Good day, and thank you for standing by. Welcome to the Vivoryon Therapeutics 2024 Half-Year Results 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 during the session, you 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 would now like to turn the conference over to speaker, Anne Doering. Please go ahead. Thank you, Raz. Good afternoon, and thank you for joining us today to discuss the company's First Half 2024 Results and Operational Updates. This morning, Vivoryon issued a press release reporting its first half 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, and Michael Schaeffer, our Chief Business Officer. We will begin today's call with opening remarks from myself. Then Michael will provide some important scientific background on the mode of action of varoglutamstat, our lead asset. After which we will move to Frank, who will discuss our understanding of the different outcomes in ViViAD between AD and kidney, to underscore the extremely encouraging results we see with varoglutamstat in kidney disease. I will then review the financial results for the First Half of 2024 and conclude the call with an overview of our corporate outlook and strategic updates. 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 program, 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. Before we dive deep into the science and clinical data, I'd like to set the stage by outlining where we stand after a time that can clearly be defined as a period of major change for Vivoryon, and I'm pleased to say that we have been able to transform a disappointing setback in Alzheimer's disease into what could be a major step forward in kidney disease. As we have described before, varoglutamstat has a novel mechanism of action, and with that, the potential to benefit patients across a range of therapeutic areas. To further explore these opportunities, we intentionally included eGFR, a prospectively defined, validated regulatory endpoint used in kidney disease trials into the ViViAD phase II-B study. Our analysis of the ViViAD data revealed a compelling effect on kidney function, one that is unique compared to other agents, and which spurred our shift in strategy towards developing varoglutamstat in kidney disease, where we have continued to make strong progress, and to reiterate, these are not chance findings. It has been rigorous scientific research and intentional clinical study design that have laid the foundation for this opportunity. We have worked hard on gaining a deeper understanding of varoglutamstat's mechanism of action and the ViViAD re-study results, and can clearly say that inhibiting QPCTL, varoglutamstat's target enzyme, is a very attractive approach to improve kidney function. This comprehensive body of evidence underpins our actionable plan to advance into a phase II study in DKD as we continue to establish our presence in the kidney disease space. The first half of 2024 was marked by continuous progress in successfully transitioning our strategy, led by compelling kidney function data. While the ViViAD results in early AD were disappointing, we have gained further insight into these results and have seen clear evidence of differences between kidney and AD outcomes from PK, PD analysis and new target inhibition information. These data are crucial for a full understanding of varoglutamstat's potential in the disease landscape, in particular inflammatory and fibrotic diseases. We observed a strong and consistent, statistically significant improvement in kidney function with varoglutamstat in the ViViAD phase II-B study. Furthermore, we were able to show a substantially higher treatment effect on eGFR with varoglutamstat in a post-hoc diabetes subgroup. These data are very exciting, and we believe that varoglutamstat's unique product profile has the potential to change the course of kidney disease. Building on this, we have decided to advance varoglutamstat into a phase II study in advanced diabetic kidney disease, subject to additional funding or partnerships. We also see potential opportunities and additional indications, which will be prioritized moving forward based on ongoing non-clinical studies. We are also continuing to understand the AD results and plan to analyze data from the VIVA-MIND study by year-end, with a view to inform next steps. So we've had a very active first half and exit the period with lots of momentum behind varoglutamstat and kidney disease. And with that, I will now turn the call over to Michael. Thank you, Anne, and welcome everyone, also from my side. Now, we have people with different levels of information on the call. Some of you have been following us for a long time, and others are new to Vivoryon, so I'd like to set the stage a bit to take all of you with us to what could be considered a fresh start. At the same time, you will see that we already have a long-standing history and expertise in investigating varoglutamstat in inflammatory disease