Hello, everyone. I'm Sten Sörensen, and I'm the CEO of Cereno Scientific. Welcome to this webcast, which highlights our top-line results of our lead drug in development, the HDAC inhibitor CS1, for the lethal disease, pulmonary arterial hypertension. So the focus of Cereno, we are passionate about developing new drugs that can improve quality of life, and if possible, extend life expectancy. So those affected by cardiovascular disease will have the ability to play with their grandkids or live a fine life despite that they have been diagnosed with disease. Next, please. Today, on this webcast, I will be joined by Dr. Rahul Agrawal, who's Chief Medical Officer and Head of R&D, our Chief Scientific Officer, Dr. Björn Dahlöf, and our Head of Preclinical Development, Nicholas Oakes. We will all share a few slides with you over one and a half hour, and approximately, and at the end of that period, we'll have a few questions that we have received from the audience, and we expect the analyst perhaps to pose one or two questions that we'll do our best to answer for you. Next. So a few words about Cereno Scientific. The company was founded in 2012, and we believe we are pioneering the epigenetic modulation through HDAC inhibition for cardiovascular diseases with a disease-modifying potential. We have two programs with HDAC inhibitor, of which we will focus on our lead program, CS1, today, where we have completed the phase II trial in PH, which has been run in the U.S. at 10 clinics. We will also refer to our second program, CS014, and some data that are very exciting for our programs, as we move forward. Our pipeline is actually three programs, so the second program, CS014, is currently in a phase I trial being run in Sweden, and we expect that trial to be done by summer next year. The third program we have is a novel preclinical prostacyclin receptor agonist, CS585, that we have licensed in from University of Michigan, with whom we've had a collaboration effort going on for four years. We're listed on Nasdaq First North Growth Market. Next, please. So looking at our portfolio, of course, as a biotech, we'd like for first and foremost, that our ambitions and hard work will result in a benefit for the patients. But the road to that benefit to the market and to the patient, sometimes it will be done through collaborations, co-developments, or even trade sales of our assets to partners in the industry. So we are developing our drugs, our three development programs, to be attractive for not only the patients, but also for collaborative partners. So if you look at our portfolio here to the right, we have a PH program, which we will focus on today with our lead drug, CS1, but we also then have a portfolio with our two programs, CS014 and CS1. In addition, we have a thrombosis prevention portfolio, where we have seen that we can prevent thrombosis without increasing bleeding risk in our animal work that has been pursued at University of Michigan on both drugs. Thrombosis is the number one killer in the world, and bleeding is a very strong unmet need on that market. Next, please. So what are the latest news? You probably, if you're in this webcast, you have seen the latest press releases. I just want to reflect on those. So in our program, in PH, in phase II, we have actually applied and gotten approval from the FDA for expanded access program of CS1 in PH patients that have completed the trial with CS1 that we just have completed. So this provides the opportunity for patients to get access to the drug way before it is introduced to the market. The judgment here by physicians in the trial and by patients willing to participate is that they have seen some benefits already in this trial and don't want to wait to get hold of the drug. We feel that that's a very strong signal that there's something positive going on with the drug in these patients, that the both the physician and the patient experience. That program was approved 30th of January, and the first patient was just dosed, and we communicated that recently. Another finding here that we have communicated from our HDAC inhibitor program is on our second development program, CS014. Last week, we released a communication that we have been documenting that this HDAC inhibitor has had a dose-dependent impact on the very dangerous changes in the pulmonary artery vessels. And we will hear more about that today by the head of those programs, Nicholas Oakes. That result, we feel, is underpinning our whole effort in this program towards the root cause in cardiovascular disease, not only PH, but specifically PH in this case. In addition, of course, Friday evening, 8:40 P.M., we released a positive top-line results of our lead program, CS1, and we will of course focus on that today. This morning, on the back of our findings, our scientific platform, I should say, supporting the whole ambition into PH with HDAC inhibitors, and then the findings in the CS014 trial, and of course, the top-line results, we communicated that we have signed a partnership program together with Fluidda, a cutting-edge and a world leader specialist on being able to visualize the reverse remodeling that could take place in arteries with our drug. We are very much looking forward to see the impact in the clinical setting from that microscope perspective, so to speak. This morning, we also communicated that we will hold a Capital Markets Day on October 17th, so a couple of weeks from now, and in Stockholm, that will also be webcast. And then, there, we will spend three hours together, and there will be more ample time to answer questions and elaborate on those. We will have guest speakers at that conference that you would be enlightened to hear more about our programs, what we've seen in the future. Next, please. Let's focus now on our PH program and the top-line results. Next, please. This program is phase IIa program. The primary endpoint in such a program is safety and tolerability. Your drug is safe and well-tolerable in a patient population, and that was met successfully in our trial. We met our primary endpoint. Another objective that we had with this trial was to harvest signals of efficacy, and we have seen very interesting data, and we're excited about those. We have seen a 45% improvement in REVEAL Risk Score, and 71% of the patients were both improved or stable. With regards to functional class, we saw 33%, of the patients improved, and 86% of the patients were improved or stable. With regards to a hemodynamic parameter, a pulmonary arterial pressure, in this case, mean, as measured by CardioMEMS, we saw that 67% of the patients had a sustained