Good day, and thank you for standing by. Welcome to the Vivoryon Therapeutics 2025 First Quarter Results Earnings 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 need to press *11 on your telephone keypad. You will then hear an automatic message advising your hand is raised. To withdraw a question, please press *11 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, Julia Neugebauer. Please go ahead.
Thank you, Nadia. Good afternoon, and thank you for joining us today to discuss the company's first quarter 2025 results and operational updates. This morning, Vivoryon issued a press release reporting its first quarter 2025 financial results and also provided an update on our progress in positioning our lead asset, varoglutamstat, in the kidney space. This press release is posted on Vivoryon Therapeutics' website at www.vivoryon.com. On the call with me today are Vivoryon, Chief Executive Officer, Frank Weber, and Vivoryon, Chief Financial Officer, Anne Doering. Our Chief Business Officer, Mike Schaeffer, will be available for questions during the Q&A session. I will begin today's call with an overview of our most recent key achievements.
I will then hand the call over to Frank, who will give a summary of our exciting proof-of-principle data in kidney disease and provide details on Varoglutamstat's unique and beneficial effects, on kidney function, as well as the relevance of EGFR, as a validated clinical endpoint. Anne will then conclude our presentation by walking you through the first quarter 2025 financials. 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 strategies. Should actual results differ from the company's assumptions, ensuing actions might 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. Despite recent advances in the field, there remains a significant unmet need for effective treatment for kidney diseases, including chronic kidney disease, CKD for short, and diabetic kidney disease, or DKD. These conditions often progress to end-stage kidney disease and kidney failure. Current standard of care therapies can only slow disease progression. They cannot halt it or improve kidney function. Vivoryon, is well positioned and on track to deliver much-needed effective therapy for patients suffering from kidney disease. The first quarter of 2025 has been another highly active period, during which we have continued to build on the already substantial body of evidence supporting our lead candidate, Varoglutamstat, as a potential game changer in the treatment paradigm for kidney diseases.
Varoglutamstat, is an oral first-in-class potent and selective QPCTL inhibitor, designed to prevent inflammatory and fibrotic processes, by blocking pyroglutamate formation. It has demonstrated outstanding benefits in kidney function in phase II clinical studies, and is uniquely positioned within the evolving kidney disease landscape. The compound is backed by a robust and compelling clinical and clinical data package and further derisked by extensive safety data. Its impact on kidney function was evaluated in two independent randomized double-blind placebo-controlled 15 studies. Results were analyzed individually as pooled data and in a meta-analysis, which was presented at the European Renal Association's Annual Congress, earlier this month. Across all analyses, Varoglutamstat, consistently demonstrated statistically significant and clinically meaningful improvements in kidney function compared to placebo.
Frank, we go deeper into this data in his presentation today, highlighting how this unprecedented large and sustained improvement in kidney function, particularly on a subgroup of patients with diabetes, translates into an actionable risk-contained strategy for a planned phase II B study, in DKD. In addition to the clinical data, Varoglutamstat, has shown synergistic effects in preclinical in vivo studies, when combined with standard of care therapies, further enhancing its potentially unique positioning within the commercial landscape. Importantly, we have also strengthened our IP position. This includes several recent patent filings covering medical use, dosing, and combination regimens, as well as the granting of a new U.S. composition of matter patent for Varoglutamstat. This patent supports market exclusivity through 2044, with the potential for further extension. With that, I'd like to hand the call over to Frank. Frank.
Thank you, Julia. Good afternoon. Good morning, everybody. Varoglutamstat, has the potential to transform kidney health outcomes. We want to look now in the next coming slides into why we believe we have outstanding data and how we move forward from our current evidence level. Our conviction that we have outstanding data is based on two randomized placebo-controlled studies, with more than 360 patients treated for up to two years, where we prospectively measured EGFR, and could show an improvement of EGFR, above baseline and versus placebo in a statistically significant and clinically meaningful magnitude of effect in both studies independently, with a much larger effect size in patients with diabetes compared to those with no diabetes in both studies. We could replicate the finding and have a very consistent outcome in those studies.
