Good day, and thank you for standing by. Welcome to the Vivoryon Therapeutics 2024 first quarter results call. At this time, all participants are in listen-only mode. After the speaker's presentation, there will be a question-and-answer session. To ask a question during the session, you'll need to press star one and one on your telephone. You will then hear an automated message advising your hand is raised. To withdraw your question, please press star one and one again. Please be advised that today's conference is being recorded. I would now like to turn the conference over to your speaker, Anne Doering, CFO. Please go ahead.
Thank you, Roz. Good afternoon, and thank you for joining us today to discuss the company's first quarter of 2024 results and strategic update conference call. This morning, Vivoryon issued a press release reporting its first quarter 2024 financial results, and also importantly, released new data reinforcing our shift in strategic focus to kidney disease. The press release is posted on the company's website at www.vivoryon.com. 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 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. On the call with me today are Vivoryon's Chief Executive, Chief Executive Officer, Frank Weber, and Michael Schaeffer, our Chief Business Officer, who will be available for questions. We will begin today's call with opening remarks from me, then quickly move to Frank's discussion of Vivoryon's clinical updates on varoglutamstat, our lead asset, where he will speak about our promising data in kidney disease. After that, I will review the financial results for the first quarter of 2024 and conclude the call with an overview of our corporate outlook. Following the prepared remarks, we will host a Q&A session. First quarter has been an important quarter for Vivoryon as we continue to make progress towards our new strategic priorities in evaluating varoglutamstat for inflammatory and fibrotic diseases.
Building on the promising results we reported in the full year 2023 earnings, we are excited to share with you today that we have been able to substantiate the data set underlying our new focus for varoglutamstat in kidney disease. Further analysis of kidney data from our phase II-B VIVIAD study revealed a statistically significant effect on a prospectively defined kidney function endpoint, the estimated glomerular filtration rate, eGFR. In detail, recent findings confirmed strong kidney function data showing significant improvement in eGFR with varoglutamstat at 600 mg twice daily in elderly patients. Importantly, we see this effect in patients with risk factors for developing chronic kidney disease, such as type 2 diabetes or hypertension. This effect has also been observed across the range of different eGFR levels at baseline in the study.
Looking at varoglutamstat's mechanism of action, results from recent biomarker analysis support the anti-inflammatory effects of QPCT/L inhibition. In today's presentation, Frank will walk you through all key findings here, emphasizing the significance of what we have learned to date and how this informs our decisions as we evolve a development path for varoglutamstat in inflammatory and fibrotic diseases. As you know, unfortunately, the VIVIAD results in early AD reported in March were not what we had hoped for, with the study missing primary and secondary endpoints. Over the past weeks, we have continued our analysis and in line with previously reported data for other subgroups, have seen no consistent effect on cognition in a subgroup of patients with particularly high CSF drug exposure. We are now waiting for the VIVA-MIND top-line data, which we expect towards the end of 2024 to inform our next steps in AD.
I will now turn it over to Frank.
Thank you, Anne. Good afternoon, good morning, ladies and gentlemen. We will focus now on varoglutamstat study kidney disease and go to the next slide, please. I want to start with an overview of how kidney disease actually develop, what are the triggers of kidney disease, and that the common pathway of many sources of kidney disease go into inflammation and fibrosis. What that means is that if you have hypertension, or if you have type two diabetes, or you have dyslipidemia, or you have a genetic peptide alteration, at the end, the kidney reacts with inflammation and fibrosis, and that leads ultimately to a dysfunction of the organ, to a change of the glomerular membrane and the tubulus apparatus. In that cascade of inflammation of the kidney, CCL2, which is a cytokine, is a validated target.
That means if you reduce the inflammatory effect of CCL2 on the kidney, then you can improve kidney function. And this has been shown by a various number of different research projects, which show that CCL2 deficiency in a renovascular hypertension model can protect against chronic renal injury. You can block the CCL2 receptor experimentally in mice, in a diabetic nephropathy model, and you protect against diabetic nephropathy. And it's also shown that CCL2 concentrations in the plasma of patients with CKD are much higher than compared to control groups. So CCL2 is a cornerstone of progression of the kidney disease into a fibrotic inflammatory, and at the end stage, an end-stage kidney disease and failure process. Next slide, please.
