Good day and welcome to the Acumen Pharmaceuticals' Second Quarter 2025 Conference Call and Webcast. At this time, all participants are in listen-only mode. After the speaker's presentation, there will be a question-and-answer session. To ask a question at that time, please press star one one. As a reminder, this call may be recorded. I would now like to turn the call over to Alex Braun, Head of Investor Relations. Please go ahead. Thanks, Michelle. Good morning and welcome to the Acumen Pharmaceuticals conference call to discuss our business update and financial results for the quarter ended June 30th, 2025. With me today are Daniel O’Connell, our Chief Executive Officer, Dr. Jim Doherty, our Chief Development Officer, and Matt Zuga, our CFO and Chief Business Officer. Dan and Matt have some prepared remarks, and then we'll open the call for questions. Joining for the Q&A session, we also have Dr. Eric Siemers, our Chief Medical Officer. Before we begin, we encourage listeners to go to the Investors section of the Acumen Pharmaceuticals website to find our press release issued this morning that we'll discuss today. Please note that during today's conference call, we may make forward-looking statements within the meaning of the federal securities laws, including statements concerning our financial outlook and expected business plan. These statements are subject to risks and uncertainties that could cause actual results to differ materially from those described in the forward-looking statements. Please see slide two of our corporate presentation, our press release issued this morning, and our most recent annual and quarterly reports filed with the SEC for important risk factors that could cause our actual results to differ materially from those expressed or implied in the forward-looking statements. We undertake no obligation to update or revise the information provided on this call or in the accompanying presentation as a result of new information or future results or developments. With that, I'll turn the call over to Dan. Great. Thanks, Alex. Good morning, everyone, and thanks for joining us today. I have a few remarks to make before handing the call over to Jim to provide some details about our recently announced Enhanced Brand Delivery, or EBD, program. Then Matt will detail our quarterly financial results before we open the call for questions. The second quarter was a productive one for Acumen marked by steady operational progress and an important strategic partnership to expand our portfolio. Following the rapid completion of enrollment in our phase II ALTITUDE-AD study in the first quarter, we continue to make great progress with the study. At the recent AAIC conference in Toronto, we received positive feedback from site investigators about the study design, patient retention, and our team's engagement. Based on this strong execution, we continue to expect top-line results in late 2026, inclusive of the key efficacy and safety measures. ALTITUDE is investigating sabirnetug, our monoclonal antibody with high selectivity for toxic Aβ oligomers. This selectivity is key to why we believe sabirnetug could unlock potentially greater clinical efficacy and improved safety relative to antibodies targeting amyloid plaques. At AAIC, we also presented data showing sabirnetug achieved the highest selectivity for Aβ oligomers over monomeric Aβ when compared to recombinant lecanemab and aducanumab. The reason why this is important is that Aβ monomer levels are approximately 7,000-fold higher than the low-abundance toxic oligomer levels found in the diseased Alzheimer's brain. Lower affinity for monomeric Aβ, which sabirnetug demonstrates, is going to increase functional selectivity because less of the antibody will be binding to monomer. I'd also like to mention that we are encouraged by the recent comments from commercial players in the space, highlighting the growth of the clinical infrastructure for diagnosing and treating people with Alzheimer's disease. Feedback from KOLs and others in the field also has noted greater easing of clinical bottlenecks. Real-world long-term data from the currently marketed products reported at AAIC demonstrate the clinical benefit of these products growing over time, further supporting their adoption. In addition, the first blood-based biomarker has been approved by the FDA, and others are being developed. We believe blood-based biomarkers will revolutionize the field by making an accurate and potentially earlier diagnosis much more efficient. We also believe they will help expand the demand for anti-amyloid treatments. It's terrific to see the field moving forward and the clinical infrastructure coming online, as well as the increased blood-based diagnostic options for the benefit of patients and their families. This momentum, we believe, sets the stage for sobirnetug and potential next-generation EBD products in the future, as there remains a very significant untreated patient population interested in receiving anti-amyloid therapy. We're excited about the potential of sobirnetug to provide a differentiated benefit-to-risk treatment option for patients and the future possibility of building on that with an EBD product or products. Moving to EBD, in July, we announced a strategic collaboration option and license agreement with JCR Pharmaceuticals based in Japan. This collaboration is to develop an Alzheimer's disease product combining our Aβ oligomer selective antibody expertise with JCR's transferrin receptor-targeting blood-brain barrier penetrating technology. We chose to partner with JCR as they are an established leader in the BBB space. Importantly, the partnership extends our portfolio and builds on our confidence in the