The company originally was founded back in 2022, very early on. We ended up licensing the first molecule, which was the anti-IL-7 receptor, crebankitug. And as we went through the rest of that year, we ended up licensing the IL-33 program, torudokimab, as well. Since then, we've raised over $200 million to advance our three programs. That includes the final one, which was tibulizumab, that was through a PIPE in early 2023, and we've had several changes within our leadership to bring on individuals with the experience needed to take us as we continue to progress as an organization. Simplistically, when you look at the three assets that we've brought in, part of what Zura has been using as the foundation is the idea of looking at dual pathway biology. A lot of assets that are currently in the autoimmune space focus really on one aspect, one signaling cascade, versus looking at a broader aspect there, and so this is where we look at tibolizumab. Tibolizumab is a novel tetravalent dual antagonistic bispecific, and we'll get into that a little bit as to what that actually means, but it allows us to start thinking about rheumatologic disease as driven by IL-17 and also antibody production. Our second asset is crebankitug. This targets the IL-7 receptor alpha, which plays a central role within both the TSLP and the IL-7 signaling cascades, and then last but not least, is torudokimab. Torudokimab looks at targeting IL-33, and you can look at the graphic there in the middle and see that IL-33 has both a ST2 dependent and a ST2 independent pathway. We will leave torudokimab for a future conversation, and we'll focus this entire presentation on the first two assets. As you look at our timeline, you can notice that there are a couple of key features that I want to bring to your attention. First and foremost is that we are looking to initiate our systemic sclerosis trial in Q4 of this year. Following on to that, based on a timing for the IND submissions, we would be looking to submit the IND for hidradenitis suppurativa and initiation of that clinical trial in the first half of twenty twenty-five. Simultaneously, you can see the anticipated external events in the bottom part of the screen, and this is where we're closely monitoring the space. As you can tell, there's a number of external catalysts, primarily related to the IL-33 programs and also to the IL-7 receptor alpha or TSLP programs, that may play a role in our development pathway and helping us to identify what is the appropriate indications to pursue, leveraging that experience and the positive success, theoretically. First and foremost, I wanted to look at tibolizumab, and just again, to reiterate the uniqueness of this molecule. So tibolizumab was actually brought together by looking at tabalumab, which was an anti-BAFF, originally in development, and then fusing the active region from Taltz to the Fc portion of the molecule. This is actually what's seen in the bottom part of the screen on the dual antagonist bispecific antibody. Why this offers a next generation approach to the treatment of these autoimmune conditions is that unlike a traditional monoclonal antibody, if you were trying to target these two pathways, you would actually have to use two independent antibodies. Or, as we've gone through in the second generation, where we had novel bispecific antibodies, where each Fab region was dedicated to a specific target, where IL-17A was on one arm, or BAFF was on the other arm, with the potential challenges of steric hindrance and trying to make sure that those ligands were in close proximity. As you think about the uniqueness for tibolizumab, the way that this is structured allows each end of the molecule to independently interact with its particular targeted ligand. So if BAFF is in circulation, we can engage with BAFF. If 17a is in circulation, we can engage with 17A, and that does not impact the binding of the other side of the molecule, which is relatively unique. This allows us to go after multiple pathways that are driving autoimmune conditions with a single asset. This illustration further graphically describe what's actually going on within that molecule. So again, you can see that the IgG form of it is the anti-BAFF tabalumab, with the ixekizumab or the single chain variable region of Taltz, fused to the Fc portion of this molecule. When you look at BAFF, BAFF exists in two different forms. There's a trimer, and there's also a sextamer. These are membrane-bound or even soluble forms, and they can engage with three different receptors, either BCMA, TACI, or BAFF receptor. The way in which we interact with BAFF, we prevent the engagement of BAFF with any of those three receptors. That allows us to then control B-cell survival and proliferation, modulating the immune responses, and ultimately down-regulating the autoantibody production. On the right side of your graphic, and this is an important note to bring to the attention of the team here, is that as you start to think about IL-17A and IL-17F, and this has come up recently with some of the other emerging landscapes and the competitive competitors in this space. Ixekizumab happens to be the most potent IL-17A antagonist, and it's because it not only blocks IL-17AA, that homodimer, right