We will present and analyze the final results from the Phase IIa AIR trial investigating buloxibutid over 36 weeks in idiopathic pulmonary fibrosis. My name is Megan Richards, and I'm the VP of Investor Relations, Communications, and Portfolio Strategy at Vicore, and I will be moderating the session today. Our speakers today will present key insights from the data for about 40 minutes, and then we will open up the discussion for Q&A. To kick things off, I will turn the conversation over to Vicore's CEO, Ahmed Mousa. Thank you, Megan, and thank you everyone for joining. Good morning, good afternoon. I'm Ahmed Mousa. I'm the CEO of Vicore since September of 2023. I'm really excited to have joined the company after the highly promising interim results of this phase IIa study of buloxibutid were revealed, especially as I'd previously worked in IPF and felt that these data reflect disease-modifying potential in an area of such high unmet need. You know, my enthusiasm for the approach also stemmed from my time in the lab, where I saw firsthand the ability of angiotensin II pathway modulation to resolve fibrosis in other disease contexts. Now, with me here today presenting are Bertil Lindmark, our Chief Medical Officer. He is a highly experienced drug developer, was previously the Vice President of Clinical Development for Respiratory at AstraZeneca, leading the approval of large respiratory franchise drugs, Symbicort and Pulmicort. He was the Head of R&D at Almirall, bringing a COPD medication to the market, and he's been the Chief Medical Officer of a number of biopharmaceutical companies leading clinical development programs, including large late-stage IPF programs as well. And of course, last but not least, we have Professor Toby Maher, who really needs no introduction. He's amongst the world's leading clinicians in the development of therapies for pulmonary fibrosis, and currently the director of the ILD Center and a professor at the University of Southern California. On the next slide, we can look quickly at the agenda. And so, first, I'll talk a little bit about the rationale for buloxibutid and IPF, why we think this approach is the right one. And next, Professor Maher will review the final phase IIa data, as was presented at ATS. And after that, Bertil will give us some deeper context on the data set, and also place it in the broader therapeutic landscape. And after that, I will make some connections between what we've seen preclinically and clinically, with respect to the mechanism, and also talk about the phase IIb ASPIRE trial that we're excited to kick off in the coming months as well. And finally, we'll of course do the Q&A, as Megan mentioned. So first and foremost then, you know, why buloxibutid for IPF? You know, we all know that IPF is a tough disease of progressive fibrosis. It essentially chokes off patients' ability to breathe with only 2-5 years of survival, you know, from diagnosis with the current therapies. There have also been a number of therapies that have, you know, not worked in recent years. So then, why angiotensin II type II receptor agonism, you know, for IPF? And if we look at this kind of schematic of the mechanism, what buloxibutid is doing is selectively agonizing on right and orange, this AT2 receptor, which is an endogenous tissue repair system that sits within this broader, angiotensin II pathway. We believe that agonizing this upstream mechanism of action provides broad anti-fibrotic and tissue repair mechanisms, and it's a really nice approach for a heterogeneous disease like IPF, as contrasted perhaps with downstream antagonistic approaches that might block collagen deposition. Just to kind of orient you to this angiotensin II pathway, when you look at the angiotensin II peptide, it signals on both the AT1 and the AT2, and these receptors sit as opposing forces in the body. The AT1 pathway is a hypertensive, pro-fibrotic, pro-inflammatory pathway, and that's actually an entirely suitable response to certain injuries, infections, insults, to make sure that you maintain a good blood pressure. It's very conserved. You see it in most species, and it's quite important. At the same time, you know, because of that importance, the AT1 pathway or AT1 receptor is broadly expressed and constitutively expressed across tissues. And so for that reason, when there's angiotensin II peptide release, the net effect is typically this AT1R phenotype, hypertension, inflammation, fibrosis, leading to the development of ACE inhibitors and angiotensin receptor blockers. What then is interesting about this AT2 receptor is it's much more selectively expressed, both in tissues and in time. So in most tissues, you don't find the AT2 receptor basally expressed. Rather, it's upregulated after there's extended hypertensive, fibrotic, or inflammatory processes, and then it becomes upregulated so that it can resolve those processes, over time. Interestingly, though, one of the few tissues where you'll find basal and constitutive expression of the AT2 receptor is the lung, and we believe that's because you're always breathing in some external particles that might drive some of these fibrotic or inflammatory processes. So it's great to have kind of the built-in system, you know, there to always kind of be resolving that. And but for whatever reason, it's there, and so our main thesis is to then, you know, basically supercharge this endogenous tissue repair system against the tough disease that is IPF. And the other thing that's then very interesting is actually the primary cell type in which you'll find this AT2 receptor expressed are these precursor alveolar epithelial type two cells. And so if we look at the next slide, we can say, "Why are these cells important for the healthy function of the alveolus, a critical compartment of the lung, you know, for breathing?" And these are really the, you know, kind of exist at the distal lung and are critical for gas exchange. And so when you look at the type two cells, you know, first and foremost, they actually differentiate into the type one gas exchange cells, which are the main cell