Good afternoon, and welcome to the ProMIS Neurosciences second quarter 2026 financial results and business update conference call. All participants will be in a listen-only mode. Instructions for the question and answer session will be given following the prepared remarks. As a reminder, this conference is being recorded. I would now like to turn the call over to Carie Pierce, Vice President, Investor Relations and External Affairs at ProMIS Neurosciences. Please go ahead. Thank you, operator, and good afternoon, everyone. Thank you for joining ProMIS Neurosciences second quarter 2026 financial results and business update conference call. Presenting on our call today are Neil Warma, our President and Chief Executive Officer, and Dr. Larry Altstiel, our Chief Medical Officer. Earlier today, we filed our quarterly report on Form 10-Q with the SEC for the quarter ended June 30, 2026, and issued a press release with our financial results. Both are available in the investor relations section of our website at promisneurosciences.com. Before we begin, I would like to remind everyone that statements made on this call include forward-looking statements with the meaning of the Safe Harbor provisions of the Private Securities Litigation Reform Act of 1995. These include, among others, statements regarding our clinical development plans and timelines for PMN310, PMN267, and PMN442, and our other product candidates. The interpretation of the significance of the blinded interim data from our PRECISE-AD trial, our expectations regarding future clinical results, and our financial position and cash runway, and our overall business strategy. These forward-looking statements are based on management's current expectations and are subject to risks and uncertainties that could cause actual results to differ materially from those expressed or implied. We encourage you to review the risk factors described in our most recent annual report on Form 10-K, our Form 10-Q filed today, and other filings with the SEC. We undertake no obligation to update or revise any forward-looking statements as a result of new information, future events, or otherwise, except as required by law. With that, I would like to turn the call over to Neil. Thank you, Carie. Welcome to all those who are joining us today to discuss ProMIS Neurosciences results for the second quarter of 2026, and also to review the recent progress across our pipeline. As Carie said, joining on the call today is Dr. Larry Altstiel, our Chief Medical Officer, who will walk us through the encouraging interim data we recently reported from our phase I-B PRECISE-AD clinical trial. I'll then provide a financial update before we open the line up for a few questions. As many of you know, ProMIS is a clinical stage biotechnology company applying our patented technology platform to build a portfolio of antibody therapies and therapeutic vaccines for neurodegenerative diseases, with a focus on Alzheimer's disease, dementia with Lewy bodies, ALS, and Parkinson's. We believe these diseases share a common biological cause. Normal proteins that misfold become toxic and kill neurons. Our platform is designed to combine protein biology, physics, and supercomputing to selectively target these toxic misfolded proteins while sparing their healthy, properly folded counterparts. Our lead product candidate is PMN310, which is a monoclonal antibody designed to treat Alzheimer's disease by selectively targeting toxic misfolded oligomers of amyloid beta. Behind PMN310, we are advancing PMN267 for ALS, which targets misfolded TDP-43, and PMN442 for synucleinopathies such as dementia with Lewy bodies and Parkinson's disease, which target pathogenic alpha-synuclein. Both PMN267 and 442 have been humanized in a human IgG1 framework and are advancing toward IND-enabling studies. We are also progressing a set of vaccine programs in Alzheimer's and Parkinson's and ALS. As we have recently discussed, the second quarter was a defining period for ProMIS. In late July, we reported positive, blinded six-month interim safety and biomarker results from our ongoing phase I-B PRECISE-AD clinical study of PMN310. Data we believe reinforce the core thesis behind our oligomer-selective approach. Larry will walk us through the details in a moment, but at a high level, the blinded interim analysis yielded a favorable safety profile across all participants and genotypes, showing no cases of ARIA-E and early directionally consistent movement in two complementary biomarkers, plasma p-tau217 and CSF MTBR-tau243, which is consistent with target engagement. We believe these data reinforce the central thesis behind PMN310, that by selectively targeting toxic amyloid beta oligomers rather than plaque, we have the potential to deliver the benefits of amyloid-directed therapy without the ARIA burden that has constrained this class of medicines. We actually hosted a live webinar back on July 28 with two independent key opinion leaders, Dr. Thomas Montine, University of Minnesota, and Dr. Michael