pressure reduction at the end of the period, which was twelve weeks. Now, CS1 study data here, together with the preclinical information that we have on HDAC inhibitors, specifically our active compound, VPA, and then now CS014, are consistent with the reversing pathological remodeling that we aim to achieve with our drug. So, based on these results, we believe we have a clear path forward. We will engage with regulatory authorities to pursue a pivotal trial, which will likely be a phase IIb/III trial, three trial. Next, please. So let's look at the agenda, and you can see we have a few points to cover. And this, again, will be fast, perhaps, but we would like to do this for you so you get more information before the Capital Markets Day already. So let's move on. So this study, the phase IIa trial, had as an ambition to recruit 30 patients and study them over twelve weeks. And in June 2028, we communicated that a decision has been made to close patient recruitment for this trial, which was done on July first. The steering committee had recommended Cereno to do so, as we believed that we had enough information from the trial to move on with the next steps of our development program. This resulted in 25 patients randomized and 21 patients analyzed for efficacy. We'll get to those numbers specifically later in the presentation, but this is the background. Next, please. Again, back to the results of the trial. Primary endpoint of safety and tolerability were met successfully. What does that mean? We had good safety and tolerability profile. No CS1-related serious adverse events, including hospitalization and mortality. No CS1-related changes in liver lab values, and no CS1-related clinically significant drug-related platelets decrease or bleedings. If we move on to tolerability, CS1 was well tolerated in the study. We'll get to more detail later on in the presentation. Next. With regards to the secondary ambition of this trial, let's look at the three main impacts that we've had in this trial, and has communicated this far. So REVEAL Risk Score, we have an improvement in nine of 21 patients. Seventy-one percent, or 15 out of 21, were improved or stable. And we will get into what does it mean to improve Risk Score? It has implications. If you're able to do that, you're doing something good for the patients, specifically when it comes to risk for the future. Now, Functional Class, we had seven out of 21 patients improved Functional Class, and 18 out of 21 stayed in their class or improved. What does that mean? Functional class is how the patient actually has physical capacity to live, and we'll get into this, and I think Rahul Agrawal will, you know, explain more what that means as we move on. Those two important parameters, REVEAL risk score and functional class, we saw quite some improvement here or stability. If we move on to a specific parameter of hemodynamics, we saw that 14 out of 21, or 67% of the patients, had a sustained pressure reduction at the end or over the period of the trial, which was 12 weeks, and this as measured by the CardioMEMS technology, which we have implanted in these patients in a collaboration effort with Abbott, who owns the technology. Very good results for us, we believe. Let's move on. Now, let's go into pulmonary arterial hypertension. It's a progressive, debilitating, and fatal disease. No spontaneous improvement. That's important to note. It's one road downhill until these patients, after seven and a half year, mean will not survive the trial, the disease. There is no cure except for lung transplantation today. Let's move on. Looking at this, so you have a healthy patient in the animation to the right. You have a healthy lung, then this patient is experiencing a pathological vascular remodeling, so the pulmonary arteries are getting more narrow, and then that creates a higher pressure in these arteries, and it's difficult for the heart to pump, so life expectancy before therapy, standard of care today, was two and a half years only. Now, with therapy, standard of care, all therapy there is seven and a half years. None of the current drugs are actually addressing the root cause of the disease in any effective way. Next, please. So what happens is that you have a healthy vessel, this is pulmonary artery, and when you get early stage, it's more narrow, and then the disease progresses, and you get a very narrow lumen and a high pressure. And if you look to the right here, the pathophysiology goes through endothelial dysfunction, inflammation, fibrosis, which causes these vessels to be less compliant or flexible, and some plexiform lesions appear, and then you have vasoconstriction, you have vascular and right ventricle, or right heart hypertrophy. And the clinical consequence of this is that the risk score and functional class in these patients deteriorates. Next, please. I should say that HDAC drive this development. Now, PH management goals is, of course, to improve the risk score measured by REVEAL, is to improve symptoms and physical capacity as measured by functional class, and it's to improve hemodynamics as measured by pulmonary pressure and other measures. So CS1, our lead drug, aims to reach the management goals by reversing pathological remodeling and achieve the goals above. Next. So more specifically, risk or status you'd like to improve. You'd like to improve the functional class. If possible, then, of course, hemodynamics. Often, the key parameter here is pulmonary vascular resistance, which makes it difficult for blood to flow and for the right heart to pump, and the mean pulmonary arterial pressure in those vessels to go down. You'd like to improve right ventricular function, and if you achieve these, you will extend survival in these patients. Next. The key unmet needs is that no drugs really address the root cause of the disease. You would like to introduce that to the patients, and you would like to do so with the safe and more tolerable treatments that are currently on the market. CS1, our lead drug, aims to address these needs. Next. What's the scientific rationale for conducting phase IIa trial? There is preclinical data. Epigenetic modulation through HDAC inhibition provides an attractive proposition to address the root cause of PH. Documentation of prevention and reversal of pathological remodeling and documentation of pulmonary arterial pressure reduction, all of this exists. Next. HDAC inhibition has the capacity and the characteristics to reverse pathological remodeling. It is an antifibrotic, it is anti-inflammatory, it's been documented to reduce pulmonary pressure, and it's a, is an antithrombotic without