type of the alveolus, so that's a very important function for them. A second key function that we highlight for the healthy function of the alveolus is the production of surfactant proteins. There are surfactant proteins that are involved in innate immune response, and there are also surfactant proteins that are critical to address the surface tension associated with water. So in the absence of these surfactant proteins, you know, there's the surface tension of water in the alveolus would drive the collapse of this compartment, and so that's quite a critical function for this cell type as well. So maybe if we push forward, then we say, "Okay, well, what happens in the disease state of IPF to the alveolus, and what happens in the disease state of IPF to the Type II epithelial cells? You see here on the left, you know, the injury to the lung that drives this fibrotic process, it doesn't spare the Type II cells, so they become dysfunctional. They undergo apoptosis, so there's a reduction in that population of cells. That injury, then, of course, cuts off the ability of this cell type to produce surfactant protein, leading to what's known as pre-fibrotic alveolar collapse due to loss of surfactant production. What that essentially means is, even before the fibrotic buildup, you know, inhibits the gas exchange, you actually have the alveolus unable to, you know, participate in that process because it's no longer has its integrity. That's a critical function. In addition to that, of course, the dysfunction of these Type II cells is gonna lead to less replenishment of the Type I gas exchange cells, which of course, are quite important. And then further than that, you know, when you have the injury to the Type II epithelial cells, it drives them to release this pro-fibrotic cytokine in response to the injury, this TGF-beta 1. And this is widely recognized to be a master regulator of fibrosis. And, you know, that, TGF-beta 1 then drives what's called this epithelial-to-mesenchymal transition, where these Type II epithelial cells, which should be differentiating more into the Type I cells, are now differentiating into fibroblasts, and then ultimately myofibroblasts, which, are the kind of key drivers of the collagen deposition and buildup of fibrosis in the lung interstitium. And then last but not least, the TGF-beta 1 is involved in dysregulation of the matrix metalloproteinases. And in particular, there are a set of matrix metalloproteinases known to be collagenases that can break up the collagen, and those collagenases are downregulated in the disease state that is IPF. So with a lot going on that, you know, drives this fibrotic process, you know, on the right-hand side, we see, you know, what buloxibutid is postulated to do, to alleviate this. And first and foremost, we're agonizing this AT2 receptor on these Type II epithelial cells to refunctionalize them, and basically allow them to continue to survive, to continue to produce surfactant, and to continue to be available to differentiate into Type I gas exchange cells. So that's going to be the first piece of the puzzle. And then the second piece of the puzzle is an inhibition of TGF-beta 1. So agonism of the Type II receptor will downregulate expression of TGF-beta 1. It will downregulate expression of TGF-beta receptor that it signals on. And also, we've shown in vivo will downregulate the signaling through the key pathways by which TGF-beta 1 drives its pro-fibrotic activity. So a significant impact on that, on that particular cytokine, which we think is important, and that ultimately will inhibit that epithelial-to-mesenchymal transition that we talked about. So stop the Type II precursor cells from differentiating into fibroblasts, then ultimately myofibroblasts. And then last but not least, we have then an upregulation also of the collagenase-type MMPs through this mechanism of action, so that we have the enzymes available to break down the fibrosis that's already built up. On the next slide, you know, when we put this all together, then this is what really underscores our excitement. We think we have the right mechanism with an upstream, you know, kind of broad approach to drive an endogenous tissue repair system. We have this really nice, you know, phase IIa signal that Toby and Bertil will talk more about. Then we have the right next experiment with a robust Phase IIb design to really demonstrate in a larger study and a placebo-controlled study the efficacy and the safety of this molecule for IPF. From here, I'll turn it over to Professor Maher, who will review the Phase IIa data set as we did at ATS. Great. Thank you, Ahmed. So yeah, it's a pleasure to be on here today to talk everyone through the results of this study. If we can move to the next slide. So people may well have seen the interim version of this data before. This is now the full and final data set. And just to remind everybody of the trial design, this was an open-label, multicenter, international phase II trial of buloxibutid at a dose of 100 milligrams twice daily, given for up to 36 weeks in treatment-naïve patients. And there are a few important parts of the study design just to focus on. First of all, as is the standard with late-phase clinical trials in idiopathic pulmonary fibrosis, all patients had to have central reading of their CT scan to confirm that they had idiopathic pulmonary fibrosis before they could enter into the trial. That's been an important sense check in IPF trials to make sure that we are actually studying the population of patients that we want with ultimately progressive fibrotic lung disease. As you can then see from the trial schematic, patients went through screening, and once enrolled into the study, underwent regular study visits. The primary endpoint of the trial was safety and tolerability. The efficacy endpoint of forced vital capacity was measured as a secondary endpoint, and as we will touch on, there were exploratory biomarker endpoints. With the forced vital capacity, again, there are a few things to focus on there. So although this was an open-label study, the spirometry