continue to advance our broader M4 franchise. We also have upcoming clinical milestones for navacaprant and NMRA-511. Enrollment is ongoing in the KOASTAL program, and we continue to expect top-line data from KOASTAL-3 in the first quarter of 2026 and KOASTAL-2 in the second quarter of 2026. Additionally, we expect top-line results from our phase I-B signal-seeking study of NMRA-511 in Alzheimer's disease agitation around the end of this year. We have made meaningful progress across our robust and growing pipeline, with multiple programs advancing toward near-term clinical milestones. With our robust pipeline and R&D efforts, we believe we are poised to bring forward novel therapeutics and deliver transformative treatments to millions of patients around the world. With that, I'll now turn the call over to Mike for a review of the financials. Mike. Thanks, Bill, and good afternoon, everyone. Our financial results for the second quarter of 2025 are detailed in the press release that we issued this morning. I'd like to take a moment to provide some context and highlight a few key points. We ended the quarter with $217.6 million in cash, cash equivalents, and marketable securities as of June 30th, 2025. We anticipate our cash runway to support operations into 2027, well beyond all of our upcoming clinical milestones. Our total net loss for the second quarter was $52.7 million compared to $58.7 million for the same period in 2024. This decrease was primarily due to a reduction in stock-based compensation and personnel-related expense and a reduction in clinical trial costs. With that, I'll now hand the call over to Helen to manage Q&A with the operator. Helen? Thanks, Mike. Before I turn it over to the operator, I'll ask that you limit yourself to one question. If you have an additional question, please feel free to return to the queue. Now, I'll turn it over to the operator to handle Q&A. Operator? At this time, I would like to remind everyone, in order to ask a question, press star then the number one on your telephone keypad. We will pause for just a moment to compile the Q&A roster. Your first question comes from the line of Brian Abrahams of RBC Capital Markets. Please go ahead. Hi, this is Joe for Brian. Thank you for taking our question. Can you talk about the preclinical study design in obesity, the type of diet, whether if you're looking to combine with GLP-1s, and what sort of comparator arms you're looking to implement in the study? Are there any certain aspects of weight loss that you're looking to demonstrate, such as better quality weight loss or maintenance of weight loss post-GLP-1 withdrawal? Thank you. Great. Thanks, Joe. This is Josh here. I'll take that question. For our program NMRA-215, which is our NLRP3 inhibitor that we're moving forward and we've announced today that we prioritize in obesity, the next step, as you've highlighted, will be to run a diet-induced obesity study in mouse. Part of the reason we're so excited about this study is we know that this model really translates between the animal setting and the human setting, and we think it'll give us a prediction in terms of how this molecule could ultimately perform in a clinical trial setting. In this study, we are going to look to run a set of studies, and across them, there's really going to be three key goals. First, we're going to assess the potential of NMRA-215 as a monotherapy treatment for obesity, and in this, it'll just be NMRA-215 dosed in the mice. We really think that this could provide a value proposition as you relate to what's out there today in terms of the GLP-1 as well as the GIP therapies. We think that this molecule could offer the potential for incretin-like weight loss with better tolerability, convenience as a small molecule, which could also result in a lower cost of goods as well. From a monotherapy perspective, we absolutely will be looking to show benefit there. We'll also be testing the product in combination as an add-on to a GLP-1 product. In this particular model, we will use semaglutide. It is known to be the standard GLP-1 used in the mouse DIO model. We will look at 215 as an add-on to SEMA in this study and ultimately to see, can we, with 215, reduce the level of SEMA that is given and ultimately increase the weight loss and the tolerability? We know in this population, there's been a range of studies out there, but we've seen anywhere from 60%- 70% of people taking the GLP-1s right now do not respond or ultimately discontinue due to lack of maximal weight loss. We think that there's absolutely room to add new therapeutics on top of this. Finally, one of the key questions is just the long-term durability of the existing therapies. We will be looking to test NMRA-215 as a maintenance treatment. You can think about this paradigm, Joe, as dosing both NMRA-215 and semaglutide in combination to reach a level of weight loss, then removing the semaglutide dose ultimately to demonstrate that NMRA-215 can maintain the weight loss over a long-term period. What this could really provide the market is a long-term, cost-effective, and tolerable option beyond the GLP-1 therapies today. We are really excited to bring this program forward, Joe, and really looking forward to providing the data from our DIO model as we move through