On this pathobiology of kidney disease, there have been previous systematic experiments which show that a QC inhibitor preventing the transformation of CCL2 in its most potent form, pGlu- CCL2, can improve kidney function. There is a publication which shows this very nicely, and we see a dose-dependent effect of the reduction of pGlu- CCL2, which is the most potent cytokine here, on the upper graph. On the lower graph, you see correspondingly, an improvement of the protein secretion, measured as the typical parameter as a urinary albumin-creatinine ratio in the urine. So we can see two things in this experiment. One is an improvement of the biomarkers, so reduction of the pE-CCL2, and an improvement in kidney function, as here shown in the protein secretion.
That animal experimental data in the kidney on the next chart, we have explored systematically in the VIVIAD protocol. So we looked again at the same things. We looked at the biomarker of pGlu- CCL2 in the serum, and we looked prospectively at the kidney function as measured by the eGFR, triggered by this basic scientific and well-known and validated approach. Next chart. Now, I'm gonna go through some data and also some new data and data which have never been published, for any other molecule. And in this chart, we show, I think, the first time, really in the world, that a QC inhibitor can reduce pGlu-Abeta in the serum of patients. And what you see here is a change from baseline, shown in the box plot.
For the placebo group in orange, for the mid-dose group in pink, and then for the 600 milligram group, the high-dose group, in dark pink. That comes from our VIVIAD clinical study. You see that dose-dependent increase of pGlu- CCL2 in the serum can be observed, with highly significant, statistically significant differences in favor of the 600 milligram group, compared to both placebo and to 300 mg. These are values which are measured at week 48 and compared to baseline. So it's not a short-term reaction. That is something which can be observed also after one year of start of treatment. That resembles very well the data in the animals I've shown you before with the QPCT/L inhibitor, which also showed a clear reduction of pGlu- CCL2.
On the next chart, we show you the reduction of the eGFR, so the kidney function in the same population. So we look here at all patients of the VIVIAD study, and we see clearly an improvement of the varoglutamstat cohort compared to the placebo cohort. The placebo cohort drops in the eGFR, as expected by about 1.5 mL/min/year. And the varoglutamstat group shows an improvement above baseline and a significant improvement in comparison to placebo. And this here is a slope analysis. And to show what that means, on the right side, you find the display of the data and the slope over two years. And you see a widening curve over the time starting to separate nicely at week 24 and then continuing over the whole period of two years.
And that is simply an over time graphical representation of what you see on the left side as a bar chart. Moving forward, we have done now a series of validation and sensitivity analysis to be really certain that what we report today is true and robust and can be replicated with various methods. On this chart here, we show you a comparison of the MDRD formula and the CKD-EPI formula. Both formula are based on the creatinine value and measure the glomerular filtration rate. And these are the same values of creatinine, just calculated by two different formulas.
You see that the effect size and the trends that varoglutamstat improves over baseline and placebo worsens at baseline is seen and proven in both formulas, and the significance level and the effect size is very consistent and comparable, whatever formula you use to calculate the glomerular filtration rate. On the next chart, we show you another sensitivity analysis, because we wanted to see whether we see the same effect of improvement when we take cystatin C as a parameter to measure the glomerular filtration rate. There are two ways, two parameter, you can take creatinine, or you can take cystatin, or you can take the combination.
And we also did here a remeasurement of creatinine with a different tool, with a different instrument in the lab, to be sure that it is insensitive to the way you measured the creatinine. And what you can see here, and these are comparisons from baseline to week 24 and 48, comparing placebo and active, that the difference in glomerular filtration rate in favor of varoglutamstat over placebo grows from week 24 to 48, independent of the method. The effect size is slightly different, whether you look at cystatin C or you look at creatinine. It looks so that cystatin C has a little bit a higher effect size of creatinine, and you see that the initial MDRD estimation of the creatinine clearance, which is the one we published first, is the most conservative ones.