I want to remind you that EGFR, was only an exploratory secondary outcome, and the primary was cognition, where the endpoint failed. In the next slide, I show you that we presented now the data the second time. This time, we were at the ERA in Vienna, recently and presented the pooled analysis and the meta-analysis, of those two studies to the scientific community. There was exciting feedback on this data. We could show that both in the pooled and meta-analysis, there is the same finding. The outcome does not depend on the statistical methodology. We find statistically significant data from week 24 onwards and can sustain them until week 96, which is unprecedented in that space.
Now, in the next chart, the ERA is also, like other scientific congresses, a good place to look around what is the trend, the scientific trend, what do other companies do, where is the world heading towards. The world is heading towards combination therapy because now we have, with the SGLT2s, the first time drugs which are recommended broadly for patients with chronic kidney disease and diabetic kidney disease, for stages up to 20 milliliter, of EGFR baseline down. This data shows on the SGLT2s, that while you have a reduction in the progression, so the speed of progression is lower, the drug doesn't stabilize kidney function. The patients still progress and get worse. This is why everybody has two additional mechanisms of action.
Here you see on the left side the rare kidney disease space, where you see various products which are under development from companies which are still doing this or have been acquired by larger pharma companies, largely in the IgAN space and in the FSGS space. There is a lot of movement. The products are largely not yet approved, but they're under development with new mechanisms of action. You see on the right side, where you are in the CKD space, where millions of patient pools are available, there are largely combination treatments or new versions of existing mechanisms of action being developed.
There is virtually only Varoglutamstat, which has a completely new mechanism of action, which is an oral therapy, which has shown synergies with standard of care available in that space to be moved forward with the aim to stabilize and improve EGFR and kidney function long term. We have an outstanding position in that field of development products in the orphan and in the non-orphan space. That is confirmed at the ERA, where no comparable data to ours have been presented or shown. On the next chart, we need to discuss a little bit about the relevance of our finding. You know that we have made the slope analysis the primary analysis of our EGFR data, for the secondary endpoint. It is important to put that in perspective, what does that mean?
EGFR slope analysis, is an acceptable clinical endpoint for phase three studies, as published already in 2018 by a workshop of the FDA, the EMA, and the National Kidney Foundation. That is also the case for albuminuria, but the data support much stronger EGFR, as a surrogate endpoint for outcomes for kidney health outcomes than does albuminuria because albuminuria is, of course, dependent on the protein transporter, which transports the protein which is filtered through the glomerulus and back in the kidney. Those can be up or down regulated. That may change a little bit the proteinuria interpretation. We can conclude that EGFR slope analysis, is a valid surrogate endpoint. Because it is a decline which goes across diseases, it is a valid endpoint for many types of chronic kidney diseases, for many causes of disease.
The regulator says that effect sizes of half a milliliter over a milliliter per year in that slope, different from placebo, is necessary and ensures a high probability of a benefit, meaning not being equal to placebo, but having a benefit. If you have about 0.5-1 milliliter in the slope difference, this is already good and likely predicts a positive outcome on kidney health. They say that two years is a likely duration of a study for an EGFR slope analysis, because you need to follow a patient for a while to make the prediction whether the slope is really stable or improving or different from placebo. This is not possible short-term data.
Knowing that regulatory assessment, of course, when you look at our data in the next slide, in the comparison also what is there, you see that the SGLT2s, have about 1 milliliter to 1.5 improvement, over long-term studies in EGFR per year. The same has mineralocorticoid antagonists like finerenone. You see Varoglutamstat, has three to four times the effect size on EGFR, compared to those products. The other products show also an improvement in proteinuria, or in other words, urinary albumin-creatinine ratios. We have not been able to collect this data in the previous studies in a quantitative way, only in a qualitative way. There we do not see an increase in proteinuria, but we will look at the quantitative way in the future studies.
In that graph, you see that there is a huge magnitude of effect for qPCT inhibitors, in the diabetes population on that slope analysis. On the next chart, it becomes a little bit theoretical and complicated. What we did here, we simulated what we would need for phase III, because when we now start the development of the product in diabetic kidney disease and chronic kidney diseases, then we, of course, need to understand what is the endgame of confirmatory studies. We see that it is highly feasible to run also a phase III program, for Varoglutamstat. Why? Because we have already two years' data and a slope analysis, conducted in the phase II. The active arm, is the dark blue line, the slope of the dark blue, and the yellow one, the orange one is the placebo.