was again performed, essentially to phase III standards, which is to say that there was a standardized spirometry device provided to each center, and that there was central overreading of all the spirometry results. Again, that's an important step in the quality control process to ensure that the spirometry that is obtained by sites has been well performed and is accurate and interpretable. And then finally, if we look at the study schematic, you will see that there was a plan for frequent study visits. In 2019, when the study was being put together, this seemed like a great idea. The goal really being to ensure that by collecting frequent FVC measures, we were gonna have a very clear impression of individual disease trajectories. Of course, with the onset of COVID in 2020, having quite so many touchpoints with the clinic actually became something of a weakness for the study. And as you'll see, this led to a number of dropouts with patients during 2020 and early 2021, often being very scared about coming up to healthcare facilities because of concerns about COVID. And so that's, that's just something to keep in mind. As we said, patients were treatment-naïve, and there were two specific visits where investigators were asked to consider whether patients should be exiting the study onto open label or onto standard of care therapy. And then, patients were ultimately followed up to week 36 on treatment. So if we can move to the next slide. So this is the study disposition. 138 patients were screened, 86 of whom screen failed. That may seem like a high screen failure rate, but it's comparable to other late-phase studies in IPF, and a lot of that screen failure is accounted for by the central reading of the CT scan. So in some ways, it's important that there was an appreciable screen fail rate because it tells us that patients were appropriately not being included in the study, if they didn't have the CT appearances of idiopathic pulmonary fibrosis. So ultimately, 52 patients were enrolled. And then, as I've alluded to, there were a reasonable number of dropouts. So 24 patients didn't make it to week 36, and the vast majority of those dropped out during the COVID pandemic, as we said, because of concerns about attending healthcare facilities during the pandemic. The minority dropped out because of drug-related reasons, and we'll come onto that on the next slide. So 28 completed the week 38, week 36 visit, and then for our safety analysis dataset, we have 52 patients. In our efficacy for analysis set, we have 50 patients. If I can have the next slide. So these are the baseline demographics of the patients. Now, in general, this looks very similar to what we see in comparable late-phase IPF trials. So we have predominantly men in their mid to late sixties. The racial disposition reflects that the countries in which the study was run. The time from diagnosis, of 1 year, again, reflects the fact that these were treatment-naïve patients. So these were patients, very early after diagnosis, who had either chosen not to go onto antifibrotic drug, or, did not have, access to reimbursed therapy. And then, if we look at disease severity, again, this is very similar, to what we see in late-phase IPF trials with, at least moderate disease severity and an FVC of 75% predicted. And then, just the final bit to point out is that, when we look at the CT pattern, and when it is centrally read, we can divide patients up into these sort of typical and probable groups. So, just over a third of patients had what we call a typical UIP appearance, while the two-thirds had a probable UIP appearance. Again, this is comparable with late-phase studies that have been run in this disease area. Next slide. As I said, safety and tolerability was the primary endpoint of the trial. If we start first on the left-hand side, with the safety, we can see that there were not any serious or severe treatment emergent adverse events that were ascribed to the drug itself. There were three TAEs that resulted to or that were ascribed to the drug and resulted in withdrawal from the trial. As you can see, there were no deaths ascribed to the drug. If we look on the right-hand side, the main side effect that was seen that can be assigned to the drug is hair loss. This was recognized in the phase I trials, and this in phase I appeared to be a dose-dependent side effect. At very high doses, occasional patients lost all body hair. At the dose used in this trial, the 100 milligrams twice daily, the hair loss that was reported was described as mild to moderate at worst, and only one patient discontinued treatment due to this hair loss. It might be noted that the current drugs in this space, nintedanib pirfenidone, have significant gastrointestinal side effects, and it's often been difficult to combine treatments that have additional GI side effects with pirfenidone nintedanib. And so it's important to note that buloxibutid didn't have any appreciable GI tolerability issues. So if we can move on to the next slide. And so this is the FVC data. And I think this is the very exciting part of the trial. Now, of course, this was an open-label study, and so we did not have a placebo group. The dotted line on this graph is a hypothetical line describing the trajectory that we would expect a standard IPF population of patients would follow. And this is really based on our 20 years experience of running clinical trials in this disease area. We know from that experience that the average IPF placebo group loses somewhere between 180-240 milliliters of FVC per 12 months. So we've just sort of put the dotted line on there as an indicator of what might have been expected from a placebo group. The green line is what was observed in the patients being treated with buloxibutid. So each time point represents the observed mean for that time point, and you'll see there's a little number under each green circle that reflects the number of patients who provided measurements at each of those time points. As we've said, there was an early dropout rate, which was primarily attributable to COVID, so we do see some