Good afternoon. Welcome to this afternoon's webcast with Cereno Scientific. For the next 45 minutes or so, we will be looking closer at the company's phase 2A results with lead candidate CS1 in pulmonary arterial hypertension. We will be hearing from CEO Sten R. Sørensen, CSO Björn Dahlöf, CMO and Head of R&D, Rahul Agrawal. You can see the agenda on your screen there. As you can see, we will finish with a Q&A session. We'll be talking to analysts from RX Securities and Edison Group, but we will also be taking questions from you, the viewer. There is a chat window on the screen where you can send in your questions, but please do bear in mind that there will be a slight delay between you pressing send and me seeing the questions. With that, let's turn to Gothenburg and CEO Sten R. S ö rensen. Good afternoon, Sten, and please, the stage is yours. I think, Sten, that your microphone is off. Can you hear me now? Now I can hear you. We are waiting for something good, so yeah, take it away. I'm super excited standing here the day that we're presenting more exciting data from our phase 2A trial with a lead compound, CS1, the epigenetic modulator, and the trial that we've done in the rare and fatal disease, pulmonary arterial hypertension. We have an exciting 45 minutes in front of us. Can I have the next slide, please? Next. Cereno Scientific has, for a few years now, pursued our vision and mission to enhance and extend lives for patients with rare and fatal diseases. We're pursuing that effort in cardiovascular and pulmonary diseases. We have three drug development programs in our pipeline, and our aim is to fill the void of the need that is in the market. We are aiming to develop oral drugs that are safe, well-tolerated, and address the root cause of the diseases. Today we're going to spend time on our lead project, CS1 in PAH. Next slide, please. Here you see first our pipeline. CS1 is a repurposed drug from the original substance, valproic acid. That's been in man for about 60 years and used for neurological disorders, mainly epilepsy prevention. Now we have completed a phase 2A trial in the U.S., and the drug has orphan drug designation in PAH in the U.S. and Europe. We have met our primary endpoint, and we've also, as you will hear more today, demonstrated the ability of reverse remodeling effects. We have an FDA-approved expanded access program, and into that program, we are pursuing a sub-study with an imaging technology by Fluidda to further evaluate our impact on the vascular bed in the pulmonary arteries in the lung. Our second HDAC inhibitor program is CS014. That's a new chemical entity, and that's pursued for the idiopathic pulmonary fibrosis disease, the rare disease, which has even shorter lifespan. We are on our way to complete our phase 1 trial. We've already seen good tolerance and safety in the first part of that trial, and we're completing the second part now and expect data by the mid-year. We will focus on the first program in our HDAC inhibitor portfolio. Next slide, please. This is an example of a patient, a very common patient in pulmonary arterial hypertension, a female, in this case, a lady, mid-life, around 50 years old. Upon diagnosis of pulmonary arterial hypertension, suddenly she has about a mean seven years to live. It goes very quickly. It's a rapid progression. Current drugs are basically vasodilators. There is a new drug on the block, but most of the drugs are vasodilators, not addressing the root cause of the pathological progression of remodeling of the vessels and the heart. What if someone could develop a drug, Cereno could develop a drug that would address the root cause, deliver an oral drug that is safe, well-tolerated, and that in addition has an impact on the vascular bed and the pathological progression, maybe halt it, maybe even reverse it? You will hear some exciting data today from my colleague, Björn Dahlöf, and Rahul Agrawal. First up here is the CSO, Björn Dahlöf, to explain more about HDAC's role in PAH, but also the HDAC inhibitor's role. Welcome, Björn. Thank you. Thank you, Sten. It's a pleasure to be here today and share some exciting data with you. Could I have the next slide, please? I am going to address epigenetic modulation via HDAC inhibition. Could I have the next slide? What is epigenetic modulation? That is alteration of the gene expression without altering the original genetic material. This is an important mechanism of disease and plays a key role in aging, cardiovascular, and pulmonary diseases. By histone deacetylase, it's easy to stumble on that, contributes to cardiovascular and pulmonary diseases via this epigenetic modulation. With acetylation, the histones can open up and DNA can be transcribed. If that is not the case, then you will have disease of different kinds. Next slide, please. A few years back, we published a paper in The Lancet Healthy Longevity, where we had gone through more than 600 references, and 100 of them were displayed in that article. It showed the potential of HDAC inhibition to untap the epigenetic modulation in both cardiovascular and pulmonary diseases. The five main pillars that could be of importance in the disease and disease modification were reverse the pathological remodeling, mainly of vasculature, antifibrotic effects, anti-inflammatory effects, reduction of pressure, actually both in the pulmonary and in the systemic