W. Weiner of UCSF, who shared their perspective on the data and its clinical relevance. For those of you who missed it, the presentation and recording of the webinar are available archived on our website. This, we believe, is truly the most meaningful clinical milestone in the company's history to date. I would now like to ask Dr. Altstiel to walk through the PRECISE-AD summary of the interim data in a little bit more detail. Larry, if you would please. Thank you, Neil, and good afternoon, everyone. I will walk through the six-month blinded interim data from PRECISE-AD that we announced on July 28. Starting with the trial design, then safety, then biomarkers, and close with what to expect as we move toward the 12-month top-line readout. PRECISE-AD is an ongoing phase I-B trial of PMN310 in patients with mild cognitive impairment due to early Alzheimer's disease. It is a randomized, double-blind, placebo-controlled, multiple ascending dose study. We completed enrollment in December 2025, with 144 subjects across 21 active sites in the U.S., randomized three-to-one active drug versus placebo across three dose cohorts of five, 10, and 20 milligrams per kilogram, dosed monthly by IV infusion over 12 months. Of the 144 enrolled subjects, 136 were included in this interim safety analysis. This is a genetically and demographically representative population. Mean age was 73.3 years, 58% of patients were female, and importantly, 61% of patients carried at least one ApoE4 allele, with 11% being ApoE4 homozygotes. That is the proportion of the very highest risk of ARIA with plaque-binding antibodies and one that is often underserved by approved amyloid-directed therapies today. As of the July 22nd data cutoff date, all 136 safety evaluable patients had been dosed for at least six months. 78% had passed nine months, and 49% had already completed the full 12 months of dosing. Safety was the primary focus of this interim look, given that PMN310 was designed as a non-plaque binding antibody with the goal of significantly reducing the ARIA risk. The results were encouraging. We observed zero cases of ARIA-E, which is the more serious symptomatic form of ARIA involving brain swelling. This result was noted across all genotypes, including in the ApoE4 homozygote population. Total ARIA, which includes the milder ARIA-H microhemorrhage finding, was 4.4%, and every case was mild and asymptomatic. We saw no treatment-related serious events and no drug-related discontinuations through the interim cutoff, and only one single non-serious infusion reaction, a rate notably lower than the infusion reaction rates reported for approved anti-amyloid therapies in their pivotal trials. These are descriptive comparisons against published data and not head-to-head studies. Directionally, this is a differentiated safety profile, particularly in the ApoE4 carrier population, where approved therapies today carry their most significant warnings. Now with biomarkers, I want to frame this next part carefully because PRECISE-AD remains a blinded ongoing trial, and these are early exploratory signals and are not efficacy readouts. We looked at two complementary biomarkers chosen to bracket different points in the Alzheimer's cascade. Plasma p-tau217, one of the earliest and best-validated biomarkers of amyloid-driven tau pathology, and CSF-mtVR tau243, a more downstream tangle-specific marker that correlates closely with tau PET imaging and cognitive decline. In untreated placebo arm patients from published natural history data, both markers are expected to rise over time as disease progresses. In our blinded pooled analysis, meaning this combines both drug and placebo-treated patients under the three-to-one randomization, we saw the opposite. Plasma p-tau217 declined approximately 15% from baseline. p-tau243 declined by approximately 13.3%, with about 62.5% of patients showing a decline. Both the direction and the proportion of patients showing a favorable response are broadly consistent with the trial's 75% active drug allocation. We think it's notable that both an upstream and amyloid-linked biomarker and a downstream tangle-specific biomarker moved in the same favorable direction at the same time point. That consistency is encouraging, although again, this remains a blinded interim look, and it is not a determination of clinical efficacy. The trial is ongoing and remains blinded. We anticipate all patients to complete their 12-month dosing by the fourth quarter of this year, and following database lock and statistical analysis, we expect to report unblinded 12-month top-line data in the first quarter of 2027. That readout will include the full safety data set, a more detailed biomarker panel, and for the first time, we will also report on clinical cognitive outcome measures, which will let us assess PMN310's efficacy in a controlled and unblinded setting. With that, I'll hand it back to Neil. Thanks very much, Larry. Again, a very encouraging set of interim data. Thanks for the presentation. Beyond