here, but it also prevents the IL-17A and IL-17F heterodimer from forming. So this allows us to actually have a significant advantage over those molecules that just target IL-17 alone, or IL-17A alone, such as COSENTYX. The reason why I bring this up is that one of the opportunities to think about, and again, I come back to our molecule could be either used as an anti-BAFF or as an anti-IL-17. What we really took pride in within Zura was to try and identify those indications where you had both pathways being active. This is actually what brought us to systemic sclerosis, and we're going to walk through this a little bit, but you start to see that IL-17 and BAFF have both been independently validated within systemic sclerosis. Specifically, there's preclinical evidence that shows that those are elevated within the individuals, but also more so, we're starting to see that there is clinical trials demonstrating a therapeutic benefit by targeting each individual aspect that we can bring together. So why systemic sclerosis? Systemic sclerosis is considered an orphan disease. It affects approximately 300,000 people across the United States, European Union, and then also Japan. It's often characterized by fibrosis of the lung and also of the skin, but can affect other organs as well. Currently, there are two approved therapeutics for the treatment of the lung disease or interstitial lung disease, but there is nothing approved as of right now to treat the all-encompassing systemic sclerosis or specifically the skin aspect of the disease. There's a number of measurements that can be used to try and understand the overall therapeutic benefit of a drug within this space, and so we'll be actually carrying those forward when we look at our clinical trial, which we'll talk about in a minute. Again, why systemic sclerosis for us is that we recently looked at a survey that was conducted within rheumatologists to try and identify those indications where there remains is still a significant unmet need. As you can see on the left part of your screen, 96% of the rheumatologists that were surveyed indicated that there was a significant unmet need, and that's a very extremely high unmet need, within systemic sclerosis, compared to several of the other rheumatologic diseases. Deeper interrogation and further questioning revealed that what they're looking for is a therapy that can treat the overall disease activity, treatment to control the fibrosis, and then treatment for the skin improvement. So again, coming back to the independent validation, when you look at the IL-17 side of our molecule and try to understand what was the rationale to go after this specifically, there's another molecule called brodalumab. It targets the IL-17 receptor antagonist, which is the signaling cascade for IL-17A and the F heterodimer. When you look at the therapeutic benefit of brodalumab in the phase III trial for systemic sclerosis, on the left side, you see the modified Rodnan skin score and the significant improvement that was induced or given to the patients by the administration of brodalumab. Additionally, you saw an improvement within lung function, albeit slightly smaller. When you look at the right side of your screen, you see the BAFF antagonist. So this was Benlysta that was tested in an investigator-initiated clinical trial, and within a twenty-patient population, they demonstrated, again, a significant improvement in the modified Rodnan score and also an improvement within the pulmonary function of these individuals. This has actually prompted and led to an orphan drug designation for Benlysta for the treatment of interstitial lung disease. But again, this only focuses for them on one aspect. It provides us the opportunity with the ability to antagonize both the seventeen and the BAFF to be able to move into an all-comer population. So when you look at the clinical trial that is planned to kick off in the fourth quarter of this year, you can see that we're looking at a single or double arm, so a placebo-controlled trial, with roughly a six-month treatment paradigm, followed by an open label extension. Specifically, we're looking for individuals that will be on stable background therapy, and then using the presence of autoantibodies to help us actually recruit the correct patients that would benefit from this type of a therapeutic. And specifically, what we're focused on, you can see this for the key efficacy endpoints in the bottom left part of your screen, is that we're looking at the skin score as the primary endpoint, and then also additionally measuring pulmonary function through high-resolution scanning, and then also the forced vital capacity as well, along with the patient-reported outcomes. The expectation is that we will see data towards the end of 2026, and obviously, that we're looking forward at the, the advantage of this in the patients with systemic sclerosis compared to the others. As you start to think about what's happened in the space for systemic sclerosis over the last several years, with the number of therapeutics that have been brought forward into this place, there's a number of things that we've wanted to highlight within our own team to try and understand how do we ensure or increase our probability of