Good day, and thank you for standing by. Welcome to the Vivoryon Therapeutics 2024 Third Quarter Earnings Call. 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 during the session, you will need to press star one and one on your telephone. You will then hear an automated message advising your hand is raised. To withdraw your question, please press star one and one again. Please be advised that today's conference is being recorded. I will now like to turn the conference over to your speaker, Anne Doering. Please go ahead. Thank you, Roz. Good afternoon, and thank you for joining us today to discuss the company's third quarter 2024 results and operational updates. This morning, Vivoryon issued a press release reporting its nine-month 2024 financial results and also provided an update on our progress, which was marked by compelling kidney function data as well as execution of important steps in implementing our strategy to advance varoglutamstat in kidney disease. This press release is posted on Vivoryon's website at www.vivoryon.com. On the call with me today are Vivoryon's Chief Executive Officer, Frank Weber. Our Chief Business Officer, Michael Schaeffer, is also available for Q&A. We will begin today's call with opening remarks from myself, giving you an overview of the key highlights from the third quarter and post-period updates, after which we will move to Frank, who will provide some details on the exciting news update we announced yesterday, which is the positive kidney function data from our VIVA-MIND phase II study. I will then review the financial results for the third quarter of 2024 and conclude the call with an overview of our corporate outlook and strategic update. Following the prepared remarks, we will host a Q&A session. I would like to remind you that during this conference call, we will present and discuss certain forward-looking statements concerning the development of Vivoryon's core platform, the progress of its current research and development programs, and the initiation of additional programs, as well as results of operations, cash needs, financial condition, liquidity, prospects, future transactions, and strategies. Should actual results differ from the company's assumptions, ensuing actions may differ from those anticipated. You are therefore cautioned not to place undue reliance on such forward-looking statements, which speak only as of the date hereof. For those that have been following Vivoryon over the last month, you know this has been a period of major change for the company. Since March of this year, we have step by step rolled out the strategic shift to kidney disease and, in particular, have presented to you the results from two phase II studies demonstrating varoglutamstat's potential to beneficially impact kidney function, which provide the foundation for this new path forward. Now, shifting to the third quarter and post-period updates, clearly the biggest development is, of course, the top-line VIVA-MIND data we disclosed yesterday, which shows a highly significant improvement of eGFR versus placebo, confirming VIVIAD eGFR results and providing a second phase II long-term data set. Frank will walk you through these data in detail shortly and show you why we can confidently say now that with the strong data package generated to date for varoglutamstat in kidney, we have a unique chance to become a key part of the treatment landscape for a number of diseases with high unmet medical needs. Another important development in the third quarter was our presentation at ASN. We were thrilled that kidney outcome results from our VIVIAD phase II study were selected for a late-breaking oral presentation at ASN Kidney Week, which is the world's premier nephrology meeting. Frank's presentation was very well received, and we have been extremely encouraged by the positive reactions we received from the community. Vivoryon hosted a virtual kidney disease KOL event in September, during which the experts provided insights into the limitations of current standard of care and new developments in kidney disease. They outlined that novel medicines are needed with MOAs suitable to addressing the key inflammatory and fibrotic pathways underlying this disease and the potential of varoglutamstat in this phase. As you can see, once again, we have had a very active reporting period marked by continued strong progress in advancing varoglutamstat for kidney disease and are poised to enter 2025 with positive momentum. With that, I will now turn the call over to Frank. Thank you, Anne. Dear ladies and gentlemen, good morning, good afternoon. We're going to move to the mechanism of action and the groundbreaking discovery we announced recently that actually the QPCT/L, or the isoQC, is the enzyme which is responsible for reducing kidney inflammation and fibrosis, and that improves kidney function. And as a short recap, the pro-inflammatory and pro-fibrotic peptides require largely pyroglutamylation, that is, a ring form at the N-terminal end of these peptides to become fully functional and potent. And Varoglutamstat is an inhibitor of that enzyme, and therefore the pyroglutamylated peptides do not occur in the same amount and are significantly reduced. And there are