I hand it over to Chris Stevo, SVP, Investor Relations. Please go ahead. Thanks, Alex. Good morning and good afternoon, everyone. I just want to remind people we'll be making forward-looking statements today, and we undertake no obligation to update those statements. If you have any questions, please see our SEC filings under Forms 10-K and 10-Q. With that, I'm very pleased to give you Richard Francis. Thank you, Chris. Good morning, good afternoon, everybody. Thank you for joining the call. Moving on to slide 4. This is a very exciting milestone on the journey to, that we started on Pivot to Growth back in 2023, to transform Teva from a pure biogenerics company to a world-leading biopharma company. Obviously, on this slide, you'll see that, that 2026 is a year of milestones. We have many milestones. I'm really excited that today we're talking about Duvakitug and the maintenance data for the UC and CD phase II study. But I just remind you that we have many more milestones coming this year with IL-15, vitiligo in the first half of this year, phase I-B top line results, celiac with anti-IL-15 as well. In the second half of the year, DARI will have the pivotal phase III study readout, and then in Remsima, the futility analysis of the phase II, and as you know, excited about the potential launch of olanzapine at the end of this year, and then finally, anti-PD1- IL-2. So a lot of exciting data coming out from our innovative pipeline. So really a key year. Now, the reason why this is so important and exciting, if you move on to slide 5, is this really has the ability to accelerate the transformation that we've started here at Teva. If you look across this pipeline, from olanzapine to DARI, Duvakitug, and Remsima, anti-IL-15 to our PD-1, these all have the ability to be billion-dollar products in their indications. And as you see, the estimated market size that we're entering is significant and growing. So not only do we have a high-quality pipeline, it is well positioned to continue to drive our innovative portfolio growth for many years to come. And I do remind you that our innovative portfolio is already growing at high double digits. So exciting times for Teva on this transition. But today's call is about D uvakitug, and without further ado, I would like to hand you over to Eric Hughes, Head of R&D and our CMO. So over to you, Eric. Thank you very much, Richard. It's exciting to be here today to talk about our Duvakitug program. And I always like to start first, you know, what is the unmet medical need here? As a physician, I know, there's a long way to go in ulcerative colitis and Crohn's disease. I think it's very important to remember that less than 50% of people, even on advanced therapies, only less than 50% achieve a clinical remission. And more importantly, that responsiveness can be lost over time, just over the first year. What does this result in? Well, about 20% of patients with ulcerative colitis still get at least one surgery in their, despite their treatment. And in Crohn's disease, in particular, over 75% of people still get at least one surgery in their lifetime. So there's more that we can do for these patients, and they need more treatments and better durability of their response. Can we go on the next slide? You know, I always like to start with this. You know, our Teva team created an antibody that's, you know, strategically designed. We made a very potent antibody that blocks the binding of TL1A to the DR3 receptor, which is the important signal of inflammation that was, you know, first related to IBD early in the days of the discovery of TL1A. But in addition, we designed an antibody that binds the TL1A trimer in a way that it allows the binding to the DCR3 receptor. This is an important aspect of our antibody because not only do we block the bad signal, but we maintain the way in which the body normally maintains the homeostasis to these exuberant TL1A responses. So I applaud the team for thinking thoughtfully about the biology and making a very potent antibody. Next slide. So, you know, what have we been showing in our program? You know, when I look back at the phase IIb study, induction portion of the study we're talking about today, you know, we were very pleased to see very robust placebo-adjusted numbers for both ulcerative colitis and Crohn's disease. And we also showed that, you know, both treatment-experienced and treatment-naive patients responded similarly, which is great for a biologic. We also showed a very favorable safety profile to date, and you'll see that we, we confirmed that as well in the long-term follow-up. One of the other important things is we showed that we had about 3%-5% anti-drug antibodies, you know, low anti-drug antibodies. Hopefully, that will show that, you know, it's contributing to our durable response. And last but not least, we've always given the entire program, and will be giving the program in phase III as a subcutaneous dose, which is convenient for patients. So if I can go to the next slide, just to review, you know, what did we show about a year ago? So a year ago, we finished up the induction portion, and we were very pleased to see that we had, in ulcerative colitis, here on the left side of the screen, you