circulation, and antithrombotic effects, all which are of importance for cardiovascular and pulmonary diseases. Next slide, please. As already alluded to, PAH, or pulmonary arterial hypertension, is a fatal disease with no spontaneous improvement. It is about progressive narrowing and pathological remodeling of the pulmonary vessels that ultimately leads to right heart failure and death. The median diagnosis is around 60 years of age, and it's a majority of females that get this disease. As Sten alluded to, the mean survival these days is around seven to eight years. That is with therapy, with today's therapy. The only cure, if you can call it the cure, is lung transplantation, but many patients never reach that. Can I have the next slide, please? Going more into depth about the pathophysiology of PAH, it is a progressive remodeling of the vasculature of the lung, mainly the small arteries and arterioles. It is about endothelial dysfunction, and you form what you call plexiform lesions, which is a kind of way for the circulation to get through these thickened vessels. Inflammation, fibrosis, constriction, and ultimately that puts a huge burden on the heart because of the pressure increase coming from the resistance increase. That gives the hypertrophy of the right ventricle, ultimately dysfunction, and finally failure of the right heart. You can see a graphic to the right, which more or less depicts this kind of progression from a healthy vessel to a diseased vessel. Next slide, please. We are developing CS1, which is the first-in-class HDAC inhibitor, which has shown in preclinic and indications in the clinic of reverse remodeling, which we think could be disease-modifying. Next slide. CS1 is a proprietary reformulation of valproic acid, as mentioned. It has orphan drug designation both in the U.S. and in Europe, and it is a class I HDAC inhibitor that acts via epigenetic modulation. Next slide, please. Just to remind you, the five pillars of effect that HDAC inhibition and VPA in particular stands on: reverse pathological remodeling, antifibrotic, anti-inflammatory, pulmonary pressure reduction, and antithrombotic, all of great importance for the pulmonary arterial hypertension. Next slide. If we go into some more detail of the different documented effects of HDAC inhibition and VPA in particular, it has been documented to inhibit cell proliferation, both pulmonary vascular cells, smooth muscle cells, and endothelial cells, to be anti-inflammatory through both TGF- beta, IL-6, MCP1, and TNF alpha, induce apoptosis, have an anti-angiogenic effect, and be antithrombotic. If you put all this together, you can see it as a combination therapy for PAH. Next slide. Disease modification, the definition is still something that we argue about. In the Lancet Respiratory Medicine, just a few weeks ago, it was published a paper coming out of a discussion at the CVCT meeting about how to define it. One definition could be that you reverse the pathological vascular remodeling, which is the root mechanism of disease progression. Either you can halt it, and then the disease maybe stays stable, or you can reverse it, and then you have maybe towards a cure of the disease. The main goals of the therapy have been said to be improve on symptoms, functional capacity, and prolonged survival. Can I have the next slide? How do you measure this in the clinic? Clinical readout in this case could be to monitor quality of life, functional class, risk scores, or the right ventricular function. How did CS1 perform in the phase 2A study? I'll leave it to Rahul to tell you more about that. Thank you. Thank you very much. Thank you very much, Björn. My name is Rahul Agrawal. I'm the Chief Medical Officer at Cereno. Based on the very exciting and sound knowledge we have on HDAC inhibition, we, of course, embarked then on clinical and accumulating clinical evidence. If I may have the next slide, please. We performed a phase 2 trial with CS1 with the main aim of looking at safety and tolerability, but also exploring some efficacy parameters. If I may have the next slide, there you see the study design. The study design with the primary endpoint of safety and tolerability and exploratory endpoints and efficacy was performed in 10 centers in the U.S. We all in all included 25 patients. At the request of the clinical steering committee, we stopped after that because the clinical steering committee felt that we had reached the goal. All in all, 21 patients were in the per protocol analyses. All the three dosage groups, we had 480, 960, and 1920 milligrams. All the groups were pooled because the exposure in the groups exceeded the estimated exposure as was found in the preclinical studies. In the next slides, you will find that we are looking at the per protocol analyses. As Björn was briefly outlining, the main goals of PH therapy are outlined on the right-hand side with improving symptoms, enhancing functional capacity. Of course, we want to slow disease progression, and with the ultimate goal, of course, to reduce hospitalizations and prolong survival. We took several of the clinical possibilities, and I'd like to share with you what we saw in the study. If I may have the next slide, please. First and foremost, the primary endpoint of our trial of safety and tolerability was met. We had no serious drug-related adverse events. We had no hospitalizations or