increased bleeding risk. Now, the majority of the data which is published has been published in The Lancet Healthy Longevity in a review article with the 100 most important articles behind this scientific platform, Next,so back here to what we would like to do and believe we are doing with our drug, the HDAC inhibitor CS1. You can see here the progression I showed before, and you see the blue line going back, so you'd like to prevent deterioration and then reverse this disease, so with the objective to improve the risk score and functional class, and this would be done by the parameters to the right, the characteristics of the drug that's already published. Looking at published data on our active ingredient, VPA, you can see to the left here two graphs that has documented that you both can prevent and reverse the medial wall thickness in animals, in rats, in PH model, and it's also measured here as vascular occlusive score, and this compared to control. And if you look to the right, the first graph, it's also been documented here that you can reduce the mean pulmonary arterial pressure in these models. Next. Now, what you'd like to do, again, if you look to the right, the goal, the clinical goal of therapy is to improve the risk or improvement of the functional class. If you could prevent progression, which is the middle here, you would stop the deterioration of these patients, and that will make them have a better quality of life and live longer. If possible, you'd like to reverse the pathological remodeling like was seen in the animal work. Next. So by that, introduction, I'd like to introduce our Head of R&D and Chief Medical Officer, Dr. Rahul Agrawal. Please. Thank you very much, Sten. Allow me to go into a few details of the design and the goals of it to put things into perspective. I would like to go, of course, first into the primary endpoint of safety and tolerability. You already heard the very good results we have had in that we have met the primary endpoint. I'd like to briefly go also into to explore the efficacy parameters and the signals of reverse remodeling, what we took, why it is important, and of course, looking at these two, and you have already heard about the good results we have, we are preparing to pursue a pivotal trial in collaboration with the regulatory authorities, the FDA and EMA. You're all aware of the phase IIa trial design. The primary endpoint was safety and tolerability, which we have successfully met. We had also, of course, introduced exploratory endpoints like the validated risk score. I'll go into more detail in there, functional class, and hemodynamics. For the hemodynamics, we used a very innovative method, CardioMEMS, which will allow a continuous measurement of hemodynamic parameters. I'll go into more detail there as well. Initially, we had planned for 30 patients, but as you heard from Sten, at the evaluation of the Clinical Steering Committee, we stopped the trial at 25 patients at 10 U.S. clinical sites. We had three dosages of 480, 960, and 1,920 milligrams. But because, of course, due to the small size of the study, we pooled the data, and number two, we also pooled it because our PK/PD, PD data indicated that we had already reached, at the lowest dosage, the maximum efficacious exposure.p Our treatment period, and please keep that in mind, was twelve weeks. Many of the studies in PH, phase III trials later on, were twenty-four weeks, so please look at it in that perspective. All in all, as we had said, we have twenty-five randomized patients. That means twenty-five patients are used for the safety analysis. For the efficacy parameters, we have used twenty-one patients. It is called per protocol. That's a technical word. What does that mean? That means, all in all, we had twenty-five patients in the trial. However, four patients did not complete the trial. There were three of them were early terminated, and one had a protocol deviation, but none of it was study drug related. One patient withdrew consent. One patient had sepsis, that is a inflammation practically of the body and of blood, so that was unrelated to the drug. A third one had symptoms for which they withdrew, and as you know, these patients are multimorbid. They take many drugs, and it was unspecific reasons for that. A fourth patient had to be excluded because of protocol deviation, as that patient was taking certain medications that were not allowed. So all in all, 25 patients were randomized, and we have used that for the safety analysis, 21 for the efficacy analyses, but the four that had to be excluded were not out of drug-related reasons. This is the baseline, if I may just briefly show. It is very representative of the PH population. We had a distribution of nearly 75% were female. We had a good race distribution. Most of the patients were, and that was inclusion criteria, in Functional Class II, 40%, and Class III, the rest, that is 60%. Allow me to briefly go into the details and also the importance of it. As you heard already from Sten, we're delighted to share that we have met the primary endpoint successfully, and we have a good safety and tolerability profile. If you look at the primary endpoint, we did not have a single drug-related serious adverse event, which you see on the highlighted gray box, which is, again, a very good news. Regarding the safety, further safety, and tolerability profile, we did not see any CS1-related serious adverse events, including hospitalizations or mortality. We did not see any CS1-related changes in liver lab values, and we did not see any CS1-related clinically significant drug-related platelet decreases or bleedings, something which, of course, everyone looks at. All in all, CS1 was well-tolerated. Let us now turn our focus to the exploratory efficacy data, and I'd like to go into three areas, which already Sten has mentioned. First of all, reduction in the REVEAL Risk Score, improvement in functional class, and reduction in a hemodynamic parameter. That is the mean pulmonary arterial pressure measured with CardioMEMS from Abbott, who we have a close collaboration with, and there we measured area under the curve, which is AUC. Let us start with the REVEAL Risk Score. There are several risk scores, but the REVEAL score has shown to have the highest prognostic power. The author of this REVEAL score is also our principal investigator, Professor Dr. Benza. Here, these data have been published. One can see that depending on in which risk group one is, the mortality, morbidity is very high already within 12 months. Something which I would like to draw your attention to is, number one, that the REVEAL