know, a delta of 27.4% in our ulcerative colitis group, and we also showed a nice dose response. And similarly, in Crohn's disease, even more impressive delta, we had about a 34.8% in the endoscopic response in Crohn's disease. So both results were very robust. Very well controlled study with a dose response. This really set us up nicely for phase III because we could make a strong, you know, modeling and simulation model that would really predict what our responses would be going to the future. So that induction phase of the study, we are very pleased to have. On the next slide, you can see how does that induction phase, you know, compare across the the treatment landscape? You can see here we, we're showing, you know, TL1As on the left-hand side with that delta I mentioned in ulcerative colitis of 27%, and all the way across with the, the IL-23s, as well as the JAKs in phase three data. You can see it's a very competitive profile in ulcerative colitis. In Crohn's disease on the right, you can see that delta we saw in induction of about 35% and see how it compares to the other TL1As in development, as well as the IL-23s and the JAKs. So, you know, when I see this, I'm very pleased by our placebo-adjusted rates being very competitive, not only for TL1As, but, you know, the treatment landscape that we see in ulcerative colitis and Crohn's disease today. But moving on to the next slide, you know, what do we really want to talk about today, and what did we have the press release this morning about? You know, I just described the first part of this study was the induction phase on the top of this slide here. We looked at 900 and 450 milligrams against placebo for that 14 weeks of the induction. Now, those people who were treated with the active drug were then determined to be either responders by clinical remission or clinical response for both ulcerative colitis and Crohn's disease. And those responders went into our maintenance phase. This is a classic re-randomization, re-randomization design to show, the durability of the response. So those, responders were then re-randomized into duvakitug at 900 or duvakitug at 450. And again, it was maintaining the blind with a re-randomization. And today, we'll be talking about, you know, that data at the 44-week time point at the end of this long treatment period. So if you can move on to the next slide, you know, this is the, this is the exciting part of today. You know, we're very pleased to see the ulcerative colitis data for clinical remission. Again, the same endpoint, for the primary endpoint we used in the induction phase. You can see, again, a nice dose response between 450 and 900, and we're very happy to see that 58% at the highest dose for clinical remission. So a great durable response over 44 weeks of additional therapy. And then now with Crohn's disease, in a similar way, looking at a very objective endpoint of endoscopic response, which is the same primary endpoint we saw in the induction phase. Again, a great number, you know, with a dose response up to 55%. Very, very robust objective endpoint. So we're very proud to see these numbers for the maintenance. You know, I mentioned when I started that durability of response is incredibly important. You know, ulcerative colitis and Crohn's disease is, are chronic illnesses that we're not succeeding in today, and people need not only the response, but a response that lasts. And I think this is, this strengthens the potential of Duvakitug. Now, if we go to the next slide, you know, what does this look like in the treatment landscape out there? There are many different things that people can be treated with, but again, people cycle through these therapies because of that durability. And what we can see here on the left is, you know, ulcerative colitis is a cross-study comparison again. So all the caveats need to be made, thought of, with that. But still, you know, how does this look like, with what people see today in the labels and in the data out there? So on the left-hand side, you can see ulcerative colitis. You know, at that top dose, we saw about 58% achieving and maintaining clinical remission, and you can see how that compares to other TL1As in development. But also, more importantly, this sees what, how we compare to IL-23s and the JAK from their phase III labels. And, you know, in ulcerative colitis, that looks pretty, what is, what's the word I'm looking for? Competitive. So I'm very happy to see that effect, you know, being maintained over a full year of therapy. But then looking at the Crohn's disease, you can see, again, in this objective endpoint of endoscopic response, very competitive, 55% response rate. And then you can see how that compares to other, TL1A, and 23s, and the JAK out there. Again, we, for clarity, we've pointed out in this cross-study comparison that the solid bars are re-randomization designs, and the hash bars are those studies which were treat-throughs. But no matter how you look at it, it looks like a very, very competitive result. And when I look at this, I think to myself, this, this is not—I don't think we just have the potential of being best in class. We have the potential of being best in disease. So that was what was so exciting