All CKD-EPI calculations, either with cystatin C, creatinine C, or CKD-EPI, are even giving higher treatment estimate and differences to placebo at both visits we measured here, week 24 and 48. As a summary, we can conclude that the results are highly consistent regarding effect size, statistical significance, and clinical relevance, using a diverse and validated set of methods to estimate the glomerular filtration rate. So we can say after these experiments, we are sure that the effect we observe is a true effect and not sensitive to methods which can be applied to measure glomerular filtration rate. Next slide, please. We have now go to the dose dependency of the effect. This is again, the slope analysis.
So here we look at slope over two years, and we can see that, 300 mg and 600 mg have different effects on the glomerular filtration rate. In patients with type 2 diabetes and hypertension, you see that, the effect size is better with the 600 mg than with the 300 mg. You also see that the overall effect size in patients with risk factors like type 2 diabetes and hypertension, is better than the overall population, meaning that if you are at risk for CKD, you profit more from varoglutamstat, or the kidney profits more from varoglutamstat, than if you would have no pathology. And on the right side, you can see the display over time.
So that is the same information, it's just not as a bar chart, but as a curve over time, so it could be understood and seen that the improvement is continuous over the period of 84 weeks we have displayed here and is significantly different. Next. In this bar chart, we compare the eGFR improvement at various baseline levels. So of course, we have in the VIVIAD study not selected patients based on their kidney function. We have selected them for their Alzheimer's disease. But some of the patients or many of the patients had already impairment of the kidney function. And here in that graph, we display that the benefit of varoglutamstat compared to placebo in the total population is very, very consistent, independent of baseline severity the patient has.
So patients with an eGFR of 30-59, per definition, are in the range of CKD 3. And there we see the same effect as in milder stages of chronic kidney disease, or in patients which actually have totally normal kidney function. So in other words, it can be concluded that the effect of varoglutamstat is consistent, independent of the glomerular filtration rate we could observe in the VIVIAD study. Next chart. Here I want to summarize the proof of concept we have achieved so far in kidney disease. And what I want to compare here is the preclinical data and the clinical data. And you see that in both settings, both in the animal setting as well as in the VIVIAD study setting, we can show a very nice dose-dependent reduction of pGlu-CCL2.
And for the kidney function, we can see the same thing. We can see in the animal, the dose-dependent improvement of kidney function, and we see the same thing in the human, the dose-dependent improvement of kidney function. And for safety, the same is true. The drug is very well tolerated in the animal, and it's also very well tolerated in the human, where we have no dose-limiting safety observations in the VIVIAD study. So the data between the animal and the human regarding kidney function and its safety are highly consistent. Next chart, please. Moving to where can varoglutamstat start to be developed and what is the market? Where does varoglutamstat fit in kidney disease?
First of all, we want to share with you the message that chronic kidney disease is a very frequent, growing disorder, which is of concern in many, many developed and industrial countries, but also in other countries in the world with a very high incidence. One of three adults with diabetes have CKD, and one of five with high blood pressure, so hypertension, have CKD. It's the third fastest growing cause of death. It's the fifth highest cause of life years lost. By 2040, it's growing from now; it's expected to grow as deeply. The treatment costs are extreme, specifically because when you have end-stage kidney disorder, dialysis and transplantation have very high annual costs, and that's the only way how you can prevent mortality.
Those costs, of course, would be better invested to prevent those disease stages than to maintain them in a stage of end-stage kidney disease. In other words, there is a high medical need to develop new medications which reduce the burden of disease in kidney disorders. Next chart. Patient selection is critical if you develop a drug for kidney disorders. The CKD is a slow, progressive disease over years, where you can measure the decline of kidney function by eGFR, and that is a regulatory and scientific parameter. The heat map I show on the left side shows that patients in stage 4, 3B, and 5, with a high albumin urine concentration or a urine albumin creatinine ratio, which is high, are at specific risk of developing end-stage kidney disease.
That is probably the population where a drug like varoglutamstat is best used when there is a risk that the patient develops to end-stage kidney disease and has a high degree of inflammatory and fibrotic cytokines moving the progression of the disorder. We are, of course, aware that there is lots of other drugs in development and already in therapeutic use for chronic kidney disease, but all approved, and probably also the major drugs under development only slow the progression of the disease in a certain population to a certain degree, but they do not stabilize the disease, and they show no improvement above baseline. So many patients still progress relentlessly to end-stage kidney disease and need transplant and dialysis. This is where we want to position varoglutamstat in future.