PMN310, as I touched on earlier, our broader pipeline continues to advance. PMN267, our program targeting misfolded TDP-43 in ALS, has been humanized in an IgG1 framework and is progressing towards IND-enabling studies. PMN442, our lead candidate for dementia with Lewy bodies and Parkinson's disease, potentially other synucleinopathies, has also been humanized and is advancing towards IND-enabling studies based on its selective binding to pathogenic alpha-synuclein. Behind those, we continue to advance our vaccine program in Alzheimer's disease, ALS, and Parkinson's, and are further developing our EpiSelect discovery platform, in which we are incorporating machine learning to accelerate identification of new disease-specific epitopes. Just turning to the financial results briefly. For the quarter, we ended the second quarter with roughly CAD 53.4 million in cash and short-term investments, compared to CAD 6.1 million as of December 31, 2025. That increase primarily reflects the roughly CAD 70.1 million in net proceeds we received in January 2026 from our private placement financing. Based on our current operating plan, we expect our existing cash and investments to be sufficient to fund operations through 2027, which importantly carries us through the anticipated 12-month top-line readout from our PRECISE-AD phase I trial expected in the first quarter of 2027. For the second quarter, we reported a net loss of roughly CAD 11.7 million, which equates to CAD 1.28 per share, compared to a net loss of roughly CAD 10.1 million, or CAD 7.26 per share in the second quarter of 2025. The improvement in loss per share reflects the increase in weighted average shares outstanding following our January financing. Research and development expenses were approximately CAD 9.5 million for the quarter, up slightly from CAD 8.7 million a year ago. General and administrative expenses were CAD 2.7 million, up from CAD 1.4 million, reflecting increased professional fees and headcount as we have modestly built out the infrastructure to support operating as a clinical stage company. For the first six months of 2026, we've reported a net loss of roughly CAD 20 million, compared to CAD 17.5 million in the prior year period. R&D expenses were CAD 16.5 million for the first half, up from CAD 14.2 million, largely reflecting full enrollment and dosing activity in the PRECISE-AD trial. G&A expenses were roughly CAD 4.4 million compared to CAD 3.4 million a year ago. Net cash used in operating activities was roughly CAD 22.8 million for the six months compared to CAD 8.8 million in the year prior, consistent with increased pace of our clinical activity. That's a brief summary of the financial results. To summarize in closing, this has, as we've laid out, really been a transformational quarter, a transformational year thus far for ProMIS. The blinded six-month interim data from the trial, we believe, provide the first human evidence supporting our oligomer selective approach. A favorable safety profile with no ARIA-E across all genotypes, including a high proportion of ApoE4 carriers, alongside early biomarker movement consistent with target engagement and a potential drug effect. We believe these data speak directly to the potential of PMN310 to offer a differentiated safety and efficacy profile in Alzheimer's disease. We're well-financed to reach our next major catalyst with the cash runway through 2027. That importantly spans the unblinded 12-month top-line readout expected in the first quarter of next year. Beyond PMN310, we continue to advance a deep and differentiated pipeline across Alzheimer's, ALS, multiple synucleinopathies, all powered by our EpiSelect platform. I want to take this time to thank, importantly, our patients, their families, and all the caregivers, our clinical investigators, and our employees for their dedication, as well as our shareholders for their continued support. We look forward to keeping you updated as we approach these important milestones. Thank you so much for your attention, and operator, I think we're ready to take a few questions, please. Thank you. We will now begin the question and answer session. To ask a question, you may press star, then one on your touchtone phone. To withdraw your question, press star, then two. For participants using speaker equipment, it may be necessary to pick up your handset before pressing the star keys. First question comes from Yatin Taneja with Guggenheim Partners. Please go ahead. Hey, guys. Thank you for taking my questions and nice progress. Congratulations on the recent results. I have maybe three questions, if I may. One broader question and two specific questions. I'll ask the broader one first. Now that you've had some time to process the data, could you perhaps talk about the KOL reaction to these data? Then what comes next for 310? I'll ask the two other questions afterwards. Thank you. Sure. Thanks, Yatin. Thanks for the comments. Maybe I'll just touch on the first one, A and B. Well, the KOL reaction and the investor