Risk Score includes all the various aspects that are important in the diagnosis and treatment of PH patients, like, which functional class they are, what are the comorbidities, vital signs. Six-minute walk test is also included in the REVEAL Risk Score. Of course, lab values, imaging values, function test, and invasive hemodynamic parameters, like the right heart catheterization, which we also had. Second thing which I would like to direct your attention to is the blue box on the right, that if one can have a one-point reduction in the risk score in 12 weeks, that is associated already with a 23% reduction of mortality at 12 months. I'd like to come back to this point on the next slide. What did we see? We saw that in the REVEAL Risk Score, keeping in mind that this is a progressive, debilitating disease where patients have no spontaneous improvement, we saw that 43% had an improvement in the REVEAL Risk Score. That means at least one point increase, and 29%, that means 29% were stable, so all in all, over 70% had either an improvement or stabilization of the REVEAL Risk Score. To put that into perspective, what I was saying on the last slide, a one-point reduction in risk score within 12 weeks, and our study was for 12 weeks, this is associated with a 23% reduction in relative risk of death at 12 months. These are very promising signs that we are doing something good here, taking the REVEAL Risk S core, which encompasses a lot of the aspects in the diagnosis and treatment of PH patients. If we look at another aspect, we've looked at the REVEAL Risk Score. How about the ability to move for the patients, which is functional class? On the right-hand side, you see the criteria for functional class. Class one is when they have no complaints at rest. Class four is they're bedridden. Class two is that there is mild complaint at movements and activity, and class three is they have marked or severe complaints at activity. So the goal is to improve the functional class. Practically, we had included two and three, so to improve it by at least one class, which would be lovely. What we see is that we had 33%, that is 7 out of 21, of an improvement of functional class. And we had, all in all, 86%, that means 18 out of 21, which either improved or were stable in their functional class. Please keep in mind again, that it's a progressive disease where there's actually no spontaneous improvement. So this is, again, a very promising sign. And functional class, of course, affects the daily activity of the patients. The more they can move, the better they feel. So this is, of course, also something very important which should be considered. Allow me maybe then to go into the hemodynamics, but before I do that in detail, I would just briefly like to tell you how we measured it. So what we did is we used CardioMEMS in close collaboration with Abbott. CardioMEMS is a device which permits daily non-invasive monitoring of the pulmonary artery pressure. It does it in that it measures it on a daily level, and then one can, in a wireless method, just, call that off. The patients have a device through lying on a certain mat, one can record it, and then build, of course, a area under the curve, because usually what one does is for 20 seconds, the patients lie on the mat. That is taken as an average, and since our trial was for 12 weeks, we have approximately 85 measurements of these. So we have all in all, over 1,500 measurements per patient, which is a lot of data, which is objective data that we have collected of these patients. And what did we get there? Sten already mentioned that briefly. We have sustained reduction of mean pulmonary artery pressure, mPAP, area under the curve, AUC, in two-thirds of the patients, that means 14 out of 21. You can see on the left-hand side of your screen, the bars that are going down, that means there's a reduction of mean pulmonary artery pressure. What does that mean? That means with the lowering of pulmonary artery pressure, the heart has sort of a less effort to work against it. This is a good sign. You see in the middle, a green bar, and that is actually the patient that we had reported approximately one year ago, the remarkable patient case. That patient had shown already a very impressive reduction in mPAP, but you can see that there were many other patients who also had even a more pronounced mean pulmonary artery pressure. Allow me to briefly just show you what that means on this slide. On the left-hand side, on the Y-axis, you see the units, which is mean pulmonary arterial pressure, area under the curve, days one to eighty-five. What we have done is we have put these all together, and then you see the number of minus four hundred, minus two hundred. What you have to do to compare to others is then divide this by eighty-five. What does that mean? That means the special patient, the remarkable patient that we had, which is the green bar, had approximately a reduction of around two and a half, three millimeters of mercury, and it goes up to five millimeters mercury. What does that mean? I'd like to put that into perspective and show you another independent trial, which was looking at the pulmonary arterial diastolic pressure, which is similar, not exact the same thing, but similar, and here it was deemed that this is an independent predictor of mortality. If I may divert your attention to the left-hand side, where you see on the black bars, which are going downwards, if one reduces the mean pulmonary arterial pressure by three or four or five, you can see the mortality goes down by 19% or 24% or 30%, and we have that in our study where we have patients who have a reduction of mean pulmonary arterial pressure of, somewhere around two and a half to up to five. So again, very promising data, which we see because a reduction of mPAP is associated with a decreased mortality risk. So all in all, allow me to summarize. Primary endpoint of safety and tolerability met successfully. We have compelling positive impact on exploratory clinical parameters, and I would like to stress here, this is already over a twelve-week treatment period. This is something to be remembered. REVEAL Risk Score, we saw that 43%, that is 9 out of 21, had an improvement in the risk score, and 71%, that is 15 out of 21, either improved or had a stable risk score, and I showed you the importance of that. Functional Class shows the level of activity possible, 33%. That means 7 out of 21 improved in Functional Class already over the twelve weeks, and all in all, 86%, that is 18 out of 21, had either an improvement or stable Functional Class. When we look at the hemodynamics, where