when we saw the results. So very happy with the execution by the team. I'm very happy for the patients in this study. So if I go on to the next slide, you know, we've gone through a number of milestones now throughout this program. First, we talked about the antibody itself. In our hands and in vitro assays, when we compare it to antibodies we make from the patents out there, we believe we have the most potent antibody in TL1A class. We have the greatest selectivity for the DR3 receptor. And in our phase II study, I believe we posted some of the lowest anti-drug antibodies out there, 3%-5%. We showed in the induction study that we started off with here some great results in both ulcerative colitis and Crohn's disease. You know, remember, these were the only well-controlled placebo-controlled studies for Crohn's disease that we bucketed together in the same study, and we saw great treatment responses, irrespective of whether they're naive or treatment experienced, and we had a favorable safety profile, and again, with low immunogenicity. And today, you know, I'm very happy to show this durability response. It's very important that we have a durable response for these patients with such a chronic disease and in a situation where you cycle through therapies. You know, our goal is to have deep, durable, steroid-free remission. You know, this hopefully will translate into fewer surgeries, fewer hospitalizations, and improved long-term outcomes for patients' quality of life. So that gives me a great hope of what we can do with this program. So and that continued favorable safety profile adds to that hope that I have. And finally, I just want to go over, you know, what are we doing now? Well, we've already moved into phase three with our partner, Sanofi, the UC program called Sunscape and the CD program called Starscape. You know, I'm very proud of the design we've put together with our partner, you know, with an open-label feeder arm, a favorable randomization to active versus placebo, and all subcutaneous treatment, you know, from induction through maintenance. So very convenient for patients and a very attractive, I think, phase III study design. So we'll be looking forward to, you know, executing as we always do. I always like to remember, we were the fastest to transfer from phase II to phase III, and I hope that excellence in execution continues. Our enrollment has already gotten off to a great start. And the final slide, you know, just to talk about more of the potential of the class. You know, it's exciting to be on a program that is a totally new biologic class. We're, you know, we're hitting a cytokine TL1A that, you know, is an amplifier of many different pathways. And I think ulcerative colitis and Crohn's disease was just the beginning of what the potential of this molecule has. You know, we look at it as buckets. There's T2 inflammation, there's non-T2 inflammation, and there's the upside possibility of TL1A having a direct effect on fibrosis. Remember, fibrotic cells actually have DR3 receptors. So a very interesting possibility here, where we're not only potentially hitting inflammation, but also potentially fibrosis. So you know, very exciting. We're excited to announce the new indications later this year, but, you know, I'm just very happy with the results we have today. And I just wanted to end with a slide that, you know, Richard started with. You know, for Teva this year, we have lots of events happening. It's a very exciting year. There's seven different events, and this is just the first step of our journey in 2026. Today, we talked about the maintenance data for Duvakitug. We'll be presenting or releasing data for anti-IL-15 in vitiligo and celiac this year. The DARI program, one of the largest studies Teva has ever run, will be reaching its final asthma exacerbation by the end of this year. Our Remsima futility analysis will be at the end of this year. Hopefully, our olanzapine approval will come in the second half of this year. And finally, we'll be having human data for our anti-PD-1 program. So very exciting year. The teams are working extremely hard. I appreciate all the effort that's going into this. And with that, I think I'm gonna open it up and hand it to Chris for our Q&A. Thanks, Eric. So for the Q&A session, we'll have Richard, Eric, and Eli available to answer any questions. And Alex, before you start the Q&A, I just want to remind people to please limit themselves to one question and one brief follow-up. And if we have time, we'll certainly let you back in the queue to ask more questions. So please go ahead, Alex. Thank you. As a reminder, if you'd like to ask a question, that's star followed by one on your telephone keypad, and if you'd like to remove your question, that's star followed by two. Our first question for today comes from Dennis Ding of Jefferies. The line is now open. Please go ahead. Hi, good morning. Congrats on the data. I had a question on ADAs. I'm curious if you have any new data on ADAs with longer treatment, if you've also looked at efficacy broken out by ADAs, and if there's any relationship there. And then number two, sort of like a bigger picture, bispecific strategy question. Seems like most of your peers are