Thank you for standing by. Welcome to the Vivoryon Therapeutics 2024 full-year results conference call. At this time, all participants are in listen-only mode. After the speaker's presentation, there will be the question and answer session. To ask a question during the session, you will need to press star one one on your telephone keypad. You will hear an automated message advising your hand is raised. To read your question, please press star one one again. Please be advised that today's conference is being recorded. I would now like to hand the conference over to our first speaker today, Anne Doering, CFO. Please go ahead. Thank you, Nadia. Good afternoon, and thank you for joining us today to discuss the company's full-year 2024 results and operational updates. This morning, Vivoryon issued a press release reporting its full-year 2024 financial results and also provided an update on our progress for the reporting period and year-to-date, which was marked by a strategic shift into kidney disease, creating a robust body of evidence for varoglutamstat's beneficial effects on kidney function, as well as significant progress both on the preclinical and clinical fronts, as well as on the corporate development side. 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 our Chief Business Officer, Michael Schaeffer. I will begin today's call with an overview of the key highlights from the reporting year and post-period updates, and will then walk you through the financial results for 2024 and 2025 year-to-date, providing details on corporate and financial updates, including our recently announced SEPA facility. I will then hand the call over to Michael, who will give very positive updates on the data fronts, where we have new preclinical information as well as news on our IP strategy. Frank will conclude our presentation with a summary and details on varoglutamstat's unique and beneficial effects on kidney function and strategic outlook. Following the prepared remarks, we will host a Q&A session. Before we start, 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 conditions, liquidity, prospects, future transactions, and strategy. 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. 2024 has been a truly transformative year for Vivoryon, as we have successfully navigated the strategic shift towards a focus on inflammatory and fibrotic diseases, in particular on kidney disease. In the reporting period and year-to-date, we have built a robust body of clinical evidence for varoglutamstat. We have concluded two independent, randomized double-blind, placebo-controlled phase II studies and analyzed the results extensively, individually for each study and in a meta-analysis. This has shown highly consistent, statistically significant, and clinically meaningful improvement of kidney function for varoglutamstat versus placebo. We have designed an efficient clinical program. The phase II B DKD study will be a small and focused study aimed to deliver results as quickly as possible and the target patient population. This has been based on a thorough statistical analysis and has been shaped in lockstep with thought leaders in the space. All along, we have had close dialogue with key opinion leaders, and we have hosted events to provide others access to their views. We have created a viable commercial strategy for our lead asset, varoglutamstat. This includes new data that we will show you today on the potential synergistic effects of varoglutamstat with standard of care in kidney disease. We also have strengthened our IP position and are sharing exciting news with you today on the recent notice of allowance for a new varoglutamstat composition of matter patent in the U.S., providing us with significantly longer potential exclusivity. All these steps are bringing us closer to realizing the full potential of varoglutamstat in this area of significant unmet medical need. At the same time, prudent cash management has enabled us to extend our cash runway, and through the recently announced standby equity purchase agreement of up to EUR 15 million, we have gained additional financial flexibility. As of May 1st, 2025, we will be expanding our executive team with the addition of Dr. Julia Neugebauer, taking on the newly created role of Chief Operating Officer and heading investor relations. All of this marks yet another extremely active reporting period with lots of updates on all fronts for us to cover today. Here we have an overview detailing the robust body of evidence generated for varoglutamstat in kidney function that underpins our strategic shift towards advancing varoglutamstat in DKD. This quarterly breakdown clearly shows the clinical and preclinical progress from the initial VIVIAD readout to where we stand today, including oral presentations at the most prestigious medical conferences, the American Society of Nephrology in the U.S. in the fourth quarter of 2024, and coming up this June at the European Renal Association Conference. Both Frank and Michael will go into further detail on the clinical and preclinical progress in our webcast today. We have decided to touch upon the financial results and corporate progress earlier on in our presentation today to also address our recently shared news on the SEPA facility. Overall, prudent spending and resource management has allowed us to achieve the strategic turnaround towards kidney disease while reducing cash utilization. As for the 2024 key figures, research and development expenses amounted to