attrition in numbers over time. But the startling thing about this line is that it, it's going upwards, suggesting an improvement in lung function over the 36 weeks of the study. And for those of you on the line who have looked at other IPF clinical trials, this is not something that we generally see. With the approved therapies, we see a slowing of disease decline, so the treatment line has tended to mirror the placebo line, albeit with a more shallow level of deterioration over time. So to be seeing a set of results where we're seeing an upward inflection in the curve is very exciting from my perspective. Clearly, we have to caveat this with the fact that it's an open label study. We do know that occasional patients with IPF who are untreated do show some mild improvements in lung function over time. But if one took a sort of Bayesian-type approach to interpreting this data, the chances of sort of accidentally enrolling 28 patients who show a persistent improvement in FVC over 36 weeks is minuscule. So I find this data to be incredibly tantalizing in terms of suggesting an effective treatment. If we can move forward. And then Vicore have started trying to dig into other data and look at some of the plasma biomarker responses, and we put here two potentially important biomarkers. So on the left-hand side, we have TGF-beta. Ahmed has already described TGF-beta as the master regulator in idiopathic pulmonary fibrosis, and certainly it's a very important pro-fibrotic cytokine. So seeing a reduction in TGF-beta levels would suggest an important effect on fibrotic pathways. On the right-hand side, what we see is an increase in MMP-13. MMP-13 is a collagenase responsible for degradation of collagen and extracellular matrix. And so an increase in plasma MMP-13 would suggest increasing collagenase activity with exposure to treatment, and again, that's something that would be considered a good thing to happen in the treatment of IPF. So if I can have the next slide. So having talked you through all the data, this is just the summary. Ahmed gave you the rationale for why targeting the angiotensin II receptor makes sense, and buloxibutid is a novel drug targeting this mechanism. We've shown you the safety profile, which I believe is very good. There is that one tolerability issue of hair loss, which has been mild to moderate, and I think in a population of predominantly older men is not something that has caused concerns with patients enrolled in the study. And finally, I've shown you the lung function data, which, as I've said, has to be caveated by the fact that this is an open label study. But really, for me, is incredibly tantalizing given how the treatment curve differs so startlingly from what we've seen in other drug trials in this disease space. I will stop there, and I will hand over now to Bertil for the remainder of the session. You're muted, Bertil. Second after you, and obviously my computer system reacted in some way. Anyway, I want to give extra context to the AIR data and to do a little bit of comparison with historical data and try to set this in perspective. It's pretty obvious if we had shown a shallower decline of the FVC, then we wouldn't have engendered as much interest as we have. But actually we, for the first time, have shown a pretty dramatic increase in FVC. So can I have the first slide, please? As Toby was saying, we took very much care to include the right patients, and when you compare here with the INPULSIS, patients in the placebo group, they were very much alike in terms of age, in terms of gender, BMI, et cetera. The lung function was actually slightly worse in the AIR trial. So patients had lost 25% of their lung function, and this is sort of the combination of HRCT and the FVC percent predicted. I think that tells the story that these patients had really bona fide IPF, and that there is a good comparison with historical data based on that. Next slide, please. So Toby showed the benefit or the good side effect profile, and I think that's... This is another sort of contrasting data set because, you know, can you, can you achieve an increase in lung function and still be very tolerable? And you look at the side effects on the buloxibutid, extremely good on the GI side, low rate of exacerbations and cough worsening, which are kind of key IPF characteristics, and then sort of comparable or much better serious, severe, or fatal AEs and non-related to buloxibutid. So given the side effect profile and given the kind of effect opportunity that we see with buloxibutid, we think that sort of you could be thinking of first line therapy, and you could be thinking of combining buloxibutid with most other sort of currently present or upcoming therapies. So this is a good starting point, sort of a tolerable therapy with potentially good disease-modifying characteristics. Next slide, please. So we've seen this graph before, and as Toby was pointing out, it sort of goes in the wrong direction. But for the patients with IPF, I think it goes in the right direction. And obviously, you can prove and unprove any approved drug with sort of cutting and slicing the data into really small buckets. But here we look at sort of the different subgroups in the AIR trial, and both in terms of gender, geography, and in terms of type of IPF. We talk about the probable UIP and the typical UIP, depending on the HRCT pattern, all end up north of the horizontal line showing improvement. And when we look at both the mean and the median FVC change, you can see that both are positive, and that tells you that this is not driven by singular patients or a subgroup of high responders. The data set is really entirely highly consistent. So that tells you that the patients had a good bona fide IPF, and they reacted completely different. It's not a single patient or a subgroup that sort of pulls this data away. Next slide, please. When we look at the percent predicted, and, you know, this is a way to link the lung function to the body size, and the length of the patients, for example. The buloxibutid again shows both a mean and a median improvement