various numbers of peptides which are involved in the inflammation fibrotic cascade and then end up creating kidney dysfunction, kidney fibrosis, and kidney insufficiencies. And we have in that slide you can see below, run and published animal experiments and pharmacology experiments which show that we reduce the markers of inflammation, including pyroglutamylation, IFN-γ, and TNF-α. We can show that we reduce Collagen III, α-SMA, and CX3CL1, which are fibrotic markers, and then we can show that we improve eGFR and reduce urea and Cystatin C in these pharmacological models. And based on this novel and groundbreaking discovery and mechanism, we now go to the VIVA-MIND U.S. study design and see how that mechanism impacted on that U.S. study. The U.S. study was an NIH-sponsored study for early AD and was a one-to-one randomization of patients between varoglutamstat and placebo. And there were those finding elements included in that study in the sense that if the 600 mg would not have been well tolerated in the DSMB interim analysis, then we would have dropped to 300 mg and 150 mg. But we announced already about a year ago that the 600 mg BID was well tolerated and could continue, and therefore no dose de-escalation to 300 mg was needed or required. And the second quarter 2024, we decided together with the ADCS to terminate that study because we saw in VIVIAD no efficacy in early Alzheimer's disease, and we did not deem it appropriate to continue the study in a nearly identical population with the same dose, just with different endpoints in this population. Therefore, we have about 109 patients now allocated to placebo and to active instead of the finally planned 414, and 180 were planned for an interim analysis. There were much less patients. That is quite important because we can see that with this little patient, we have highly significant ADAS-Cog p-value. Just to remind you what those patients were, these were patients selected for early AD with an MMSE of 20 to 30, a CDR sum of boxes between either 0.5 or 1, and an age of 50- 89 years old. We had objectives to look at the safety and tolerability as well as the efficacy for Alzheimer's disease, and the primary endpoint was CDR sum of boxes, and that was, of course, different than the VIVIAD study where we have an ADAS-Cog. Then we had an interim pre-planned analysis after 180 patients were treated for up to 24 weeks to look at interim efficacy using EEG and a normal psychological test. Kidney function were prospectively defined, eGFR being a safety parameter, and we did not change that because we didn't deem it appropriate after we saw the VIVIAD data to do a last-minute post-hoc evaluation to efficacy. We thought that is a kind of cheating. Therefore, we left it as a safety prospective parameter, and as such, it is reported here. Going on, I just want to remind you that the top-line data are always preliminary and may be subject to minor changes on additional analysis and quality check, which you always have. That should not change the overall interpretation of data, but there can be some numbers changing, of course, always to happen until we have final, final data. Going to the next chart, this is the distribution of patients between active and placebo, and it starts, unfortunately, with a little bit of a confusion because we have 53 patients and 59 patients. In actually should be 58 and 52 and 57, and that is due to a patient which was initially randomized to placebo but got one single dose of varoglutamstat, which was an error and administration error by the site. But that, of course, made the patient still in the efficacy group in efficacy in placebo, but for safety, you needed to put him into the varoglutamstat group because he had exposure to the drug. That should not change any interpretation of the results, just a small detail. So you see that the groups were well equilibrated regarding sex and age. The average treatment duration is probably quite important, is 45 weeks in the study. The CDR sum of boxes at baseline was 3.35 and 3.29. So in the early stages, the eGFR was around 77 for both groups. Then you see how the study rolled out as it was planned to have everybody 72 weeks in it. It would not be prematurely terminated. We had only 25%-33% completing the 72 weeks, and the rest of the patients were either prematurely terminated by the sponsors, that is, our decision to stop the study, or by withdrawal of the subject or all other together. So we look here at data, which are, of course, much shorter and much smaller than in VIVIAD. Next slide, please. So we, first of all, want to discuss the results on Alzheimer's disease. And at the pre-specified primary, key, secondary, and relevant endpoint of ADAS-Cog, we saw no clinically meaningful and no statistically significant differences between varoglutamstat, BID and placebo. And I want to remind you that additional data will come, EEG, biomarker data in the CSF and in the blood, but they will only be available in the first quarter 2025. In that respect, VIVA-MIND fully replicates the finding in VIVIAD, where we had the same outcome for Alzheimer's disease. So on the right side, you find some specificities of which I have already talked about. So we can jump to the