success by understanding what's going on. Through this, we've actually engaged with several individuals that are a part of our scientific advisory board, that include Dinesh Khanna, for example, who is a world-renowned expert in the space of systemic sclerosis. We've gone through and reviewed the challenges that have happened within the systemic sclerosis clinical trials. Through this entire process, through a combined internal and external effort, have gone through and identified what some of these challenges may be and the ability that we can overcome those. As we move to the next indication, one of the other roles where we see both a combined IL-17 aspect and also a BAFF or a B-cell targeting therapeutic approach, is in the space of hidradenitis suppurativa. This has risen a little bit in prominence over the last several years, with a number of IL-17 antagonists that have been brought into the space and have shown some therapeutic benefit to those individuals suffering from hidradenitis suppurativa. And so we're gonna walk through a little bit of the data, what's the benefit that we offer with by targeting the BAFF in addition to the IL-17 as we go forward with this. But it's a significant opportunity. As you think about HS as a whole, it starts off with a follicular occlusion of the hair follicle, and you get an infection that ultimately triggers an inflammatory response. This most typically appears in the armpits, breast region, and in the groin areas. And so it can be incredibly painful for the individuals. It's actually one of the reported outcomes for those individuals, is the pain associated with this. And the challenge with HS is that it often takes up to seven years to get a proper diagnosis to be able to treat those individuals. As we go through, and I'll address that bottom right piece, is that when you start to think about the therapeutics that have been in development for HS, obviously, the only approved therapeutics at this point are adalimumab, an anti-TNF, and secukinumab or COSENTYX, an anti-IL-17A. When you start to look through this, and you see the placebo-adjusted scores for the HiSCR50, and the HiSCR is actually the clinical endpoint that's used by the FDA. It includes a measure of the abscesses and the nodules, with no worsening of the actual draining fistulas or the draining tunnels. And this becomes really important, and we'll talk about that in a second. But when you look at the placebo-adjusted scores, you can see where secukinumab, for example, has about 11% of patients above their placebo that reach a HiSCR50, and you max out with the other IL-17s, roughly around 35%-38% or 40%. As you go up to a higher stringency with a HiSCR75, so this is an improvement of 75% in those patients, again, you're maxing out at around 30% of patients who experience a benefit compared to the placebo. What this indicates is that there's still a significant need within those other populations. So, the extrapolation is that about 65%-70% of patients are left with an unmet need beyond that IL-17 axis. And this is what actually prompted the investigation by a number of companies trying to explore the role of B cells. And so earlier this year, we saw the data reported out from Novartis for remibrutinib, where they looked at the BTK inhibitor, which would actually be downstream of BAFF signaling, and they demonstrated a significant benefit in those patients. And again, you can see the data here, where even at the HiSCR of 75, there was a 24% delta in those individuals that responded to a BTK inhibitor, supporting the idea that antagonism or disruption of B-cell signaling would be therapeutically beneficial in those individuals. So based on that data, a combination with the translational efforts that have further elaborated a role for BAFF, specifically within HS, we are moving forward with a phase II trial. This would be two doses along with a placebo control, specifically looking at the moderate to severe patients in early stages 2 and 3, using the HiSCR as the primary endpoint. But again, I want to come back just briefly to one of the other efficacy endpoints, which includes the IHS4, which is another new scoring system currently in validation, that allows the ability to incorporate the effect on those draining tunnels. And why those draining tunnels become important from a Zura perspective is that what we've learned through some of those translational studies is that there is a high level of BAFF being produced by the neutrophils within those draining tunnels. And that is left unresolved at this point in time through a lot of the IL-17 targeting therapeutics, which gives us an opportunity to potentially show superiority. As you think about tibulizumab as a whole, we're incredibly excited. There's a number of factors that will obviously influence the company over the next several months as we look at initiating two specific clinical trials, one in systemic sclerosis, again, at the end of this year, and then in the first half of next year, looking at hidradenitis suppurativa as a follow-on indication. And this gives us an opportunity to be positioned as a potential first-in-class dual pathway biologic for the treatment of these autoimmune conditions. The next therapeutic I want to discuss a little