EUR 14.1 million versus EUR 17.6 million in 2023. The decrease is primarily attributable to lower third-party expenses, mainly due to lower clinical and manufacturing costs following the ramp-down of the VIVIAD study. We have seen a decrease in general and administrative expenses with costs of EUR 6.9 million in 2024 compared to EUR 8.6 million in 2023. This EUR 1.7 million decrease was largely due to a decrease in personnel costs and costs for non-executive board members, driven largely by a decrease in share option expenses relative to 2023. All of this resulted in a net loss for 2024 of EUR 20.6 million compared to EUR 28.3 million for 2023. The company held EUR 9.4 million in cash and cash equivalents as of December 31st, 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 in 2024 reflects the intensive investment period in VIVIAD and VIVA-MIND, especially in the first six months of the year, as well as investments to support the advancing of the kidney program, some of the newest results of those efforts we are sharing with you today. Costs from VIVIAD and VIVA-MIND are largely completed. However, spending continues to occur on preclinical studies and evidence supporting the kidney strategy. This brings us to an updated financial guidance. We are very pleased that we have been able to navigate 2024 successfully with a positive outlook also for 2025. As a result, we are extending our cash runway given the improved outlook, now expecting our cash and cash equivalents being sufficient to fund our operating plan for the full year 2025 and into January 2026, provided there are no unforeseen circumstances and without taking into account potential additional financing transactions, if any. We have been diligent in spending and have invested where we believe it makes strategic sense to strengthen the kidney disease strategy. During this period, we have built the clinical evidence of varoglutamstat and its impact on kidney function. We have expanded the pipeline with the progress of our new molecule VY2149, and we have also strengthened our IP position. We still have our planned phase IIb study in DKD in sight, for which we will need further funding and our partnership. Now, I would like to move on to the standby equity purchase agreement with Yorkville Advisors, which we just announced last week. The SEPA is one piece of our financial strategy towards starting our phase II-B DKD study. It is with Yorkville Advisors and provides us with access to additional capital of up to EUR 15 million over 36 months. We can use this facility at our discretion, and there are mechanisms in place that provide a level of control over the amount and timing of tranches. We have not yet issued a tranche under the facility. The program can be stopped at any time. Strategically, it allows us to keep open the various potential paths we see going forward. Importantly, the SEPA does not pose any restrictions on other fundraising or partnering options, meaning that we can continue the active pursuit of the optimal solution to fund the phase II-B DKD study. We have always been and continue to be fully committed to doing what is in the best interest of our shareholders and the patients we strive to serve with the medicines we are working tirelessly to develop. I'd like to conclude my remarks with an exciting announcement. We are very happy to welcome Dr. Julia Neugebauer to our executive management team. Julia will join as Chief Operating Officer on May 1st, a new role within Vivoryon. She brings to the company nearly 20 years of experience in the biotech industry. Many of you will know Julia from her long tenure at MorphoSys, where she spent over 10 years in R&D before transitioning into investor relations, most recently as Vice President, Global Head of IR and Sustainability of MorphoSys. As Vivoryon's COO, Julia will be heading investor relations and communications activities, spearhead our market analysis, and lead other corporate functions. As a seasoned industry expert combining scientific expertise with business acumen, she will be an excellent addition to the company's management team to support Vivoryon in executing its strategic goals. With that, I will hand it over to Michael. Yeah, welcome, everyone, also from my side, and thank you for starting us off. Let me continue with some details on very exciting recent findings and developments in the preclinical space, as well as some significant progress we have made on the operative level related to intellectual property. Starting with varoglutamstat's mode of action and QPCT, QPCTL inhibitors in general. As a reminder, Vivoryon's groundbreaking discovery underlying our most advanced development program is that inhibition of the glutaminyl cyclase QPCT and QPCTL reduces kidney inflammation and fibrosis and can significantly improve kidney function. Varoglutamstat is a potent and selective inhibitor of glutaminyl cyclase QPCT and QPCTL, which I will refer to as QPCT/L from here on out. These two enzymes are the only ones in the human body enabling pyroglutamate formation in the substrate proteins and peptides. This pyroglutamate formation is per se a physiological event that we all need for our bodies to function normally, as it leads to stabilization and/or full potency of the glutaminylated substrate protein. However, in disease conditions, disease-relevant molecules, including glutaminyl cyclases, are overexpressed. Increased levels of pathologically relevant proteins cause additional or accelerated