Thank you, [Rachia?] .

Good morning or good afternoon, everyone, and thank you for joining us today for Vivoryon's third quarter 2025 results call. Earlier today, we issued a press release reporting our third quarter 2025 financial results and business updates, which can be found on Vivoryon's website at www.vivoryon.com.

On the call with me today are Frank Weber, our Chief Executive Officer; Marcus Ilsfeld?] , our Acting Chief Financial Officer; as well as Michael Schäfer, our Chief Business Officer.

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 programs, 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. On slide 3, you see the agenda for today's call.

I will begin by highlighting our progress throughout the reporting period and recent weeks as we continue to build a robust body of evidence for varoglutamstat in kidney disease and beyond. I will then hand the call over to Frank, who will provide an overview of how we are advancing steadily on our strategic priorities, including a very interesting new data analysis that further substantiates the potential for varoglutamstat to become a convenient, widely available new oral therapy to transform the treatment of kidney disease.

After that, Marcus will review the third quarter financial results. As previously reported, Marcus has assumed the role of acting CFO during Anne Doering's temporary partial leave of absence.

You will have seen in our financial results press release this morning that Anne will be stepping down as Vivoryon's CFO in December 2025. On behalf of the entire management team, I would like to thank Anne for her exceptional work and her invaluable contributions to Vivoryon over the last 2 and a half years.

Marcus will succeed Anne, taking over the role of permanent CFO. Prior to taking the acting CFO position, Marcus has been a strategic consultant to Vivoryon since December 2024, and is an experienced finance executive with deep life science expertise.

We would like to welcome him to the team in his new capacity, and thank him for the excellent support and collaboration over the past months. Following the financial update, I will wrap up the call, and then we will move to Q&A, where we will also be joined by our Chief Business Officer, Michael Schäfer.

The compelling data that we presented so far for our lead program, varoglutamstat, in kidney disease is clearly outstanding. It continues to create very much interest and excitement within the scientific and medical community, and this is reflected in our interactions with international nephrology experts.

In early November, we presented a late-breaking poster in Houston at the American Society of Nephrology's Kidney Week, the world's premier nephrology conference. As a reminder, so-called pyroglutamated peptides produced by QPCTL are a central part of the pathways that mediate inflammation and fibrosis in kidney disease.

Varoglutamstat works by blocking the production of these molecules. The poster at ASN 2025 showcased additional analysis from the total study population from our Phase 2 study, VIVIAD, assessing on an individual patient basis how levels of one of these pyroglutamated peptides, the biomarker pE-CCL2, correlate with kidney function as measured by eGFR slopes.

Notably, a reduction in pE-CCL2 was significantly correlated with improved kidney function, providing yet another strong data point towards explaining why we see the exceptional results we see with varoglutamstat. Today, we will share results from a new analysis that addresses the key question: how do patients with impaired kidney function respond to varoglutamstat?

Frank will walk you through the findings in detail, but in short, we observed a consistent and meaningful treatment effect across all patients, and importantly, this benefit was also evident in those with more impaired kidney function. These results further reinforce our confidence in our plan to advance varoglutamstat into a Phase 2b study in Stage 3b and 4 diabetic kidney disease.

Building on the beneficial effects on inflammation and fibrosis that we're observing with varoglutamstat, we see potential of this promising drug class to be relevant across a broader range of immune-mediated diseases. Our core expertise and differentiated platform of oral small molecule QPCTL inhibitors allow us to selectively explore additional development and partnership opportunities alongside our primary focus of advancing the DKD program.

Concluding the key achievements with a brief corporate update: in October, we successfully completed a private placement of new shares to existing and new shareholders with gross proceeds in the amount of €5.1 million. With these additional funds, we now expect our existing cash to support our operating plans well into the third quarter of 2026.

We continue to see increasing momentum both within the kidney space and beyond, with interest from a broader set of biopharma companies and strategic investors. With that, I'd like to hand the call over to Frank, who will cover our strategic priorities in more detail.

Frank?

Thank you, Julia, for your nice presentation. Dear ladies and gentlemen, we look at our strategic priorities, and ASN as well as constant exchange in the expert field of nephrology allows us also to look where does our product stand compared to others, and we conclude at the current point in time that there is rightly the search for products which stabilize kidney function and partially reverse it, and the field moves to combination, but none of those approaches has yet shown to really halt or reverse the kidney function impairment.

Best data shown at ASN were Phase 2 data of an autologous cell therapy, which had an effect size of around 4.5 ml in diabetic kidney disease, and keep that number in mind when you look at later analysis of our data from Phase 2. The medical need still is for convenient therapies to stabilize and improve kidney function in those patients who progress to end-stage kidney disease.

Varoglutamstat is a premier opportunity for those patients in the future to be used, as the current data are highly promising and show a very pronounced effect. I want to show you in the next slide what we mean by this.