settings. So to bring everyone on the same page, at Vivoryon, we are tackling a cellular process, which is called pathological post-translational modification or PTM. Now, what does this mean? PTM is a process that helps to functionalize proteins. For example, introducing an on/off switch for the activity or enabling proteins to bind to each other. There are several different ways in which proteins are modified and various types of PTMs, which are depicted here on the right side of the chart. PTMs are catalyzed by a large group of specialized enzymes, many of which are important drug targets. The PTM we are tackling with our oral small molecule inhibitors is a so-called pyroglutamate formation, which means that the ring is formed at the very beginning of the substrate protein at the N-terminus. And this happens when it starts with either a glutamine or glutamate residue. This cyclization has emerged as a central process in different diseases, including neurodegenerative, inflammatory, fibrotic diseases, and cancer. In the human body, the pyroglutamate formation is catalyzed by only two variants of enzymes called glutaminyl cyclases, QPCT and QPCTL. And exactly these two are the drug targets of our candidate, varoglutamstat. Whereas QPCT is secreted into the extracellular space, QPCTL is localized within the cell in so-called Golgi vesicles. Here, it finds its substrate proteins and converts them into pyroglutamate or pE versions. While QPCTL remains within the cell, these pE versions of target proteins are released into the extracellular space where they are active. Important target substrates of QPCTL include chemokines, like, for example, members of the pro-inflammatory, pro-fibrotic chemokine family, including CCL2 and others. P E formation on these chemokines significantly increases their activity, potency, and stability. Now, with varoglutamstat, we can efficiently inhibit QPCTL activity to block pE formation on these chemokines, thereby reducing their activity. Vivoryon has been actively working actually in this field for many years already. We've authored and co-authored several publications with groundbreaking results on the application of glutaminyl cyclase inhibitors in inflammatory diseases, some of which actually date back to ten years or more. So you see that there already is quite some history and knowledge accumulated at Vivoryon on this approach. In recent years, the number of publications on targeting chemokines like CCL2 to treat conditions of the liver and kidney, and especially the concept of regarding such conditions as inflammatory, has dramatically picked up. You can see this here in the graph. There has been an exponential increase in the number of publications in the past decade. This slide lists only a very few examples of important publications, but taken together, all of the research in this area makes it clear to us that we are at the right place at the right time with our anti-inflammatory approach to treat these diseases, for which, despite advances in therapy, an extremely high unmet medical need still remains. With that, I'd like to hand over to Frank, who will now guide you through the most recent analysis of the ViViAD study data and elaborate on what these exciting results mean for varoglutamstat development moving forward. Frank? Thank you, Michael. Thank you, Anne. My name is Frank Weber. I'm the CEO of Vivoryon, and we have a couple of slides now coming, which are highly scientific and shed a light on understanding the outcomes of ViViAD. ViViAD, the phase II-B study we conducted, was clearly the main activity and highlight of the first half of 2024. After this presentation, it will allow everybody to understand why we have a very positive outcome in kidney and failure in Alzheimer's disease in the same study. There are four charts and items I will lead you through. The first one is the concentration of varoglutamstat, which we measured in the study, both in the serum and in the CSF, and both at the 300 and 600 mg level. The charts number two and three deal with the enzyme Michael just introduced to you, and that is the extracellular QPCT, so-called QC enzyme, which we can measure in the serum and CSF, and the intracellular QPCTL, or also called isoQC, which we cannot measure directly, of course, in the cells, because the cells are in the brain or in the kidney. But we can measure a substrate which is only produced by these cells, and this substrate is secreted then in the serum, as Michael told you in the previous charts. So we show you the inhibition of the intracellular QPCTL. And what is new, we can also show you the reduction of pyroGlu A-beta 40 in the CSF, which is the target peptide for Alzheimer's disease. And the aim we set out is to significantly reduce the pyroGlu A-beta 40 in Alzheimer's disease patients, and I'll show you results on this. Next chart, please. Here, these are the concentrations of varoglutamstat in the serum and the CSF