pathological changes like inflammation and fibrosis, ultimately leading to kidney function decline. Now, glutaminyl cyclases have a rather broader number of substrate proteins, many of which are involved in fibrotic events, extracellular matrix remodeling, and inflammation, like the ones you see in this illustration here on the right. For example, several chemokines and collagens, in addition, M1 macrophages are recruited to the site of inflammation and stimulated to polarize into pro-inflammatory states by CC chemokines, again, out of which some are also substrates of glutaminyl cyclases. Thus, inhibiting glutaminyl cyclases strongly reduces pyroglutamate formation on these inflammatory and fibrotic effectors, making them less active and ultimately leading to reduced inflammatory processes and fibrotic responses, for which, for example, alpha-smooth muscle actin is a marker and a reduction of kidney injury, for which KIM-1 would be a marker here. Importantly, it also leads to an improved glomerular filtration rate, which is indicative of improved kidney function. In this context, I'd like to highlight that QPCT/L inhibition is modulating substrate activity rather than completely blocking it, which is just one of the several major differences to earlier anti-CCL2, CCR2 antibody approaches, for example. I'm making this clear distinction here because it is important to understand that this modulation of the activity of many different key inflammatory and fibrotic players with a beneficial trajectory is very different from a full block of just one more or less dominant disease pathway. Taken together, varoglutamstat and QPCT/L inhibitors have a unique and new mode of action, which also makes them, in addition to being used as monotherapeutic agents, a very interesting component to be tested in combination with existing therapeutics. I'd like to highlight on the next slide for you why this is of special importance in the kidney space. For that, let us have a look at standard of care in DKD, as it is laid out nicely in the recent KDIGO guidelines. KDIGO stands for Kidney Disease Improving Global Outcomes, a nonprofit foundation with a mission to improve the care and outcomes of people with kidney disease worldwide through the development and implementation of global clinical practice guidelines. In the KDIGO guidelines, we see that SGLT2 inhibitors, which prevent glucose reabsorption in the kidney, are now defined as a standard of care in DKD. SGLT2 inhibitors are now recommended very broadly for CKD DKD patients with eGFR equivalent above 20 milliliter per minute. Today, three SGLT2 inhibitors are approved and recommended for use in DKD. Nevertheless, the risk of disease progression is only reduced at best by 34% under SGLT2 treatment, still leaving a major need for approaches that can effectively halt or even reverse disease as a single agent or acting on top of SGLT2 inhibitors. With this in mind, we believe understanding the potential additional benefit of QPCT/L inhibitors on top of SGLT2 inhibitors is essential for development and commercial success. This has prompted us to investigate combination treatment of varoglutamstat with SGLT2 inhibitors, namely dapagliflozin. I'd like to show you some of the exciting results we had in preclinical models. Before I go into the data, I'd like to briefly introduce the model I was speaking about today. The adenine-induced animal model of chronic kidney disease, ADICKD model for short, is well established in the industry. At the same time, it is also known to provide a high hurdle for showing efficacy due to the manner in which kidney inflammation is triggered here. In the ADICKD model, a specific metabolic product, 2,8-DHA, accumulates and crystallizes in animals fed with an adenine-rich diet, ultimately leading to kidney inflammation. To investigate potential combination effects and also compare once daily versus twice daily dosing, we conducted a series of experiments in several groups, including dapagliflozin alone and dapagliflozin with once or twice daily dosing varoglutamstat on top. Treatment duration was three weeks, and readouts included a broad panel of blood parameters and immunohistochemistry markers in kidney samples to analyze inflammatory and fibrotic events in kidney function. The most exciting outcome is that we found quite impressive synergistic effects for the combination treatment of dapagliflozin and varoglutamstat over a broad panel of markers. You can see here on the graphs on the right side that the combination treatment, which are the green columns, achieves statistically significant improvement versus dapagliflozin-only treatment group, which is the purple column. Just as examples here, on top is CD11c, which is a known surface marker for the pro-inflammatory M1 macrophage subpopulation and indicates beneficial impact on inflammation. In the middle, strong collagen III reduction shows the strong antifibrotic effect exerted by the combi treatment. On the bottom, you see clearly reduced plasma cystatin C levels, which are indicative of increased kidney function. Moreover, when comparing the dark green column, which is the combination of varoglutamstat twice daily and dapagliflozin with the control in light gray, you see that the combination nearly normalizes pathology for these domains. Furthermore, comparing both green columns, which is once daily versus twice daily versus twice daily dosing, you see they are quite similar, in particular the domains of fibrosis and kidney