Good morning and welcome to the ABG Investor Days. My name is Alexander Krämer. I'm a biopharma equity analyst here at ABG. Today I have the pleasure to host Sten Sörensen, the CEO of Cereno Scientific. Welcome, Sten, and the stage is yours. Thank you, Alexander. So it's a pleasure to be here at the ABG event and to meet the investors both here in the room and digitally. Cereno Scientific was formed in 2012, and we are based in Gothenburg. We are on Nasdaq First North, market cap SEK 1.7 billion approximately and 10,000 shareholders. We are passionate about developing new drugs that can meet unmet needs. And specifically, we are focusing on rare diseases. And that's a pivot that we've done over the last few years. And I'm very happy to share the exciting news and progress for the company that we've had this year. So we are focused on rare cardiovascular diseases and pulmonary diseases. So this picture actually illustrates three different patient categories. And we are aiming to address the root cause of these diseases. And we call it disease-modifying capacity with our compounds. This lady is around 50 years old. You can imagine she has probably a family, married, kids, and everything is going fine. Suddenly, she gets this diagnosis: pulmonary arterial hypertension, and this is actually the lung vessels, and this is a very rapid progressive disease. When you are diagnosed, you have a mean seven years to live. That's approximately similar to severe cancer forms. What happens is that the pulmonary artery, the artery between the right heart and the lungs, the muscles in that grow very fast, and the tube becomes very narrow, and you can see the tightening of these vessels here in the plexiform lesions in PAH in this picture, so the current drugs, they actually only dilate vessels. And that's a temporary relief, and it has helped these patients to go from two and a half to seven years life expectancy, symptomatic relief. It doesn't really halt the disease. What if we could develop a drug that could halt the disease and maybe reverse it? That's what Cereno is about. So this is another disease, idiopathic pulmonary fibrosis, mostly affecting, in this case, men compared to PAH, which is mostly women. This is actually even more severe, three-to-five years life expectancy, and it's fibrotic development in the lungs. Suddenly, you're diagnosed, you're three-to-five years to live. The current drugs don't do much when it comes to quality of life or prognosis. So there's really a high unmet need in this field. What if we could address the underlying cause of this disease, fibrosis, maybe halt and reverse? We're trying to do that at Cereno. Third patient category: this is the most common cause of death on the planet, thrombosis, mostly hit the brain and the heart, stroke, myocardial infarction. All the drugs out there cause dangerous bleedings. Three out of 100 patients die of the medications. 25 out of 100 end up with bleeding such as you see on this picture, hospital care, et cetera. Current drugs cause this. What if we could develop drugs that don't cause bleeding and can add to the efficacy? We are trying to do that at Cereno Scientific. Two of our programs: we are pioneering HDAC inhibition, epigenetic modulation into two diseases. I will review why and how we're doing that. Why are we focusing on HDAC inhibition and epigenetic modulation? The reason is that there are around 500 - 600 articles published that document that you can reverse pathological remodeling. They have anti-fibrotic efficacy, anti-inflammatory agents, can reduce pressure both systemically and in the lung circulation, and also can block thrombosis without causing bleeding. This is all documented and published information. Most of it's in preclinical work. We have two programs with HDAC inhibitors. One, the first one you see is one, and we have just reported phase II-A data in patients with PAH that are very positive. We did that this fall in Q3. It's a repurposed drug that's been in man for 50 plus years for neurological disorders such as epilepsy prevention, and we've taken this drug into pulmonary arterial hypertension in a new formulation, so phase II data was reported in Q3. We also got approval by FDA after a physician had requested us to ask FDA if we could get expanded access program approved. We call it compassionate use here in Europe. So the physicians can opt to use the drug now, way ahead of us reaching the market. And this is what requested us because of the investigators in our trial saw what they saw in benefits of adding this to current standard therapy. So what's the milestones coming up? Well, we are going to go to the regulatory authorities and get the next program accepted, discuss it and accepted. And that's going to happen in H1, so first half next year. And we're going to get readout from this compassionate use program, long-term use with our drug on top of standard therapy under protocol that is between the patient, the physician, and Cereno. And then we're going to start that program, a phase II-B program or a phase II-B3 program. It depends on our discussions with FDA and what's best for Cereno. That's going to start in 2026, first half. The second program is a novel HDAC inhibitor. We call it CS014. It's actually a modified version of the first drug. It's