at week 48. And you see four columns. On the left column, you see the concentration in the serum at 600 milligram dose, and you see it's around 300 nanogram per milliliter. At 300 milligram, you see it's around 100 nanograms, so about a little more than one-third. And then the CSF at 600, it's again, a little bit lower, it's around 80 nanogram per milliliter. At CSF in 300 milligram, it's around 30 nanogram per milliliter. These were all measured, and these are geometric mean concentration of the free varoglutamstat, so the protein unbound fraction between hours two and six post-dosing. And what you can conclude from this is that the blood-brain barrier reduces the concentration of varoglutamstat in the CSF compared to the serum, and that was known before. And, also, you see a dose-dependent concentration of varoglutamstat, which is fully consistent with previous published results. So here there is no surprise in the ViViAD study compared to what we published before in the SAPPHIRE study or in the phase I. Next chart, please. So now we come to the inhibition of the extracellular QPCT enzyme, which basically is a free-floating version of the enzyme in the serum and in the CSF. And we can measure the QPCT activity at baseline and after we give the drug, and we can calculate the inhibition of that enzyme depending on the dose. And then we go to the display, and what you see is that at all doses in the serum and at all doses in the CSF, we have a strong inhibition of the QPCT enzyme, both in the serum and in the CSF. So we have about 90% or 85% in the serum. At 600, we have about 80, at 300 or 85. In the CSF, we have 80 at 600, and at 300, we have around 65% at 300 dose. So this we can measure basically directly. What we can conclude is that at the doses we applied in the ViViAD study, we found a strong and significant inhibition of the extracellular QPCT enzyme. Basically, at all doses we used, both in the serum and the CSF, and that is also consistent with published data, and we have shown you previously some PK/PD models we have established based on phase I and II-A data, and this data exactly match what we predicted. Next slide, please. Now, Mick introduced to you a basically sister version of the QC enzyme, the so-called isoQC enzyme, and that is the enzyme which sits in the Golgi apparatus in the cells and pyroglutamate peptides, which are just synthesized before they get secreted into the bloodstream and the serum. Here we can measure the reduction of the pE version of CCL2, which is only produced intracellularly, either in macrophages or in the brain and glia cells, and then secreted as a pyroGlu version directly into the CSF and serum. The production, the pE production, happens by the IsoQC in the Golgi apparatus, so intracellularly. Here we can see, when we go back to the graph, the reduction at 600 milligram in the serum is strong and highly significant by 38% around. At 300, we have only around 13% of reduction of pyroGlu CCL2 from baseline in the serum. A similar value we have at 600 milligram in the CSF, around 15% to 60% reduction. And the CSF at 300 milligram, we basically see no reduction of pyroGlu CCL2, so the levels are unchanged at week 48, compared to baseline. These effects are, of course, consistent with the concentrations we have with the drug in the serum and the CSF, and those which are then, of course, translated into intracellular concentration as well. Next chart. We have newly been able to also measure pyroGlu A-beta in the CSF. That was our aim, to reduce the pyroGlu versions of A-beta in order to improve the outcome of Alzheimer's disease, because we believe that pyroGlu A-beta is more toxic species, which triggers and makes progression of Alzheimer's disease. Now, here, in the first set of 36 samples, you see that the reduction of pyroGlu A-beta in the CSF was only 13%. And that is, of course, not sufficient to have a broad and robust clinical outcome. This shows that we have a target engagement, that we can interact successfully with the production of pyroGlu A-beta, but the dose of the drug in the cell was not high enough to stop that production of pE A-beta. The assay was actually developed together with a company called Alamar. And the effect size, what is interesting here, is very comparable to the pE CCL2 reduction in the CSF we measure. So in other words, the pE CCL2 in the CSF we measure, which is only produced in the cells, shows a very similar decline as the pE A-beta, where we didn't know really whether it produced actually in the cells or in the CSF. But these data here point very strongly to the fact that the pE A-beta is actually produced in the cells and not in the CSF, in the plaques, because in the CSF, in the interstitial fluid, we had much higher QC inhibition data of the free-floating QC. And if that QC would have had inhibited and produced the pyroGlu A-beta, then we would have a much higher reduction of pyroGlu A-beta 40. So these