we have a continuous monitoring, so very exact measurement of the hemodynamics, we saw that 67%, that is 14 out of 21, had sustained pressure reduction, so very much in line with what we already reported earlier, one year ago, and this is, of course, again, very promising in this small study. I would like to maybe share with you a quote, and we're also going to hear from Dr. Kucher, who is one of the most active investigators in our trial, who was very pleased with it, and due to the results of what he saw in his patients, he's also someone who very much wanted his patients, and the patients also voiced that, they wanted to be in the compassionate use. Actually, all of his patients have said that they want to continue the treatment with CS1, and maybe we can just briefly share what Dr. Kucher has to share with us. I am very pleased with the positive outcomes we are seeing in our patients following treatment with CS1. Their improvements in health and well-being are encouraging and reflect the potential effectiveness of the therapy. This progress reaffirms my commitment to advancing treatments that can make a meaningful difference in patients' lives with PAH. Okay, so thank you very much for playing that, and this shows actually, and he's only representative, and we have heard that from other investigators as well, the positive impact that they see, and they would like to continue their patients in the Compassionate Use Program, so we are seeing very encouraging signs in the clinical trial, in this phase IIa trial. What I would like to now go is, and hand over to my dear colleague, Nick, who is Head of our Preclinical Development, on where we see some evidence, and that we would like to share with you. Nick, allow me to hand over to you. So thank you very much, Rahul. It's a really great pleasure to be part of this webcast and share some more insights that we've gained from both combining our preclinical data with our clinical data, as well as diving more deeply into some of the clinical data that we have. So just to sort of go through in brief what I'm going to talk about in this section, I will refer to some very recent in-house evidence of reverse remodeling from preclinical data. I'll then talk about pulmonary vascular resistance, which is our indirect measure of reverse remodeling from the CS1 phase II trial, and also then go into a group of remarkable responders that we have in this study, showing evidence consistent with reverse remodeling and also improved right ventricular function in the CS1 phase II trial. And then also, I will just finish off with some data that suggests that perhaps, you know, we have already achieved the therapeutic exposures needed to obtain this reverse remodeling at rather low doses. So next slide. So first of all, I want to share with you some really beautiful preclinical data from a very closely related compound, CS014. Why do we think this is relevant? Well, because this compound has equimolar potency to CS1, and we know from a lot of preclinical data that not only is it equipotent on the primary target, which is HDAC1 or HDAC inhibition, but it is also equipotent in several other measures of efficacy. This slide speaks to a particular pathophysiologic feature of PAH, which is really a hallmark of the pathophysiology of PAH, and that's shown in the histological pictures on the right-hand side. If we compare the healthy situation, which is the picture on the left, you see that what's depicted here is a cross-section through a small artery of about 100 micrometers in diameter, and that's in the center of the field that you see, and surrounding that are the terminal air sacs that make up the lung tissue. And you can see that this artery is basically very empty there. It has a thin wall, and there is no obstruction to the blood that would be flowing through it. In contrast, what you see to the right in this figure is a so-called plexiform lesion. Now, here, the endothelial cells have proliferated and occupied this central lumen of the artery. They make it very difficult for blood to flow through this vessel. And again, this is really a classic feature of clinical PAH. And if we now look at the data where the occurrence of these kinds of vessels has been quantified, in a well-used animal model, so this is the Sugen hypoxia rat model, which has been used for basically every principal clinically used today for PAH. What you can see is leftmost histogram is the normal, healthy animals, where the occurrence of these is practically zero. And then in the untreated, placebo group, you can see that there is a high occurrence of these plexiform lesions. And then when we treat with this, well, the active ingredient of CS1's analog, CS014, we see a very nice and robust dose-dependent reduction in the occurrence of these plexiform lesions. Next slide, please. Oh, I should also say that in that histology, we also noted a marked reduction in fibrosis in the surrounding vessels. Sorry about that. So next slide, please. Now back, I want to take you back to the clinical trial results with CS1, and we can't, in this data that we have today, speak about plexiform lesions, but instead, we talk about a parameter that reflects the degree to which the vessels are obstructed in these patients, and that parameter is the pulmonary vascular resistance, as Rahul mentioned previously. Basically, on the left-hand side of this diagram, you see the progressive obstruction of vessels with the pathogenesis of the disease, and then underneath these sort of cartoon diagrams of the small arteries being blocked, you see our hypothesis that CS1 will reverse this pathological change so that we will have more open vessels, precisely as I've shown you from preclinical data. PVR is the hemodynamic parameter that best reflects reverse remodeling. Okay, to the data on the right-hand side, what you see in this figure is all of the data for all the individuals, all the individual patients, plotted here for PVR. What's shown on the X-axis is the pre-treatment baseline value of PVR in Wood units, plotted against, on the Y-axis, the end treatment PVR in the patients, so that if there was no alteration in PVR with treatment and no variation, then all of these points would lie along this diagonal line, the red line. So if we take as an example, there's a minus 50% shown here. This individual patient had a value in Wood units of 12 before being treated and six at the end of treatment, and actually, this is absolutely remarkable change in PVR that we saw in this individual, and there were several other patients who also showed very large changes. Next slide, please. And what