death, no clinically significant abnormalities in either hematology, clinical or chemistry, urinalyses, and also no abnormal ECG findings. We met the primary endpoint. On the next slide, I'd like to share with you some of the exploratory efficacy parameters. We had already previously on the Capital Markets Day shown you that the REVEAL Risk Score, which is a very powerful prognostic risk score, there we had shown improvements. In 43% of the patients in a progressive disease, we showed an improvement. Allow me to remind you that publications have shown that a one-point reduction in this risk score already within 12 weeks, and that was the duration of our study, translates into a 23% reduction in relative risk of deaths within 12 months. When we looked at the functional class, that means how were the patients feeling? We showed a 33% improvement, but all in all, 86% of the patients either improved or were stable within these 12 months. If we look at hemodynamic parameters, in this case measured with CardioMEMS, a non-invasive measurement, we saw that two-thirds of the patients had a reduction in mean pulmonary artery pressure, again showing that on the one hand, REVEAL Risk Score, which correlates with a better prognosis, functional class, which correlates with the well-being of the patient, and a reduction in mean pulmonary artery pressure, which mirrors the effect on the right ventricle, all pointing in the same direction. These are very encouraging results. We explored further. On the next slide, I'd like to share with you what else we saw. We saw that within these 12 months, if you on the left-hand side, you see the REVEAL Risk Score, on the right-hand side, the functional class, we saw a gradual improvement over time in both these parameters. In the green bars, you see the improvement. In the blue, you see the stabilization, and in gray, the worsening. As you can see in this progressive disease, you see a continuous improvement in the REVEAL Risk Score from week four to week eight to week 12, from 20%- 43%. Very similarly, you see also an improvement in the functional class from week four, 10%- 33% after 12 weeks, again indicating that we have an impact on disease progression. If I may have the next slide. Here we see further signs on what is happening to the right ventricle. Because as you may have heard, pulmonary arterial hypertension leads to right ventricular dysfunction due to the pressure overload, and this has a fatal outcome for patients. Allow me to just translate that briefly, and this is also shown on the left-hand side and illustrated on the right-hand side. Through this pathological remodeling of the pulmonary vessels, which happens in pulmonary arterial hypertension, this leads to a pressure overload of the right ventricle. What happens then? What happens then is that there is a start of, if you like, leakage of the tricuspid valve. Blood goes backwards, which again increases the overload of the right heart. This leads to a bulging of the right ventricle, and in the end, it leads to right ventricular failure, which ultimately leads to death. This is something which is then, if you like, the natural course of pulmonary arterial hypertension and then right ventricular failure. The goal has to be to in some way stop or slow this progression. On the next slide, I'd like to show you what we found. We looked at some of the signs of reverse remodeling of the right ventricle. Why is that important? Because that improves patient functionality and, of course, the prognosis. Two of the key parameters that one looks at are the so-called right ventricular global longitudinal strain, and I'll go into a little more detail what exactly that is, and also tricuspid regurgitation. That means flowing backwards of the blood. This is again, both the parameters are closely tied to disease severity and prognosis. On the next slide, I'd just like to briefly explain to you exactly what global longitudinal strain is. What one looks at is in how far does the muscle in the longitudinal stretch. The more it stretches, and you see that shown on the right-hand side on this diagram, the more negative, if you would like, the values are. The stretching. What we are seeing here is in the diagram on the baseline, that is the X-axis, at base how they were, and the patients after 12 weeks how they were. In the green field, you see either they were improving or stabilizing. As you can see, most of the patients over these 12 weeks showed either an improvement or stabilization of the so-called right ventricular global longitudinal strain. This is an indication that the right ventricle function is either stabilized or improving. On the next slide, I'd like to show you what exactly the regurgitation means. Regurgitation, again, as I was saying, is something which is clinically apparent and is a sign of worsening. If regurgitation increases, that is also a sign that the right ventricular function is actually deteriorating. What did we find in our study? On the next slide, you see that we saw in this progressive disease, and allow me to repeat this fact, and we should always keep that in mind. PAH is a progressive disease where patients deteriorate. Here we see in one-fourth of the patients an improvement of the tricuspid regurgitation, and 70% were stable. All in all, over 12 weeks, 95% of the patients were either stable or improved, which is again