the rest of 2025. Your next question comes from the line of Paul Matisse of Stifel. Please go ahead. Hi, this is Matthew on for Paul. My question is on NMRA-861. Could you perhaps provide more description on what gives you confidence that this would be safer than the MNRA-266 molecule, which was also from the Vanderbilt deal? Thanks. Yes, absolutely. Joe, this is Josh here. I'll take the question first, and then I'll pass it over to Nick to provide some specifics. I think, Joe, one of the things to really remember about our M4 franchise is that all of our compounds are structurally distinct. As we think about the convulsions that happen with NMRA-266, NMRA-861 and NMRA-898, which is our third M4 PAM that we announced today, are all structurally distinct from one another. Nick, maybe you can provide some added details just on what gives us confidence on the safety of NMRA-861 as it relates to what we saw with NMRA-266. Thanks, Josh. Yeah, Nick here. Matthew, yeah, good question. Just stepping back, if you remember, with 266, we had unfortunate and unexpected convulsions in rabbit. As we brought these structurally distinct compounds forward, that was really the main barrier for us to achieve. When you look at the basic pharmacology, have a look at our current corporate set, the molecules look really good, in particular NMRA-861, NMRA-898. Critically, we've taken both those compounds into rabbit, with push doses and exposures, which have exceeded where we saw convulsions with NMRA-266. Moving forward, we've truly de-risked the issues on NMRA-266 with both of these molecules. We feel like we're in a really good position now to push both of these forward and obviously very excited as we announce we've started our phase I study with 861 and more news to follow on NMRA-898. Thank you. Your next question comes from the line of Yatin Suneja of Guggenheim Securities. Please go ahead. Hey, guys. Thank you for taking my question. Exciting announcements today. Maybe just a couple on the KOASTAL program first, if I may. Any color on screen failure rate you can provide on the two studies or any parameters that might give you confidence that the site quality is good here? If you can also comment on the male to female ratio that you might be targeting or you might have enrolled so far. Just a quick one on the NMRA-511. Obviously, those data are going to come, you know, relatively soon. If you can maybe help us set expectation, what we should be expecting and what will be considered good for you to move forward. Thank you so much. Yeah, this is Bill. Good to speak with you again. We are really pleased with some of the benefits we're seeing from the added measures we've put into place with KOASTAL 2 and 3. As you recall, we took three steps when we paused the KOASTAL- 1 study. Number one, we enhanced the medical monitoring. Second, we added in Verified Clinical Trials. Third, we reduced the overall number of sites that were participating to focus on those that had more experience in MDD. The first of these steps, which was enhancing the medical monitoring, included partnering with MGH, RITIO, FAVA, the SAFR Group, and CTNI. We are seeing that independent verification of the diagnosis is helping to ensure that appropriate patients are being randomized. The VCT approach, or Verified Clinical Trials, is a screening database that's helped us to ensure that the subjects being considered for the study aren't enrolled at a different site or in a trial that would serve as exclusionary, for example, in a TRD study. That is also providing some added benefits. We are pleased with what we are seeing with the measures we've put into place, and the trial is progressing in that regard. With respect to male to female ratio, I'll just simply state that we are seeing more females already enrolled relative to males in KOASTAL 2 and 3. We won't get into specifics today, but we are pleased to see that is, in fact, more consistent with the prevalence of MDD and historically what's been enrolled with sex distribution across the studies. Lastly, with NMRA-511, as you'll recall, this is a signal-seeking study that's not powered to demonstrate statistical significance between active and placebo. Part A of the phase I-B study was designed to evaluate the safety, tolerability, and the PK in healthy elderly participants. We completed Part A in 2024. NMRA-511 was well tolerated in those participants. We subsequently moved on to Part B and expect to have results towards the end of this year. Part B is designed to evaluate the safety, tolerability, and efficacy in people with AD agitation. The primary endpoint is the change from baseline to week 8 on CMAI. Although the study is not powered to show statistical significance, we believe the data will help us better understand the drug's effect in AD agitation, including the domains of agitation that it affects, and then we'll proceed with further steps around clinical development based on what we learn. Your next question comes from the line of Douglas Tsao of H.C. Wainwright. Please go ahead. Hi. Good morning. I'm just curious in terms of NMRA-215 and your thoughts in terms of development in obesity. Obviously, this is a very competitive space, and once you get past the preclinical stage and even phase I, things start to