next slide, which is safety. And we see in VIVA-MIND a very good safety and tolerability profile. We did not see any additional safety, and here it is important that VIVA-MIND exclusively used an accelerated, faster titration regime starting at 150 mg and going to 300 mg and 600 mg, whereas VIVIAD started at 50 milligram and it took a longer time to come to 600 milligram. So it is a more convenient and accelerated regime we tested here, but it did not impact negatively on safety. Actually, the safety are quite equilibrated with a similar number of related treatment adverse events in both groups. Also by severity, there are no major differences. Also, the serious and the related serious treatment adverse event didn't show any difference. There is also for patients with drug modification, there is no difference, and for drug discontinuation, there is a minor difference, but not a lot. I want to remind you that there were two patients dying which were unrelated to the drug in the study, one because of gastrointestinal bleeding and a surgery for this and a complication of the surgery thereafter, which happened many weeks after stopping of treatment, and the second patient having a fall down the stairs and having a patient's provision not to have intensive reanimation done and therefore was dying thereafter. Then we come now in the next slide to the kidney data, and we see here on the left side the difference between placebo and active for the totality of all patients and all visits. So what we did here is we simply took all the data around the treatment and subtracted active and placebo, and that is the difference between it. So you see it's a little bit about 4 mL average difference across all visits. At each visit, active is better than placebo. And that is highly significant, as you see with the p-value. And I said that is all patients, all visits. So there's no subgroups, no division, no post hoc here. That is the totality of the data. And then you look on the right side where we divided the efficacy parameter into periods, one in the starting period where the drug was titrated and a little afterwards of the titration, that is between week 4 and 16. And you see that the effect size versus placebo is already significant, but with around 3 mL, 3.3 mL, of course, much smaller than later between weeks 24 and 72, where you basically reach a plateau of efficacy of above 5 mL difference of active versus placebo. What it means is that each of these visits, the average of the active was more than 5 mL better than the average of placebo. And that's, of course, a huge effect size, which is three to four times higher than everything you saw with approved drugs used for the treatment of kidney diseases these days. Next slide. We want to dive a little bit in the sustainability and now here on this slide, sorry. This is, first of all, the slide where we compare two calculations as we did in VIVIAD. So we look at MDRD and CKD-EPI, and while there is 1 mL difference, the significance level and the effect size is very comparable. It's just a different formula to make sure that we're not chasing only one thing and forget another one. We see that the data is robust, comparable, and consistent. Next. Now going to the comparison of VIVIAD and VIVA-MIND because in the following charts, I want to present you a little bit more about the consistency between the VIVIAD and the VIVA-MIND study. So first, before we go into the data, we need to understand that the studies have similarity and differences. So the study completion, of course, VIVA-MIND is a smaller data set, it's a discontinued study, and VIVIAD is a completed study as per protocol. The mean age is quite comparable in VIVA-MIND a little bit older than in VIVIAD, and you saw that the upper age range in VIVA-MIND was 89, whereas in VIVIAD was 80. So that is explained by this. The number of patients treated, I said, is smaller in VIVA-MIND and VIVIAD by 2.5- fold, actually. In VIVA-MIND, we only tested 600 mg, as explained, because we did not need to down-escalate the study, whereas in VIVIAD, we tested up from 300 mg and 600 mg, and then we decided that 600 mg is good, and we moved everybody to 600 mg. The dose escalation is different. So in VIVA-MIND, we started fast with 150 mg BID, and we reached 600 mg at week nine, whereas in VIVIAD, we started slow with 50 mg, and we reached 600 mg at week 13, so four weeks later. Mean treatment duration was also shorter in VIVA-MIND than in VIVIAD, 46 and 76 weeks. Or you can put it in other words, the longest treatment duration in VIVA-MIND, the 72 weeks, is still four weeks shorter than the average in VIVIAD. So we have a shorter treatment set. Based on this result, based on these facts, the results are actually, I think, mind-blowing in terms of the robustness and consistency. The number of patients with eGFR results week 36 and later were 73, sorry, excuse me, and 73 in VIVA-MIND and 246 in VIVIAD. So about a third with long-term data. Next chart. When you now compare what the results are between VIVA-MIND and VIVIAD, and you compare comparable patients, meaning only patients treated with 600 mg in VIVIAD and, of course, all of VIVA-MIND, you see that numerically there is even a slight advantage