With the Jefferies Healthcare Banking Team, and it is my great pleasure to introduce Ahmed Mousa, CEO of Vicore Pharma. Thanks, Jason. Thanks to the Jefferies team for inviting us. I'm really excited to tell you more about Vicore Pharma and what we're working on. We'll refer to our typical forward-looking statement disclaimers. Vicore Pharma is a publicly listed company out of Sweden on the Stockholm and Nasdaq exchange. We have about a $230 million market cap and about a $100 million cash position as of the last quarter. We have a team based in Sweden, in Denmark, and also in the United States. We're fortunate to be backed by some of the leading specialists in the healthcare sector in both the United States and Europe. What we're working on at Vicore is a novel mechanism of action in the angiotensin II pathway, and a great deal of our effort is dedicated to advancing a novel therapy for IPF that's currently in phase two development, and also considering and actively working on earlier stage compounds in multiple other indications in the fibrotic and pulmonary space. Now, why have we selected IPF as the lead indication for our approach? I think it really starts with the unmet need. IPF is quite a terrible disease. The prognosis for this disease after diagnosis is survival of only three to four years. You're talking about a disease that's worse than most cancers, which is quite terrible. There are only two drugs that are available for this disease, and unfortunately, that survival that I just mentioned is in view of those available therapies. In addition to having limited effectiveness, they also, unfortunately, are really tough to tolerate. They cause really significant side effects, GI side effects, nausea, diarrhea, and other side effects that make them really difficult to take. For that reason, only about a quarter of patients who have IPF ever even start taking these drugs, even though this is such a deadly disease, which is a little bit shocking. In addition to that, the average time on therapy is only 10 months, which means that many people discontinue because that therapy has not been effective for them or because they cannot tolerate the side effects. Now, even though I have said all that, the market is still already huge and can grow significantly if you can offer a better tolerated or more effective therapy. Last year, the market was over $4.2 billion, and that's with these two standard of care therapies that I mentioned, pirfenidone and nintedanib. Now, the additional point to this is even then when you look at the pipeline in development, it's quite limited in terms of the number of therapies and quite limited in what, unfortunately, is expected to come from these therapies' contribution to kind of meeting that unmet need. This slide actually represents the total kind of sum of the phase threes and 52-week phase two Bs that are ongoing in this disease space. Boehringer Ingelheim has a phase three program that reported phase three data showing incremental improvement over a standard of care, still only slowing the decline of lung function with GI tolerability issues. United Therapeutics has therapy that they're advancing in phase three. Based on the experience with this drug and prior data, it has tolerability issues as well as kind of more of an approach that's more tailored to pulmonary hypertension than pulmonary fibrosis. Finally, BMS also has a phase three program. While that one does have a favorable tolerability profile in the phase two setting, it also has a very incremental effect that was observed in phase two. We are hopeful that these therapies can reach the market, but are expected, even if that's the case, to offer more incremental advancement for patients suffering from IPF, which is what makes us very excited about the approach that we're advancing in this field. Now, why we're so excited about this approach starts with the mechanism of action. It's quite different from the other programs that have been advanced in this space. Both those are ongoing and those that have previously been attempted and failed in this space. I'll talk more about that. That nice upstream mechanism of action has led to a significant clinical signal in a phase 2a setting where we've shown the ability to improve lung function rather than just slow the decline of lung function and also shown a very nice tolerability profile. What we have now ongoing is a large and robust phase 2b trial to really confirm the efficacy of this molecule with the regulatory endpoint in a global study. Now, as I'd mentioned, this mechanism of action we think is the right way to go after this disease. In a simplistic way, what we're talking about is activating a natural tissue repair system that exists within the body to drive resolution of fibrosis, reduce inflammation, and cause vasodilation or expansion of the vasculature. This is the AT2 receptor that's shown here in orange on the right-hand side of the slide, and our small molecule buloxibutid is designed to activate that receptor. This AT2 receptor, in a simplistic way, sits as the opposing force to the AT1 receptor system, and that's the body's rescue system which drives hypertension, inflammation, and fibrosis. That's, of course, a very suitable response to infections, injuries, insults. Knowing that this kind of system with this sort of two sets of pathways exists, we've actually had a lot of success as an industry in kind of blocking this AT1 system. ACE inhibitors and angiotensin receptor blockers, or ARBs, actually block AT1 signaling, and we think that equally or even more potent in terms of therapeutic efficacy across a range of indications can be activating this natural tissue repair system in the AT2 receptor. Now, then taking this into the context of the lung and say, okay, what happens when you activate this AT2 receptor in the lungs? Really, first is then confirming that this target is highly expressed