function. This clearly supports the once daily investigation of varoglutamstat in our planned clinical study. I'd like to reiterate that the efficacy bar in this model is pretty high. All this is extremely encouraging and once again makes varoglutamstat and QPCT/L inhibitors a very attractive development program in the kidney space, both as a standalone therapy in its own right and also in combination with SGLT2 inhibitors. To provide further proof points, we are currently investigating additional animal models, including a DKD model, and results will be presented in one of our upcoming reporting events. Taken together, these exciting findings pave the development path for QPCT/L inhibitors in combination with SGLT2 inhibitors, and the effect observed on top of standard of care SGLT2 inhibitors could substantially de-risk our DKD clinical development program. Based on this outstanding effect, we very recently also have filed patents for the combination of QPCT/L inhibitors with SGLT2 inhibitors. This leads nicely to the next topic I'd like to update you on today. This is how we are protecting our findings and strive to extend our leading position in the field. Now I'd like to give you a brief update on our IP strategy and patent status. Let me start off with the most exciting news here in Light Blue. The accelerated examination process we have been applied for in the U.S. regarding the new composition of matter patents for the actual polymorph and the drug product of varoglutamstat has been completed, and this was a positive outcome many months earlier, actually, than expected. We've received the notice of allowance just recently, and I'm very happy to report that the examination process went extremely smoothly, and the investigators had only very few minor formal remarks. We have completed all final administrative steps on our end, and we expect the final granting letter to arrive within the next month. The nationalization phase to the rest of the world will be due and starting by end of this year. In addition, we have filed further patents on medical use, dosing measurement, as well as the combination therapy of varoglutamstat and SGLT2 inhibitors, covering not only varoglutamstat but also our follow-up candidate VY2149, as well as other QPCT/L inhibitors and all of their polymorphs, which actually provides additional layers of protection. In line with the potential application of QPCT/L inhibitors in a broad range of diseases, we also have secured a large number of medical use patents and other indications, as you see here in the dark blue section. As of today, overall, our patent portfolio is comprised of 22 patent families and over 400 patent application issue patents with composition of matter patents on QPCT/L inhibitors representing the clear majority thereof. Now, what does this mean in terms of timelines regarding the IP protection of our assets? As you see, varoglutamstat is now protected until 2044 with a potential extension under the Hatch-Waxman Act to 2049, which obviously is a major added value on top to the natural runtime to year 2031 under the original patent. Patent filings for dosing, medical use, and combination add a year on top of that. As I said before, if granted, it will provide an additional layer of protection from competition for varoglutamstat and also the follow-up candidate VY2149 and other QPCT/L inhibitors of our portfolio. I would now like to conclude my remarks today with a quick summary of where we stand with varoglutamstat. Let me point out here, very importantly, what you see is not an aspirational list. These are statements reflecting the body of scientific and clinical evidence we have generated to date about the profile of varoglutamstat to demonstrate that this compound has the potential to become a convenient new treatment option to fill the existing gap in kidney diseases. Varoglutamstat is a single-agent oral compound with additional preclinical evidence for highly synergistic effect with SGLT2 inhibitors. Rooted in a first-in-class mechanism of action addressing key pathways in inflammatory and fibrosis, varoglutamstat treatment has proven to result in a statistically significant and clinically meaningful improvement of eGFR in two independent double-blind placebo-controlled phase II studies with an effect size substantially larger in the diabetes versus non-diabetes population. Frank will go on into the clinical data in more detail shortly, outlining the clearly differentiated profile with about 70% of patients showing improvement on post-stabilization of eGFR in the diabetes subgroup, as well as the excellent safety profile consistent across two years of study duration. I have just updated you on our important recent success on the IP front, putting us in an excellent position with not only varoglutamstat but also our other product candidates. With that, I would like to hand over to Frank for the clinical data deep dive. Frank? Thank you, Mike. Thank you, Anne, for this very nice presentation. This is a special day for Vivoryon. It is about one year ago that we announced the first time that we had fantastic data on improving kidney function. We have a year behind us, and I will shortly review where we are today and give you an outlook on what is happening in the next year and where our ambitions go. Next shot, please. Chronic kidney disease is a very severe and unreversible progressive disorder where there are treatments out like SGLT2 inhibitors to which Michael spoke before, but