are the new findings. Now, let's summarize these complicated things in a more easy way, in a summary chart. Next. Before we want to go the summary, of course, this translates, of course, to efficacy. And here comes the efficacy data for kidney and for AD. You see here the slope analysis for eGFR on the left side, and this slope analysis are nicely dose-dependent. The 600 milligram improves eGFR above baseline, and, the 300 milligram just stabilizes it, and placebo shows a drop of eGFR, as expected by the natural course, in these patients. On the right side, you see the Alzheimer's disease results, and you see a drop in the placebo group and a very identical drop in, the active arm. And the interpretation of this, and the conclusion is, that we need high concentration of varoglutamstat, which leads to a clear pE peptide reduction of intracellularly produced pE CCL2 and pE A-beta, and that results in a profound effect on kidney function. But of course, as at pE A-beta, we didn't find a strong effect with only minus 13% reduction, and the concentration of CSF is lower than in the serum, and then in the cells, of course, it will be again lower. We didn't see here an effect at the dose we used in the ViViAD study for Alzheimer's disease, and that explains the different outcomes in AD and in kidney. Next chart, please. We can confirm after these results that varoglutamstat is a potent and strong inhibitor of QPCTL, and this is an attractive target in kidney disease. Beyond the efficacy in eGFR, we could provide much more evidence with ViViAD for our future development. We found that the concentration profiles of the drug, which we already intensively studied in phase I, were confirmed in the ViViAD, so-called the pharmacokinetics. We also showed that we have a strong inhibition of the QC enzyme at all doses. This is the enzyme which is in the serum and CSF free-floating, but it does not correlate with clinical effects and benefits, neither in AD or kidney. We only see clinical benefits when varoglutamstat concentration is high enough to inhibit the intracellular QPCTL or so-called isoQC, and that is proven by the 600 milligram BID, which showed a clear reduction in pE CCL2 in the serum, and a strong effect on eGFR. The 300 milligram BID showed a minor effect on pE CCL2 in the serum, and consequently, only a minor effect on eGFR, so a stabilization. Varoglutamstat concentration in the CSF at 600 milligram BID shows only a minor reduction of pE A-beta, around 13%, and of pE CCL2 at the same magnitude of effect, and showed no effect on AD. Those results suggest that the majority of pyroGlu A-beta is actually produced intracellularly in the brain cells and not in the CSF or interstitial fluid around the plaques. In sum, these findings suggest that intracellular QPCTL is a more important target to drive efficacy. Next. Beyond this, I think, very interesting PK/PD findings, which allow us to focus and very precisely continue development pathway forward, we found other things in the ViViAD study. The first one is that the effect on eGFR was robust, independent of the analytical method or the formula for creatinine. And, whether you take creatinine as a substrate or Cystatin C, we came to very identical outcomes in terms of benefit. We also showed that the effect on eGFR persisted until the last dose of treatment for up to two years. We showed excellent tolerability and safety in more than 400 subjects in phase I and phase II studies. We also analyzed whether hyperfiltration could be a potential effect and concluded that is very unlikely, because we didn't see any worsening of proteinuria. We saw a reduction of diastolic blood pressure and mean arterial pressure, a slow onset of action, three to six months until the full dose effect. The dose response, we, connect very plausible with the mechanism of action and shows that 300 milligram BID is not sufficiently potent and robust for kidney disease. It just leads to a stabilization, but not to an improvement of eGFR above baseline, and the results in patients are also very consistent with the outcomes of animal studies, which we have published and conducted before. Next chart, please. Here is just a graphical display of the various methods of analyzing eGFR using the CKD-EPI formula or the MDRD formula, and taking cystatin C or creatinine, or a mix of both in calculating eGFR, and while the magnitude effect, depending on the formula and the substrate, of course, is a little bit different, the overall benefit and significance level is maintained through all different types of methods and analysis. Next chart. We also went further on in the first half of twenty twenty-four and looked at various subgroups within the ViViAD population, to understand whether the treatment benefit was similar distributed in various patient subsets, or it was differently distributed. We found that patients with diabetes had a more, at least a double or even more effect size