I've done in this slide is just to highlight the patients that had large changes, and these are shown encompassed in this rectangle. And these individual patients showed reductions in PVR of between 35% and 51%, with a mean of 45%. Now, of those patients that responded like that, four out of five of them were actually in the low-dose group. Now, how likely is it that we would see changes like this? Well, it turns out that it's extremely unlikely that we would see these by chance. In fact, we compared these reductions with standard of care treated placebo groups from a much bigger trial, the STELLAR study, which had hundreds of patients instead of our trial, and we're able to conclude statistically that the chances of this kind of reduction are extremely small. So next slide, please. Now, when we actually take those patients who responded and try and understand what else happened in these patients that stood out, and specifically, was there any evidence that right ventricular function was improved in those patients? So we could see that there was a very strong inverse relationship between the change in stroke volume in those patients and the reduction in PVR. And this group, we're calling the remarkable responder group. And so if we just take a look at this figure that is shown here, what we've plotted is the change in stroke volume on the Y-axis versus the change in PVR on the X-axis. So those patients who responded remarkably are shown in this green field on the upper left-hand side of the figure. So what you can see is that as PVR was reduced in those individuals, the stroke volume markedly increased. And if we try and understand were these changes in stroke volume significant? Yes, they were, because we know from the literature that changes of greater than ten milliliters in stroke volume are clinically significant, meaning that those patients have improved outcomes. And what we could see was that the changes were greater than ten milliliters in all of these patients. So we can conclude then that reduction in there we saw in these PVR remarkable responders, a reduction in PVR, and an increase in stroke volume. They were clinically meaningful in magnitude, the increases in stroke volume, and that we have evidence that remodeling results in increased PVR, so this is the impact of the disease and worsened right function. That's shown by this red constriction in the diagram below, and that CS1 reduces PVR and improves right heart function. Next slide. Now, just bringing together all of the data that we have, so the preclinical data as well as the clinical data, and reminding ourselves, CS014 is an equipotent analog of the active ingredient of CS1. So what we've done in this slide or in this diagram to the left is to compare the exposures that were needed in order to see the reverse remodeling effects, including the reduction in the plexiform lesions. So that that's represented by the green field at the bottom of that graph, and the upper line in the green field represents the maximally efficacious exposure needed to achieve this reverse remodeling. And so what we could see was, if we compare these exposures to the preclinical studies against the exposures that were achieved in the clinical studies, we could see that we are far above the exposures needed at the high dose and slightly above them at the mid dose. So the maximally effective preclinical unbound exposures correspond to the low to mid-dose levels in our phase IIa clinical trial, and the majority of these remarkable PVR responders are actually in the low-dose group. So next slide. So just to summarize what I've told you here then, so recently obtained preclinical data with CS014, again, a very close analog, equipotent to the active ingredient of CS1, demonstrates a dose-dependent reversal of remodeling of lung resistance arteries in a PAH model, a dose-dependent reduction of plexiform lesions, a reduction of fibrosis associated with pulmonary arteries, and maximal efficacy at equivalent exposures to CS1 phase II trial, lower dose range. 24% of the patients responded to CS1 with remarkably large reductions in PVR, consistent with the proposed reversal of pathological vascular remodeling, and these reductions in PVR, between 35% and 51%, were strongly associated with robust increases in the right ventricular stroke volume of greater than 10 milliliters. So next slide. So with that, I'd like to hand back to Sten to wrap up the meeting. Thank you very much. Thank you, Nick. Excellent presentation. Now let's go to the conclusions. So we have positive top-line result of the phase IIa trial with the lead candidate, CS1 in PH. Next. And you have heard this data several times. I won't repeat it, but basically saying that we have met successfully the safety and the tolerability. We have, both in REVEAL Risk Score, which is very important for prognosis, functional class, which is very important for quality of life, and mPAP, which is a prognostic factor for these patients, very good data. CS1 study, together with preclinical information, is consistent with reversing pathological remodeling. So we have a clear path forward, and we are engaging with regulatory authorities to... with the aim to pursue a pivotal trial of this drug in PH. Next.... So what is the path? Well, we're gonna complete the analysis of the trial. We have announced a Fluidda's collaboration, compassionate use, what's happening with that, and then regulatory path. Next slide, please. So we will complete the analysis of the PH trial, possibly come back with more data to the market, and we'll of course take that data in our discussions with the FDA. Our regulatory path is to aim for a pivotal trial, but this data and our aim is also to get faster regulatory processes, if we can, for the drug. With regards to compassionate use, we have one patient dosed so far and communicated that, and we aim to have that data to show us clinically and other parameters, what will CS1 be able to achieve if we have achieved this in twelve weeks, what we will be able to achieve in longer studies, six months or a year? That will be very exciting to follow. Fluidda partnership to document the impact of our drug on reverse remodeling, which Nick so elegantly has communicated with you today. We'd like to see the drug studied with the cutting-edge technology on the pulmonary arteries in man, in the clinical setting, and we aim to do that over long-term use, and some of these patients will be the compassionate use patients, so that will be excellent to see. Next. So this is the technology, and just showing you the press release to the left this morning of the collaboration