compared to baseline. And we've added in the untreated patients from the INPULSIS studies and the nintedanib patients just for comparison, and we've interpolated down to 36 weeks. So here again, a percentage predicted, it's consistent with an increase in absolute FVC and tells the uniqueness of the intervention. Next slide, please. When we look at the sort of patients that outperform the change in FVC, when we compare with standard care, the INPULSIS data with nintedanib, buloxibutid wins, sort of outperforms 75% of the patients. And when we compare with the untreated in the same study, we outperform against 82%. So it's really a population shift that we accomplish with the buloxibutid intervention. Next slide, please. Here we look at the percentage of patients with improved lung function versus baseline. And of course, you know, as Toby was saying, how likely is it that you would in a population like this, 52 patients, that you would see an accumulation of patients with vastly improved lung function? Well, if we compare with the untreated, that's about 9%. So you would think of 5 patients maximally or maybe 10, but it would still be much less than what we saw in the AIR trial. Standard care, 25%, also not doing as well as buloxibutid. And there is sort of internal consistency data in the data. There is the loss of lung function, the previous loss of lung function, saying that these are bona fide IPF patients that actually increase in lung function. Next slide, please. So we had in the trial, we built in a risk-benefit evaluation at week 12 and week 24. And the physician was prompted to think about whether or not it was the benefit-risk was okay and whether or not it was indicated to start anti-fibrotic therapy. One patient in the whole study went from inside the study into anti-fibrotic therapy, and overall, 97% at both time points kept going in the study, and it was felt that the benefit-risk was fine. So what I've tried to say today is basically we have a population that looks similar to previous populations and where we have a completely different side effect profile, extremely well-tolerated, and with no, you know, gastrointestinal side effects to be mentioned. Really, however we cut the data, the internal consistency and the comparison with historical data outside of the trial is really sort of telling that we have potentially a drug that could be extremely well sort of put in both for patients in the first line, but also in combination with other therapies that might be approved in the meantime. So with that, I'll finish my talk and hand over to Ahmed. Over to you. Yeah, thanks very much, Bertil. And, you know, so we have Professor Maher who talked about the clinical data, Bertil, who put it into a broader context. And before I talk about the phase IIb design, I'd just like to relink, you know, what we saw in the clinic with our postulated mechanism of action and even a couple of pieces of translational data that we have. So on the next slide, you know, it's just a reminder of what Professor Maher showed, the decrease in plasma TGF-beta trend, as well as the increase in the collagenase type MMP. But exactly what does this mean, and why are these important, and how does it link to our kind of preclinical data set and why we think this mechanism's important? So just on the next slide, really, you know, again, kind of reinforcing the importance of this pro-fibrotic cytokine, that it stimulates the extracellular matrix formation, drives these transitions of the type II cells to ultimately myofibroblasts for collagen deposition, and also plays a role in the MMP imbalance associated with disease progression. So it's been very nice to see very consistently in the preclinical and translational data sets that buloxibutid inhibits the expression of TGF-beta 1. And on the right-hand side, this is an ex vivo study in human IPF precision cut lung slices, but we've generated similar data in vivo and other models as well. And in addition to kind of the effect on the levels of TGF-beta 1, we also have very nice data in vivo, reflecting inhibition of the signaling pathways, the SMAD2/3 signaling associated with TGF-beta 1's pro-fibrotic drive. So for us, this kind of correlation between what we see in the preclinical and translational data set, in the blood biomarkers, and in the ultimate kind of lung function has been very exciting for us. And then maybe if we move to the next slide, there's also, right, as we said, this kind of increase in collagenase type MMP-13. And there have been a number of studies that have shown that this is an important matrix metalloproteinase for breaking up the collagen matrix. On the right-hand side, you'll see a study where they knocked out MMP-13 in mice and then bleomycin challenged them, leading to a greater level of fibrosis and damage to the lung. So this is an MMP that's known to decrease collagenase activity, sorry, sorry, to increase collagenase activity and to promote resolution of lung fibrosis. And so it's been very nice to see then the correlative kind of a plasma biomarker work that's consistent with the importance of this type of a matrix metalloproteinase. And this is also consistent with our translational data sets showing increases in the collagenase type matrix metalloproteinases. And then the third slide, this is also the third piece of the puzzle, which I think is not to be forgotten, right? This is the impact on the type II epithelial cells and the surfactant production. Again, here, just, you know, kind of showing a small study in vitro on the left-hand side, where you co-culture the type II epithelial cells with bleomycin. Essentially, you're simulating that injury, that I was talking about that occurs in the alveolus in the IPF disease state, and that'll lead to apoptosis and cell death in the type II epithelial cells. Here we see that C21 or buloxibutid, in a concentration-dependent way, is able to inhibit that, bleomycin-mediated apoptosis. What should that lead to, right? That should lead to an increase in these surfactant proteins that can address the surface tension and prevent or