GLP-1 agonists which do not reverse the disease but just slow it down. There is a huge unmet need to change the trajectory of that disease, and there is currently nothing out there which looks as promising, I would say, as varoglutamstat does with the data we have seen in the past and by Michael, and which I will present to you. Our evidence is based on two clinical studies which we were running in the year 2021 to 2024. One is the European VIVIAD study, and one is the American VIVA-MIND study, both double-blind placebo-controlled randomized studies initially targeted in an elderly Alzheimer's population with prospective measurement of kidney function. What we saw is that there is, on the next chart, consistent highly significant improvement of eGFR in both studies independently replicating the positive effects on different continents with different CROs with different investigators. We have a very robust finding for our drug based on these two clinical studies. To give you some idea, the effect size we observe here in the total population we studied is three times higher than compared to SGLT2 and GLP-1s observed versus placebo in diabetic patients. That is a conservative statement because in diabetic patients, our effect size is much higher than in the total population, as can be seen in the meta-analysis on the next chart. We conducted the meta-analysis, and we compared the effect of diabetes patients with non-diabetic patients in those two studies. What you can see is that the bar charts are much wider away from the zero line in the diabetic population than they are in the non-diabetic population. Both are significant, but when you compare then the effect size, you come, of course, much higher than threefolds to what you have observed so far for the SGLT2s and GLP-1 inhibitors. While there are all statistical models, I think so far, we have never shown the observed case MMRM by visit data. These are the pooled observed data from baseline to last visit for VIVIAD and VIVA-MIND. You see here in the pink line the active compound, and then the placebo is in orange. What you can see is that, as we always said, varoglutamstat increases slowly over six months or 24 weeks and then has a plateau of efficacy always clearly above the baseline value. What you see is that the patients treated with placebo have a mild decline. The efficacy is clearly maintained over two years, and the effect is highly significant in the population, in the total population. When you move to the next chart, we have also done the same chart for the diabetes population. As you can see, for the diabetes subpopulation, the active is in the blue, and the placebo is in the yellow color. The placebo is a little bit noisy because there are very few patients in the placebo arm. There is only 16, 14, 30. What you can see clearly is that the drug effect is very consistent and maintained over two years against starting at about six months of treatment. The effect size actually is larger in diabetes patients than is in the total population. It is a little bit confusing here. I apologize for this, but the scales are a little bit different. This is a smaller magnification scale. The effect size seems to be small in diabetes patients, but actually it's much higher because when you look at the real numbers, of course, the difference is much bigger than in the previous chart when we corrected just for the scale of the presentation. Overall, we have a very consistent and very meaningful effect in the total population and even more in the diabetic population, which we then analyzed as well whether it comes from only a couple of patients or the majority of patients' profits. We did a responder analysis. In the responder analysis, we can clearly show that at the high dose, 72% of the patients have a sustained improvement of at least two minutes above baseline, whereas that effect only occurs in 24% of patients in placebo. We can state that about three-quarters of the patients using our drug at 600 mg twice daily have a sustained improvement of kidney function as measured by eGFR above baseline. These are data so far, I think, have not been presented scientifically or in a presentation at that stage and that length and that robustness. It is a unique finding. Efficacy is one part of it. The safety is another part of it. While you see big differences in efficacy, there are only very minimal differences in safety. There are some patients who have more gastrointestinal or have more skin and subcutaneous side effects, but these are very small, and these are minor, and they do not lead to drug discontinuation or to SAEs. The product is very well tolerated. Beyond these safety data from the phase II studies, we have also a large phase I study. We have completed an ADMA study. We have done our long-term safety tox studies of six and nine months in rodents and mammalians. We have a very complete and safe data package for the use of the drug in diabetic kidney disease and kidney disease. In 2024, we already started designing the next study. The objective is now also forward-looking to bring the drug now to patients with chronic kidney disease and diabetes stage 3B and worse. Those patients which progress relatively fast to end-stage kidney disease, those patients which then require either transplant or dialysis are in dire need of additional treatments improving their outcome. With the data Michael showed today, we are very confident that we can add substantial benefit on top of the current