a deuterated version. It has a better profile than the first one because we believe that the field is so big for these drugs that we can pursue this for several indications. That's in phase I. It was initiated this summer, and we're going to complete that study by the first half of next year and then move to regulatory for a phase II study acceptance and start that also in the first half of 2026. The third drug is an IP receptor agonist that's very potent, very selective for the IP receptor. We licensed that from University of Michigan and the innovator Mike Holinstat, and we have complete development commercial rights for that. That's in preclinical work. I will address these three drug development programs here. I'll start with the first one. Back to the lady that got diagnosed with this, seven years to live. What if? What if CS1 could halt and reverse this disease? It's this narrowing of the vessels in the lung. And it's difficult to breathe. It's difficult for physical activity. And eventually, you die of right heart failure. It's too heavy for the right heart to pump. Now, HDAC inhibitors with these characteristics that I mentioned here, reverse pathological remodeling, anti-fibrotic, anti-inflammatory, pulmonary pressure reduction, and anti-thrombotic fits very well with the pathological progression of this disease. And you can see in the middle here how the artery is narrowing as a progression. There's documentation in animal work that you can actually reverse this progression of the muscle, both the muscle and fibrosis, as well as the heart muscle. You can reverse the hypertrophy, and you can lower the pulmonary pressure. That's why we have pursued this now into man. I'll review with you what we have seen. This drug has orphan drug designation. It's protected seven years in the U.S. and 10 years in Europe after introduction. It has been proven to have good safety and tolerability in our phase one trial. Now we documented good safety and tolerance in the phase II-A trial and very strong signals of efficacy. We have this expanded access approved. What we also have released this fall is our new compound CS014, animal work that you saw this on the slide. This is the origin of disease, the plexiform lesion. We published or communicated here in Q3 that our novel HDAC inhibitor has a dose-dependent impact reduction of plexiform lesions. So the origin of the disease. So HDAC inhibition and our drug seems to work in the animal work. And we also saw reduction of fibrosis in that study. So very encouraging data. Now, the study that we have pursued on CS1 in the states together with the major company, Abbott, was run in 10 centers and had 25 patients included. And we had three different dosages. And our drug was added to current standard of care therapy. And we had a 12-week treatment. The primary objective was, of course, safety and tolerance. And then we looked for signals of efficacy. But I want to review with you what happened during the year that we ran this trial. One investigator came back to us and said, "My patient is a remarkable improvement. We have 30% improvement on the pressure in the lung. We have 43% improvement of total pulmonary resistance, the resistance in the artery, so lower the resistance. And we had normalized cardiac output the way the heart can pump." So we wrote, or the investigator wrote an abstract to American Heart, but we eventually released it to the market instead because we couldn't sit on it for four months. So this was the first clinical indication that we saw that something good is going on when we add our drug to standard of care. Then we did a review halfway through the trial, and we saw that two-thirds of the patient would reduce pulmonary pressure sustainably with Abbott's wireless remote technology, CardioMEMS. And then, of course, at the end of last year, investigators approached us and said, "Can you please apply to the FDA for compassionate use? We don't want to let go of your therapy for our patients." So we did that and got that approved in January. Now, the results that we communicated in Q3 from this phase II-A trial showed very good safety and tolerability of a drug in these patients. So we expected that because the drug has been in man in much higher dosages for neurological disorders. So we were happy with that result, but we expected to pass it well. What we didn't know was what kind of efficacy we would see in this trial as we add this to standard of care. But what we saw was that in 43% of the patients, 9 out of 21 patients, we saw a reduction of a REVEAL Risk Score. That's a 10-grade scale. And if you reduce a score with one point, you actually improve. You lower the risk of mortality with 23% in one year. And we did that in 43% of the patients just by adding our drug to other therapy. Very pleased with that outcome. The second thing that physicians do in their office, they use REVEAL Risk Score, but they also use something called Functional Class. That's a scale of four. So you can see that to the right, class I, II, III, IV. If you have Class I, you hardly feel the disease. So it's easier for the patient. It's in the beginning of the diagnosis. If you have Class IV, you can't leave your bed. You're bedridden. So very severe. What we saw in our study was that 1/3 of the patients improved their functional class just by adding our drug to their current therapy. They moved to a lighter class. So physical capacity in these patients deemed by the physician was improved with one class in 1/3 of the patient. 