for VIVA-MIND, but overall, it's pretty consistent, around five or above 5 mL average benefit in the period where you have a stable dose reached. This is 24-72, respectively, 36-96, and it's adjusted to the slower treatment titration period in VIVA-MIND. So what you see is, sorry, in VIVIAD. So what you see is the data are when you compare apples with apples, so the same dose and a comparable period post-full dose, you see exactly the same results, and that is an average 5 mL for each visit and each patient better on active than placebo. Going, and it's, of course, significant in both studies and similarly significant. Next. And here is what I announced before. We look at week 60s and 72s because what is important not only is to see the effect size, but also whether this effect size is sustained across the whole study. So on the left part of the chart, you see the week 60 results. That means we compare here the effect size observed only at that single visit, and you see in VIVA-MIND, we had about 5.5 mL, and in VIVIAD, we had about 4.5 mL. And, of course, in VIVA-MIND, we have much less patients at that time point than in VIVIAD. And, of course, here we also only compare the 600 mg. And on the right side, you have the 72 weeks results, which are the last visits in the VIVA-MIND study, but it's not the last visit in the VIVIAD study because VIVIAD went until week 96. But we compared week 72 in both studies just to see how the effect is sustained in VIVA-MIND and in VIVIAD. What you see is, despite only having 13 and 20 patients in VIVA-MIND, at that time point, we have a p-value of 0.002 and an effect size at that visit day of more than 6 mL difference between active and placebo. In VIVIAD, the data were correspondingly a little bit about 5 mL and also statistically significant. What we can conclude from that analysis is that in both studies, the effect size was sustained in the midst of the second year and to the end of the second year. There was no lowering or reducing of the efficacy over time. The efficacy was fully maintained and was significant until the last visit. Next chart. I want to summarize the finding of our phase II program in this chart. We now have two double-blind placebo-controlled studies, one conducted in Western Europe and one in the U.S., totally different investigational sites, totally different CROs, not connected to each other, and both show a consistent, very comparable, statistically significant, and clinically meaningful improvement for eGFR for varoglutamstat, sorry, versus placebo. In both studies, eGFR was improved above baseline and stabilized across the whole treatment period for up to 96 and 72 weeks, respectively. These results provide a robust, and I want to say a very robust, evidence of the treatment benefits. We have good safety results in VIVA-MIND with the accelerated dose escalation scheme, and that provides a very good pathway for a convenient and commercially viable dosing schedule. And what is also important looking forward is that VIVA-MIND, with this small patient number of 109 patients, of course, supports a sample size planning of 120 patients or less for the next planned study in diabetic kidney disease, which we announced before. And so the sample size assessment we did before, I think, was very solid, and probably we need a couple of less patients, but we will follow up on this in a later conference when we have fully digested the VIVA-MIND data. So we will continue to analyze the data. We're here at top line only data, first view on it, and with that, I want to hand over back to Anne. Thanks, Frank. Let me take you through the key figures for the period. R&D expenses in the first nine months of 2024 amounted to EUR 12.6 million versus EUR 10.4 million in the same period of 2023. This increase of EUR 2.2 million was largely attributable to the increase in clinical costs from the VIVIAD and VIVA-MIND studies, as well as investments into kidney-related research and analysis. We have seen a decrease in G&A expenses with costs of EUR 4.9 million in the first nine months of 2024 compared to EUR 6.8 million in the first nine months of 2023. This EUR 1.9 million decrease was largely attributable to higher compensation of non-executive board members in 2023. All of this resulted in a net loss for the first nine months of 2024 of EUR 17.4 million, the same amount as we had in the first nine months of 2023. The company held EUR 12.5 million in cash and cash equivalents as of September 30th, 2024, compared to EUR 28.6 million, which includes cash and cash equivalents and term deposits within financial assets as of December 31st, 2023. Cash utilization for the first nine months of 2024 reflects the intensive investment period in VIVIAD and VIVA-MIND, especially in the first six months of the year, both of which are expected to continue to ramp down in the months ahead as both studies conclude. Our reduction in cash and cash equivalents for the third quarter was less than half, seen in each of the first and second quarters. We updated our financial guidance and expect our cash and cash equivalents being sufficient to fund our operating plans into the third quarter of 2025. Looking ahead into the upcoming months, we will continue to