standard of care of SGLT2 in this patient population. Let me conclude now and our situation of Vivoryon in 2024. What we did is we had completed in time and in budget two clinical trials with about 400 patients, around 370 patients. We created robust evidence of efficacy for improving the kidney function, and we designed a specific study. Now, from now onwards, we will focus on ensuring that we have a clinical and commercially viable product in the market. With the new composition of matter, which has a letter of allowance for the largest pharmaceutical market in the world, the U.S., we are quite confident that we can get there. We also find additional medical use patterns. The data with SGLT2 inhibitors in combination not only provides a huge opportunity, they also de-risk the development program and the next clinical studies, making it much more likely that we see success in the future studies. We also, which has not been mentioned so far, were busy in the last year completing the characterization of a novel follow-up compound with improved characteristics which can follow the pathway of varoglutamstat with a few years of delay. Finally, with those facts, we want to point out that our values and the way we operate is based on strong scientific foundation. In the year after we saw the first kidney data until today, we provided a huge amount of scientific, intellectual, and also organizational evidence and competence to move the product to chronic kidney disease. QPCT/L inhibitors are likely to become a cornerstone in chronic kidney disease, something which was not imaginable 12 months ago. We have a clearly defined commercial strategy. We have a large population with a huge unmet medical need. We have only limited competition in that space with a unique product profile, an oral simple administration with a huge IP runway, and a very attractive time to market because we are a mid-stage clinical development company. There are not decades to come. There's a couple of years to get to the market, but it's not decades like in an early-stage company. Of course, we want to secure the value of the shareholders and the companies in our future pathway forward, moving the product now to patients with diabetic kidney disease and chronic kidney disease. For that, part of that strategy to improve our financial situation was the conclusion of the SEPA agreement with Yorkville, which allows some additional flexibility if needed. We additionally, and don't misunderstand us, pursue additional financing and partnership opportunities that will be the cornerstone of the next months coming forward. We, of course, in parallel enhance the management capabilities and breadth. With that, I want to also welcome personally Julia, looking forward to working with you. Not forgetting, of course, the team of Vivoryon who has carried forward that program in their brains and hands and hearts and bring the product where they are today. With that, I want to thank everybody for listening, and we're ready for Q&A. Thank you. Thank you, dear participants. As a reminder, if you wish to ask a question, please press star one one on your telephone keypad and wait for your name to be announced. To withdraw a question, please press star one one again. Please then bow or compile the Q&A row studies. It will take a few moments. Now we're going to take the first question. Just give us a moment. The first question comes from the line of Joseph Hedden from Rx Securities. If your line is open, please ask your question. Good afternoon. Thanks for taking my questions. Congratulations on the IP and the new preclinical data. I guess I was just trying to dig in a little bit more onto any of the partnership discussions you may have been having recently, maybe from the perspective of you've got this quite solid data in kidney disease now. You've compounded the preclinical package. The IP is important. You seem to be getting a lot of things in place. I'm just wondering, is there anything else you see that a potential partner might be looking for that is still yet to come, or do you now see yourself in a very solid position? Thanks. We always commented that we can't comment on ongoing due diligence and discussions. It is a principle policy. Also, I don't know what is in the brain of the people looking at our data. They may say something. They may think another thing. What I think we can say is that we have now, as you thankfully also mentioned, I think, a very solid case for any partnering and collaboration in the future because how usually things get looked at is by net present value. The net present value is the value which the compound has in the future for the commercialization period. That depends largely on the market exclusivity of the compound. With the IP allowance letter, that period in the largest market in the world, of course, is much longer with, of course, increases in the net present value in each calculation of a company looking into our portfolio. It gives us also a little bit more time to go to the market. We are not so stressed whether we lose a year or not because the net present value still will be fantastic and we have a very long market exclusivity. For us, that is one of the homework we had to do. We got very successful, very fast, I have to say. I want to thank the team for this outstanding effort and the result. We are much more confident that we can do something reasonable in terms of moving this forward into the clinic, to the patients, and into the market. Let's