on eGFR than all subjects, the total population. In the diabetes group, we also saw a trend of improving transaminases by about six units, at average. At week forty-eight, we saw a mild weight loss. We saw lowering of diastolic blood pressure and mean arterial blood pressure, which would all be very positive for event outcome in the cardiovascular space. The adverse events were comparable in the diabetes population and the total population, and the overall data clearly support advancing varoglutamstat in diabetic kidney disease. Next. So what are we targeting in diabetic kidney disease, and why would inflammation be a very attractive, mechanistic target in diabetic kidney disease? The situation today is that the standard of care targets metabolic parts of it, like SGLT2, which secretes glucose, or GLP-1, which controls glucose levels, or looks at hypertension through either ACE inhibitors, or angiotensin receptor blockers. Direct addressing inflammation in diabetes has not been yet achieved, so various programs have been launched and stopped, and there is a new call for looking at inflammation. Why? Because the activation of pro-inflammatory proteins and pathways is a hallmark of DKD pathogenesis. It drives the disease, inflammation is what makes the kidney worse. So stopping inflammation would have a positive effect on the kidney outcome. Varoglutamstat can directly attenuate pro-inflammatory signaling through reduction of pE-CCL2 and other pyroglutamylated cytokines, and thereby destabilizing key inflammatory molecules. This means less inflammation and therefore better kidney outcomes. The mechanism of action, of course, is different and complementary to those of SGLT2s and GLP-1s. We can focus in the future that patients progressing on the current standard of care are not eligible for those medications because either too advanced or too risky in this situation. We can treat with varoglutamstat. This is, as said, in line with a strong need of developing new therapies for patients with diabetic kidney disease. To further corroborate our current evidence, we are planning to conduct a phase II-B study in advanced stage 3b/4 diabetic kidney disease patients on top of standard of care. This study would meet the expectation of industry and key opinion leaders to address the key questions of how good varoglutamstat is in the more advanced patients with diabetic kidney disease, which were not systematically studied in the ViViAD study. The study design is that we would select these patients based on their CKD stage. They should have significant proteinuria as well. The treatment of varoglutamstat will be on top of standard of care. Patients would be randomized one-to-one between the varoglutamstat dose of 600 milligrams, which we have already identified, and the treatment duration overall would be per patient 15 months. We will need 220 patients to find, with 80% power, a treatment difference of 5 mL/min and the minimal effect size, which would be significant to 3.5. Endpoints are eGFR slope, albumin-creatinine ratio in the urine, and biomarkers of inflammation of the kidney and also of the liver, as well as safety. We can conduct an interim analysis in the study to further de-risk the study and give some results in between to see whether we're on the right track and right target. Finally, next chart. We are now having a target product profile of varoglutamstat in diabetic kidney disease with a strong potential to improve kidney outcomes. Based on efficacy, with a robust and clear improvement of eGFR over baseline, independent of baseline eGFR, and we studied already a range of eGFR rates between 45 and 120 milliliters in the ViViAD study. We have identified a subgroup, and this is a very strong subgroup of patients with diabetes, having diabetic kidney disease, where we see reduction of diastolic and mean arterial pressure, which is favorable for any cardiovascular outcome and event rate. We see a reduction of liver transaminase, which is favorable for frequent comorbidity of non-alcoholic fatty liver disease in DKD patients. And we see a weight reduction, which is favorable for overall and cardiovascular outcomes. This is the, I think, a very attractive target product profile from an efficacy point of view. From the safety and administration point of view, we as well find varoglutamstat very attractive. It has an excellent tolerability and safety, no worsening of proteinuria, with a potential of improvement to be assessed in more advanced patients in the next study. Also, it is a simple oral treatment of 600 milligrams twice daily, a morning and an evening dose, and no need to visit the doctor for injections or follow-ups. And the position in therapy will be that, the treatment effect through inflammation and anti-fibrotic mechanism is complementary and non-redundant to the current standard of care of metabolic and glycemia-based therapies. And varoglutamstat, of course, and that we shouldn't