We have analyzed the data of our Phase 2 studies for patients with the most severe impairment of eGFR at baseline. You see on that slide, on the left side, the total population in our Phase 2 program for varoglutamstat and for placebo, and you see a slope analysis where you see the annual rate of decline in the placebo arm of around 2 ml, and the active arm improves of around 1 ml per year.

That makes a difference of 3.2 ml in the total population, which is, of course, highly significant. Then we looked on the right side in the worst 33% of the patients, those with the 33% at baseline which are the worst.

You see an identical picture: patients in the placebo group decline, and patients in the active arm improve, and the effect size is nearly identical, and the p-value is highly significant. That means the drug works as good in impaired patient as in the total population.

More importantly, we did another analysis in our core indication, which is diabetic kidney disease, and you see that graph in the next slide. Here we did a very similar analysis: we looked at the worst 50%, worst 33%, worst 25%, and worst 20%.

So 20% is really the worst of the worst, and 50% is the half of the worst, basically. What you see, you see that the worse the population gets, when you look at the lower part of the chart, the eGFR, the mean eGFR of that population, of course, drops.

The worst 50% have a 65 ml eGFR at baseline, the worst 20% have only 55.8 and are in the middle of Stage 3a diabetic kidney disease. Then you look at the graphs and you see what the drug does in terms of improvement, and you see what the placebo group does in terms of worsening.

What you see is that the active arm continuously shows an improvement between 3 and 4 ml, independent on how severe the population is. Even in the most severe population, we can show an improvement of about 3 ml.

Whereas the placebo arm, of course, gets worse the worse the baseline is. That's clear that patients who have a bad baseline have a much higher progression than those which have a normal baseline, because those with a bad baseline have, of course, really inflammatory and fibrotic kidney disease, and they progress much faster, far faster than those at the beginning of the disorder.

That shows you the placebo group is, of course, worsening the worse the baseline is. When you look at the difference between the blue, what the active does, and what the yellow, what the placebo does, you see you come up with about 7 ml difference between active and placebo for those who are really affected by diabetic kidney disease.

Now I come back to the loop. That is, of course, much better than any so far published Phase 2 data in diabetic kidney disease.

This comes from, of course, placebo-controlled study our data, and was an exploratory endpoint, these are robust and, I think, very comforting finding for our drug. On the next chart, you're going to show our priorities, and we have evolved a little bit our priorities because we see beyond diabetic kidney disease, and don't misunderstand me, diabetic kidney disease is our core indications, we see very promising data, this is where we see the biggest and the fastest value for the company, but we need to evolve the company further and see what other opportunities we may have with our compounds and our platform.

As previously said, we're working continuously on orphan kidney diseases as a near-term opportunity, including Fabry, Alport, FSGS, and cystic kidney diseases, where we continue our preclinical research in order to come up with a strategy how to approach those rare kidney diseases in the clinic. We also see mid-term opportunities in other immune-mediated diseases because QPCTL inhibition has a major role in immune defense, inflammation, and fibrosis.

We have already data in-house for various compounds where we see improvement of metabolic-associated steatotic liver disease in a mouse model, we also see benefits in cardiovascular diseases in a mouse model, we see benefits in inflammatory bowel diseases in a mouse model and in septic arthritis, and even in an MS model. There is opportunities for QPCTL inhibitors much beyond what we are currently looking at diabetic kidney disease.

As a small company, of course, we need to keep the focus. We need to do first things first, and that is focusing on moving diabetic kidney disease forward, researching other rare kidney diseases, and then looking at a broader application: what can QPCTL inhibitors else do, and where are they unique, and what can they provide?

With that, I hand over to Marcus welcome fully to the team. You were always part of the team, but now you're on front stage, and, yeah, up to you.

Thank you very much, Frank. I will now walk you through the financial figures for the first 9 months of 2025.

Research and development expenses amounted to €3.7 million in the first 9 months of 2025 versus €12.6 million in the first 9 months of 2024. The reduction of €8.9 million was largely attributable to a decrease in clinical development costs from the VIVIAD and VIVAMIND studies, as well as a reduction in production costs.

R&D expenses in the reporting period mainly occurred for kidney-related research. We have seen a decrease in G&A expenses with costs of €4 million in the first 9 months of 2025 compared to €4.9 million in the same period last year.

The decrease was largely due to lower personnel costs resulting from a reduction in non-cash effective share-based payments. All of this resulted in a net loss for the first 9 months of 2025 of €7.6 million compared to €17.1 million for the first 9 months of 2024.

By the end of September 2025, the company held €2.5 million in cash and cash equivalents compared to €9.4 million at the end of 2024. As already mentioned, in October, we completed a private placement of new ordinary shares to selected investors with gross proceeds in the amount of €5.1 million.