a very good sign that the right ventricle is sort of not deteriorating and the function is being stabilized. On the next slide, I'd like to share with you further things, how that translates also to quality of life. One accepted quality of life questionnaire specifically for pulmonary arterial hypertension is a so-called PAH- SYMPACT Quality of Life Questionnaire, where you see the four columns on the right-hand side. Another very commonly used life or heart failure questionnaire, quality of life questionnaire, is the so-called Minnesota Living with Heart Failure Questionnaire, which you see on the left-hand side. Again, you see a very consistent picture here. Consistency in that patients, to a large extent, either improved or were stable. You see in the Minnesota Living with Heart Failure Questionnaire on the left-hand side that 75%, sorry, 71% improved. All in all, three-fourths were either improved or stable. In the PH Symimpact, and there are several criteria here, overall, the patients were either improving or improving and stabilizing, again showing that the hemodynamic changes that I showed you, the risk profile that I showed you, the functional class that I showed you, also is pointing in the same direction as an improvement in quality of life. All in all, these data are very consistent and showing and pointing towards the right direction. If I may have the next slide, please. All in all, the key results are we have met the primary endpoint that our CS1 is safe and well tolerated, and it's an oral drug, if I may say. Again, it's an oral, safe, and well tolerated drug. We have very encouraging signs of reverse vascular remodeling, which we saw. We saw a gradual impact over time, as I shared with you, on the REVEAL Risk Score and the functional class. We measured and see and saw, sorry, an improvement of right ventricular function of the heart with two of the key parameters. On the one hand, right ventricular global longitudinal strain and improvement in tricuspid regurgitation. We also saw an improvement of quality of life, both in PAH- SYMPACT and the Minnesota Living with Heart Failure Questionnaire. Very, very promising results. I'd like to share with you briefly on the next slide, the next steps that we are having. We, as Sten was already mentioning, have an expanded use program where half of the patients have already enrolled. The first patient was dosed in August of last year. Interim readout, we're expecting middle of this year. We're also performing a sub-study in the expanded access program where we're using a very innovative imaging technique, and there the patient enrollment is about to just start. We're going to do several CT scans there over 12 months, and the results we'll be sharing beginning of next year. We are, of course, interacting with regulatory bodies, with the FDA, and we'll keep you updated there. We're planning already now for the next steps. That means for the phase 2B trial, but we'll keep you updated there as things develop. If I may have the next slide, please. With that, I'd like to hand over to Sten and thank you very much. Sten. Thank you, Rahul and Björn. I am again back and excited to share with you that CS1, as you heard, has shown potential to reverse pathological vascular remodeling to improve quality of life and potential to extend life expectancy of these patients in pulmonary arterial hypertension. We are very excited at Cereno. Can I have the next slide, please? Now, we believe that our drug, CS1, will transform treatments for PH. As you've heard, it's rare, fatal, and very progressive, and there is a high unmet need to address this vascular remodeling that's happening. The market has a void of safe and well-tolerated treatments that are oral and that are addressing the underlying pathophysiology of PH. Combined preclinical and phase two data, which you've heard today, is consistent with a reverse vascular remodeling potential for CS1. It is oral, safe, and well-tolerated, as we have seen in this and our phase one trial. In preclinical and now in clinical data, we see potential for reverse vascular remodeling effect for this rare disease. Our drug has a patent protection, three patent families, plus orphan drug designation market exclusivity of seven years in the U.S. and 10 years in Europe, EU, upon approval. As you know, with such an unmet need, the market size is big. Next. We are way on our way to deliver on our vision and our mission. As you heard, we are pursuing our process with regulatory authorities, FDA. We hope to start our study phase 2B in next year. Yeah, next. Of course, we believe that our portfolio, and now especially our HDAC portfolio of the two programs, CS1, the repurposed drug in PH, which we focused on today, but also our new chemical entity, CSO14, which is targeting another rare disease, idiopathic pulmonary fibrosis, is becoming an attractive collaboration or acquisition opportunity for Cereno and, of course, for potential partners or acquirers. We are looking forward to continued talks with potential partners here, and we will revert back when we have something to say about that. With that, I think I have concluded my talk and our talk, and we are leaving this open now for Q&A. Thank you. Thank you so much, Sten and Björn and Rahul for that presentation. Like you said, we will be moving on to the Q&A part of this webcast, turning first to the