on the lung. The data here on the right-hand side are a demonstration of the high expression level of the AT2 receptor in healthy human lung tissue. Actually, a number of academic groups have confirmed even upregulation of this receptor in a disease state like pulmonary fibrosis. In addition to that, through single-cell work, we know that this particular receptor is highly expressed on a stem cell in the lung called the alveolar epithelial type II cell. That could lead to the question, what does this type II epithelial cell do in the lung? It has really two key functions. This epithelial cell sits in the air sacs, the alveoli, millions of these at the end of the lung, critical for breathing. The oxygen would come through the alveoli, through the interstitium, and then oxygenate your blood by diffusing into the vasculature. These type II epithelial cells, they actually are the ones who create or differentiate into the type I epithelial cells, which are the gas exchange cells of the lung. They are critical for that reason. They're also the ones that maintain the integrity of the alveolus by releasing surfactant proteins, which break up the natural surface tension of water. In the absence of surfactant proteins, these air sacs would collapse on themselves because of that surface tension. Maybe taking this then to the context of IPF and saying, what happens in this disease and what does our drug do about that? On the right-hand side, you see, sorry, the left-hand side, you see kind of a schematic of the air sac, the interstitial space, and the vasculature. What you'll see is that in IPF, you have a disease where you have injury to the air sacs, to these alveolus. It drives a runaway wound healing process that causes fibrosis to build in the space in between the alveolus and the pulmonary vasculature. You also have a narrowing of the blood vessels and a thickening of those blood vessels. How this practically then happens is when you have this injury to the air sacs, you have apoptosis or death and dysfunction of the type II epithelial cells that have our receptor. When these type II epithelial cells become injured, they can no longer replenish the type I epithelial cells, and the type I epithelial cells are also becoming injured and dysfunctional, which means you have less gas exchange capability. Now oxygen is actually not able to diffuse out from your air sac into the interstitium, into the pulmonary vasculature. In addition to that, you have this phenomenon called prefibrotic alveolar collapse, which causes a loss of lung function. What this is, is when you have the surfactant proteins that are no longer being produced by these type II epithelial cells because they're dysfunctional, you then also have the inability for those alveoli to actually participate in the gas exchange process. Even before you have any build of fibrosis in IPF, that's having a real impact on patients as well. In addition to that, the injury to these type II epithelial cells is actually what triggers and orchestrates the wound healing process. The type II epithelial cells, when they're injured, they're the ones that trigger the scar formation, the fibrosis formation in the interstitium, and that's via a cytokine that they produce called TGF beta-1. Essentially, that TGF beta-1 drives the activation of fibroblasts, which become myofibroblasts and deposit collagen in the interstitium, which builds into a fibrotic matrix. Now, on the right-hand side, you see our view on what our mechanism does in the context of this disease. First and foremost, what we're doing is we're refunctionalizing and driving a proliferation of these type II epithelial cells, which essentially allows you to continue producing these type I epithelial cells, the gas exchange cells, allows you to continue producing surfactant proteins so that you can maintain the alveolar integrity, and it cuts off or attenuates the TGF beta-1 production and signaling. You can essentially stop both the wound healing process, the fibrosis build, but also repair the parts of the lung that were injured. It addresses the disease at its core when many of the other mechanisms that have been advanced for this disease only address the fibrotic build in the interstitium, which we think is not an invalid way to go after this disease, but perhaps an incomplete one. This is just some data reflecting some of the pieces that I mentioned. We're able to protect these type II epithelial cells and drive their proliferation and increase the production of surfactant proteins. We've done these experiments in human IPF lung tissue, ex vivo, as well as in in vitro experiments. We also show here that we're able to reduce that profibrotic cytokine, that wound healing signal, TGF beta-1 in the human IPF lung tissue, as well as reducing the collagen production. In addition to that, we also show that we're able to significantly increase a set of enzymes called collagenase MMPs. And these collagenase MMPs, like MMP-13, can actually break up or digest existing collagen or fibrotic matrix. And so this is actually a way of not just slowing down or stopping new fibrotic build, but actually dealing with what's already there. This is in line with the natural function of this AT2 receptor as an endogenous tissue repair system. In addition to that, we've also looked at our drug compared to some of the others that I mentioned at the very beginning. Nintedanib is one of the two available standard of care. Nintedanib is the phase three BI program. We ran an experiment where we took these fibroblasts and we exposed them to a profibrotic cocktail, so compounds that would basically drive these fibroblasts to start building the fibrotic matrix. That fibrotic matrix is built in basically pieces of ProC3, which are kind of the building blocks for that. Basically, what we were able to see here is that buloxibutid, our therapy, is able to significantly reduce the ProC3 