We believe that we can explore the effect in more severe stages in CKD in a smaller study to show all the needed evidence in that advanced patient group. If we want to move to the market, there is, of course, larger programs needed with two pivotal study of 1,500 patients together and, of course, two years of follow-up of each patient. These are the regulatory requirement for the pivotal studies in CKD. Next, slide shows that we have also options in kidney disorders, which are often diseases like Alport syndrome, which is a collagen genetic disorders which has a fibrotic and inflammatory component, and where there are no specific treatments are available for preventing end-stage kidney disease, which happen in many of these patients who have Alport syndrome.
There are about 150,000 patients only in US and Europe, and they have a high or at least moderate degree of kidney failure. In such an indication, of course, a phase II/3 study with about 180 patients probably can show. Can be considered pivotal and show robust efficacy and safety. I just want to remind you in that context that we have shown in the subgroup of patients with hypertension and type 2 diabetes, which are about half of our patients in VIVIAD, is around 130. We showed p-values of 0.001 for glomerular filtration rate, so a study size of 180 is probably realistic to show a benefit.
I want to end, or my second last chart, is to summarize where we are today for kidney function and kidney disorders. We are a first-in-class glutaminyl cyclase inhibitor, and we believe that we have very broad potential opportunities in CKD, including orphan diseases, but also CKD. We have promising proof-of-concept data, very consistent between animals and humans. We hold the full rights to those assets in Europe and U.S. We develop and try to identify follow-up compounds in preclinical development, and we now have a very extensive data set of phase I and phase II data showing the safety and the tolerance of varoglutamstat. I want to finish with where we are and where we want to go as a company.
Based on our robust statistical and consistent data, and the evidence of the dose response, and the effect across the whole baseline range of glomerular filtration rate and the safety data, the main clinical development goal and the next step is to show an effect size in stage 4 CKD and in orphan kidney disorders, to show a robust effect of albuminuria in humans. We have showed that in animals, but we haven't measured that in humans yet. We also want to show a sustained efficacy post-discontinuation of the treatment, so if a patient stops the treatment, that he still has sustained benefit. And of course, we want to show that the event rate of end-stage renal disease has been reduced.
And we are also considering a supportive package with further additional biomarker analysis and investigation of the mechanism of action in a specific target indication, like Alport and later stage of CKD. With this, I want to turn over to Anne for the financial results and the closing remarks. Thank you.
Thanks, Frank. Let me take you through the key figures for the period. We didn't record any revenues in the first quarter of 2024, nor in the same period in the prior year. R&D expenses in the first quarter amounted to EUR 7.4 million, versus EUR 3.1 million in the first quarter of 2023. This increase of EUR 4.3 million was largely attributable to the increase in clinical costs from the VIVIAD and VIVA-MIND study. We have also seen a slight increase in G&A expenses, with costs of EUR 2.1 million in the first quarter of 2024, compared to EUR 1.9 million in the first quarter of 2023. This EUR 0.2 million increase was largely due to higher expenses for share-based payments, as well as legal and consulting fees.
All of this resulted in a net loss for the first quarter of 2024 of EUR 9.3 million, compared to EUR 5.1 million in the first quarter of 2023. The company held EUR 22.2 million in cash and cash equivalents as of March 31, 2024, compared to EUR 28.6 million, which includes cash and cash equivalents and financial assets as of December 31, 2023. As we highlighted at our full year results a few weeks ago, we have maintained prudent resource allocation on VIVIAD activities, and these will be ramping down as it approaches its conclusion. We are discontinuing VIVA-MIND in the second half of 2024 and stopping the VIVALONG preparation activity, as well as streamlining manufacturing and API development costs.
These measures reflect an overall reduction of cash utilization that extends our cash runway into the second quarter of 2025. Further funding and our partnerships would, of course, be required to support potential additional clinical studies and/or to extend our cash runway beyond the second quarter of 2025. I would like to now wrap up with our strategic priorities. You know, we are very excited about the strong kidney data we have presented to you today. The data reinforce our strategic shift to focus on kidney diseases, and we see this as a further step towards securing the company's future. We have three areas of activities ahead for us. Most importantly, we will be pursuing an actionable plan to establish our presence in kidney disease.