reaction, Larry and I have had a busy couple of weeks since the release of the data. I think overall, the overall reaction response has been very positive. I think we set expectations going into the interim analysis, and we were careful how we set those expectations. I think the data we saw from a company perspective, we certainly met our expectations and probably even exceeded them a little bit. The safety was extremely encouraging. The target engagement signal was, again, encouraging as well. I think this was reflected very much by the external stakeholder groups, the KOLs, the investors, the shareholders, all were quite buoyed by the interim data. So we were pleased with that. I think that reflected from the webinar, the two KOLs, the independent KOLs we had on our call, were quite supportive of the data as it related to their neurology practice as well. As far as what's next for PMN310, thanks for that question, we're certainly not just sitting and waiting for the data to read out in Q1. We're looking forward as to how we manage the life cycle of PMN310 all the way to market. Contained within that internal program, if you will, is what potentially is the next clinical trial that follows this one if the data is successful. Larry, certainly, and the team are working hard on designing the next clinical trial. We believe that if the data are positive and continue to be positive and read out positively in the top line, we anticipate stepping into a single registration study. The clinical development plan is certainly being refined for the next clinical study. The regulatory path, we expect meeting with the FDA. We do have Fast Track designation for this program. We expect meeting with the FDA shortly after the final data set's together. The regulatory path is important to us. We're also developing, or looking at developing a subcu, subcutaneous formulation. That program is ongoing right now. It's monthly IV dosing. Getting to market with a subcu formulation is very important to us, so that's also in the works as well. We're also looking, as Larry said, this patient population we're addressing now is that MCI early Alzheimer's patients. There's a lot of interest in the asymptomatic preclinical AD patient population. We're also looking at that expansion or label expansion, if you will, as to how we address that market because we think having a product like PMN310 that ideally delivers better efficacy, but importantly, much better safety profile, that preclinical AD population is one that we could address quite well with a very safe and effective product. There's multiple prongs here that are being internally assessed and evaluated and prepared. Really is that life cycle management for PMN310. In addition, obviously, we're having discussions with strategics. There's a lot of interest from the pharma companies in what we're doing. Looking at how to work with them potentially in the future, or potentially looking how to fund the next study ourselves. Those strategic options are also part of the discussions internally. Very good. That was excellent, Neil. Perhaps the two follow-up questions. One is on the biomarker, then the one is on the safety. With regard to the biomarker or the blinded biomarker, I understand, I think you and Larry have emphasized that we should not be overreading it at this stage. But to us, the target engagement is pretty clear, at least, or pretty evident, because we don't think there is any reason for p-tau217 to decline in an untreated AD population. The question is, how should we think about target engagement for 310? On the safety side, yes, I think it's very clean safety and tolerability. The question is, with regard to ARIA-E, does it reflect the front-loaded fast pattern, or does it hold beyond six months? Love your answer on both of those. Thank you. Maybe I'll turn that over to Larry. Larry, if you want to speak on the, kind of what do we feel about the target. I think we're pleased with the target engagement signal. Yeah. Maybe you can speak a little to that and then to the safety as well, please. Yeah. I think we're pleased with the target engagement signal. Again, we're happy to see a robust decline in p-tau217, really beginning at the first month, and then continuing on and increasing up to six months. As Neil pointed out, the natural history of p-tau217, if it's unopposed by any sort of therapy, is to increase over that period of time. So we were happy with that result. We were also happy with the p-tau, the MTBR-tau243 result because that really represents the onset of tauopathy. When tauopathy begins, that's really the onset of frank clinical decline. So we were happy with both of them. Because they bracket two ends of pathology, of oligomer-based pathology, that is, one, increasing tauopathy with p-tau217, and then the increase in abnormal phosphorylation of tau going on to neurofibrillary tangles. We think that that's an interesting sign of potential target engagement. Now with the safety. The safety data were not really cut off