forget, has the potential in orphan kidney disorders, where we currently study this in non-clinical studies to see their profile. And with this, I hand over back to Anne. Thank you. Thank you, Frank. Let me take you through the key figures for the period. Research and development expenses in the first quarter amounted to EUR 10.3 million, versus EUR 6.3 million in the first half of 2023. This increase of EUR 4 million was largely attributable to the increase in clinical costs from the ViViAD and VIVA-MIND studies, as well as early investments into kidney-related research. We have seen a decrease in general administrative expenses, with costs of EUR 3.5 million in the first half of 2024, compared to EUR 4.4 million in the first half of 2023. The EUR 0.9 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 quarter of 2024 of EUR 13.6 million, compared to EUR 10.7 million in the first half of 2023. The company held EUR 15.3 million in cash and cash equivalents as of June 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 six months of 2024 reflects the intensive investment period in ViViAD and VIVA-MIND, both of which are expected to meaningfully ramp down through the second half of 2024 as both studies approach their conclusion. We reiterate our guidance, expect our cash and cash equivalents being sufficient to fund our operating plan, including any additional financing, into the second quarter of 2025. Further funding or partnerships would, of course, be required to support a phase II study in DKD, any potential additional clinical studies, and to extend our cash runway beyond the second quarter of next year. Thank you, everyone, for joining us today. And I'd like to conclude by reiterating that based on the compelling efficacy and safety data in people at risk of kidney disease, and in particular in a diabetes subgroup, we are very well set up to target the high unmet need in DKD with a phase II study planned in phase III, IV- B DKD patients on top of standard of care. A strong scientific foundation and new PK/PD data provide a key information on the mechanism of action and demonstrates varoglutamstat is a robust molecule, which we now better understand. We are excited to build on this momentum in kidney disease, driven by the rigorous analysis and comprehensive body of evidence we have seen with varoglutamstat. It has been a very active year for Vivoryon, and we have digested the setback in AD and put the science and operational elements in place for a successful future in kidney disease. We look forward to keeping you informed of our progress, and to that context, we'd like to cordially invite you to join us for a virtual kidney disease KOL event later this month, on September 30th, where we will be hosting key experts in the field. Professor Tobias Huber, Director of the Third Department of Medicine of the University Medical Center Hamburg-Eppendorf. Florian Jehle, CEO of Vifor Fresenius Medical Care Renal Pharma, as well as Dr. Kevin Carroll, CEO of KJC Statistics, will be there for a detailed discussion of varoglutamstat potential in kidney disease, with an emphasis on DKD. And 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. Thank you. We are now going to proceed with our first question. The questions come from the line of Lucy Codrington from Jefferies. Please ask your question. Hi there. Thank you for taking my questions. Just to begin with, I guess now you know what you know from the additional analysis of ViViAD, what are you hoping to find out from your findings when you analyze VIVA-MIND? Just try to work out what could be incremental there. Secondly, I think on the last call, you acknowledged that partnership discussions had not included the additional data in diabetics that you were presenting. So since that data were disclosed, could you update us on how your partnership discussions have progressed? And then finally, on the design of the study for diabetic kidney disease, will patients be stratified by GLP-1 use? Just considering the fact that the proposed kind of anti-inflammatory effect of these looks to be independent of the weight loss, so just not to kind of mix up any anti-inflammatory effect of those with that potentially of varoglutamstat. Thank you. Yeah, maybe I take your question. Thanks a lot. Very good questions. So first of all, the last one first. We will stratify on standard of care, so GLP-1, SGLT2, and not only because we want to avoid a mix-up of weight loss and effect of inflammation. From our analysis standpoint, there is none, but because the penetration of GLP-1s and SGLT2s is not a very homogeneous high. There's a lot of patients who get it, but there's also a lot of patients who don't get it for various reasons. And as we do the study on top of standard of care and standard of care is different in each patient, we need to stratify by this. This is very clear. Then the next question was on the partnership discussions. You understand