address the prefibrotic alveolar collapse. Our ex vivo human IPF precision-cut lung slices data are consistent with that, with an mRNA upregulation in key surfactant proteins B, as well as, C in order to address that, that phenomenon. So on the next slide, if you take this and you put it all together, you know, what that means is that you're hitting the fibrotic drive from two ends, right? You're reducing, hopefully, the level of fibrosis with this postulated mechanism of action through the TGF-beta 1 inhibition of expression and signaling, but you're also then impacting the fibrosis that exists through the upregulation of the collagenase-type MMPs. And then, as kind of a slightly separate categories, how we see it, you know, you're impacting also the alveolar integrity and addressing prefibrotic alveolar collapse due to loss of surfactant production. Those are some of the reasons why, you know, we believe we've seen this exciting clinical signal, and why, you know, we're excited to push forward to the phase IIb study. Maybe on the next slide, we can do a quick overview of that one. Again, this is really intended to be, you know, a robust phase IIb with kind of the regulatory endpoint in mind, so that we really demonstrate as much as we're able to, the safety and the efficacy of this molecule for IPF. It's randomized, double-blind, placebo-controlled study. It'll include IPF patients now who are on the standard of care, nintedanib, or not on standard of care, whether that be treatment naive or treatment intolerant or otherwise. It'll be a 52-week period where we're measuring as the primary endpoint change from baseline FVC at 52 weeks. We'll include 270 patients, and we'll also include two dose levels, 100 milligrams twice daily, same as in the phase IIa AIR study, as well as a 50 milligram twice daily dose, relative to the placebo, placebo group as well. On the next hand slide, we'll just put into a little bit of context what it means to enroll 270 patients based on our statistical powering. So while I've been very excited to see this improvement in lung function, in the phase II AIR trial, and we see that as a clinical signal of activity, certainly something that could stabilize lung function, especially something that's safe and well-tolerated, would be a huge win for IPF patients, would address a really high unmet medical need, and, you know, would be also, you know, a significant commercial opportunity. And so from that perspective, we've ensured that by including 270 patients in our trial, we have the statistical power to be able to detect a stabilization of lung function out to 52 weeks, under the assumption of kind of, you know, the most mild of placebo/standard of care arms, that have been observed in IPF trials. So really trying to make sure that we power this in a conservative way for success after seeing this nice phase IIa clinical signal. And then on the right, just depicting that we, you know, are going for a broad geographical footprint as we advance to phase IIb, including significant enrollment in the United States, with twenty to thirty percent of this study being anticipated to enroll in the U.S. And then from there I will hand it over to Megan for the Q&A. Great! Thanks, Ahmed, and thank you all for an engaging presentation. We'll now open up the conversation for questions, and we'll start with the analysts on the phone and then move on to questions in the chat. 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 Dan Akschuti from Pareto Securities AB. Please go ahead. Thank you very much for taking my questions, and congratulations again on the great data. I have mainly questions for the Phase IIb trial now. When are you expecting the trial start, and how do you see your data enabling you in kind of marketing to get the patient enrollment up and fast? Because there's still quite some competition, as you know, with other modalities. Thank you. ... Yeah, that's a, that's a great question. So on the timing side, we'll make the regulatory submissions to initiate the phase IIb starting next month. So we're, of course, compiling the final phase IIa data set to include as part of those. We've identified the 97 clinical sites that we'd like to include in the study across the 14 countries, and so we're already engaged with them. Maybe on the point of, you know, how enthusiastic investigators might be, maybe I'll turn that over to Professor Maher and see if he has any perspective on, you know, what this data set might mean for, you know, enthusiasm amongst the clinical community, as we, as we kick off the phase IIb as well. Thanks, Ahmed. Yeah, and I think as was alluded to in the question, it is certainly a competitive space at the moment for clinical trials. We've got at least one phase III study and a large phase IIb study running. That said, as a disease area, we've become much more experienced at recruiting patients, and the timelines, even at phase III for recruiting patients, have got shorter and shorter over the last decade as more and more centers have become involved in clinical trials. I think for phase II studies, you know, one of the keys to engaging interest is really having both a good rationale and having as much good data as possible. I think Vicore are in an excellent position with the data that we've just described to really engage with investigators and patients and patient support groups to really drive enthusiasm for this trial. And you know, my expectation, given the data that I presented today, is that recruitment should be as easy as it gets in a phase II IPF study, given what we can tell patients about the drug to date. Okay, thanks. And I would have one follow-up for you, Toby Maher, if I may. I listen to your presentations quite frequently, since you present a lot of other data sets from other companies as well. So I wonder how, how—because many of these data sets are 12-week based, and even in Vicore's data, we don't see much at 12 weeks. How do you compare kind of the significance of those 36 weeks data versus 12 weeks of going...? Thinking about the trajectory that Vicore now has for... How