expression in this model relative to the available standard of care as well as emerging therapies, which we think is a nice reflection of the potency of this mechanism of action. In addition to that, from the safety side of things, this mechanism as a natural tissue repair system, we think has a different risk-reward or risk profile in terms of having safety or tolerability issues. In addition to that, the receptor is very limited in its expression in healthy individuals, which you can see on the left-hand side compared to some of the other targets that are sitting on fibroblasts or myofibroblasts or other cell types that have been targeted by other therapies that are approved or in development. We think that provides for a better kind of risk profile on the safety side as well. That is in addition to also having tested actually buloxibutid in hundreds of patients to date for up to nine months and observed that the therapy is quite well tolerated as well. Now, maybe taking this from the preclinical to what we've seen now so far in phase two A. We ran a phase two A study with treatment naive IPF patients, and we looked at their lung function, which is again the regulatory kind of marker endpoint over a 36-week period in these patients. The patients that were enrolled into the study, we called it the AIR trial, were quite similar to what you would expect from a phase two or phase three study in IPF. The comparison here is to INPULSIS, which are the phase three studies that led to the approval of nintedanib. In addition to then observing having a patient population that was quite in line with what you'd expect in these clinical studies for IPF, we also observed in our treatment really nice safety and tolerability profile. In the right-hand side here, you can see the treatment emergent adverse events. You don't have the diarrhea issues that are associated with the standard of care, and you can see that on the left-hand side, nintedanib causing in the majority of patients diarrhea, other types of side effects that are not apparent with buloxibutid. In addition to that, we had no drug-related serious adverse events as well, which was great to see over the nine-month study. In addition to then a really nice tolerability profile, which by itself is attractive, we've also demonstrated in our initial clinical signal something transformational on the efficacy side. As I'd mentioned, typically what's happening in the development of IPF therapies is slowing the decline of lung function, whereas here we're demonstrating the ability to stabilize and maybe even improve lung function over an extended period. What's really nice about this data set is not only that we're improving lung function by over 200 milliliters on that 36-week period, but also that this is not an outlier-driven data set. It also reflects a median improvement of 63 milliliters, which means the majority of patients had improvement in lung function over this 36-week period. In addition to that, we've also seen in comparison to the historical standard of care as well as kind of patients who are left untreated, very different types of outcomes. Buloxibutid, again, improving lung function in 65% of patients at 36 weeks relative to what you'd expect with the standard of care, 25%, or untreated population, 9%, a very different result. In addition to that, one thing that we did in our open-label study after completing it is developed a synthetic control arm to contextualize the signal that we observed. Here we took a database of over 10,000 IPF patients, filtered them based on the inclusion criteria of our phase 2a study, and then actually matched them on the baseline characteristics, and then compared basically a large number of placebo arms to find the ones that matched ours best. It took those top matching 408 placebo arms and basically compared them to our own data set. What you see here is this is the baseline matching reflecting that the placebo arms were nicely matched in baseline characteristics to the buloxibutid treatment arm in our phase 2a study. Here is a reflection of the difference in treatment effect between what you'd expect in a placebo group for baseline matched patients versus what we produced in our phase 2a AIR trial. This data set is also imputed according to that placebo arm. What we have seen here is basically a statistical significance of or a p-value of 0.0025. This is a reflection that basically of those 408 synthetic placebo arms that were generated that matched closely on baseline characteristics, 407 of them were inferior in terms of the effect relative to what we observed in the AIR study. In addition to seeing these nice clinical signals on lung function, we also nicely see a trend in decreased TGF beta-1 and an increase in collagenase matrix metalloproteinase 13, which again is a reflection of the ability to digest collagen and also then to reduce that fibrotic drive. From here, what we are doing and what is now ongoing is a phase two B study, which has the regulatory endpoint, 52-week change in lung function. This one does have a placebo group, and it's double-blind and also has a second dose level, 50 mg dose level. We're now allowing patients who are on standard of care and nintedanib or not on standard of care. It's also relatively large in size for this rare disease at 270 patients. How we've thought about that 270 patient count results in a conservative powering of our study for even stabilization of lung function, assuming that we have a mild placebo arm in the study. This study is being run in 14 different countries across over 100 clinical sites, and enrollment here is well underway. We're excited to continue to keep folks updated on how the study progresses and very pleased to have significant investor support after financing late last year, where we're now capitalized to produce this readout and move forward thereafter. Thank you, and appreciate your time.