thoroughly analyze the VIVA-MIND data and expect to disclose additional results, including biomarker data related to varoglutamstat unique MOA, as well as preclinical data on orphan kidney diseases from our scientific collaboration. In 2025, Vivoryon plans to start a phase II study in DKD, which we have outlined previously and see as the next natural step given the strong VIVIAD and VIVA-MIND data. Depending on anticipated preclinical results from our collaboration with Professor Huber, Director of the Third Department of Medicine, UKE Hamburg-Eppendorf, we are also looking into potentially launching a small orphan disease study. As a reminder, all potential future clinical studies are subject to additional funding and our partnership, which we continue to actively explore. Beyond 2025, we anticipate upcoming meaningful milestones to include interim and full data readouts from the planned DKD phase II study, which we have also outlined previously in detail. As you can see, we have lots in store for 2025 and beyond that will build on our current momentum. I'd like to conclude by reiterating that despite the setback in AD earlier this year, we have been able to successfully generate compelling efficacy and safety data in people at risk of kidney disease from two independent double-blinded placebo-controlled phase II studies, and we are now very well set up to become a key part of the treatment landscape for a number of diseases affecting the kidney with high unmet medical needs. Backed by our strong scientific foundation, varoglutamstat's novel mechanism of action and confirmed target engagement, the extensive safety data package with convenient dose escalation scheme, as well as compelling dose-dependent long-term kidney function improvement, we have a focused development plan in place. Furthermore, based on new filings, we anticipate composition of matter patent protection to be extended to beyond 2044. In addition, we have been active in strengthening our patent protection in the kidney field in general. We actively pursue funding and BD opportunities to realize the full potential of the significant commercial opportunity in DKD and beyond. With that, we will now open the call to take questions. Thank you. Thank you. As a reminder to ask a question, please press star one and one on your telephone and wait for your name to be announced. To withdraw your question, please press star one and one again. Once again, please press star one and one on your telephone and wait for your name to be announced. To withdraw your question, please press star one and one again. Please stand by while we compile the Q&A roster. This will take a few moments. Thank you. We are now going to proceed with our first question. The question comes from the line of Natalya Davies from Intron Health. Please ask your question. Your line is open. Thanks for taking my questions, and congratulations on the encouraging data. Just a couple for me. Firstly, can we expect any additional subgroup analysis from the VIVA-MIND study or any additional data on transaminase levels or weight loss, diastolic blood pressure? Any of those would be great. And yeah, any further analysis that we can expect on both of the trials. And then the second question is just on the kidney opportunities outside of diabetic kidney disease, such as Fabry disease. Has the preclinical analysis started, or is this subject to additional funding? Thank you. Yeah. So first of all, we are, as you said, we are at the beginning of the analysis of VIVA-MIND. We are happy that VIVA-MIND is consistent with VIVIAD, but of course, we are not through all the analysis of VIVA-MIND. We're just starting with it. So we will take our Christmas holidays and dig into the data and come up with all the things you have asked for. And yeah, of course, that will be then published and said and disclosed at the next webcast of press release. And the same is true for diabetic kidney disease. We are convinced that this is a very good indication based on VIVIAD. We still need to do some analysis in VIVA-MIND, but there are not so many patients with diabetes in VIVA-MIND, so let's see what that brings. But given the overall results are positive, I expect that similar things would happen for diabetic patients, but I haven't seen the data personally, so I cannot make any promises here, to be very clear. But we are looking forward to digging deep into the data and come back to you with all the results we will have. Did I answer your question, or was that not what you asked? Oh, and sorry, and just on the opportunities outside of diabetic kidney disease, are there any updates on that front? Currently, we have not yet the updates on the orphans and other indications, but we work on this, and we will come relatively short in this. These are partially academic collaborations, not necessarily run by the week, probably more by the month. And so we are also waiting for that. I don't know any update material on this, but it will come. Great. Thank you so much. We are now going to proceed with our next question. The questions come from Lucy Codrington from Jefferies. Please ask your question. Your line is opened. Hi. Thank you for taking my questions. So just following on from that, you