analysts that we have with us. We will start with Joseph Hedén, I'm sorry, Joseph Hedén, to speak properly, the Senior Equity Analyst at RSecurities. Good afternoon, Joseph, and please ask your questions. Good afternoon, and thanks very much for taking my questions. It's great to see really interesting data coming out of the trial. I'm just wondering for some context on RVGLS and TR as well. Have you seen in previous trials of PH drugs these kind of effects, even minor effects on these measures of heart health or across the broader spectrum of cardiovascular diseases? Has these kind of changes been documented before? Rahul, please. Yeah. Thank you very much for that question, Joseph. Usually, the global longitudinal strain has been used for left heart failure, and it is a very strong prognostic factor in that. In PH, when one looks at it, this has not been really widely published so far, but there are several publications in this direction. The tricuspid regurgitation factor is something which already, since, if I may put it that way, before the imaging, also clinically was a very important factor, which one looked at. Usually, one subdivided into moderate, severe, and mild, and then one looked at if there was an improvement or not. This is a very widely used parameter to look at the function of the right ventricle. Are you measuring that via CardioMEMS, or is there another approach that you're— No, no, this is— Sorry. This is an imaging technique via echocardiography, so readily available, and every patient is usually also investigated with an echocardiography. In the top-line data, or maybe in the subsequent release, you talked about some subgroup of remarkable responders where you defined as great, quite significant reductions in arterial pressure. Do you find that the degree of improvement on these newer endpoints that you're talking about today, RVGLS and TR, is there a correlation between the effect size of those endpoints and the effect size that you see in those remarkable responders? Do they have the greatest improvements? Yeah. Just to maybe outline briefly for all, these were five patients who had a remarkable PVR reduction, and we looked at them, of course, very closely. Some of them, and this was only five patients, that's why they were to some extent, if you like, all over the place. There are some who showed an improvement, some were relatively neutral. Okay. Okay. Perhaps turning towards what this means in your efforts, your kind of business development efforts, what additional information do you think you need to generate now, or what's left to kind of build this into a package that you can partner with? Hi, Joseph. Good to see you. Yeah, it's a good question, right? We will hear that from our potential partners. There are meetings going on, of course. This data is very new. It's the first time we go public with it. We haven't discussed these findings with any partners yet, potential partners. You can do a deal on phase one data; that's done more now, I think, than before because of the competition after phase 2B placebo-controlled trials. It depends on the view on our data at this point. The next step, of course, we are very encouraged by the data, and we think that numerous beyond the platform of HDAC, as involved in the disease pathology progression here, we see that intervention there with our program is doing something good. The potential here is tremendous, of course. It depends if potential partners want to go in and do talks with us now and collaboration, or want to wait for a phase 2B trial where you have more patients and can conclude more succinctly what we are seeing here now. I should also say that the global longitudinal strain data here is on the whole group, right? You mentioned this super performers, if you will, or responders, but here you have that impact on the whole group. I hope that answers your question. Okay. Thank you. Perhaps a final one just for now. You're highlighting starting phase 2B next year. It seems like a kind of long timeline to start that study when the conversations with the FDA are ongoing and you've got probably a reasonable idea of the design and it's rubber stamping it with them. What's accounting for the timeline? Maybe I'll let Rahul in here, but we have learned through experience that the startup phase, even when you have defined your centers, normally to run trials of the size here, you require maybe 50 centers around the world. To get those assigned and then to actually get the ethical approvals and contracting done with various parties takes a fair amount of time. Beyond the regulatory process initially to get the protocol discussed and then approved or accepted, you then pursue these multi-center global discussions and eventually contracting and ethical approval. You can start to actually recruit patients. That takes time to do, actually. There is data on how long time it takes and so on for these larger trials. Yeah. Okay. Thank you. Thanks, Sten. Thank you. Thank you. Yeah. Thank you, Joseph, for those questions. We will move on to Jyoti Prakash, the Director, Healthcare at Edison Group. Good afternoon, Jyoti. Yeah, fire away. Good afternoon, all. Thank you for taking my questions. It was indeed quite heartening to see the additional positive data. My first question is if you noticed any unique characteristics for the patients who showed improvement