potential treatment benefit of targeting toxic Aβ oligomers. We've been working closely with JCR for more than a year, and I'm very excited at the potential to develop a differentiated next-generation treatment option for patients and shareholders alike. We expect to make a development decision for up to two product candidates in early 2026 based on non-clinical data. I'll now turn the call over to Jim to expand on our progress and our EBD strategy. Thanks, Dan, and good morning, everyone. Thanks for joining us today. I'd first like to build on Dan's comments about AAIC and the positive sentiment surrounding current Alzheimer's disease therapies and the potential for next-generation treatments. A number of KOLs have recently commented to us that if a patient's appropriate for one of the available monoclonal antibodies and makes the decision to begin treatment, compliance with the IV infusions and MR monitoring is very high. When used in clinical practice, the safety profile of amyloid-targeting antibodies appears similar to what's been reported from placebo-controlled clinical trials. That said, additional improvements in the modest efficacy and reduced need for safety monitoring with the current drugs would be welcomed. One of the major challenges for treating neurological disorders like Alzheimer's disease is the restriction of many therapeutic agents from entering the brain in high enough concentrations to provide therapeutic efficacy. The blood-brain barrier, or BBB, is a system of epithelial cells that line the blood vessels in the brain that very effectively limit entry into the brain for many therapeutic agents. Selectively leveraging a process called receptor-mediated transcytosis has become an exciting technology to improve delivery of therapeutic macromolecules from the bloodstream into the brain. Receptor-mediated transcytosis takes advantage of natural systems that selectively transport specific proteins into the brain, thereby delivering substantially higher amounts of enzymes or antibodies to where they need to be. We have recognized for some time that this approach could benefit our program at Acumen by delivering oligomer-targeted therapeutics to the brain in a safe and effective manner. Although a number of receptors have been identified that can serve as access points for RMT technology, we have chosen the transferrin receptor as the appropriate carrier for our program based on clinical experience and the potential to mitigate the risk of ARIA associated with amyloid-targeting therapeutic approaches. We conducted an extensive search and evaluation process to assess many technologies, and we're drawn to JCR because they are an established leader in the blood-brain barrier space with an approved therapy in Japan using their technology that is associated with low rates of anemia. J-Brain Cargo technology is a proprietary JCR Pharmaceuticals drug delivery system that efficiently delivers drug to target tissues, including the central nervous system, through receptor-mediated transcytosis. It's applicable to various modalities, including antibodies, enzymes, oligonucleotides, lipid nanoparticles, gene and cell therapy, peptide, and decoy receptors. The first drug developed based on this technology is approved in Japan for the treatment of lysosomal storage disorder and exhibits an established safety profile. We have worked with JCR for more than a year on feasibility studies, and in July, we announced a collaboration license and option agreement to investigate the combination of our oligomer-targeted antibodies with their transferrin-targeted blood-brain barrier technology. As you heard Dan discuss, we believe selectivity for synaptotoxic Aβ oligomers is a key opportunity for both safe and effective next-generation disease-modifying antibody therapy. Pairing this differentiated cargo with JCR 's validated carrier technology may offer an attractive next-generation product candidate for Alzheimer's patients. We're investigating both sobirnetug and other oligomer-selective antibodies from our library and exploring both single-chain and variable heavy-domain antibody constructs with JCR, which we consider cutting-edge approaches in the blood-brain barrier space. A non-clinical data package inclusive of a non-human primate study is expected in early 2026, at which point Acumen has an exclusive right to exercise our option to deliver up to two development candidates. Now I'll hand the call over to Matt. Thank you, Jim. As a reminder, our second quarter 2025 financial results are available in the press release we issued this morning and in our 10-Q we will file later today. As of June 30th, we had $166.2 million in cash and marketable securities on our balance sheet, which is expected to support our current clinical and operational activities into early 2027. R&D expenses were $37.1 million in the first quarter. Apologies, in the second quarter. The increase over the prior year was primarily due to an increase for manufacturing and materials for the ALTITUDE-AD clinical trial, as well as an increase in clinical expenses now that we are fully enrolled. G&A expenses were $4.6 million in the quarter, roughly flat to the same period in the prior year. This led to a loss from operations of $41.7 million and a net loss of $41 million in the quarter. Finally, I would like to note that our collaboration with JCR Pharmaceuticals is a highly capital-efficient way to expand our portfolio of oligomer-targeted candidates. Under the terms of the agreement we announced in July, in addition to an upfront payment that JCR received, if Acumen exercises our exclusive option to develop up to two development candidates, JCR will receive an additional option payment of $9.25 million. JCR