become more expensive in terms of the studies. Obviously, as a sort of CNS-focused company, you know, obesity is maybe a little bit out of your sort of primary focus. I'm just curious, is this something that you would want to take to a certain stage of development and accrue a certain amount of clinical data before potentially finding a partnership? Yeah, Doug, this is Josh, and thanks for the question. I think in terms of how we view the obesity indication for us at Neumora, we're really committed to following the science as we advance our pipeline. There's been this increasing body of evidence that really supports the role of centrally acting drugs for treating obesity. We've even seen it with some of the GLP-1 therapies. It's clear that some of the appetite suppression is working through central mechanisms. What we think NLRP3 offers is really a distinct approach for the treatment of patients with obesity, different than the incretins or some of the other mechanisms that are in clinical development. We've seen that through multiple sponsors having generated preclinical data in the DIO model supporting the role for NLRP3 inhibition in obesity. As we looked at this opportunity, we really felt like this fit within the scope of what Neumora was set up to do, which is tackle large population health challenges at scale that require expertise in developing chemistry that can act centrally. That's what we've done. I think you've seen through some of the data we've put out today, Doug, that we absolutely believe we have the best-in-class NLRP3 inhibitor in terms of CNS penetration. From a development perspective, we're not going to comment right now in terms of whether we're going to partner and/or move the program forward on our own at various stages. What I can say is that the progression of NMRA-215 through the DIO model and into phase I is contemplated in our spend that's associated with cash runway into 2027. It is currently in our operating plan to move forward under our own theme. Doug, we're really excited about this announcement today and really looking forward to what's going to what we're going to bring forward over the rest of this year in terms of some of the preclinical data for NMRA-215 in obesity. Your next question comes from the line of Myles Minter of William Blair. Please go ahead. Hey, guys. Thanks for the questions. The first one's on NMRA-15. One of your peers that you list as a molecule on slide 28 in your presentation did have a diet-induced obesity model showing 15% body weight decrease as a monotherapy. Just curious, as you comment that efficacy is related to increasing brain exposure and you're greater than twofold that compound according to your data, are you expecting efficacy in that preclinical model to be greater than 15% weight loss in a monotherapy setting? That's the first question. Second question is, has your confidence in KOASTAL two or three changed at all since we've seen the Ventura one and two trial data at ACNP? Believe those showed a 0.9-0.5 point improvement versus placebo on the MADRS, respectively. Just wondering whether views have changed since you've actually seen that data. Thanks. Hey, Myles. This is Josh. In terms of NMRA-215, we've obviously looked at the weight loss that has been generated by competitors across the DIO model quite substantially. I think as you look at the weight loss that's been achieved by NLRP3 inhibitors to date, I think it's showing in general about 10%- 15% weight loss as a monotherapy. From our perspective, that is quite compelling weight loss, particularly as we think about the translation from mouse models to humans. If you look at it in comparison, semaglutide, which is a very well-known molecule that's typically used as a controlled GLP-1 in these studies, tends to generate in and around 20% weight loss. As we sit here today, I'm not going to provide a specific numerical guide in terms of what we would expect for NMRA-215 in the DIO model, but we absolutely think that the potential of these molecules is based on their activity centrally. We believe based on the data that we put out today showing that NMRA-215 has best-in-class brain exposure, that we have a chance to show some really compelling data within the DIO model. In terms of your second question on confidence around K2 or K3 post-ACNP, I don't think our confidence or conviction in the study has really changed since we announced the changes that we're making to the study in the March timeframe. Maybe I'll turn it over to Bill right now just to comment on how some of those changes have really come into play and what we're seeing out of it. Hi, Myles. This is Bill. As you'll recall, navacaprant is far more selective for KOP, where it's a mu opioid receptor, so there's a difference in pharmacology between navacaprant and itinquaprant. Ours is a monotherapy development program in contrast to the adjunctive setting. With those fundamental differences between the molecules and the programs, we remain confident in our program. The steps we've taken post-K1 also are proving to be quite helpful with enhancing the medical monitoring and the application of the verified clinical trials database, as well as having gone to the sites that are most experienced in major depressive disorder and having stopped