that bodes kind of for the 52-week trial? And if you can share anything else that you think is really standing out here in a positive or negative way. Thank you. Yeah, it's a good question. My general view is that 12 weeks will give us a reasonable impression of the potential efficacy of a drug. I think it's unlikely that we will miss an effective drug by running 12-week studies. And if you think back to the data I showed today, you know, at 12 weeks, there was stabilization of FVC with buloxibutid. So, that in itself, you know, would have been considered quite exciting in comparison to some other studies. You know, I think clearly having longer-term data is advantageous. As you've alluded to, the regulatory expectation is that phase III studies will be run over 52 weeks. So ultimately, decisions about efficacy will be made at the 52-week time point. So, where we have more than 12-week data, I think it can only build confidence further that the signal is sustained. And as you've seen from the shape of the curve with buloxibutid, perhaps the advantage of having run the study a good distance beyond 12 weeks is that we've seemingly begun to see a cumulative benefit. So, you know, when I'm talking to companies about study design, I tell them that I think 12 weeks is sort of the bare minimum, and it is enough, but if we can go further, then it can only build confidence that there is durability of treatment effect. Okay. Thank you very much. Appreciate it. The next question comes from Sushila Hernandez from Van Lanschot Kempen. Please go ahead. Thank you. Congrats on the results, and thank you for taking my question. Also, a question for Toby. With all these developments in the IPF space, what about, buloxibutid, profile excites you the most? Thank you. I know—I think two things. I obviously, you know, I... One always has to caveat one's enthusiasm about the improvement in FVC that we see over the 36 weeks, given that it's an open label study. So I, you know, don't wanna get... sound like I'm getting too carried away. But on the other hand, the lung function trajectory that we are seeing is completely different to anything that we've seen before. So to have a treatment, you know, let's say, that plays out in the phase IIb, to have a treatment that genuinely improves lung function over time, would really be a paradigm shift in this disease area. So I think that's reason for, you know, cautious excitement. I think the other important factor is the tolerability profile. You know, our existing drugs and several of the drugs in development are potentially very difficult for patients to tolerate. And with nintedanib, we see when nintedanib is used in community practice, about 50% of patients discontinue therapy at 12 months because of gastrointestinal side effects. So what we've seen with Buloxibutid suggests to me that it should be a drug that is relatively easy for patients to take long-term. So that combination of efficacy and good tolerability really makes this a very exciting program. Okay, thank you. The next question comes from Patrik Ling from DNB Markets. Please go ahead. Thank you, guys. Two questions, actually, more for Ahmed, I think. First, can you say anything about what you expect the phase 2b trial will cost, and if the financial resources that you have in your balance sheet right now is sufficient for you to bring that trial to completion? Yeah, no, great, great, great questions, and thank you, Patrik, for joining. We currently have a cash runway that takes us into 2026, as we've guided kind of publicly. So we really have kind of a strong balance sheet to push forward in a significant way, and of course, it's been really great to also build the support with the deal with NS Pharma, where we've outlicensed regional Japanese rights. But of course, that brought in upfront payments. It'll bring in milestone payments and also some cost-sharing for both the non-clinical, like the CMC cost, a portion of those, as well as the late-stage clinical development costs as well. Okay, great. And then also another question when it comes to the trial. I mean, in the AIR trial, you had several interim readouts. Will you have anything similar in this trial, or will we just have to wait until the trial is completely finished before we get any sense of direction from the trial? Yeah, absolutely. It's a great, it's a great question. So for both, like, regulatory reasons, and because now this will be a placebo-controlled study, there are limitations around what can be, what can be done in order to make sure that, you know, we're able to have the right regulatory interactions with the FDA. Our hope and anticipation is that with a positive phase 2b readout, we could engage with FDA to facilitate having only one phase 3 trial in order to get the drug approved. And for that reason, as well as some others, we won't have an efficacy kind of interim analysis. There will be an interim analysis for futility built into the study, though. Okay. And then lastly, I mean, since these patients might be on nintedanib as well, I mean, how do you handle if the patients drop out? Because as Professor Maher said, I mean, most patients drop out within 12 months of treatment with nintedanib. Yeah. So also a great question. So as part of our powering calculation, we have assumed a particular dropout rate, and that is in line with what's been observed in prior clinical studies that included nintedanib, including IMPULSS itself, but also including, you know, kind of other phase 2 and phase 3 studies. So we've made a baseline assumption of kind of what we expect for a typical study, the dropout rate to be. It's consistent with what, for example, the post-12-week or even a little bit more conservative than what the post-12-week dropout rate was in the phase 2a AIR trial. And in addition to that, we'll be able to observe in a blinded basis the dropout or withdrawal rates. So if there's any kind of shift from the assumptions and a need to think about adjusting the powering, there is that opportunity built into the protocol as well in case something unanticipated does