mentioned that there was a small proportion of patients with diabetic kidney disease in this study. Can you tell us how many, if any, patients did have diabetic kidney disease across the two arms? And then just related to that, any of the patients, were they on concomitant SGLT2 or GLP-1s, both within VIVA-MIND and in the VIVIAD study? And then just on the final comment or comment toward the end about extending the composition of matter IP, just what's driving confidence that that will be feasible for varoglutamstat? Thank you. You want to start, Mick, with the IPs? I can. Hi, Lucy. This is Michael. I can start with the IP. Yeah, I mean, it's probably always not straightforward to say in an IP process, but what I can tell you is that, I mean, if you ask about our level of confidence, it's pretty high that we have a good chance here to get the patents we have filed also granted. So I also want to note that actually in the whole field of QC inhibitors, all the patents we have filed have been granted in the past, and we have no intention that this will change. Yeah, maybe I can add to this. I mean, filing a patent to get it approved is a process. That process runs as by the books, and we will have some updates in the future on this. Once there is the time to update you on this, it's probably not so far away. So, of course, until that point is happening, we cannot give you any information, but we're in the process as it should be, and there are no bad surprises so far. As you know, we are patenting the compound we're using under a specific contingency, let's say, and that was a genius move from the past, and I think we let it there until we can fully speak about it in the public. Regarding diabetes patients, I mean, the process we do is that we by hand check the identification of diabetes and prediabetes patients, and we're currently trying to understand what is a prediabetic patient, so some with disturbed hypoglycemia or hypoglycemia and disturbed glucose tolerance versus the full diabetic patients. We expect the number of full diabetic patients to be something between 10 and 20, but that separation is currently ongoing to really identify the groups properly and to reinforce the number, so I cannot give you a more precise number because while a patient may have a history of diabetes or impaired glucose tolerance, that needs to be checked with the laboratory data and the concomitant medication and the history accurately, and we have top-line data now, so we're, from a timing perspective, not fully through this, so I cannot give you more precise information on this. Of course, we will disclose the concomitant medication, but the patients who had diabetes did have the typical co-medications, including some patients' SGLT2s. How many there are, I have to wait until the data are fully mature and QC. Did that answer, Lucy? Was that? Yeah, I think so. Thank you. We are now going to proceed with our next question. The questions come from the line of Joseph Hedden from Rx Securities. Please ask your question. Good afternoon. Thanks for taking my questions and congrats on this positive, consistent data. Just on the plan for the phase II DKD study, the fact that you've seen that these data are quite consistent with VIVIAD, does that change the plan in any way, the recruitment size or any factors of that study? And then secondly, on the cash runway and the streamlining that you've been doing to extend it, has that affected any of the preclinical work that you were doing? Is there anything there that's now not being explored that was previously part of the program? Thanks. We actually did more in kidney than we ever planned, but of course, there are limitations because, as you can imagine, the opportunities are infinite to do exploratory pharmacology in animals or in cells. You could do thousands of things, but we have neither the manpower nor the money to do everything, but all the critical activities have been started, and we haven't restricted the evidence generation in non-clinical based on our financial situation. Of course, we are careful with our spending, but that doesn't mean that in that area we would have restricted. What we have restricted is investments in Alzheimer's disease, clearly, because currently we have these results and VIVA-MIND confirmed with the current dosing regimen. No way forward for Alzheimer's disease. Now we are looking, of course, in alternative options, but the mainstream is diabetic kidney disease, and the experiments for kidney disorders are fully run. That's one thing. The other thing of the sample size, as I've announced, we have not recalculated the sample size based on the VIVA-MIND results and the consistency thereof, and that is because the results are fresh from the press, and we could not make a statistical model including VIVIAD and VIVA-MIND data. As you see, they are totally homogeneous. There is no difference between the data that, of course, will facilitate or no meaningful difference between the data. Of course, there's minor differences. Sorry to correct this, but there's no meaningful difference between the data, so that helps, of course, planning the next study, and probably will more reduce the sample size needed, but on the other