at six months, but actually reflected the total safety data, which we review every day, by the way, up to the time of the interim analysis, which was July 22nd. A substantial number of patients had crossed the six-month threshold. Almost half of the patients had finished the study. We think that, again, the absence of ARIA-E is certainly due to the fact that we engineered PMN310 to avoid amyloid plaque. It does not bind to amyloid plaque in the brain and also in the vasculature. So we think that that's principally the reason why we're not seeing any ARIA-E. The ARIA-H data probably represents the baseline increase that you see in Alzheimer's patients due to cerebral amyloid angiopathy. This is what is commonly seen in patients who are not being treated with drug. You will see a small amount of ARIA-H that increases over time. Again, I think that with the ARIA, we were quite gratified to see that signal. Also too, safety and tolerability do not really end with ARIA. We did not see any serious adverse events related to drug therapy. We did not see any dropouts related to treatment. Also, the infusion reaction rate was actually quite low, with just simply one case of a mild infusion reaction that did not require a change in dosing. All in all, I think that our impression is that the safety is really quite remarkable, and that we do have evidence of target engagement. To your point also, Yatin, the importance of six months, I think is also kind of emphasized when we know that the majority of ARIA cases, ARIA-E and ARIA-H, but certainly when you look at our graphs on our presentation, the majority, 90%-plus of ARIA-E cases occur in the first six months of dosing. To see zero cases in, as Larry said, six-plus months, half the patients have actually completed 12 months of dosing, so it kind of goes beyond six months. Again, that 6-month threshold, when we know typically from the donanemab and lecanemab studies, 90% of the cases occur, we are that much more pleased with our zero cases over the first six-plus months. Excellent. Thank you. No, thanks, Yatin, for the questions. Operator, I think we can take a couple more. Next question, Pete Stavropoulos with Cantor Fitzgerald. Please go ahead. Yeah. Hi, Neil and Larry. How are you? Congratulations on the updates and progress for the quarter, and thank you for taking our questions. One question is, though, whether you have target engagement when dosing these humans in PMN310. You did present some data at AAIC about a month ago. Can you just talk about this assay and the outcomes, and when can we expect to see a similar analysis for the Phase Ib? Will we get any additional biomarker data from the blinded interim look before 1Q 2027 readout? Yeah, Pete. Yeah. I'll start with your, kind of work backward through your question. We'll have a much more fulsome presentation of all the biomarkers in the clinical trial, along with the clinical outcomes when we unblind the data after the study is concluded. With respect to the assay that you were speaking about that we disclosed at AAIC, this is an assay to detect A-beta oligomers in cerebrospinal fluid. The A-beta oligomers, although they're extraordinarily toxic, are present in very low concentrations, in picomolar concentrations, 10 to the -12. So they're very hard to detect. Other companies have used an antibody saturation level to look at antibody saturation of them, but no one has really, to date, measured the exact thing itself, that is, the A-beta oligomers. I think what we showed here for the first time, in conjunction with our colleagues in Germany, was to show that we actually measured the concentrations of A-beta oligomers. We did this in a phase IA study. These are patients who were otherwise healthy, but nonetheless had low amounts of A-beta oligomers. We were able to detect a dose response with that, even after a single dose of PMN310. This assay is still being refined, but we expect that it will be used, and we will present the data again when the study is completed. Yeah, I think the importance, and thanks for the question, Pete, and your comments. The importance of that assay, as Larry said, is really to kind of elucidate the mechanism of action that we have been predicting, if you will, over the number of years since we have been developing PMN310, that being the binding to the oligomers and the removal of those oligomers. As Larry said, that has not been possible because there has never been an assay sensitive enough to measure these oligomers. Now that we have shown early data that we can indeed develop an assay that is sensitive enough to not only measure these oligomers, we also show that in the presence of PMN310, the actual reduction of these oligomers from circulation. Again, this was done in our 1a samples, but it really is kind of connecting the dots around the mechanism of action. This assay will be implemented into the phase IB study so that we can look at pre-treatment and post-treatment results to see whether or not indeed we actually are able to reduce