that we cannot reveal specific names, sort of our policy on names and status. What we can confirm is we're in discussions with other pharma companies and the solidity of science and evidence which we can provide now with all these analysis, of course, helps us and is much more convincing than if you compare our situations in probably April or May, where we had just the first kidney data, but had not a conclusive view on the mechanism and how exactly Alzheimer's and kidney would lead to different outcomes in the same study with the same drug and the same mechanism. This will, from our point of view, help a lot. We feel in a strong scientific position, we are unique and certainly are a leader in anti-inflammatory research in kidney disease these days. So that puts us in a good position. And the first question is, what can we expect from VIVA MIND? VIVA MIND was like ViViAD, initially targeted as an Alzheimer's study, and the population and the dose is identical, more or less, or 95% identical to ViViAD. What was different was the outcome parameter for the Alzheimer's assessment. So whereas in ViViAD, we had more modern contemporary outcome parameter, in VIVA MIND, we had more the classical CDR-SB sum of boxes and ADAS-Cog. For that was different. But we stopped the VIVA-MIND study, as it had the same patient and the same dose as ViViAD, and we expect, of course, no different outcome in Alzheimer's disease in VIVA-MIND, so we haven't seen the results. And therefore, the study only has randomized 110 patients of what about 80 patients went to week 24 and later. So it's a quite small study. So what we expect here, eGFR, then in ViViAD, and of course, it would be a second study showing the same magnitude of effect, but 80 patients, of course, are not powered for a P value, as was in ViViAD, where we knew that the power was sufficient to show high P values if the drug would work. From a magnitude effect, we would expect very similar outcome in VIVA-MIND compared to ViViAD for both Alzheimer's and kidney. Thank you very much. Did I answer your question? Yeah, that was great. Thanks. Okay. 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. Thank you. We are now going to proceed with our next question. The question comes from the line of Christian Ehmann from Warburg Research. Please ask your question. Your line is open. Hello, and thanks for taking my questions. I would like to have a question regarding the patent life. So under which circumstances would you be able to extend the patent protection to two thousand and forty-four, as you've mentioned in your slides? And what kind of patent protection would this entail? Are we talking about additional composition of matter patents, or is it more like in the area of the method of delivery and so forth? Thank you. Yeah, maybe I take that question, and Mick can add to this. We have filed these patents, both a new composition of matter patent and also indication patents already a year and a half, one and a half ago. We're in the process of getting those reviewed and agreed. So we are confident that that will happen. And once they are granted and published, we can go in further details on this. But we worked hard on it. So, Christian, you can believe that we worked hard on it because not only because we are now switching varoglutamstat in as a first priority to kidney. Also for the Alzheimer situation, the patent life would have been relatively short. So we made a very strong effort to allow a market exclusivity into the mid-forties based on very strong composition of matter, because that is what counts, and that is also what other pharma companies would look into. What's a reasonable timeline to expect a decision on this? Oh, we are in the review process, so of course, the patent reviewers are not necessarily totally bound on timelines, but I cannot give you a granting and a publication date. But we are in a Q&A with them, and it looks, I would say, promising. Thank you very much. Thank you. We're now going to proceed with our next question. The next question's come from the line of Joseph Hedden from Rx Securities. Please ask your question. Good afternoon, and thanks for taking the questions. You presented some interesting data on, you know, PKPD profile of Varo from the ViViAD study today. So what dose do you think you would need to have a significant effect in reducing the intracellular pyroGlu A-beta? And do you think that's feasible given that eight hundred mgs twice daily in severe, you know, led to some tolerability issues? It's a good question, but I and we have asked our question ourselves, but we are not yet there to give you that answer because we showed you today an initial data set of 36 out of probably 200 samples we have, and we want to measure that completely, and we may even measure other pE A-beta constructions, which, which float in the CSF because it's only only pE A-beta 40. There are oligomers, there's pE A-beta 42 and others. So