see how others see it because, of course, this is a partner decision and not our decision only, whether we do something with them or not. Great. Thank you. Perhaps just one on the equity line. You talk about it providing you more strategic flexibility. Are there any obvious wins, perhaps, that you anything left that you can kind of get the phase II-B trial in a better position for? What's the position with the manufacturing of the drug product? Can you remind us, is there anything left over from the VIVIAD and VIVA-MIND programs, or are you needing to run a manufacturing campaign for the next trial? Is that perhaps something the equity line can help? Thank you for the question. We have drug product available for the study we have outlined in this presentation. That is available and can be packaged and shipped. We do not need a new production campaign for this. Of course, if you do much, much larger studies, much, much longer studies, at a certain point in time, we need to restart production. No question. For that study outline or for a study, a small to medium-sized study, we have material available. Yeah. I don't know. Did I miss another part of your question, or? No, really. It was just on how might the equity line be used to get towards that phase II-B trial? The equity line was primarily not directed to financing the phase IIb study. As you've seen, it's about EUR 50 million max over three years. That doesn't help to finance the DKD study or any phase IIb study, which we previously announced to cost probably around EUR 10 million alone. When you do the numbers, it doesn't help. As you've seen, the markets have been really stable in the past couple of months. It's a little bit of a turbulent environment. We thought it is good to secure the operational basis of the company with that standby agreement in case we would need it. The primary purpose is not to use this to largely finance our future studies. For that, we need additional financing as laid out by Anne or alternative partnership. That is now on the to-do list for the next period. Got it. Thank you, Frank. Thank you. Now we are going to take our next question. The question comes from the line of Susheila Hernandez from Van Lanschot Kempen. Your line is open. Please ask your question. Hello. This is Sam calling for Susheila. Thank you for taking the question. There are three from our side, if we may. The first one is, if you could remind us how much funding you would need for the phase II-B trial in DKD and on the financing agreements with Yorkville. Has Yorkville already requested a tranche? On the meta-analysis to be presented at the ERA in June, is there anything new compared to the data disclosed in January this year? I'll start with the last one. Leave the Yorkville to Anne. The meta-analysis was submitted. Based on the data we have presented, but of course, the scientific presentation will always add a little bit of color here and there. It is not the same, let us say, high-level presentation as we usually do for investors. The scientific presentation goes always more into details and more into science. The purpose here is clearly to get feedback and get into interaction with the scientific and clinical community with our drug. There is not totally new data because the meta-analysis is, of course, done. Also, the data are submitted in the abstract submission, so the data will not change. Of course, the granularity and scientific rigor and the way we present will be different. Regarding the clinical study we have in this presentation and we portrayed before, we have settled as a reasonable potential size of the study around 90 patients to be randomized and to be treated for about 30 weeks based on the meta-analysis and the current knowledge and also with the SGLT2 data. We have always said it is about EUR 10 million-EUR 12 million cost for the study. That did not change either. I leave the middle question of Yorkville and the requesting of tranches to Anne and to put that in a. Just to make sure we have the same understanding, Vivoryon actually submits a request for the tranche. We can actually proactively do that. No, we have not yet issued a tranche under the facility. I hope that addresses your question. For us, it is important that we get the message across. It is a management security safety belt we have put with Yorkville into place. We steer it. This is not an automatic trading system which you have with some other providers where shares get dumped regularly in the market. That is not our purpose. We will use it consciously if needed, very carefully in bridging or special situations. For us, it's important to have it in place because it's a little bit of a lifeline if needed. That is not our primary financing strategy, to make it very clear. Thank you very much. Thank you. Dear speakers, there are no further questions. I would now like to hand the conference over to the management team for any closing remarks. Thank you for listening and joining us in this year of birth of the chronic kidney disease program. I think the baby is born. It's alive. It's kicking. We want to keep it healthy and growing in the next years and, yeah, make the program a successful program and with the objective to help these patients who have progressive kidney disease and no other treatments available. That is what we want to achieve. Hope you join us in that effort. Thank you. This concludes today's conference call. Thank you for participating. You may now all disconnect. Have a nice day.