the level of these circulating oligomers. Then ideally, that lines up with the clinical evidence we see at the end of the study and ideally with the biomarker evidence. So having that mechanism of action piece is significant for our own use, but certainly when it comes to regulatory authority approval as well. There will be no unblinding or blinded data presentations prior to the final results coming out, Pete. Okay. A couple of follow-ups. Current formulation in the phase IB is IV administered. How are you thinking about the potential subcu formulation? Is it feasible? Are you working on it? What formulation would you actually like to bring it forth, assuming the phase IB is positive? Yeah, that's a good question. We touched on it a minute ago a little bit, but it's important to us to deliver the product to market in a subcu formulation. I think we're expecting to have improved efficacy versus products in the market, certainly improved safety. So what we want to ensure is that we'll have improved patient compliance, if you will. So entering the market with a subcu formulation of PMN310 is certainly in our sights, and we've actually started the formulation development of that program. We've actually hired somebody on board to really lead the effort on the subcu formulation. We haven't presented any data results on that. We'll give some clarity as we get going with this program. We think it's quite possible. Again, others have gone before us and formulated antibodies as a subcu formulation, so I don't think it's overly complicated. Understanding what's required, viscosity, volume, we need to understand the PK/PD and dose from the clinical study. But all of that seems very possible. Again, without giving too much away until we do the actual data and the work, it does seem like it is possible. Then we need to understand how to roll it into that next study such that we can get it to become commercially available as soon as possible. But it is very much a priority for us, developing this over the next couple of years. All right, great. And last question. You did touch on it. You do have early-stage candidates. Just curious to hear how you're thinking about these assets and which may enter the clinic next, and what's going to be the driving factor for those decisions. Yeah, the driving factor is certainly going to be, and thanks for the question, we really are excited about the pipeline as well. Although we obviously remained, as they say, laser-focused on the execution of this study to deliver the results on time, and safely as well. But beyond that, there's some very exciting products coming along. I think our EpiSelect platform is unique and differentiated in that I think we've proven we can develop very selective antibodies to these misfolded proteins. So as we said, coming close behind is the antibody targeting misfolded forms of TDP-43, which is implicated in most of the ALS patients. So ALS is another candidate indication we're going after. And then the misfolded forms of alpha-synuclein, whether it be dementia with Lewy body or Parkinson's disease, is also very interesting to us. So we are actually advancing both those candidates pre-clinically. We would like to get additional preclinical proof of concept for those candidates as well. It will be important if we can generate data, obviously with the Alzheimer's program clinical data, but then also have some preclinical proof of concept data in the follow-on assets that all read out in the same time. We want to demonstrate that we have a robust discovery engine, if you will, and a viable pipeline beyond Alzheimer's. The goal is to advance these towards the clinic, the two pipeline candidates towards the clinic over the next six to nine months, such that they will be ready for IND-enabling studies and can enter the clinic within the next year or so. That is very much a goal of ours is to advance these. Again, we are selective. What is the driving factor will be data, obviously, as it always is, and resources. Again, the bulk of our resources is focused on the Alzheimer's program, so we are careful how we allocate resources beyond that. We are modestly allocating certain resources to advance a couple of the pipeline candidates as well in order to generate value and get those to the clinic for the patients as soon as we can. All right. Great. Thank you, Neil and Larry, for taking our questions, and have a good evening. No, thanks so much, Pete, really appreciate it. No, thank you. Thanks, Pete. Next question, Fozia Ahmed with Brookline Capital Markets. Please proceed. Hi, team. Thank you for taking my question. Hi, Fozia. Hi. My first question is, I see on the press release you will be presenting at the upcoming CTAD meeting. If you could share what would you be presenting at that meeting, that would be great. Then I have a follow-up. Sure. CTAD, for those of you who do not know, Clinical Trials for Alzheimer's Disease, is a medical conference focused on Alzheimer's. That takes place in mid-November. It is really the