bit is crebankitug. So this pathway, we originally in-licensed this molecule specifically from Pfizer, where they had gone through and utilized the phase I studies in the type 1 diabetes population. And what they demonstrated very early on is the impact that it had on CD4 and CD8 effector cells. So as you start to think about the autoimmune function, a lot of these autoimmune diseases are characterized by overactive T cells. The other part that was really unique to the IL-7 receptor alpha blockade in the pathway is the role that it plays within TSLP. Obviously, there's been a lot of interest over the last several years with the approval of an anti-TSLP in the space of severe asthma, other therapies that are coming forward and demonstrating therapeutic benefit in other conditions as well. One of the challenges is that primarily, those treat the TH2 forms of the disease, and that there are other aspects that are left unmodified. And so by going after both the IL-7 and the TSLP, it gives you the ability to look at epithelial alarmins, so disruption of the epithelial surface, and to be able to have that IL-7 component, which is also going to dysregulate the T cell-driven aspects of the disease as well. And again, this just further illustrates, as you look downstream, and you see where IL-7 plays a central component with the IL-7 receptor alpha for both the IL-7 side of the graphic there and also for the TSLP side of this. And so this gives us a number of indications that we can start thinking about pursuing, that would be either led by TSLP signaling or also by the IL-7 receptor alpha signaling. Specifically, it gives us an opportunity to start thinking about what that competitive landscape looks like. And so this is data that we previously presented at the World Allergy Congress in 2023, where we did a comparison between some of the existing competitors in the space. So there's crebankitug on the right, tezepelumab, an anti-TSLP receptor, and an anti-CD127. CD127 is the same, it's synonymous with IL-7 receptor alpha, so it's an analog for, say, the Q32 and OSE assets. What you can see in that graphic is that we are significantly more potent at disrupting the TSLP activity compared to all of the other molecules. That includes the anti-TSLPs themselves and the TSLP receptor, along with the CD127. So when you combine that with the data on the left, that shows that we are similarly to Q32's molecule in disrupting the actual IL-7 side, that gives us the opportunity to be the best-in-class therapeutic, targeting both the TSLP and also the IL-7 components that signal through IL-7 receptor alpha. So as you start to think through the emerging landscape and the external catalysts, we are closely looking at the data that's being generated by some of the competitors, specifically in the spaces of atopic dermatitis, alopecia areata, ulcerative colitis, and severe asthma. And this gives us an opportunity to think about how those could inform our development path as we go forward. Simultaneously, we have internal efforts that are being led by several groups within Zura, and also external groups as well, evaluating what are the other opportunities where TSLP biology and IL-7 biology could play a significant role, whether those are common autoimmune diseases or they're not, they're orphan autoimmune diseases. And through that evaluation, we'll be able to go through and communicate at a later time what those lead indications would be potentially for crebankitug as we learn a little bit more. This just highlights a little bit more for you, understanding that there has already been PK/PD within this therapeutic, and that there's safety that's been generated for 93 patients. It was incredibly well tolerated and gives us the opportunity to truly move forward into a phase II within whatever lead indication we identify. As we close up the conversation here, just wanted to reiterate just again, as Zura has gone through its growing process, our mission is still there, that we're driving scientific breakthroughs, looking for transformative life-saving therapies to treat patients with autoimmune and inflammatory conditions. Our goal is to demonstrate with our pipeline that we have a significant advantage. When you look at tibulizumab, it has the opportunity to be the best in class as a first-in-class dual antagonist. And then as you look at our other therapies as well, with their dual pathway biology, positions us very nicely to start thinking about how do we treat broader indications. As you start to look at the upcoming catalysts that'll be reported out over the next year or so, they play a significant role as we learn from those and what we want to identify as our path forward as well. We are incredibly well-positioned. Again, so our current state, we have approximately $188 million that allows us to take these therapies through development until the end of 2027, and so we're incredibly well positioned. With that, I'd like to thank the organizers yet again. I'd like to thank our internal team, who helped to generate a lot of the information here, as well as our internal stakeholders that have contributed to what we've seen for a successful couple of years with Zura up to this point. I'll take this time to answer any questions.