The difference is 5 milliliter. Over two years, we have a p-value of 0.002 in already 94 patients only. If we run a phase III and want, as a simulation, only see a difference of 3 milliliter because we can make, of course, the point, the phase III, the magnitude effect may be a little bit lower because the population is a little bit wider and not so consistent, then we would need 260 patients in the study to complete one phase III study. If you go down to smaller effect sizes like the SGLT2s have or the GLP-1s or finerenone, you see that studies become, of course, more difficult to be conducted with EGFR, as an endpoint because you need already thousands of patients to do this. If you go for the regulatory minimum, you need a couple of thousand patients to power a study adequately.
In other words, Varoglutamstat, is specifically suited for a phase III development program with phase III studies, in the range of 250-350 patients in a single study conducted over two years to meet that regulatory endpoint. That encourages us, of course, to now start the development program, first of all, in the phase II B study, and then confirming this data and these simulations, and then running the phase III program accordingly. Going to the further story of the ERA and what is currently state of the art, as said, these SGLT2 inhibitors, and none of the single agents being out there today can stabilize kidney function or even slightly recover kidney functions.
This is why everybody looks at additive effects of existing approved treatments like the combination of finerenone and empagliflozin or dapagliflozin, that we had the CONFIDENCE study, just published at ERA, or similarly with other products under development in combination being either mineralocorticoid receptor antagonists or endothelin receptor antagonists or aldosterone synthetase inhibitors, which are known mechanisms of actions. Those show, of course, an additive effect in the reduction of proteinuria, but there is no evidence that long term they stabilize EGFR, or significantly defer the act. There are some indications of EGFR, being quite similar to the single agents, but the studies they have conducted are, of course, not long enough to make any interpretation on the EGFR, on the slope.
The medical need of a stable outcome in chronic kidney disease, is still out there, and new therapies and new mechanisms are needed, those like the glutaminyl cyclase inhibitors and Varoglutamstat. Next chart. This is why our data we generated in the pharmacological model on top of gliflozins or SGLT2s, are so important because gliflozins are, of course, the standard of care and given to many patients now with chronic kidney disease and diabetic kidney disease. Of course, we wanted to show and demonstrate that glutaminyl cyclase inhibitor, Varoglutamstat, on top of these gliflozins, gives additionally a boost and an improvement of the kidney function. We look here at inflammation, at fibrosis, and at kidney function.
You see that, of course, the gliflozin alone in this model has an effect, but if you add varoglutamstat, you see that the pathology nearly disappears, and the green bars, are about the same height as the gray bar. The gray bar, is the non-diseased healthy animal. The black bar, is the diseased animal. The green bars, you see is the combination of SGLT2 plus Varoglutamstat, which is a highly promising finding. We patented this finding because of the fantastic synergies we saw here in the combination of those two treatments. A highly promising finding for future clinical trials. In the next chart, you see that we filed that patent. That is the last line, but we also have a composition of matter granted in the U.S. with a runtime of 2044.
When you see of all medical use in kidney dosing regimes, we filed our patent span is now to the mid-2040s, to the end-2040s, which allows us a sufficient market exclusivity for the compounds in the future to leverage our scientific findings. In summary, this is probably the most promising compound to be a convenient new oral therapy and has a potential to transform really the treatment of kidney diseases, making these diseases stable and less progressive and preventing ultimately kidney failure and kidney replacement therapy for many patients. The medical need is products that really stabilize or improve kidney function for the majority of patients. Varoglutamstat has, based on the current finding and the future development plan, huge potential to show and leverage that.
We have now a clear development pathway forward, which is based on regulatory discussions and findings, and future programs can be based on our currently robust available evidence based on the statistical findings on EGFR, on the two independent studies, on a huge effect size, on an excellent safety profile, and on the synergy with the gliflozins. With that, I want to hand you over to Anne, for the financial part. Thank you.