with Fluidda and how it looks if you have a healthy pulmonary artery grid of vessels around and in the lungs, and you can see what happens to the right to these vessels in PH. So this is what we'd like to see. Can we prevent progression or reverse into the left picture, perhaps? Next. So, concluding there, the communication around the top-line data and in-depth analysis, let's look at Cereno and the path forward for the company. So of course, we had, as I mentioned up front, a portfolio of, programs, and, let's look at some key upcoming milestones that are interesting. Next, please. Yes, so I showed this up front. So we have this portfolio, our PH program, which is getting exciting, more exciting by the day, I would say, CS1. And then we have our portfolio, and now we have some very interesting data beyond reduction or prevention of thrombosis without bleed with CS014. We also have, impact, a dose-dependent impact on, plexiform lesions in the pulmonary arteries. So the portfolio is to, from our perspective, hot. And then, of course, thrombosis prevention, we have documented for our novel agent from University of Michigan, a prevention of thrombosis without increasing risk of bleed, as has been done also with CS014, as I mentioned. So we hope, and we believe that this will be an attractive portfolio to discuss with possible partners, discussions that are already ongoing, I would say, without going into any details. Our company and our portfolio has been exposed to several or many companies, I would say, over this year in the start and as we have moved into the fall, expecting our top-line data. Next. So key upcoming milestones, the Compassionate Use Program, long-term data in the first part of next year. CS1, FDA pivotal study approval, we expect to get, on the first part, we hope so, of next year. Reverse remodeling impact of a drug in human pulmonary arteries, as measured with Fluidda's technology, in the beginning of next year, or, beginning of the year, I should say, in the spring. And then CS014 phase I completion is targeted for end of Q2, and CS014 phase II approval by the end of next year, and of course, continued partnering, collaboration, or M&A activities. Next. So by that, you know, I'd like to conclude the presentation, and, hope you found it, interesting or, and you're all excited. I'll let open up the webcast Q&A session. And before we actually go into that, I'd like to mention here that we have quite a short session here, in respect to the time that we have available. But you would also be welcome to send questions to this email here, our IR responsible, Henrik Westdahl, henrik.westdahl@cerenoscientific.com, and we'll do our best to answer those to you, and publish them in some frequently asked questions on our website. In addition, as communicated here, we have a Capital Markets Day, October 17th at 1:30 P.M. in Stockholm. That will also be streamed, and we expect to have an extensive session on questions and answers with our people that are active, either over Teams or on stage that day. Now, let's open this for questions from the audience, analysts first. If you wish to ask a question, please dial pound key five on your telephone keypad to enter the queue. If you wish to withdraw your question, please dial pound key six on your telephone keypad. The next question comes from Joseph Hedden from Rx Securities. Please go ahead. Good afternoon. Thanks for taking my questions, and congratulations on this very encouraging data, so Sten, I think you alluded a bit at the end to it would be great to see what happens with longer treatment periods, so I was just interested if you could share any details about how quick were the reductions in pressure that you saw in responders in the trial, and did you see deepening responses over the course of twelve weeks, indicating that maybe with longer treatment periods, these patients could be doing even better and better? It's a good question. I want to give this over to Dr. Rahul Agrawal, our CMO. And I should, you know, of course, point out here that the pressures that you see as measured with AUC is actually the pressure load. So, you know, the mean PAP here reduction that you see multiplied by days measured is the load on the right ventricle. And that's why the documentation here of two or three to five has a significant impact from 20%-30% reduction in mortality over a period as Dr. Rahul Agrawal mentioned. But, Rahul, please, take the question forward. Sure. Thank you very much, and this is, of course, a very important aspect we are also looking into. Keeping in mind, and I think you were alluding to that, we have only used 12 weeks so far. So we are really capturing promising signals, and we have received them, especially with the CardioMEMS technology, which has allowed us to really capture a lot of data. And as I was saying, over 85-90 days, we have captured nearly 1,500 data sets for these patients, and yes, we see very promising results. And if one keeps in mind, this is a progressive, continuous disease, we hope to see, of course, better and even more pronounced results over a longer treatment period. Absolutely. Okay, great, and perhaps if I could just follow up on the patients where you saw the most impressive effect on PVR and the ones who you're calling the super responders. Do they correspond exactly to who has the biggest improvements on or who improves on REVEAL Risk Scores and who Functional Class? So is everything perfectly aligned in that respect? Again, I'll leave that up to you, Rahul, to- Sure - to comment on. Yes. I mean, in the best of worlds, we would have said everything is aligned, all the parameters are, but of course, patients react differently. As I had said, this is a very small trial. It's a phase IIa trial, so, several patients did show, also the reductions in hemo or improvements in hemodynamics in the right direction, but we're talking here, as Nick had very nicely shown, about five, six patients currently, and we hope that in a larger group, we have a much more sustained sort of effect, and we can show that, in a more reliable fashion. Okay. So- Thanks I hope that was helpful, Joseph. And do we have other questions from the analyst audience? The next question comes from Aaron Aatkar, from Edison Group. Please go ahead. Hi there. Thanks very much for the presentation and for taking my question. So your press release has sort of mentioned engaging with authorities for a pivotal trial. Just wanted to get your thoughts on if you think that one randomized trial will be sufficient for regulators based on the fact that Sotatercept had two late-stage trials. Thanks. It's a