will also be eligible to receive future milestone payments of up to $40 million related to development and up to $515 million related to sales for a total of up to $555 million, as well as single-digit percentage royalties on sales of any products that emerge from the collaboration. We are excited for the optionality and potential value this deal provides and await preclinical candidate data in early 2026. We are also confident in our strong execution of ALTITUDE-AD and look forward to sharing top-line results, which are expected in late 2026. We remain dedicated to delivering potential next-generation treatment options for the benefit of patients, caregivers, and shareholders. With that, we can open the call for Q&A. Operator? Thank you. As a reminder, if you'd like to ask a question, please press star one one. If your question has been answered and you'd like to remove yourself from the queue, please press star one one again. Our first question comes from Jason Zemanski with Bank of America. Your line is open. Good morning. Thanks so much for taking our question and congrats on the progress. I wanted to talk to you a little bit about AAIC. Specifically, if you look at Roche's similar sort of brain-shuttling technology, the trontinemab initial results there, and how to benchmark a potential brain-shuttling technology around sobirnetug. I guess secondarily, given the overall plaque reduction seen in those patients, what does that mean for your epitope given kind of the focus on the oligomers? Thanks. Thanks, Jason. Great question. I guess I'd like to direct that to Jim initially, and Eric, you may have some comments as well. Yeah, absolutely. Thanks, Jason. We've obviously been paying close attention to this entire space, including Roche's program. I think where I'd start is where we see the opportunity for this technology is to significantly enhance the ability to deliver your therapeutic target to the targeted areas in the brain. You see that certainly with the trontinemab, they see a significant change in the overall profile of the molecule from the days of delivering it directly as cantaniramab to what they're seeing now when combined with the shuttle to allow them to increase their brain concentrations. I think we see the same kind of opportunity with sobirnetug, where, of course, their difference is in the fundamental targeting of the molecules. We believe very much that these toxic synaptotoxic oligomers are directly toxic within the brain during the progression of Alzheimer's disease. Being able to robustly target that, we think, is a mechanism that's going to lead to improvement for patients. Of course, we also see some effect on plaques, and there's a complex biology there, the amyloid biology, although we all refer to amyloid as the target, and it certainly is. Amyloid biology is pretty complex, and so there are oligomers associated with plaques, and that's a much longer discussion. I think where it really lands is that we see the technology as enhancing the ability of sobirnetug to really effectively access soluble oligomers, and we think that is going to be a mechanism that will be beneficial to patients. Eric, I don't know if you want to add anything to that. Yeah, the only thing I might add to that is just in terms of where we are in development. I mean, Roche has done a great job in terms of their phase I study, and they're obviously starting to phase III studies, which will take a while to read out. On the other hand, we're really looking forward to our ALTITUDE-AD study with 542 patients that'll read out the end of next year. They're doing a great job with their development plan, but it's early. They're in phase I right now, and we're looking forward to the results of our phase II ALTITUDE study. Thanks so much for the color. Thank you. Our next question comes from Jeff Meacham with Citi. Your line is open. Hi, guys. It's Russ on for Jeff. I just wanted to understand a little bit more what you guys are hearing about the pTau217 screening assay used in the screening process, just what you're hearing or any feedback or color on that from physicians in the practicing end. Thanks, Russ. If you want to handle that, maybe mention the AAIC poster and some of the traction that we were getting from how we used that assay in ALTITUDE. Yeah, sure. Thanks. A great question. Really appreciate that. We, as you probably know, use that as part of the screening process in our phase II ALTITUDE study, and it worked really well, I think. We actually, in our phase I study, when that wasn't available, over 60% of the PET scans that we obtained as part of the screening process were negative for amyloid. When we used the screening process and got a pTau217 level first and then allowed people to go on the PET, only 17% of the scans were negative. We didn't really want to have 0% negative because then you were too conservative in your set point. In the poster that we had, we actually showed that as part of the screening process, that actually reduced the cost by about 40%. I think equally important, it reduces the burden for patients and their families because now you have far fewer patients going on to unnecessary PET scans and lumbar punctures for spinal fluid. It worked very, very well in our study, and we're pleased with those results. More broadly, to kind of get to your question, you know, we're hearing a lot of positive comments from clinicians in terms of the utility of this blood test, and there will be probably other blood tests that will become available, but this is the first one to actually get FDA approval. In the future, I think you'll see a lot of clinicians applying these blood tests as a screening procedure, and that even includes primary care