Thank you, Frank. I will now walk you all through the first quarter 2025 figures. Research and development expenses, amounted to EUR 1.2 million, in the first quarter of 2025, versus EUR 7.4 million, in the first quarter of 2024. The decrease is primarily attributable to lower clinical and manufacturing costs, following the ramp-down of the VIVIAN and BEAM aligned studies. We have seen a decrease in general and administrative expenses, with costs of EUR 1.3 million, in the first quarter of 2025 compared to EUR 2.1 million, in the first quarter of 2024. This EUR 0.8 million, decrease was largely due to a decrease in personnel costs, as well as legal and consulting costs. All of this resulted in a net loss, for the first quarter of 2025 of EUR 2.4 million, compared to EUR 9.1 million, in the first quarter of 2024.
The company held EUR 7 million, in cash and cash equivalents, as of March 31, 2025, compared to EUR 9.4 million, as of December 31, 2024. Our cash runway, into January 2026 does not include any funds from the standby equity purchase agreement, announced in April 2025. There are only minimal costs, remaining from VIVIAN and BEAM studies. Our spending plans continue to support the kidney disease strategy and the strengthening of our intellectual property position. We continue to actively pursue additional financing and partnership opportunities to primarily fund the phase II B study. As shown throughout today's presentation, we have been working on all fronts to drive the company forward and develop a much-needed treatment for kidney disease. The cornerstone of our strategy and steps forward has been based on Varoglutamstat's, breakthrough clinical results in this indication.
Varoglutamstat, is a unique asset targeting inflammation and fibrosis, which are key drivers of kidney disease. Our approach is differentiated from standard of care, not only with regard to how it potentially works, but also from the substantial beneficial impact on kidney function that we have reported. The phase II kidney function data, for Varoglutamstat, which has been observed in two independent phase II studies, show that we have the potential to stabilize and even partially recover kidney function, not just slow the progression of disease. We could even have a synergistic effect on top of standard of care. Let's also not forget we have an extensive safety data package supporting Varoglutamstat. In terms of convenience, we are talking about an orally available medicine.
To move forward, we have established an actionable development path to reach the market in diabetic kidney disease with the next step of phase II B study, in this area, building on the data seen thus far and extending it into a more advanced patient set. We see significant market potential in diabetic kidney disease and also in chronic kidney disease and even in rare kidney diseases. We have secured further patent protection to fully take advantage of these opportunities. Simply put, we believe we are well equipped as we aim to transform the treatment and, more importantly, outcomes for patients suffering from kidney disease. Before we move to Q&A, I would like to take the opportunity to thank the extended team of Vivoryon, who have enabled us to reach where we are today. I want to thank everybody for listening, and we're ready for Q&A.
Thank you, dear participants. As a reminder, if you wish to ask a question, please press star 11 on your telephone keypad and wait for a name to be announced. To withdraw a question, please press star 11 again. Mr. Ball will compile the Q&A roster. This will take a few moments. Once again, if you wish to ask a question, please press star 11. Now we are going to take our first question, and it comes from the line of Romy O'Connor, from Van Lanschot Kempen. Your line is open. Please ask your question.
Hi. Thank you very much for your presentation. I have two questions. The first, I'd like to know what steps you can currently take with your current cash position to prepare for the planned phase II B and TKB, and also what you consider optimal funding solutions for this trial. Secondly, regarding partnership progression, how are discussions going, and are you reaching a more advanced state? Thank you.
For the progress of the clinical trial, we are in in-depth protocol design discussions with CROs and experts. As you have seen in the last quarter, we put a significant emphasis on understanding the full development path until the end of phase III, and how we get to the market because we need to keep the phase III, program in mind when designing the phase II B program, to make it a reasonable intermediate step. Our efforts were directed to understand the regulatory environment and the product environment and the competitive environment as displayed today to really fine-tune the protocol and to make it a success and to de-risk it. That is where we are. We also look, of course, at study medication and financial parts and so on. We try to get ready for really starting the study, and we are relatively advanced.
I'm not fully there, but we are in advanced protocol design discussion. I think that answers you the first part of the question.
Yes. Perfect. Thank you.
Regarding partnership, of course, we need to be always careful in disclosing what we do, not to make confidential disclosures to the public. I can confirm that we are in conversations with interested pharma companies, and they continue. As I always say, we need to see what comes out and whether such a partnership is in the best interest of the company at the end, also for our shareholders or not. This is another decision we need to take. This is ongoing, and we are confident. We have a significant interest in that program because we have unique data. We are going to see what is the best for the company to move forward.