86% of the patients were stable or improved. Very good information to know before we go into the next program. The third thing that you want to know is that you can reduce the pulmonary pressure. We saw that in 2/3 of the patients. That's the scale to the right as measured with CardioMEMS, Abbott's technology. Now, very important, we had high responders. We call them super responders in this trial. So five out of these 21 patients, around 24%, had a reduction in pulmonary vascular resistance between 35% and 51%. So the narrowing was released in these patients. And that's a very good result and promising result for us. And these patients had a corresponding improvement of cardiac output, the heart's ability to pump. Now, if you look through the various measurements in this trial, REVEAL Risk Score improvement, Pulmonary Vascular Resistance improvement, Functional Class improvement, stroke volume or cardiac output, as well as pressure reduction, you can see here that these patients are aligned with those kinds of improvement. And that's a very encouraging sign for us. What we have done since then is that we also communicated in Q3 here at our Capital Markets Day that we have signed an agreement with Fluidda, a company that can measure impact on structure in the lung with a CT scan technology. The founder is a respiratory professor, and the son comes from NASA, you know, the space business. And they have created this company that you can look at this. This is available in 500 clinics now throughout the world. And we will study this structure change in our compassionate use patients and look for information in H1. That's the first patient and the first drug. Second patient group, idiopathic pulmonary fibrosis. So you saw this, the fibrosis development in the lung. This is not muscle now. This is the connective tissue in the lung. What if we could impact this, which has three to five years to live, mostly men? And here we have CS014. We believe this will be disease modifying for this patient category because there's documentation that HDAC inhibition with a compound that's the mother compound here, VPA, can reduce fibrosis development. And we also saw with CS014 here, as I mentioned before, that we have impact on fibrosis. With this HDAC inhibition and our second program, we believe we can halt the progression of pulmonary fibrosis, maybe reverse it. We will have to see that in the trial. This targets a $7 billion market in 2034. This is a new chemical entity, CS014. We have received patent in the U.K. this year. IPF is an orphan disease, and we will likely get an orphan designation eventually. That's our hope. Let's move on to our third compound, CS1. Most common cause of death, infarction and stroke, bleeding is the key issue here and unmet need, but also efficacy as it's the most common cause of death. Here we have our CS585 in license from University of Michigan, very specific to the IP receptor. Now, 22 million people die of cardiovascular diseases by 2030 on an annual basis. 80% are due to thrombosis, attacks in the heart, and stroke, and 60% experience bleeding of the current therapies. Because physicians are afraid of the bleeding risk and you can't use high dosages, and some patients don't even take their medication, but so there is really a need for new strategy here that you can add to or use alone in these patients to prevent thrombosis from happening or recurring, and we have documented with this new drug that has a receptor, IP receptor, that's very specific and potent for that, that we can prevent thrombosis without causing bleed in models of mice that's very translatable to man. If you don't bleed, if you are effective preventing thrombosis in mice, you will be effective in man, and if you don't bleed, it's most likely that you don't bleed in man. So this is still in preclinical work, and we aim to put it into phase one in 2026. Now, if you can look at our portfolio then, so you can say that we have a PAH program with CS1, orphan disease. We have an IPF, idiopathic pulmonary fibrosis program with the second HDAC inhibitor. That's in phase one. We'll go into phase two in beginning of 2026. And we have an, you can say we have an HDAC portfolio then. And then we have a thrombosis portfolio because both our HDAC inhibitors have proven prevention of thrombosis without causing bleed. So this, we believe, is attractive for pharmaceutical partners eventually. And we are in talks with various pharmaceutical players about our programs. Now, we are based in Gothenburg at the new healthcare environment, and we are on the fourth floor here, GoCo, moved in there this year. This is a team, a lot of experience from the pharmaceutical industry here, and we run the programs from here, but most of our programs are actually in the U.S. Here's our scientific advisory board, and it's quite prominent players in the field, and we're happy to work with them. Cereno is not a small company. You saw just a few people here, but we work globally. You can see here all our collaboration partners. Abbott is one of them. Fluidda, the lung detection