physicians. We're starting to see now. Certainly, the specialists that we all talk to, KOLs, they will use this. I believe the utility of this method will become much more broad, which will get more people into the pipeline to get to these disease-modifying therapies. I'll leave it at that. Thank you. Thank you. Our next question comes from Paul Matteis with Stifel. Your line is open. Hey, this is Julian on for Paul. Thanks so much for taking our question. Just again, thinking about comparisons of the JCR t echnology to what Roche has shown. Just curious how you think you guys could potentially be differentiated, particularly even on the safety side, if you have any commentary on that. On the same topic, just wondering what you think, you know it's early, but what the phase II development could potentially look like. Sort of separately, just a broader question. There's been a lot of attention in the investor community on the early Alzheimer's studies, pre-symptomatic studies being conducted by Lilly and Novo. I'm just curious what you guys think of these trials and if you have any commentary there. Sorry, Lilly and [APPHI] is what I meant there. Thanks. Thanks, Julian. Yeah, I think I'll lead out. Maybe Jim, you want to comment a little bit more on the safety differentiation, and then Eric, you can comment on what we're sort of thinking about from a clinical development standpoint. As we envision the JCR collaboration, there are two points of differentiation. It's principally both on the carrier element and the way the JCR transferrin-binding carrier technology may lead to better safety relative to other transferrin-mediated delivery modalities that actually induce a level of anemia. I think that's one area of interest to us to exploit and potentially validate. The other is, and Jim mentioned this in his prior comments, around the cargo and the preference of oligomer-directed antibodies to avert even further reduced ARIA or other safety elements. Those are kind of the two primary modes of differentiation we see based on the synergistic partnership we've established with JCR. Jim, I don't know if you have more comments to make, and I think we probably should talk a little bit about reference, kind of the potential future clinical design for an EBD-directed product. Yeah, absolutely. Happy to. I think there are a number of elements that could impact a safety profile that we think, and it's part of the reason we're excited about this approach. At a high level, we see the opportunity to really lower the delivered dose because you're going to get a higher fraction of the circulating dose into the brain if the technology works as it's intended, which I think is overall a good thing. When you think about safety profiles, you can look at it from the perspective of target-associated things like ARIA. That's obviously something that's top of mind for anyone developing an amyloid-based antibody approach. We're overall pleased with the profile we see for sobirnetug when it comes to ARIA rates, and that comes from our phase I study, which we've talked about a number of times. It is interesting when you look at the work coming from the Roche group that in their case, their antibody, the ARIA rates are much, much lower when you convert trontinemab to trontinemab. There's a scientific hypothesis around that based on where the transferrin receptors are localized, which can change the entry points for where the antibody is getting across the blood-brain barrier. That's an interesting hypothesis and offers the opportunity to even further enhance what we think is an already attractive profile for the potential for ARIA risk with sobirnetug. As Dan mentioned, there are the transferrin-related risks associated with things like anemia, and that's certainly an element that's been reported in the Roche program to date. It's also been seen in other programs targeting the transferrin receptor, something we've thought a lot about and obviously went into our evaluation process. We've landed with JCR because we believe that based on their clinical evidence, they've seen very low amounts of anemia with their marketed products. The reasons for why that might be, I think there are a number of different things we could get into, like affinity ranges for the transferrin receptor. Also importantly, a number of different shuttles target the transferrin receptor, but they don't all necessarily target the same epitope. I think we're learning a lot about how this technology works, but we see opportunity here to really significantly alter and improve the safety profile that we see with sobirnetug. By the way, it's a profile we're already pretty proud of. We think there's opportunity there. I think we can talk about phase II study design. It is early days, as you say. The one thing I would point out is that Eric and the team really did a fantastic job in putting together a progressive study design for sobirnetug in phase I. I think we can benefit from the approach that we took, looking at both fluid and imaging-based biomarkers in AD patients with an EBD product. I think beyond that, we'll have to see. We've got plenty of work to do before we get to that stage. We're very proud of the work that the team did in phase I, and we think that there are some insights that came out of that design that we can apply to the next program in the chain. I'll leave Eric to address your question around what we think about the preclinical studies that are ongoing right now. Yeah, thanks, Jim. I think, yeah, definitely for shuttle technology that phase I even may be inpatient. You say it takes some learnings from sobirnetug. To get to your question about the preclinical studies, that's something that's under active