We have gotten this far due to the rigorous scientific research in the field of QPCT/L inhibition, despite the Alzheimer's disease setback, which has been laying the foundation for this opportunity in kidney disease. We have outlined for you today potential clinical development paths in kidney disease and will decide on the most effective path to move forward with, sharpening those clinical stage plans in chronic kidney disease and/or in orphan kidney diseases, and continuing to enhance the dataset. Also important, we are already active in building our presence with the scientific and medical advisors in the nephrology community. We have an active dialogue with key opinion leaders in the field.... Although kidney disease is of utmost priority for us, we don't want to lose sight of our Alzheimer's disease program.
We plan to complete the phase II program, discontinuing the VIVA-MIND study in the second half of this year, as announced in April, from which we expect to have top-line data towards the end of 2024 to inform next steps in AD. In order to support our strategy, we will continue to actively pursue funding and business development opportunities that align with our objectives. Our prudent cash runway ensures financial sustainability, maintaining our cash runway into the second quarter of 2025, and we have a highly dedicated team in place to drive this transformation for the company. We look forward to keeping you updated on our progress as we continue to move forward with our strategy. With that, we will now open the call to take questions.
Thank you. As a reminder, to ask a question, please press star one and one on your telephone and wait for your name to be announced. To withdraw your question, please press star one and one again. Once again, please press star one and one and wait for your name to be announced to register for questions. Thank you. We are now going to proceed with our first question. The questions come from the line of Luisa Morgado from Van Lanschot Kempen. Please ask your question. Your line is open.
Hi, team. First of all, many congrats on these results. Very exciting to see and explore a bit more. My first question is, as Anne just mentioned, you've been having some discussions with KOLs. I wanted to know, what is their feedback on these results in kidney function?
KOL.
Yeah, of course, we started disseminating the data, and I would say very excited. Surprised that that can be shown, and because the world hasn't seen such a thing so often, actually, very rarely if at all. And it's also a new mechanism of action in kidney disease, which, which KOLs are not really yet fully aware. So we will continue dissemination of that novelty and innovation, but the effect size are clearly clinically meaningful, and highly appreciated.
Very clear. And maybe, a few questions, questions packaged into one. In terms of your current cash running, how far does that take you into, the research into kidney disease? And you've mentioned perhaps going into CKD or rare diseases. Is there any of the two that you are more inclined to? And what magnitude of financing do you, estimate, if you estimate anything at this point, that you would need to proceed with the, with one of the two directions?
Well, there is really many questions in one.
Yeah, sorry.
So first of all, we have not finally defined our development pathway. We know that we have very good options, both in CKD and in rare diseases, but we have not finalized our program and decided definitely where we go first and second. The second is that our cash runway, the current cash is going into the second quarter of 2025, but already the timelines are not sufficient to start and conclude a new clinical study in that period. So we cannot start new clinical studies with the current cash. We would need additional financing for this.
Okay, makes sense.
We will continue research activities and some-
Yeah
mechanistic and profiling activities. I think not so many are needed because the evidence level currently is already very high, so, we can do some more supportive activities. But, of course, the next big step is a clinical trial.
Makes sense. And when do you expect to share more information on which path you're taking?
Yeah, I mean, this is a very good question as well. I think this should be done within the next, yeah, I would say, several weeks to probably up to three months, we should be able to come up with a clearer development outline. The situation is here that, of course, any clinical trial we would conduct is dependent on the amount of money we have available, and the more money you have, the bigger the study gets, and the more you can do. So, it's dependent also on the financial resources we can generate for moving forward.
Okay, makes sense. Maybe one final question. You mentioned perhaps partnering. What would be the right partner in this indication? So which, let's say, characteristics would you be looking for to be able to have a partnership there?
I think we don't want to comment on specific partners right now, and I think we should not speculate too much. But partnership arrangement with other pharma companies or other institutions, in our situations, of course, a pathway we evaluate. But we cannot go at that stage much further and want to share things which are not facts, but speculation. So, be a little bit short on this question, please.
Okay. Thank you for taking my question. That's all.
We are now going to proceed with our next question. The question's come from Lucy Codrington from Jefferies. Please ask your question.