next one. As you all know, we attended the AAIC in July, and this is the next one following the AAIC coming up in November. We are submitting abstracts similar to what we have presented already, Fozia. So we do not have any kind of acceptance yet of abstracts, so we are careful what we are saying we are going to do at CTAD. We are at CTAD. We are going as a team. It is in Boston this year, where we are located. We plan on being at CTAD certainly to engage with KOLs, to engage with pharma companies, and with interested parties. Ideally, we would like to present similar data that we presented a couple of weeks ago around the interim analysis. Again, we are not looking to present additional data. If we are given the platform by the organizing committee at CTAD, it would be nice to stand on the podium and present again. Again, we have not been given that yet. They have not decided on all the speakers. We will be there in force to talk to folks and ideally to re-present, if you will, the interim analysis that we presented a couple of weeks ago. Thank you. My next follow-up question is on the subcu formulation. I just wanted to see if you could shed a little more color on, assuming that phase I-B study is positive, how do you incorporate subcu? Would it be part of the potentially registration study, or would you expect to establish efficacy with the IV formulation first and then bridge to subcu separately? Yeah, those are things we're asking ourselves internally. As I said, we're building out that plan now. The important thing is we get it to patients as quickly and safely as we can. Assuming the data's positive, a lot depends on clinical trial design. That in part depends on FDA feedback. There's a lot of moving parts, Fozia, on is it a separate arm of a registration study? Does it follow? Does it come before? We really haven't given any guidance yet on that. Again, a lot of these questions we're asking ourselves internally and with our experts. As soon as we have some clarity around how the subcu folds into the next clinical development piece, we'll certainly update the folks. But right now, as I said, there's a lot of questions that we need to answer first around dosing and viscosity and some of the stuff we're advancing now just to understand a little bit more. Again, viscosity is an easy one to mention because that's something that needs to be done early. These are the studies we're doing in order to understand. We're also looking at devices and is this an auto-inject pen, for example, does that make sense? Again, a lot of questions to answer first before we know exactly how it plays out in the clinical development picture. But it is our intention to have a subcutaneous form of the product to patients as quickly as we can. Thank you. I appreciate it. Sorry, can't be more specific. Again, there's a lot here, but we'll clarify. It's not trying to avoid the question. It's just, as I said, we're determining a lot of this ourselves with our experts. No, I understand. Thank you so much. Thanks, Fozia. Next question, Gail Mckay with Chardan. Please go ahead. Hi, Pete. Neil, thinking forward to 2027 and assuming the Phase Ib data reads out positively. As you're thinking about the design for the registrational study, what can you learn that can inform the design of that study from the Phase III studies of lecanemab or donanemab, whether it's patient inclusion/exclusion criteria or your choice of the primary endpoint, whether that's CDRSB or IADRS. What are you thinking there, and how might those studies be helpful in your design? Larry, I'll follow, but Larry- Sure. You might have some thoughts around that. Yeah, I think the outcomes will be pretty clear. The FDA really recommends the CDR sum of boxes as the primary clinical outcome measure because it includes both functional and cognitive assessments. Then with the ADAS-Cog and ADAS-Cog composite scores, like the IADRS, as secondary outcomes. I think that we're pretty well fixed on what the outcomes will look like. In terms of what the trial design will look like, we think that obviously the trial will have to be of a large enough size in terms of patients and a long enough duration to make some credible statements about affecting disease progression. It has to be large enough that we can power it to see a credible change in the CDR sum of boxes, which will be the primary outcome. It is important to note that, again, the primary things that are involved in getting an approval are, one, safety, and then two, a positive clinical outcome. I think that we can learn something from their studies and something from their recruitment strategies and something about the time that it takes to enroll such a study. I think that, again, what we will learn probably most of all is what is our effective dose from our Phase IB study? What kind of clinical signal do we see in our Phase IB, which will help us power that larger Phase III study? Yeah. We will give a little bit more color around that, Gail, too, as we decide. Yeah. Again, those