looking at TL1A and IL-23 bispecific, though both are going after P19, while Pfizer and Roche, they're going after P40. So I'm curious how you're thinking about the two and the puts and takes between one over the other, and when do we expect Teva to unveil its own TL1A bispecific strategy? Thank you. Great, Dennis. Thank you for the question. So first, thanks, Dennis, for the question. So first, with regards to the ADAs and the efficacy. So, you know, we have to batch those things, and this is just a top-line report. So we actually haven't run the later batched samples yet. But, you know, looking back on the beginning of this study, you know, we only saw about 3%-5% when it comes to ADAs, depending on the indication. So, you know, with such a low number of ADAs and with such high response rates, right now, it's hard to make any correlation. So I don't anticipate that to be a significant correlation, but we'll report that when we get the data with regards to the efficacy. Now getting on to bispecific. So, you know, we're always encouraged by the fact that so many people are now interested in TL1A. I think that, you know, given the, you know, the good safety profile we're seeing to date, is encouraging when it comes to the concept of combination therapies. I think combination therapies are something that will continue to develop. I would remind you that, you know, Teva makes a lot of antibodies. We've made a lot of biosimilars. We've been leaders in making the TL1A antibody. So our ability in our labs down in Australia, this is their sweet spot. They can make bispecifics very well. In fact, we have a great bispecific for TSLP and IL-13 in development right now. And, you know, suffice it to say, we are looking at many different combinations. But I think that the fact that there's such great interest in this possibility, it shows you the strength of this biologic class. ... Got it. Thank you. Thank you. Our next question comes from Louise Chen of Scotiabank. Your line's now open. Please go ahead. Hi, thank you for taking my question here, and congratulations on the data. So I wanted to ask you, how do you think your induction and maintenance data read through to your phase III UC and CD studies? And as a quick follow-up, wanted to ask you, what do you think would constitute a commercially and clinically meaningful outcome in those studies relative to what we saw today? Thank you. Richard, I can take that one. Yeah. Okay. So, thank you, Louise. Yeah, so the read-through to phase III. So there's aspects of the phase III program that I'm very encouraged by. You know, our modeling and simulation for our dose selection, I think, is very strong, based on the fact that we had, you know, a great dose response, great PK, and well, anti-drug antibody. So, you know, our translation in the phase III, I think, will be robust. So if I think we see data that's similar to what we're showing from the phase II, I believe this program will be extremely competitive in IBD for both ulcerative colitis and Crohn's disease. I hope that answers your question, Louise. I think the second part was around the commercial competitiveness. Eric? Oh, yes. I'm sorry. Yeah. So thinking about how that translates, if this translates to phase three, is, I think, the commercial competitiveness, as you can see by, you know, the comparisons we've made from what's in the, the literature and what's in the labels, the U.S. labels, for, you know, the many of these different programs that are doing very well in the commercial space, we're competitive. So I expect that, you know, we will continue to show deep, durable, and steroid-free remission. That will translate into great value for, for payers, you know, fewer surgeries, fewer hospitalizations, and I hope to show all of this with increased quality of life for patients. So those are all things that people will value and that payers, I think, will, you know, be willing to pay for, because I think this will have an impact on the disease. So yes, I think we have a great opportunity in the commercial world. Yeah, and if I could add on to what Eric has just said, it is worth remembering that this is a $38 billion market, and so, you know, what proportion of that Teva can take, I think, in such a sizable market, which is growing, and as Eric has highlighted, has significant unmet medical need. I think it's an exciting opportunity with the efficacy we're showing, but just the size of the market makes it an important opportunity for Teva. Next question, please. Thank you. Our next question comes from Glenn Santangelo of Barclays. Your line is now open. Please go ahead. Oh, yeah. Thanks for taking my question. Hey, Eric, I just want to follow up on the report today. So the dose response clearly looks good, and I'm just kinda curious to get your take, and you sort of touched on it in your prepared remarks, but is sort of looking at the Merck 50-week trial may be the best comparison here, and how should we account for the differences in the dosages, the dosing between the two different studies? So you know what? I always talk about the dose response. The dose response is important because when you come to making a model and you're trying to simulate responses, you wanna be on a