occur. Okay, great. Thank you, guys. Thanks. There are no more questions from the phone conference, so I hand the conference back to the speakers for any written questions from the chat and comments. Excellent. Thank you for those great questions on the phone. Turning over to the chat, we do have a lot of great questions coming in. So first, I want to start off with a question from Jeff Jones at Oppenheimer: "Can you comment on the impact of outlier patients on these mean FVC results? Yeah, I think, Bertil did a great job talking through that. Bertil, why don't you recap, you know, some of the discussion you did on that point? Yeah. We saw 65% of patients sort of improving the lung function. And obviously, when we look at the mean and median, the mean improvement was 216 milliliters, and the median was, I think, from memory, about 63. So this really shows that the majority of patients sort of improved the lung function. Obviously, in a study like this, you will have patients improving and patients not improving because that's the nature of the disease. But as a cohort, we can say for absolutely, clearly, and when we cut the data material into gender, geography, type of IPF, we think that the data is internally consistent, and it's not driven by single or a small number of outliers. Excellent. Thank you, Bertil. Looking at the next couple of questions, we're actually getting a few similar ones from folks in the chat, so I'll consolidate them here. When do you expect the Phase IIb study to start, and have you received any feedback from investigators? Yeah, absolutely. So, we would expect to, again, make the regulatory submissions to initiate the study, next month, and then you would start screening, and enrollment following kind of regulatory clearance in the months, thereafter. So, we're really excited to kind of push, push forward. You know, Professor Maher talked a little bit about the reasons why, you know, people might be excited for this study and why, you know, it might kind of be, you know, relative to the competitive landscape that is IPF, and that it's a rare disease, you know, kind of a, an efficient enroller in that context, and we certainly hope that'll be the case. We're getting good initial signals at that front. We had kind of a packed room for our investigator meeting at ATS with some of the phase IIb investigators who were attending the conference. As I think I'd mentioned, we have 97 clinical sites, so that means we've already kind of aligned with those sites that we would like to include them, and they would like to participate in the study. And at least for now, that'll be kind of the number of sites that we have. So, you know, now we're kind of generating a little bit of a waiting list or kind of a list of others that maybe we can think about expanding in the future if it is needed. I would say that the early signals on enthusiasm are quite nice, and I think it is this, you know, first and foremost, having a safe and well-tolerated drug that's easy for patients to take, especially since we're going on top of the nintedanib standard of care. Then on top of that, having this promise of potential efficacy based on the phase IIa signal, that's getting some of the investigators excited as well. I think the initial signals there are quite good. Excellent. Another question from the chat here: What is the reason behind the hair loss seen with Buloxibutid, and how does this impact the profile of the drug? That's a great question. Should I- Maybe I'll hand that over to Bertil. Exactly, yeah. Yeah, no. As I mentioned, this is seen in a minority of patients, and we saw one patient stopping therapy because of the hair loss. Excuse me. The exact reason why we see it is not known, and we have started a program to look at the sort of the background, whether or not it's on target or off target. We think that is manageable. I think it's mild and or moderate. And as to Professor Maher, mentioned, the sort of the population group that we're looking at here, sort of male- predominantly males, 60, 75, etc., probably can tolerate some of this hair loss, especially if we improve lung function. But it's... At this point in time, the jury is out on the exact mechanism. Excellent. It looks like we have time for about one or two more questions, so, I'll go with a provocative one: Why do you think that you will succeed where others may have failed? That's a great question, and I think, you know, some of the discussion, you know, that I did at the top and the bottom really encapsulate that. You know, that you're going after a disease with an upstream mechanism of action that drives an endogenous tissue repair system, quite distinct, I think, from some of the other approaches that are downstream, antagonistic, and block collagen deposition. That you're also able to impact fibrosis in multiple ways, you know, reducing buildup and driving the breakdown, but also that you're able to have this impact on surfactant production, which is, you know, in a way, broadly being recognized as an important piece of the, you know, puzzle in IPF. So we think each of those pieces is important. I think the other, you know, thing that you might notice if you look at the literature in the IPF space is a lot of, you know, kind of scientists and academics are focusing in on these type II alveolar epithelial cells. And the refunctionalization of these cells, you know, we think is a quite an exciting thing to do, and we think, you know, that drives kind of a broad range of beneficial, beneficial effects. And I think, you know, that, those things give us hope that we can do something, you know, different, based on this initial signal and the translational data that we have. Excellent. Well, it looks like that is all the time that we have today for this session. So thank you all for taking the time to join. I know we had a lot of great engagement in the chat, and we were not able to get to all of the questions, but we would love to follow up with you, so please feel free to reach out to us after this meeting. Thank you so much for attending, and enjoy the rest of your day.