discussion. I think based on our phase I data, sobirnetug would be a good candidate for a preclinical trial given its relatively low ARIA rates in our phase I study. We are having active discussions about how that might be done. I think you could take the approach that you could use a blood-based biomarker, and that's all you would need to get into a preclinical study. I'm not sure if that might be just a little bit too aggressive, but it's one of the things we've talked about. The other thing is, rather than just going straight to a PET scan, you could do essentially what we did in our ALTITUDE study, where you use a screening test, a blood test first, and then depending on the result of that test, then you go on to either spinal fluid or a PET scan. The other piece to this that is really evolving nicely, I think, is maybe doing sort of a phase II study for preclinical patients and looking at biomarkers. You would look at things like pTau217, but also GFAP, a number of other measures. Before you do the very large and very long phase III preclinical study, you get some good evidence that your biomarkers are going in the right direction. You're having the kind of effect you want in a smaller phase II study. Based on that, make a decision to do a much larger phase III study, which would be at that point a registration trial. It's something that's under active discussion at Acumen right now. Thanks, Eric. I'll just comment, Julian, that I think the rationale for an oligomer-directed agent in that preclinical population is very strong, given the elevated levels of oligomers that present and persist in that early preclinical phase of disease progression. We're excited about that future opportunity. Thanks very much for the detailed responses, and congrats on the progress, guys. Thank you. Thank you. Our next question comes from Chuang Nguyen with UBS. Your line is open. Morning, guys. Thanks for taking the question. Just following up on the asymptomatic question, and you touched upon the blood-based markers identifying this population. How do you see that being integrated into trying to find patients? How do you see it being covered by payers? Is this something that you'll see covered readily along with PET scans? Thank you. Thanks, Chuang. Eric, do you want to take a first cut at that? Sure. Yeah. There's a lot actually baked into that question. It's a good one. When you think about payers, now you're talking, of course, about something that's available commercially, and will payers pay for these things? What we're hearing anecdotally is that payers are reimbursing for this pTau217 screening assay, the one that's FDA approved now. I would expect that that would continue to be the case once you have a drug that you know has a positive clinical effect in this preclinical population. In other words, you want to delay the onset of symptoms. It is a different study design. It's not slowing the rate of decline because these people are impaired. It delays until you start to have cognitive decline. I think from a payer standpoint, and this will require some discussion, from a payer standpoint, it's to their benefit within the Medicare population, let's say, that it's to their benefit to delay the onset of cognitive decline because that's where healthcare costs start going up. I think there's a lot of potential for this to play out clinically. The first step, obviously, is we've got to do the study to show that this strategy actually works. I think it's got a lot of potential. Great. Thanks. Thank you. Our next question comes from Pete Stavropoulos with Cantor Fitzgerald. Your line is open. Hi, Dan and team. Congrats on the progress, and thank you for taking our question. As you were mentioning before, there was a lot of excitement around biomarkers, some of which show change in biomarkers start to appear far in advance of symptoms, as well as some of the underlying pathology, like various path species. How do these updates, including new biomarker data at AAIC, inform your approach and assumptions about clinical studies? Are there any that stand out to you as ones you may look at with samples at ALTITUDE studies that you haven't disclosed before or incorporate into a phase III study? Also curious to know if you're seeing ARIA rates from the ALTITUDE study on a blinded basis, and if so, any commentary around that? Thanks, Pete. A lot in that question. I'm going to direct it to Eric for a quick comment on biomarkers at AAIC and future development opportunities. Yeah, sure. Let me just talk about the biomarker question first. I mean, as much as we all are impressed by the pTau217 screening assay, there's a lot of additional work going on with additional biomarkers. pTau is one of the ones that is getting a lot of attention right now. We continue to just watch that field very, very closely. The results that we've had with the pTau217 screening assay were, I think, quite good. As you know, in our phase I study, we also looked at pTau181. We looked at GFAP. We looked at the Aβ42 over 40 ratio. I mean, there's a whole series of these biomarkers that you can look at. One of the strengths of doing that, actually, is when directionally they're all going in the direction you want them to move, I think that's good evidence that you're having a right effect on the biology of the disease. To get to your question about ARIA, we're obviously in the midst of an ongoing blinded phase II study. What I can tell you is that we've not seen any data that are inconsistent with what we reported for our phase I study. That's what I can tell you at this point. Yeah, and Pete, maybe I can layer a little bit on the biomarkers. As Eric was saying, I think you know there are more and more biomarkers that