hand, we don't want to do a totally minimalistic study. That means our aim is not to invest as little money as possible because we want to have a meaningful study and robust data at the end. So a too small study may not be convincing either. Even from a statistical point of view, it would be feasible, but I would not recommend to go down to a minimum. So we try to find that good balance between evidence generation and statistical sample size, and I think we are in a good spot to assume that other two situations are the max, max, max, and likely it will go more down, but if it's too small, then, of course, everybody scratches their head even near the p-value of the relevance of this. So that's a little bit between the two where we are trying to find a solution in the upcoming weeks. Then, of course, the final product will have to go again through the KOLs and need to be tested, and then we're going to publish it and discuss it with you. Okay. Great. Thanks very much, Frank. Thank you. As a reminder to ask a question, please press star one and one on your telephone and wait for your name to be announced. To withdraw your question, please press star one and one again. We are now going to proceed with our next question. The question comes from Luísa Morgado from Van Lanschot Kempen. Please ask your question. Hi, team. Thank you for taking my questions. First of all, of course, congrats on the data confirming your earlier findings. My first question, in terms of the VIVA-MIND study analysis, what are the main motives behind withdrawal by the subjects themselves? Yeah, if you could elaborate on that. This is an Alzheimer's study, and it's done in the U.S., and you know that the distances from study sites to where the people live are meaningful, and if the patient, the burden of the study is much higher than the patient thought initially, or there are problems with the relative taking care of it, patients drop out. The other part, which was a withdrawal reason, is that lecanemab became commercial in the midst of the study, and we had a couple of patients who elected to leave the double-blind placebo-controlled study because they could be on placebo for one and a half years and elected to go to commercially then available lecanemab, which was at that time approved, so we had a couple of those, and that explains a little bit the number. Okay. Clear. That's quite helpful. And in terms, maybe a question more for Anne, in terms of the expenses over the next quarters, what can we expect here and when will the VIVA-MIND trial completely terminated altogether, or when will that happen? Thank you. Hi, Luísa. As you've seen, the progression of our sort of cash burn or cash usage over the entire year so far has gone progressively down. So we've had a lot of expenses in the first six months of the year related to VIVA-MIND and VIVIAD, and then you've seen a step down in the third quarter. And so as those studies do come to a conclusion, we should see that ramping down. And we've also had the additional update today of our guidance into the third quarter, and that also reflects that ramp down. Probably to be a little bit more concrete, we haven't paid everything of VIVA-MIND. There are still some remaining expenses coming also because there are additional subgroup things and statistics and so on. So there will be some more expenses, but I think the vast majority, of course, of the costs have already been paid. So there are some things to come, but largely phase II program is paid a little bit to come. And then we have the typical operational expenses of the company plus some non-clinical activities for the kidney disorders, I said. So that's probably it, but our confidence in financial planning and the team's financial capabilities is good, and this is why we made today the announcement that through the third quarter cash with what we have today is the new guidance. Okay. All clear. Thank you for taking my questions. Thank you. As a final reminder to ask a question, please press star one and one on your telephone and wait for your name to be announced. To withdraw your question, please press star one and one again. We have no further questions at this time. I will now hand back to you for any closing remarks. Yeah. First of all, I want to thank you for your attendance, and I want to close with a remark that repetition and replication is the name of the game, and consistency of data is really important to make scientific and medical judgment and look at the scientific merit of the data. I think we are largely through a transformation of the company from a hopeful Alzheimer's disease to a validated and confirmed kidney company with additional opportunities. So having seen that in very well-conducted, high-quality, robust, randomized placebo-controlled studies, which both are long-term of 72 respective to 96 weeks, I think gives us a very solid foundation for moving forward, and happy to have you on the next call and see how we are progressing, and with that, I wish you a very happy festive period and Christmas period and good relaxation period, and see you back next year. Thank you. This concludes today's conference call. Thank you all for participating. You may now disconnect your lines. Thank you.