curve where you have differentiation between the doses. So that data helps us, you know, predict, you know, how we can see doses going forward. The more data, obviously, the model gets better. You know, I don't wanna co-comment too much on, you know, the comparators that we have in TL1A. You know, I would remind you that for both ulcerative colitis and Crohn's disease, we have a well-controlled study with a good dose response. So it gives me confidence in how we can predict our dose going forward. And there's also a differentiation in how I started this whole story, Glenn, is that, you know, we have a different antibody. We bind in a different way. We block the DR3. We allow the DCR3 receptor to engage the biologically active trimer. So we believe that we're actually clearing more TL1A along the way. So when you compare doses between programs, you have to... There's a lot of caveats there because there's different potency, there's different selectivity, there's different ways in which it's being cleared, there's different anti-drug antibodies. So our dose, I'm confident in the dose we select, and I think that our data stands to really predict that well. Thank you. Our next question comes from David Amsellem of Piper Sandler. Your line is now open. Please go ahead. Hey, thanks. So I wanted to come back to combination therapy and bispecifics, but wanted to introduce the, the topic of biomarker-enriched populations here. So on, on one hand, the space, in terms of drug development, seems to be moving towards these novel combinations that are being tested. But on the other hand, we hear a lot more about biomarkers and biomarker-enriched populations, where potentially there could be monotherapy cases to be made in biomarker-enriched, subgroups. So with that in mind, how are you thinking about that, Eric, in, in terms of testing, biomarkers, in other words, high TL1A expression? I know your phase three program is all comers, but as you think about Duvakitug down the road, how are you thinking about biomarker-enriched populations? How are you thinking about the evolution of drug development in IBD towards these, these kind of patient enrichment? Thanks. Thanks, David. Yeah, so, you know, just quickly to comment again on combinations. Combinations, I think, are exciting. I think there's a great potential there. Always the goal is to increase efficacy while maintaining a safe profile. So those will develop. They're early in the process. Certainly, we're looking at that, and certainly some of our competitors are looking at that as well. So that's something that's way down the road, but exciting nonetheless. With regards to the biomarker, so I always joke, I got into this business 20 years ago, actually as a biomarker development guy, in the early space. Biomarkers are challenging, and one of the interesting things about TL1A, though, TL1A was really kind of discovered as a novel cytokine that was actually highly associated with Crohn's disease and ulcerative colitis. So the history in this field is very enticing. Throughout my career, though, I've learned that you need a lot of data to be confident of a biomarker. So that's why we've always planned to do this program as an all-comers. And, you know, you need thousands of patients before you have a confidence that you have a strong association with a biomarker. I certainly see that as a hope. You know, if we do identify one that has a high sensitivity and a high specificity, that's something I would be happy to develop, and then you could actually increase your potential for monotherapy. So I think that that's always a possibility, but we always need to have more data to be able to be confident in that. I think we're in the early days, and we have some great biomarkers that we're working on now and testing in our studies, but we need to be confident before we go out there and say, "This is something people should use to choose." 'Cause remember, these patients are cycling through therapies. You don't wanna disabuse someone who's failing on a therapy, the chance, even if it were low, to get on a new treatment, because we wanna prevent those surgeries, and we wanna prevent those hospitalizations and those relapses. So that, that's my take on it, and I think it'll just be a matter of time before we have enough data to confidently say we have a good biomarker. Thank you. Our next question comes from Umer Raffat of Evercore ISI. Your line is now open. Please go ahead. Hi, guys. Thanks for taking my question. I have a couple here on this trial, if I may. Perhaps first, the doses. I think one of your slides indicates you have two doses in phase three. I saw ClinicalTrials indicates three doses, but I couldn't tell if it's three doses or three cohorts. The reason I ask is because I think one of the more important things in this data today is perhaps what's not shown, which is, you took a bunch of responders from induction, which were on either 450 or 900, and then they were re-randomized, meaning you technically have data in here on patients that went from 900 in induction to 450 in maintenance. That's my question: What did the response rates look like in those? Because when we look at Roche data, it looks like stepping down in dose from