Including the proceeds from this private placement, we now expect that existing cash and cash equivalents will be sufficient to fund our operating plans well into Q3 2026. Our spending plans continue to support the kidney disease strategy and the strengthening of our intellectual property position.

Furthermore, we continue to actively pursue strategic financing and partnership opportunities, primarily to fund planned Phase 2b study. Before we come up to the Q&A session, I would like to hand the call back to Julia for wrap-up.

Thank you, Marcus. As said, before we move into Q&A, I'd like to conclude with a few comments.

The kidney space is highly dynamic, but as Frank mentioned, despite recent advances in the field, there remains a substantial unmet need for therapies that can stabilize or even improve kidney function. Our lead program, varoglutamstat, is well positioned to address this gap.

We have compelling data from two Phase 2 studies in an elderly patient population, and new analysis demonstrates a consistent, beneficial effect in patients with impaired kidney function. Importantly, this profile is paired with convenient oral dosing and patent protection extending at least until 2044, making it a unique asset within a dynamic space.

Beyond the planned study to evaluate varoglutamstat in patients with diabetic kidney disease, we've also seen rising interest in our platform of oral small molecule QPCTL inhibitors for other indications. We will continue engaging actively with the scientific and investment communities, including at several upcoming international medical and investor conferences in the first quarter of 2026.

With that, we would like to open the Q&A session. [Rachia?]

?

Hiya. Thank you very much for taking my questions.

Just going back to the data you showed in terms of the patients with the lower baseline eGFR, I guess, can you tell us what their average eGFR was in that lower tercile of patients? Then, perhaps I'm misunderstanding, but I think you kind of confirmed it with your comments on the diabetic patients in the next slide, why was it that the decline in eGFR was less in the patients with impaired kidney function relative to the total population?

I would have thought, based on what you then said about the diabetic patients, that you would have expected a greater decline in the patients with more severe baseline disease. Then just when it comes to your discussions with potential partners, is the focus on the fact that you've shown this eGFR increase, is that what they want to see replicated in a Phase 2b, or is their general acceptance that a stabilization of eGFR will be considered good enough based on precedent so far?

Thank you.

Lucy, thank you for your question. The first one, I think we have to be a little bit in a dialogue because I didn't fully get it.

When we showed two data charts, and what I understood is, what is the baseline on the first chart, basically on the all patients, what is the baseline in the worst 33% tercile? That is written down in the chart, it's 72 ml.

The worst 33% patients of the all patients, independent of what type of disease, diabetics and non-diabetics, everything included, has 72 ml, whereas the all patients have 80. The worst 33 have 72 in average, all on the left side have 80.

That's an explanation. There's not a big difference in the mean of this, there's 8 ml difference, and you see that the effect is also very comparable between the two.

If you go down by 8 ml or 10 ml, you see the same effect. That's probably the explanation for the first chart which I showed with the two graphs.

Did I answer that question, and then we go to the diabetics one?

There wasn't a question about the diabetics. It was just more that when you looked at the decline in the placebo group, 1.85 in the patients with the worst kidney function, is actually less than the decline you saw in the overall population, and I would have thought you would have had a greater decline in the patients with the lower baseline eGFR, which is what we did see, I think, on the next chart, where you show that the patients with the lower baseline eGFR have a greater decline relative to those.

This is only the difference between 80 and 72. I would think it is a very similar population.

If you go in the worst 33% in the total population, you're very similar to the average, to an 80. There's not a big difference.

Of course, we can drive it more and more down, but if we drive it more and more down, let's say we take the last 20% of the total population, you basically land more or less in the diabetic population. This is why we then showed the diabetic population.

In the diabetic population, the difference, of course, is much bigger in the baseline, because the diabetic population, the total diabetic population in our studies has also a baseline of 80. The worst 50 have only 65, there's a 50% 15 ml difference.

The worst 20 have 55, there's a 25 ml difference. Here you can drive down the eGFR in the worst population quite a lot.

Then, of course, you see the placebo group really reacting. You also need to acknowledge that the placebo group in the worst 50 and 33 actually doesn't drop.

If you look at correspondingly the total population, look at the worst 33%, it's very similar to the total population. If you look it into diabetes, the worst 3 33%, it also only declines by 2.1, which is very similar to the total diabetic population.

That means only really bad patients with a baseline probably below 60 have a higher decline. That is in line with what you expect in the science.

Patients who have manifest diabetic kidney disorders like 3a and worse, they show the worst decline. This is what our data show in the placebo group, and this is why I think they're credible, and this is why we show those data.

Only by cutting the baseline a little bit by 8 ml, you do not worsen the population significantly. I think that's what you want to comment on, and I would say I agree.

By going from an 80 to a 72 mean eGFR, you don't change the population much, and you basically have a very similar picture. Only if you drive the eGFR down below 60, then you see, of course, a much higher placebo drop.