those sites that have just less experience. Things are progressing per plan, and we're on track for K3 in the first quarter and K2 in the second quarter of next year. Again, as a reminder, if you would like to ask a question, press star one on your telephone keypad. Your next question comes from the line of Ami Fadia of Needham & Company. Please go ahead. Hi, good evening. Thanks for taking my question and apologies if this was already asked. My question is regarding the NMRA-861 molecule. You mentioned earlier that it's obviously different from your earlier M4 PAM, but could you give us any color on any preclinical work that you may have done that gives you confidence around its safety profile? Thank you. Thanks, Ami. This is Josh. What I'll start off by mentioning is that, just a reminder, all of our M4 PAMs are structurally distinct from one another, including NMRA-266, NMRA-861, and NMRA-898. I'll turn this over to Nick right now to provide some more specifics on your question on NMRA-861's safety profile. Yeah. Hi, Ami. Nick here. I think the critical preclinical information we have is work we did in vivo in the rabbit. As you recall, it was unexpected seizures in the rabbit, which put us on clinical hold with that molecule. We've done a lot of work in the last 12 months with NMRA-861 and NMRA-898 in the rabbit where we've taken and we've dosed those compounds and achieved exposures, which is the part where we were with NMRA-266, and we've not seen any evidence of any convulsions. We feel very confident we have de-risked both molecules as we move forward, alongside their really encouraging overall pharmacological profile and other data we have. We're really encouraged about moving both of them forward. Yeah, and as I mentioned earlier, really excited about having NMRA-861 back in phase I clinical development. On J.P. Morgan. Please go ahead. Hi, team. This is Maryam on for Tess. Thank you for taking our question. What synergies do you see between your existing neurofocus pipeline and obesity? Along these lines, how did you come about deciding that this was the right next indication for Neumora? Can you help us reconcile what your cash runway does and does not include in terms of R&D initiatives? Thank you. Great. This is Josh, and I'll take the question. I think as I mentioned previously, as we were looking at indications to take NMRA-215 into, we are really committed, as I highlighted before, to following the science and the growing body of evidence highlighting that the drugs that are being developed and brought forward to treat obesity really are working through central mechanisms. We feel like obesity is an indication that fits squarely within our mandate of bringing novel mechanisms and novel approaches forward to patients suffering from a range of large population health disorders that are driven through central mechanisms. We really feel like NMRA-215 into obesity is an opportunity for us to develop a new therapeutic that we believe could be best in class for that area. We think there are a lot of synergies in terms of the team's expertise in designing and developing molecules that are highly brain-penetrant as really the critical step to unlock the potential of this class and target. In terms of cash runway and what's included, what I will highlight is that we have a strong cash balance as we sit here today. Mike highlighted about $217 million on the balance sheet as we ended the second quarter. This gives us runway into 2027. That fully funds all of our critical programs where we provided public guidance through the clinical stage gates. We think that with each of the four most advanced programs, we will be able to deliver meaningful clinical milestones for each of them within the current cash runway period. We're really excited about what we have moving forward and, frankly, the opportunity we have to bring forward six potential clinical catalysts in patients over the next 18 months. That ends our Q&A session, and we appreciate your participation. I will now turn the call back over to Paul Berns, Chief Executive Officer, for closing remarks. Please go ahead. Thanks, Operator. Thank you again to everyone for joining us this afternoon. As you can see, this is an exciting time at Neumora with up to six distinct catalysts anticipated over the next 18 months, each serving as a critical inflection point with the potential to create significant value across our portfolio. These include preclinical data with NMRA-215 in obesity and the initiation of clinical studies with this program, initial clinical data from NMRA-861 in schizophrenia, the phase I-B data in Alzheimer's disease agitation, and phase III data from navacaprant in the KOASTAL program. We are well positioned to achieve all upcoming milestones, which reflect the strength of our pipeline and caliber of our execution. Most importantly, it reflects our commitment to the millions of people who are in need of better treatment options. We are working with urgency to bring forward the next generation of novel therapies and ultimately unifying drug development in neuroscience. Thank you again for your continued support, and that concludes our call this afternoon. Ladies and gentlemen, that concludes today's call. Thank you all for joining. You may now disconnect.