probably with that technology we have now our hand, we can do more of this. And once we have a complete understanding and also can make a PKPD model for those because you know, we have patients with a higher concentration of CSF and a patient with a lower concentration of CSF. So while the mean concentration is very clear, there's of course some variation between patient and patient, and we can look at the variation of the patients and the concentration and their outcome of pGlu A-beta reduction. Once that homework is done, which we expect probably when we have also VIVA-MIND data, we will conclude on if anything can be done in Alzheimer's disease and if yet, at what doses. And of course, there is also technologies to improve the penetration of the blood-brain barriers for small molecules and others. And of course, we are looking into these technologies, but it's much too early to give a public statement of whether that would work and what we would need to do. So we are still in the, I would say, making of the data. What is important from our point of view today, is that we have now a clear understanding that our target with varoglutamstat is the intracellular QPCTL or isoQC. And if we hit and inhibit it, this enzyme, we see clear effects in the kidney. And we expect to see also clear effects in the brain if we can come to reasonable concentration in the cells of the brain, and not only in the CSF. So this is what we can say today. What the dose would be and how we get there is still, I mean, these research questions are ongoing, but, as this data are very, very new, and of course, we cannot provide yet a full answer on this one. Okay, understood. Thanks, Frank, and then perhaps if I could just have one on the kidney opportunity. Alongside the primary plan in DKD, in July at the time, you also mentioned extra preclinical work to explore other opportunities, and specifically, perhaps leading to a market study in 60 patients or so. But no mention of that in the release today, so are those plans shelved, or are they very much still on the subject to financing? No. When I understand you correctly, whether we initiated this and we can pay for this? Yes, we initiated it. Yes, we can pay for that. That's in the budget. That's also within the runway, which Anne mentioned. We expect those data coming probably by the end of the year or the next year. Also, animal studies take a while until they are authorized. You need ethics committee for this, you need to set it up and so on. So this is not super quick, but we expect this coming, yeah, probably in the next four to six months, and then we can show you the results. Okay. And then again, at the time, you specifically singled out Alport syndrome and Fabry disease as potential orphan indications with a kidney component as potential targets. Is that because there's data that you'd previously seen that you need to build on, or is there any kind of commercial reasons that you've perhaps looked at those areas first? I really don't understand your question, but it's acoustically. I don't hear you very well. So if you can rephrase. What I understood, Fabry and Alport, we mentioned, and there is the research has been initiated. We need research data in order to justify a clinical trial. We expect this research data, at least the first one, to come up in the time frame I told you. They are financed and then the runway included which we published and mentioned. So we just have to wait. And of course, it's in a collaboration with Tobias in Hamburg. We don't have these models ourselves, of course, in our small R&D team, but it's a collaboration with Tobias and let's see when he can show some data. Okay, great. Thank you. And I also want to use that opportunity, by the way, to thank our Vivoryon team and our R&D team for their relentless work on finding out what happened in ViViAD, of doing all this additional analysis and these calculations. So we have full transparency and clarity where we are today and how we can move forward. So thank you to the team. 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, it's star one and one for any questions. Thank you. We have no further questions at this time. I want to hand back to Mr. Frank Weber for closing remarks. Thank you. Thanks, everybody, for following us. We had a very exciting and turbulent first half of twenty twenty-four, and, when we look today, we stay strong and on very good scientific foundation. We understand the Alzheimer data, and we understand also the kidney data. We have a very logical explanation of how things happen, which provides an excellent base and future for further continuing development, primarily in kidney disorders and in Alzheimer. We will conclude once we have VIVA-MIND data and further analysis on biomarker completed. Thanks a lot for your interest. Goodbye. This concludes today's conference call. Thank you all for participating. You may now disconnect your lines. Thank you.