company, the latest here. But we have a number of collaborative partners around the world and advisors, so we are busy. Now, next upcoming milestones. This is, I think, my last slide, so positive CS1 top line in PAH presented in phase II, Q3 this year. We've strengthened our focus and identified idiopathic pulmonary fibrosis for the second HDAC inhibitor, CS014. We did structured finance alone on SEK 250 million a couple of weeks back. So we have secured funding and operations into 2026. We're very happy with that. And then upcoming milestones is CS1 phase II-B, or pivotal trial to be accepted by FDA by the first half of next year. CS1 extended access program or long-term clinical use on top of standard of care we have approved, and we will see some readouts in the beginning of next year together with the Fluidda technology and CardioMEMS and other standard measurements. So that's CS1. For CS014, we complete phase one in first half, and we get approval in the second half. And then CS585 will still be in the preclinical work, but we aim to complete that in the first half of 2026. So that concludes my talk. Thank you for listening. I hope you find it interesting. Thank you very much, Sten, for this very insightful and interesting presentation. Now, I would like to ask you some questions, and maybe we can discuss a little bit. I mean, it has been a very eventful year this year for you, and I would like to look forward a little bit into 2025 to your next milestones that you will reach, and maybe to start with CS1, I mean, you said today you will have interactions with the FDA, and could you provide some color what kind of meetings you're going to have with the FDA and if you already have some dates with the FDA fixed, and also maybe could you comment on, you said in H1, we expect different things for the FDA outcome we expect, but we also expect Fluidda and EAP, and do you think that the FDA wants to see that data? So does it need to come first, Fluidda and the EAP data, or does the FDA decision is only based on your current data? Yeah, thank you. Very good questions, of course, but yeah, so we don't have our clinical study report yet, so that's been worked on, and we expect to conclude that by the end of this year, and then we'll move with that information and our discussions with the FDA. We don't have a specific date yet set, and there are different kinds of meetings that you can pursue. We haven't decided exactly what kind of meeting wants to run first, but it's advisory meetings first, and then you go into more serious discussions, and so first meetings, normally you ask questions to the FDA and they answer, so that's how it works. We expect to conclude those discussions by mid-spring and obtain an approval by the end of the first half of the year. We don't expect the FDA to want to see the Fluidda information. When you move forward, it's basically safety concerns that the FDA is looking for. Because the drug has been in man for a long, long time in higher dosages, and we had a clean, basically a clean side effect and tolerance profile in the phase II-A trial, we should be fine with FDA and moving forward. It's more the structure of the study that we'll pursue. The Fluidda and other information that will come on long-term use with our drug on top of standard of care will be very interesting to look at. You should remember that this trial was only three months long, and we saw what we saw in that trial. So we expect to see more important and hopefully positive information in further direction of benefits for the patients with long-term use. Very interesting. And then my second question, maybe I would shift a little bit to CS014. Very interesting that you made this move this year or relatively recently into IPF. And here my question would be like, do you already have some ideas and could you provide some color on a potential phase II design, like what kind of timeframe we are looking here at? And also maybe a little bit in relation to what your local peer, like Vicore, has done. I mean, they also have run a phase two. Do you believe that you could run something similar with CS014? I think you should always separate yourself from others because you have a different mode of action, etc. So you look at the bench and you see what others have been doing and how both the investment community and the regulatory community, how they appreciate the various studies and setups, etc. So I think the learnings is that you should, if you can, you should try to do a study that's placebo controlled. And I believe, and I hope we will be able to do that. That would be our target. So it would be different than what Vicore did initially. And it depends also what kind of information you have with you when you pursue a trial. So we haven't gone public with any design or anything like that. But when we get, we have to see our phase one study coming out. It's progressing very well. We started in the summer, and we aim to conclude that and have the study report by end of the spring, so to speak, before the summer, and then we'll take that information. During the spring, we'll design our protocol. Great. Thank you very much, Sten, for this very interesting presentation today. For the sake of time, I will close now the presentation, and thank you for listening. Thank you.