Thank you. Now we're going to take our next question. The question comes from the line of Joseph Haddon, from Rx Securities. Your line is open. Please ask your question.
Good afternoon. Thanks for taking my questions. Two, please. Firstly, just on the evolving treatment dynamics in DKD, just wondering what proportions of patients in the U.S. and Europe, now are receiving the SGLT2s. Then secondly, in your recent attendance of the ERA Congress, just wondering if there are any key takeaways for you or learnings that you can incorporate into the phase II B, trial design or whether that's solidified now or indeed competitor programs. Thank you very much.
As you know, the SGLT2s, were broadly recommended in the KDIGO guidelines of 2024. That is probably based on the evidence there. The KDIGO, Kidney Outcomes Consortium, made a huge recommendation. Since then, I think it's really picking up. I would say we're probably north of 30-35%, of the potential population getting SGLT2s today, and it's strongly increasing. There was a time needed until everybody was convinced that SGLT2, is the right thing to give because you have initially a strong dip in EGFR, which looked a little bit like a worsening.
There were people thinking that that is a bad thing happening, but it turned out that there was a certain recovery after a couple of weeks, and then there was a stabilization or a slower decline later, which compensated the initial dip that made it a little bit a long shot in terms of market penetration. Keep in mind, these are all compounds which make north of $1 billion in turnover. These are not small compounds. Of course, the market penetration to reach more than half of the patient will take a while, also because the diagnosis of patients in 3A and 3B chronic kidney disease, is not perfectly done in practice these days. There are huge gaps in identifying those patients still. Many patients only are seen in stage four or five by a nephrologist, who then initiates treatment. Sometimes it's already too late, unfortunately.
This will take time, but it plays into our cards because as an add-on to SGLT2s, in probably four or five years, that will be penetrated. It is not an issue for the commercial perspective of our drug. For the clinical trial subject availability, it is also not an issue. You see that combination studies are ongoing and done. We find plenty of patients who take SGLT2 inhibitors, for many years and who are progressing their disease. I can confirm by talks to CROs and experts, there is sufficient patient out to run our phase II and III program. As you see, we have a relatively efficient program, so we do not need thousands of patients for showing efficacy. We need probably thousands of patients for showing tolerance in big parts because of big disease.
For the efficacy study, we can stay in a very efficient program, what we have communicated today. The second question I asked were our ERA learnings. It is interesting because you always, I mean, it is a little bit sloppy, but you always need new experts and new views. The reaction overall is, wow, this is very interesting. It is a very supportive, interesting statement, but then people have different views on what we could add as additional parameters in the trial, how long the trial should go, how many patients there could be. Overall, we have, let us say, on the key parameter, we have clearly seen that we should, in the randomized study, not go below 20 milliliter EGFR. Probably we should also include some 3A patients, and not make too hard cut on 3B.
They encouraged us to say, "Look, with improving diagnostic, more and more patients are diagnosed earlier, and there are patients in 3A, with high degree of proteinuria, which have a high risk of fast progression, which you should not include." Of course, not everybody with 3A, we should include, but those with a very high degree of proteinuria, have very bad perspectives, and those we should include. There is a little bit of movement, let us say, in the in-exclusion criteria right and left, but overall, I think we have pretty much nailed down what we do, and that is confirmed that the ERA, where you see, of course, a lot of people doing similar things.
Yeah. Okay.
Yes, yes, it does. Thanks, Rave.
Thank you. Dear participants, as a reminder, if you wish to ask a question, please press star 11 on your telephone keypad. Dear speakers, we'll just give one moment for our participants. There are no further questions for today. I would now like to hand the conference over to Speaker Frank Weber, for any closing remarks.
Thank you for your continued interest in the company. We are starting now really a new promising area to move forward in chronic kidney disease. We have a clear plan laid out. We are working on executing that plan and happy to walk with you forward together. I want to thank the team again who contributed to this fantastic turnaround of Vivoryon . Thank you.
This concludes today's conference call. Thank you for participating. You may now disconnect. Have a nice day.