are coming out. You know, at a fairly high level, what I see is an improving resolution to be able to understand disease progression. We know that Alzheimer's disease is a progressive disorder. Patients progress over time. Existing diagnostics can sort of help do that diagnosis, but it's a relatively low resolution. As more and more markers are being studied, of course, they're all peaking at different points in the disease course. Over time, multiple groups' work is going to pull together, I believe, a much more high-resolution ability to understand where a given patient is in their progression of disease. Hopefully, that leads to more differentiated treatment. I think that's the long-term opportunity that I'm seeing in the blood-based biomarkers coming along. Of course, it goes without saying you've also got the benefits of convenience and cost savings and things that go along with that. It is that ability to sort of understand disease progression at a much higher resolution that I think ultimately is going to be the biggest impact. All right. Thank you for that, college. Just one more question, if you don't mind, on the blood-brain barrier technology. Any commentary around optionality in terms of the design to find an optimized candidate? Will you be grafting sobirnetug's FAB fragment onto JCR's FC backbone, or will you graft the transferrin receptor binding domain onto your antibody? Any details would be helpful. What were some of the non-clinical data or data from the feasibility studies that you found encouraging and influenced the decision to enter the agreement? Thanks, Pete. Go ahead. I think that's for you, Jim. Yeah, thanks, Dan. Absolutely. Yeah, Pete. I think the opportunity here that we see, and this is why we talk about it in terms of combining the cargo from the Acumen side of things with the carrier from the JCR side of things. JCR's technology is somewhat flexible. It allows us to investigate coupling different carrier molecules that are going to have different properties. We're looking at things like the overall PK profile that is generated, the rates at which the drug enters into the brain, things like that. Obviously, you're always interested in understanding safety profile. On the cargo side of things, sobirnetug is, of course, our flagship antibody, but we do also have other antibodies in the library that sobirnetug came from that all have their own properties that we've characterized over time. You can imagine at this stage in the collaboration, we're looking at what are the best components to put together. You know that we've talked about looking at single-chain variable fragments. We've talked about looking at VHHs. I think combining numerous different flavors of carriers with a couple of different possible cargos is the exercise that we're going through. It's a really very interesting exercise because it really offers lots of different optionality. That will be the process we need to finish up to make some decisions about which, if any, molecules to take forward. From a little bit of color around the types of studies, we're obviously interested in ensuring that we haven't altered the properties of the cargo by coupling to the carrier. We also want to make sure that the carrier is giving us the right targeting when it comes to PK and to brain penetration. There are a number of studies that are ongoing in preclinical species that will include a primate study to really kind of give us the characterization of the different possible combinations to pick the best ones. All right. Thank you very much for taking our questions, and congrats once again. Thank you. Again, to ask a question, please press star one one. Our next question comes from Tom Schrader with BTIG. Your line is open. Good morning. This is Jenny on for Tom, and I want to ask a couple of questions on your trial. Would there be any data on the range of MMSEs in your trial, and how often are cognition tests given? Is it every six months, or is it more often than that? Thank you. Yeah, I think. Do you want me to go ahead and take that? Please, yeah. Yeah. We will have MMSE as the secondary outcome. As you may know, our primary outcome is a scale called the IDRIS, which combines a cognitive measure and a functional measure. We'll also be looking at the CDR sum of boxes that are frequently used in trials. We have a number of other secondary outcomes that affect things like quality of life and that sort of thing. Most of the main cognitive assessments are done every three months in the study. Of course, we'll also have a lot of biomarker data just to put that out too. We're looking forward to really looking at a package of data. One thing I might mention in terms of our data readout at the end of next year, all the data don't become available at exactly the same time, especially some of the biomarker data. It takes a while to run those assays. Our top-line result will include top-line efficacy and safety. Some of the other more detailed biomarker results may take a little more time to become available. When we do have our top-line results, again, we'll have top-line efficacy and safety, but we'll also have some additional, especially biomarker results that will be rolling out in the subsequent weeks. I hope that answers your question. That does. Thank you very much. Thank you. I'm showing no further questions at this time. I'd like to turn the call back over to Alex Braun for closing remarks. Thanks, Michelle. Thanks to everyone for joining us today and taking the time to listen in. If you have any further questions, we are always available at the company, so please contact us. Have a great day. Thank you for your participation. This does conclude the program. You may now disconnect.