Hi there. Thanks for taking my question. So just again, on that, the strategy, again, I've not been fully decided yet, but if your additional work supports going down the orphan route, would this be something you would like to do alone? Or ideally, would you seek a partner regardless of if you went down the orphan versus CKD stage four route? And what else do you think you need to show in order to get a partner, and can this be done with current cash? And then, I guess, just on the basis of deciding between the two, given the different pricing between an orphan versus a general kidney route, you know, it seems like you need to choose one or the other, and it's not a case of being able to keep one and partner out the other.
Are there any backup compounds that potentially could be used for, for instance, Alport syndrome, that then still enable you to pursue a wider kidney use? And then, apologies if I've missed this, have you now abandoned the thought on potentially there still being a route forward in Alzheimer's with a higher dose, and the focus is now purely kidney, or is there still that hope? Thank you.
Well, I'll start with the Alzheimer's, that I can remember. So we still have VIVA-MIND ongoing, and we expect VIVA-MIND's top line data in the fourth quarter this year. And the dose in VIVA-MIND is 600 mg, so it's identical to the higher dose in VIVIAD. But the endpoints are... the population is comparable, but the endpoints are different. So that study, of course, has not been completed. It has been prematurely stopped due to the VIVIAD results, but nevertheless, we need to look at the data. What we have communicated today is that we looked in a subgroup of patients, which have a higher CSF drug concentration.
So from all the patients who got VIVIAD, well, varoglutamstat, we could identify a set of a little bit about 30 patients, where the concentration in the concentration of the drug in the CSF, which we measured, was higher than in the average patient. And we looked whether we could see a treatment signal in cognition or in EEG there, but that was not the case. So that is what we communicated today. So there is no current plans to go back to 800 mg. Of course, we wait for VIVA-MIND data, and then we make, of course, some more, what I call PK/PDs or pharmacokinetic pharmacodynamic calculations. And then see what we can do in Alzheimer's.
But the primary focus going back is now kidney, because we have seen the benefit of the drug in an endpoint, which is a primary endpoint for kidney development. So that is very good. So we have basically shown the effect over two years on the final endpoint of kidney, and that is, for us, it's a huge gain, quantum leap. Now, the question is, given the potential drug price difference between orphan and CKD, would you not be better in orphan than in CKD and then go with a follow-up compound? That is also one of our thoughts. Nevertheless, there is also a population in CKD 4 with high albuminuria. So these are the patients who have a very high urinary albumin-creatinine ratio, which lose a lot of protein, who are at very high risk of end-stage kidney disease.
If you select such a population, you can think about in two years, probably one quarter to one fifth of the patient going to either transplantation or to dialysis. In such a, let us say, high risk, high medical need population, probably you could also go in parallel. The price probably would not be identical you get, but is, not far away. If you would position the drug in, let us say CKD 3, of course, there you compete, with a lot of other drugs, and, probably the ability to have a price like an orphan is, is not, is not feasible. Also, because the population is, is huge with CKD 3. It's about, I think it's about, tenfold higher in CKD 3 than in CKD 4.
So that's what the epidemiology tells you. So, yeah, how do we make decisions? I think decisions need to be made based on science, on the mechanism of action, on the evidence, on the feasibility, on the having the best opportunity for the drug to work, and we are still trying to fine-tune the program in this respect. We are just 2.5 months after AD results in VIVIAD, and we are probably only less than two months away from the kidney data, the first, or even six weeks only. So we need probably another couple of weeks to come to a valid conclusion on this.
Okay, thank you.
Thank you. We are now going to proceed with our next question. The questions come from the line of Joseph Hedden from Rx Securities. Please ask your question.
Good afternoon, and thanks for taking my question. You speak about QPCT/L inhibition as being a first-in-class approach in kidney diseases, obviously. But in terms of other ways to modulate CCL2, CCR2, is there anything in the clinic or any program that has been before that has you know attempted to modulate this axis to treat kidney diseases? Could you give me information?