induction to maintenance, they lost, whereas keeping the dose flat helped. So conversely, if you actually did retain all those responses going from 900 to 450, that starts to be the, perhaps the most direct defense here. Thank you. Great. Thank you, Umair. I appreciate the question. And let me clarify, I think you, your interpretation of the phase III is right. There's three cohorts, but there's two active doses in phase III. So you know, we're actually—I'm actually very excited to have two doses, that is interrogated in the phase III, so it gives us more optionality for, patients potentially in, in the future. So that, just as a clarification, it's two doses, in the phase III program. Now, with the re-randomization design, so re-randomization designs are very common. You can also do treat through. Both are, acceptable to health authorities. And you're right, you know, people go in either having received 900 or 450 in the induction, and then they're re-randomized. So there's four different pathways that people go. They go from 900, re-randomized to the high and the low dose, or they go from 450, re-randomized to the high and the low dose. And, you know, I'd love to talk about that all today, but I have to limit myself to what was in the press release with regards to the data, and we'll present that, you know, in the conferences coming up in the future. Suffice it to say, as we say in the press release, you know, the, what we've seen in the primary endpoint has been consistent across many of the different efficacy endpoints. Thanks, Umair. Thank you. Our next question comes from Ash Verma of UBS. Your line is now open. Please go ahead. Oh, hey, guys. Congrats on all the progress here, and thanks for taking our question. So, just maybe, like, in terms of the commercial, what do you think about your potential order of entry versus other TL1A competitors? Is that something of a disadvantage, or you don't necessarily think that way? And just, like, secondly, on this phase III, UC and CD design, so can you confirm, like, is the, is it going to be a Q4W dose, or is it going to be a Q2W? Because that's another differentiating aspect versus some of the other programs that we've seen. Thanks. Great. So yeah, I, I can address that question about the commercial order of entry. So, you know, the rule of thumb that I have is that if you're within an 18-month window, the order of entry actually doesn't matter. It's the efficacy that matters. So we're well within that 18-month window. I think we're even a better position for the Crohn's disease. So I'm not so much worried about the order of entry at this point. I'm making sure that, you know, we maximize the efficacy on this program, and, you know, it's about execution. I, I mentioned that, you know, we transitioned from phase II to phase III the fastest with our partner, Sanofi, and we're off to a great start with our phase III program. With data like this, you know, it does make people think carefully about which study you want to go into. Do you want to go into a study that's, you know, looking like it has great induction and durability? So I think it comes down to execution, and we're in a good position with regards to the order of entry, and it's gonna be dependent on the efficacy. Now, with regards to the Q4 versus Q2 in the response, all I can say today is that this study looked at Q4, so we're very confident in a competitive profile of a monthly dosing, and we haven't announced yet what we have in our phase III program. But I'm pleased to see that today, you know, Q4 dosing works, seems to work very well. Thank you. Our next question, our next question comes from Jason Gerberry of Bank of America. Your line is now open. Please go ahead. Hey, guys. Thanks for taking my question. Mine is, as you think about the evolving data that you're generating here, how do you think about future head-to-head trials against market leader IL-23 in the IBD space? You know, when we look at AbbVie, the most successful company in this area, they got head-to-head trials against prior generation biologics up and running prior to approval of the lead indications, and so what I wonder is, you know, when I look at this data, it seems like maybe worst case, you'd be non-inferior, but there's a really big upside case that warrants doing head-to-head trials here. So curious, you know, if you're seeing things that way, and anything you can say on that front would be much appreciated. Thanks. Thanks, Jason, for the question. I actually love this question. You know, head-to-heads are, you know, an important way of assessing programs. You know, we're gonna have to look at the evolving data and, and decide, you know, whether, you know, that's something we want to do. I think that even asking the question is a great thing today. But again, you know, we'll have to look at the data very carefully and, you know, see what the benefits and pros of doing that in the future. You know, I'm just happy with the results we're showing today. You know, with these cross-study comparisons, I think that we're in a good position to have a great option for patients in the future, and it's all about the efficacy we can generate in Phase III. Thank you. Our next question comes from Matt