very good question. Thanks for being present and, you know, I'm sure, here again, Rahul will answer. I can mention that, the approach with this kind of two A data, the aim is likely to be three trial. So but again, I'll leave that to Rahul to comment on. Thank you very much, Sten, and yes, this is a very important question. Please keep in mind that we're talking about a rare orphan indication. We already have orphan drug designation, so the authorities are very open to discuss, especially if the data points to towards a safe and well-tolerated drug. As you know, there is experience with the key component of CS1 for many years, and we have shown good results. So we think we have very good data to go there and engage the regulatory bodies, and I have previous experience from my times when I was at larger pharma companies, also in PH, where one can approach them, and they're very open for an adaptive trial design phase II, phase III, as Sten was mentioning, and we think we have some very good arguments here. So we'll pursue this, absolutely. Any more question here? Thank you very much. And one more, if I may. So in terms of the next phases of development, we see that you're open to sort of M&A options and licensing partners. Appreciate it's pretty early stage, but with the sort of two HDAC inhibitors that you've got in your portfolio, how do you see discussions playing out with sort of potentially interested parties? Is there a chance this could be for both assets, or do you think that you'll see these as individual programs going forward? Thank you. A very good question, and, you know, there is, of course, a strategy behind Cereno pursuing these two assets that is five, I would say five, six years old. So we have our, you know, business and development strategy, and we have obtained what we have decided to pursue many years ago. So what you're seeing here playing out in data from the PH trial with CS1, and you see data playing out in thrombosis with CS014 before, and now plexiform lesions, it's all part of a plan that we keep close to our chest. But we believe that this will be an attractive HDAC portfolio for the majors pursuing cardiovascular disease, with the ambition to be able to address the root cause of the disease progression in several indications. That's our plan, and exactly how those discussions will play out, we will have to see. We haven't really disclosed the end or, you know, we're not discussing the end of these programs and the full totality of what can be pursued of these programs. We have previously communicated to the market and also to potential partners the many indications that you can pursue if you have an impact on inflammation, endothelial dysfunction, fibrosis, and vascular remodeling in the vessels and the heart. There are many patients in cardiovascular diseases that have this complex pathophysiology in various degrees. Agents that can do what we have seen so far with HDAC inhibition would be, and will be very attractive, I think. Thanks very much. No more questions, and congrats again on the positive data. Thank you. Additional questions, perhaps? There are no more questions at this time, so I hand the conference back to the speakers for any written question. Okay, thank you. I don't know if I'm on. I have some questions that I've gotten into my phone there with me. I think many of these questions have been responded. I'll see here. So could you please comment on the conclusion of the optimal dose being found in the lower dose, and what's the hypothesis of this? I think Nick, Nick Oakes referred to this and to some extent here. So I think that question has already been answered. Why did you pool the doses? Is another question here, and perhaps, Rahul, you could take that question. Sure, very gladly. I had mentioned that briefly also in my presentation. We have pooled it, A, because we had seen the PK, PD, that means pharmacokinetics, pharmacodynamics data, which were pointing in that direction. And number two, because of the small sizes in each group, we thought it is best to pool the data. So those were definitely good reasons to do so. Good. Thank you, Rahul. And do you expect to see further improvement over a longer treatment period? I think that was just asked and answered. Now will you be sharing more information of the exploratory efficacy parameters as we move on, you move on with your analysis? That is likely to happen, and we are planning, hopefully planning here a publication in a good journal or several about that data. And we'll get more data coming out of the trial when we finalize the analysis into final report. What are your next steps? When do you foresee that the pivotal trial can be initiated? Well, we hope that we'll be able to get a regulatory approval for our programs moving forward, and we are aiming for a pivotal trial. We hope we'll get that approval by the first half of next year, and then preparations going on from now and moving towards a start of such a trial, which we haven't really disclosed yet when that would be. I would offer here that it might be, you know, in the early 2026. So possible sub-questions: What will the collaboration with Abbott look like after the trial? We've had a very good collaboration with Abbott here in this trial, and we think one part of the very interesting data we have here is the CardioMEMS sustained clinical reduction of mean pulmonary arterial pressure over time with these 1,500-2,000 measurement points for each patient. Now, the question is, of course, how will that CardioMEMS technology be useful as we move forward in the programs? I'll wait with that until we have defined how that could be useful in our programs for getting this drug eventually to the patients through a pivotal trial. I think those are the main questions here. I don't know if we have any other questions to address. I think we perhaps should close the Q&A session for now, and just thank everyone for being part of this webcast, and especially the shareholders for supporting our journey to provide, develop and provide valuable therapeutics to patients that are in dire need of those, and especially addressing root causes of diseases with safe and effective therapies. Please send your questions to this email, henrik.westdahl@cerenoscientific.com, and we'll try to answer them. And of course, we'd love for you to show up at our Capital Markets Day, either digitally, because it will be streamed, or in person at Posthuset in Stockholm, 1:30 p.m., October the 17th. And by that, I'd like to conclude this webcast, and I hope you share the excitement of this data and Cereno's future with our programs. Thank you.