trials are certainly formative and give us some colors to a little bit of precedence. They were done a number of years ago. Also keep in mind that we certainly expect to go to the agency, the FDA, with a much differentiated product, certainly with respect to safety profile. When you look at the numbers of patients that the donanemabs and the lecanemabs, Eli Lilly and Eisai had to build for their safety database, we are expecting ours does not have to be that large if all continues well as we have seen. Patient numbers might be less, again, powered for efficacy, not because we need a large safety database. Again, we are not expecting a black box warning. Ideally, our ARIA-E and safety profile would prevent that from happening. There are certain things we can certainly learn. But I think our product is going to be differentiated in a very positive way, such that there will be elements of our clinical trial that make it more streamlined and such. We do expect to run a global clinical study. We want to make this product available to patients around the world. That is one of our philosophy here at the company. Also, market size globally is interesting for us as well. We will give more clarity around the trial design as we interact with the agency. Again, we have Fast Track, so we can do that in a pretty expedited way. But I think it is going to be differentiated in a product that we might be a little bit more streamlined in our approach. Well, great to hear. We will look forward to hearing more about that. Thanks so much, Gail. Really appreciate it. Operator, do we have one more? Yes. Next question, Raghuram Selvaraju with H.C. Wainwright. Please go ahead. This is Yan Zhai sitting in for Ram. I have two questions. The first is, at top line, what magnitude of p-tau217 or MTBR-tau243 change could you consider beyond assay and within patient variability? And how will that placebo separation and dose exposure response factor into your interpretation? Yeah, I mean. Well, I think that Go ahead, Neil. Yeah. Well, I will just start quickly, and then you probably speak to this better than me, Larry. Again, as far as kind of expectations and what do we expect, we are kind of really being careful not to go into the next six months in top line predicting what might happen. Again, we are expecting and we are hoping to kind of continue along the same framework here with clean safety, and a strong clinical signal. So predicting what expectation is tough at this stage, and we want to be careful not to give any guidance on these are the numbers or this is the level of separation. I think we want to be at least as good as, from an efficacy perspective, what is on the market. When you look at expectations and biomarker movements and percent biomarker movements, again, we do not want to give any expectations here. I know, Larry, maybe you can speak to the holistic approach of the biomarkers, and I think we are very expansive with the panel of biomarkers that we are looking at. So that is more important for us to think through mechanistically how the drug might affect some of these biomarkers rather than leading with, we expect to see this percent change. But Larry, you can maybe speak to that a little bit. Yeah, I think, Neil, that's correct. We look at the biomarkers in their totality. We chose them really to reflect a lot of the biology that is affected by A-beta oligomers. We expect them to move at different times and at different magnitudes. But we think that they will tell the total story of what PMN310 is doing. I think it probably doesn't make a lot of sense is to tie success or failure to a particular percentage of p-tau217, especially at this stage in the study. Again, we look at the biomarkers in their totality, and again, that will give us a more fulsome notion of the biology of PMN310, and also really help guide us in our subsequent studies as well. Got it. Thank you. My next question is actually speaking of biomarkers. With SV2A, what controls, I'm curious, have you run the rule out PMN310 interference with assay capture or detection? Just, for example, so that a lower signal reflects lower oligomer burden. Yes. The answer to that is yes. Again, with our new assay that we have, that's being optimized right now, so I think we're in pretty good shape with that assay. Got it. Thank you. Okay. Thank you. Thanks, operator. I would now turn the floor over to Neil Warma for closing remarks. Yeah. Again, I'd like to thank everybody for your attention this afternoon. It's been, again, an interesting call. Thank you also to the folks for their very interesting questions. Appreciate that. Thanks for your attention, your interest in ProMIS and our programs. We look forward to presenting more updates over the remainder of this really an exciting and pivotal year for us at ProMIS. Thanks again for your attention, and we'll continue to update you as we progress. Thank you. This concludes today's teleconference. You may disconnect your lines at this time, and we thank you for your participation.