Dellatorre of Goldman Sachs. Your line is now open. Please go ahead. Great. Hey, good morning, guys, and congrats on the data. Maybe just on the potential of this mechanism to have an impact on fibrosis, you touched on this a bit briefly, but could you share if there's anything in this study data that you saw that either increases or decreases your confidence on that aspect? And then maybe just kind of in conjunction with that, what's the likely venue for the full data? Thanks a lot. Yes. Thank you, Matt. That, that's a great question. Scientifically, it's the most interesting question for me. You know, we don't have proof yet that we're having a direct effect on fibrosis. It's gonna take some time. Usually, you know, in the work I've done in fibrosis in the past, it's really based on the biopsy data, and that can be variable at times, so but we're gonna monitor that. We'll look at serum markers, we'll look at biopsy markers, we'll look at everything we can do to show an actual direct effect on fibrosis. You know, if I were to speculate, the most interesting thing is the fact that we're having such good responses in Crohn's disease. I mean, Crohn's is, I would describe it as almost a hyperfibrotic disease. If we're seeing these great effects on the objective endpoint of an endoscopic endpoint, you know, that gives me hope that maybe we do have some direct effect on the fibrosis. That still needs to be shown, and it's gonna require a lot of data to get it there. You know, there'll be more indications coming out in the future that should, you know, looks directly at fibrosis. That's where we're gonna really get a good sense of whether there is a direct treatment effect on fibrotic pathways itself. But it certainly is the clear upside in this biologic. You know, it's the first time, as I said at the very beginning, where we're potentially not only hitting inflammation but, you know, directly having an effect on fibrosis. Particularly in Crohn's disease, you know, in my opinion, that's where, you know, that could be really beneficial to patients. Thanks for the question. Thank you. Our next question comes from Les Sulewski of Truist. Your line is now open. Please go ahead. Good morning. Thank you for taking my questions. You noted hypertension as a pooled AE in the maintenance portion. Was this signal dose dependent, and were these events transient, or do they require intervention? And are there any concerns regarding systemic vascular remodeling that could lead to a label of restriction? And then second, for the open-label feeder phase III, how are you mitigating the risk of functional unbinding? And then for the phase III, are there any changes to the subq auto-injector, or is it identical to the one used in the RELIEVE study? Thank you. Okay, so, and I'm just writing down your questions. You had multiple ones. I might have to follow up. But, you know, when it comes to the safety, the safety is exactly the same we saw in the beginning, in the induction part of the phase of the study. You know, the common, most common AEs over 5%, I think we said were, nasopharyngitis and, you know, respiratory illness, and then hypertension. There's no dose dependency of any of this. There was no interventions for this. These are, these are common AEs that we're, you know, we're more measuring hypertension throughout the study. So there's really nothing in the, in the safety that we can see at this point that was very similar to the induction. Your question about the vascular, I think, effects, we do not see any signal of vascular effects at this point. So, I'm confident in the safety so far, and we'll, you know, have a full data set, you know, over 1,000 patients in each of the indications from phase III. And you may, you asked a question of functional unblinding. Could you ask that again? Could you explain that again? Is that in the maintenance you're talking about? Yeah, it's this open label feeder into the phase III. Essentially, how are you mitigating the risk of functional unblinding, or, or I guess, patient expectancy bias in the maintenance portion? No, that's a very good point. And so the open label feeder is not baked into the blinded portion of, and the statistical analysis of the common comparison to placebo. So that really, remember, the functional open label feeder is just really building up our safety database that allows us to, you know, reach the numbers that you require for any submission with regards to your total safety exposure. So yeah, they're treated differently in the phase III study. And I missed your last question. What was your last question? The drug device combo, is it the same for phase III? Oh, yeah. It wasn't RELIEVE. Yeah. So, you know, I always like to emphasize our program has always been totally subcutaneous, so we have direct correlation from our phase II program to our phase III. Our phase III is using a prefilled syringe that will then enable our auto-injector, which is using the same syringe. So we're locked and loaded and ready for launch with an auto-injector. Thank you. At this time, we currently have no further questions for today. Therefore, that concludes today's conference call. Thank you all for joining. You may now disconnect your lines.