versus who had stable disease from the phase two data. Yeah. Thank you very much for that question, Jyoti. What we would like to share is, I mean, the global longitudinal strain that, as you could see in the graph, most of the patients were pointing in the right direction, either improving or being stable. Again, this was a 25-patient trial over 12 weeks. We saw these encouraging signs. What is really the most positive thing is that they are pointing all in the right direction. We definitely need to do that in a larger context with the phase two B. We will be doing that. That is what we are aiming to as a next step. Okay. This leads me to my next question. Given the positive sign of reverse remodeling, how does this impact your plans for defining the primary endpoint for the phase two B or phase three trial? Does it have an impact, or do you have it set out already? Maybe a short comment from me, and I'll let the experts in. As Rahul mentioned here, I think maybe both Rahul and Björn mentioned the recent publication in Lancet Chest, which was published after a discussion at CVCT, a major cardiovascular conference in Washington every year. Two of the members of that are actually on the scientific advisory board of Cereno Scientific, Dr. Pitt and Dr. Faiez Zannad. The involved parties there were both regulatory parties, patient groups, and cardiovascular and pulmonary experts. They deliberate on what is to be studied, documented in relation to the positive impact for this patient group, PH. I think we have seen signs here in our phase 2A trial that points in the direction of what both the experts and regulatory authorities are looking for. Of course, the outcome of what we actually will put into our trial as primary endpoints and secondary endpoints will be discussed with FDA, and that's not disclosed at this point. Do you have anything else to add? I might add one thing, and that is that in the article, there were several ways of trying to find out disease modification and discussed because no one has really defined that. The jury is still out on exactly how to do that. The technique we are using in our expanded access program, the Fluidda technique, where you have a CT and with a sophisticated software approach, you can find the volume of blood in the small vessels as an indirect sign that you have an improved circulation. You can also see the vessel wall thickness with another approach. That was discussed as one of the approaches that could highlight the reverse remodeling, which is the root mechanism of disease progression. We are there. We are collecting this kind of data, and hopefully, at the end of the year, we can give you more on this. Of course, FDA is looking for patient outcomes that ultimately result in enhanced life, so quality of life, mobility, as well as extend life. That is the ultimate goal of the therapy. The connection between what you're seeing structural-wise and parameters-wise to outcomes has probably been avoiding the actual clinical trials in PH. They had quite soft endpoints for regulatory approval. I think that will change now with they will require more of substantial signs that you affect morbidity and even mortality. Maybe not mortality studies in itself because they are quite large, but signs that indicate mortality. Yeah, such as, for instance, impact on risk score. Risk score. I think what you're seeing is a change at the regulatory authorities in the direction actually that we have taken already at Cereno with our different measurements here. It plays in our favor, I would say. Yes. Sure. The paper had actually authors that have been with the regulatory authorities, the previous head of the division that looks at trials and approvals of PH drugs. Okay. For the Fluidda sub-study, will all the 10 patients in the extended access program be part of that study as well? Hopefully, yes. Maybe nine. I can't remember, but I think it's nine that will be part of it because they are more locally organized in one center, around one center. For simplicity, one patient will probably not. It will be nine patients. Okay. Just one final question from my side. The next study can either be phase 2B or phase 2B3. Will your strategy change in terms of looking at partnering opportunities if it were phase 2 versus phase 2B3, or is the strategy going to be the same? Good question. We have actually communicated the change of strategy or maybe more defined strategy. Our strategy that we have chosen is to pursue a phase 2B. Earlier, we were not defined, so we said 2B3. We have decided strategically that it is better for Cereno to pursue a phase 2B. There are many reasons for that. You have actually a shorter time to next key leverage point with a larger trial, etc. That is good. It's shorter, and it's less capital-intensive. It fits very well with a biotech that wants to change the world. In terms of the study design and size of the phase 2B study, what can we expect this to be? I think that's after we have the discussions with the regulatory authorities, that's proper to discuss that. We previously said maybe somewhere around 100 patients or more. That is up to that discussion and exactly what parameters we're going to select for the trial. Thank you again, and congratulations again for the positive data. Thank you. Thanks for good questions. Thank you. Thank you, Jyoti. We will turn to the audience questions. We've