Then you see, comforting enough, the same effect size of our drug. I think these data are highly credible and predictive for the next study.

The reason why we did these data is actually to look on the translational value of this data for the new study, how much can current study data predict the outcome of a future study, and this is why we did it. Did I answer your question?

The first part. I think the data are consistent and in line with what you expect from clinic and science, and they're very consistent between diabetics and non-diabetics when you look at the 33 percentile, which you rightly have.

The question is, what do the partners say? What do companies want to see?

I think the attractiveness of our company is that we are best in class. Medically, you would say it's enough to stabilize patients fully.

If you don't see a decline anymore in average, that's the best outcome for the patient. An improvement by 3 or 4 ml, like we showed here in our graph, is neither feelable nor meaningful.

Whether you have 3 ml or 4 ml or 5 ml, nobody can feel a 5 ml or 3 ml eGFR improvement. In the terms of a best-in-class data set, that becomes relevant because you can, of course, promote it, and you can also see that this mechanism leads to a partial recovery of the kidney function.

That means that the anti-fibrotic and anti-inflammatory effect we see in the kidney actually translate into a better kidney function that the patient has before, and that again is relevant from a conceptual point of view. When you look at from a patient basis, you would say stabilization is good enough.

You look at from a mechanistic positioning of the drug, a best in class which can lead to a partial recover of the kidney function is a unique feature which I think is highly appreciated by everybody. That's a little bit of complicated answer on a simple question.

I'm sorry.

Got it. Thank you very much.

Are we doing more with the data? We're currently constantly working on the data, and this is not because we only have new ideas, but of course, we get external input.

Part of those analysis, of course, are requests from other parties, I would say, and of course, we want to share that with you in order to be very transparent where we are and what is the current state of discussion. There will be more analysis, I'm sure, because there will be more ideas what to do.

The second thing is, do we progress in the Phase 2b preparation? We have progressed in the sense that we have internally decided with which CRO we would go, but we don't disclose it, but we have done a CRO selection process, and we have also a synopsis, a fully fledged synopsis in-house for the study, and now it's a little bit the fine-tuning with third parties to that synopsis in order to execute it.

Great, thank you.

Good afternoon. Thanks for taking my questions.

Just going back to slide 9 where you show the participants with diabetes and reduced kidney function, is this kind of pattern of response do you think unique to varoglutamstat, or would you expect to see this kind of response across declining eGFR groups at baseline with SGLT2s, for instance? Thanks.

That's the first question.

That is a relatively easy answer. I think this is a completely unique situation that you can preserve kidney function independent on the severity of the pathophysiology or the disease progression.

We have seen that many drugs basically reduce the progression, but still there is progression of about 3 ml, 4 ml, that you go in these very progressive patients which have 4 ml, which is a typical decline of those progressive patients. It's nothing unheard of when you look in the literature.

In Stage 3 and 4, 4 ml is a typically observed eGFR progression per year. You look into what currently GLP-1s or SGLT2 do in this, there is probably a benefit of a milliliter or 1 and a half above the 4 ml.

They may decline 2 or 2 and a half. None of the drugs has ever shown to be above baseline or at baseline for a year or two, and this is of course 2 years' data.

These are not short-term data of 6 months. We show here data with a treatment duration up to 2 years, I think is very unique data set, and it comes to the best-in-class approach we are pursuing here.

Thank you. Then just on potential applications in orphan diseases, subject to financing, is the idea there that you could still proceed with a basket trial to kind of tease out which indications might be best suited?

Thanks.

I think is a very good question, and that's really also in our mind, and we haven't really made the decision whether the basket trial is the best solution or from our preclinical data we can pick one or two of the orphans where, from a mechanistic and preclinical perspective, the data set is the most compelling and the likelihood of success is the highest. We are like, shall we really go for a basket?

Basket study is, of course, attractive because you cover more indications, but the interpretability of the data sometimes is not so easy. Whereas if you say, look, we go for one or two, and we focus on those, you can, of course, make a much more precise study, and the interpretation and the value of the results usually are higher.

The guidance on how we come to the decision what kind of study we do will be delivered ongoing additional preclinical evaluation, which probably reach until the first or maybe the second quarter of next year, that's the current timeline, and I hope we are then in the situation to make a final recommendation and decision on how to move forward in the orphans. The data so far are very promising.

The mechanism seems to fit to a couple of orphan in renal disorders which are currently not in the center of the market hype. That some orphan kidney disease, there are many compounds currently either developed or already commercialized.

We're focusing on those where is very little or none, and we have a couple of really good, I would say, results and concepts there, and data, and then we will make this decision when we have the maturity of everything, and of course, we will share that.

Thanks very much.

Thank you for your ongoing interest and support. With clear progress and growing momentum in the kidney disease space, we remain firmly focused on driving the next stage of our growth.

We appreciate your time today and look forward to updating you again soon. Goodbye.