There have been antibodies before. There have also been dimerization inhibition approaches, which are still under development by some companies. There is other pathways to interact with the CCR2 pathway. I think the strength of our data is that we clearly show that the pGlu-CCL2, which is a much more potent, much more degradation-resistant molecule, can be reduced with our drug. And the same is true for fractalkine, which was also a pGlu version, and there are some other cytokines which come in the pGlu version. So I think, regarding the approach and the mechanism, we don't fear really competition. I don't think there is a problem in terms of somebody else goes into the CCR2 and, you know, takes the market. This is... Yeah, we don't see this.
Okay, thanks very much.
As a reminder, to ask a question, please press star one and one on your telephone and wait for your name to be announced. Once again, it's star one and one for any questions. Thank you. We are now going to proceed with our next question. The questions come from the line of Christian Ehmann from Warburg Research. Please ask a question. Your line is open.
Hello, and thanks for taking my question. I'm looking at the graph on slide 13, and regarding the patient population with the higher amount of risk factors compared to the overall population. That looks like a little bit that the effect you have in the beginning is actually quite strong until week 30, 36, and then kind of collapses downwards towards more baseline development, which is similar to what we see in pre and middle grounds. So I was wondering if you could share anything regarding potential patient stratification you thought about as a preparation and any more details you'd like to go for. I appreciate the fact that you want to go for a stage 4 chronic kidney disease, but any more color on this would be really helpful.
My second one would be regarding potentially surrogate data you have for the impact of your drug on any inflammatory biomarkers. Thank you.
So, regarding the slide 13, I have to say I not fully share your analysis of the data. We put in the various data measurement points, and you see, of course, a peak at week 36. But if you would just ignore that one, it steadily still goes upwards and the other goes downwards. When you look at eGFR data over time, and we have here 250 patients overall, this is a very low fluctuating number for 258 patients. And the p- value of 0.001 tells you that the data are extremely robust for the slope. I think there haven't been a study at that size which has shown more robust statistical values for eGFR and more consistent data points at each visit than this one. eGFR is a fluctuating parameter.
I mean, it changes, let's say, from day to day, but it's fluctuating depending on what you eat. Specifically, if you need to create a need, it depends on your muscle mass. It is not a very stable parameter in a patient. And I think this, and this is why we show these dots, it's probably a realistic and actually very good trajectory. And you see at no time point, we cross the line, which can happen, which could happen theoretically due to the fluctuation, but it never happened. So, from that point of view, actually, we are very comfortable that it develops this way. We're also very comfortable that we see a cystatin C and a remeasurement of creatinine and take another formula, the results even look better.
So that's the most conservative display of our data. We can have from all what we had. We didn't select the best, we select the one we initially defined, which is the most conservative one. Regarding the color, patient selection is extremely important when you run or when you for every clinical trial, but for kidney, even more. And, of course, we want to select patients on their clinical phenotype of their, for their risk of progression, and end-stage kidney disease. Those are usually defined by their baseline level of eGFR, and usually, you should go below 60, and CKD, probably you go below 30. In Alport, you probably go a little bit higher, and then you look at the progression rate.
A good surrogate for the progression rate, as I said before, is the degree of albuminuria. This patient lose a lot of protein subsequent to tubular dysfunction and reabsorption problem, and of course, a higher filtration. Normally, you don't. You always filtrate some proteins, but you reabsorb them. If you have a kidney disease, you can reabsorb them, and you lose them through the urine, and you can measure that. And the higher your protein loss in the urine is, the higher is your likelihood that you progress. Of course, we work on additional biomarker and targeted approaches, but that is subject, first of all, to further analysis, and second, of potential patent filings. And so I cannot be very explicit on this, but a targeted therapy, of course, would be an additional advantage in that setting.
I agree if you meant that. So I cannot be more precise here, but we are working on that. I cannot guarantee success for that, but we're working, trying to nail down and further narrow down the population where our drug works best.
Okay, thank you very much.
So with that, no further question?
We have no further questions at this time, so I'll hand back to Mr. Frank Weber for closing remarks. Thank you.
Oh, thank you for your continued interest in Vivoryon. I hope we have answered and clarified where we are. As a clinical stage biotech company now with a validated endpoint in patients, we are looking forward to further develop the assets, and we thank you for your attention. Goodbye.
This concludes today's conference call. Thank you all for participating. You may now disconnect your lines.