touched upon some of them in the analyst questions. In the interest of being fair, we will ask all the questions, and you may just have to repeat yourself a bit, gentlemen. We have a question here on the phase 2B trial. This audience member says that the phase 2A was 12 weeks long. Are you planning a longer phase 2B trial? Maybe Rahul. Yeah. Thank you very much for that question. We are planning for a longer trial, presumably 24 weeks. As Sten was alluding to, we are in discussions, and we will discuss the design, the duration, the endpoints with the authorities, with the different authorities. Of course, we will be more than happy to share the details. We also have a question on the Fluidda study asking you to sort of summarize what you expect to see from this study and how it can support CS1's efficacy profile. Yeah, you can. I mean, as I alluded to in my presentation, the, I should say, definition of disease modification is still not given. That is a discussion. Disease modification can be seen as you have stopped the progression. You can see that you have reversed the progression. At the core of the disease progression is the remodeling of the vasculature. Of course, everyone knows you can't go and biopsy lung vessels like that. You have to have some indirect measure of that. I think one of the most innovative of these measures in imaging is just the Fluidda technique because it's based on a CT scan, high-resolution CT. With software, you can visualize both the content of the vessels and the actual wall of the vessels. That is actually the possibility to see reversal of remodeling. If that can be shown, you can kind of claim that you have modified the disease in either stabilizing or even reversing the progression of the disease. That is one way of doing it. You remember that we used to work with vasodilators. A vasodilator is a drug that can expand on the lumen somewhat that reduces the pressure, reduces the resistance to pressure, and the burden on the heart. It is dependent on a continuous drug dosage. If you discontinue the drug, it goes back again. One other way of disease modification is that you can stop drug, and you can still be stable. These are the two ways that are discussed. We are looking at the Fluidda now. We might also go into the other, who knows, but there is no decision on that. Yes. Thank you, Björn. I should say, again, the connection between what you see in the vascular bed and the heart together with quality of life, physical capacity, etc., and risk score. I do not think it is going to be enough for anyone to just see impact on vasculature. You need to see benefits to the patient. You have to link it. Thank you. For a final question then, this viewer wants to know if you can disclose if any big pharma or other potential partner, buyer is in your data room under an NDA or a CDA at the moment. No, we cannot, unfortunately, not disclose any of our discussions. Maybe fortunately, I do not know. Anyone who wants to find out needs to hang on. That is a good cliffhanger to end the Q&A session on. Thank you for answering the questions. Before we end the webcast, I would like you, Sten, to ask if you would like to leave the viewers with some final words on Cereno's journey. Yes, I would like so. Maybe I could get a few slides. Again, thank you, Rahul and Björn. Next slide, please. I can see it. I think you're at the end now. You should probably go back a few slides. You're getting the presentation again without words, guys. I don't know what's going on. The last three slides in the presentation. At the presentation, not only. There we go. Go back. One more. Go back. No, you're going forward instead of back. Here, let's just stay here. There was one more slide before this. This is not the slide, so. Let's end with the next slide then. Here. One of the questions, the last question actually in the Q&A, was regarding our discussions with potential partners. This is something that's for many biotechs that are nearing or in clinical development is continuous dialogues with potential interested parties. We've had those for a while, not a long while because we haven't been communicating clinical outcomes or data, I should say, signals of efficacy, safety, tolerance, and now signs of reverse remodeling, including also progressive impact and improvement of quality of life. We expect these discussions to continue and maybe intensify depending on the interest here over time. There are a fair amount of companies that are interested in cardiovascular diseases, rare diseases, and pulmonary rare diseases. The field is quite large. Of course, disease-modifying capacity can be expanded outside of rare diseases. We expect these discussions to continue. We believe that we have moved our company, and especially CS1 and the HDAC program, to even more attractive assets based on the data we have presented here today. Sorry about the slide here in the end, but I hope you stayed on for my concluding. I would like to thank everyone that has been taking the time to listen to our new data and our presentation, and also to you there at BioStock. Thank you. Thank you, Sten, and thank you to everyone at Cereno for your presentations, and of course, for the analysts for calling in with the questions. Of course, to the viewers for sending in your questions in the chat. Thank you so much, and thank you so much for watching. Thanks.