Hello, everyone, and thank you for joining us today for the IL-15 celiac disease phase II-A Top Line Results conference call. My name is Sammy, and I will be coordinating your call today. During the presentation, you can raise your question by pressing star, followed by one on your telephone keypad. If you change your mind, please press star followed by two on your telephone keypad to remove yourself from the question queue. As a reminder, if you are using a speakerphone, please remember to pick up your handset before asking a question. I will now hand over to your host, Christopher Stevo, Head of IR, to begin. Please go ahead, Christopher. Thanks, Sammy. Good morning and good afternoon, everyone. Thank you for joining us for these celiac disease results for TEV-408, our anti-IL-15. The materials are posted to our website this morning in the investor relations section as always. Please see those. Before I turn the call over to Richard Francis, I would like to remind everyone that we will be making forward-looking statements on this call. The company cautions investors that any forward-looking statement involves risks and uncertainties and is not a guarantee of future performance. Actual results may differ materially from those expressed or implied in the forward-looking statements due to a variety of factors. These factors are described in our earnings press release and our most recent Forms 10-Q and 10-K filed with the SEC. Any statements that we make are only as of today, and we undertake no obligation to update these statements subsequently. Now, it is my pleasure to give you Richard Francis. Thank you, Chris. Good afternoon and good morning, everybody, and I do appreciate you joining the call. Today marks another major step forward for Teva as we continue to execute on the Pivot to Growth strategy. A strategy that was launched three and a half years ago to transform Teva from a world-class, pure-play generics company into a world-class biopharma company. As many of you will know in the conversations and interactions we have had, a major part of this was expanding our innovative portfolio. In fact, that was pillar two of the four pillars of the strategy. This was about stepping up innovation. I think you will see today that we continue to make great progress on stepping up innovation here at Teva. If you go on to the next slide. We set out this year to have seven milestones. But we had to update that, and it became eight milestones as we had the transaction and ecopipam came into our pipeline. But for a world-class biopharmaceutical company, I think this is a very impressive lineup that we have here. We've made significant progress on executing on these milestones. Already, we've had the duvakitug maintenance data. As I mentioned, we've had ecopipam where NDA was accepted. We've had the top-line results of vitiligo. As of today, you'll be hearing from Eric about the celiac disease phase II-A top-line results. But I will remind you, there's still quite a lot more to come this year with the DARI and emrusolmin, olanzapine LAI anticipated approval in Q4, and finally, the anti-PD-1 IL-2. So what does this all mean for Teva? If you go on to the next slide. It means we have an opportunity to have five submissions in five years. It's worth pointing out that these products, these programs, and their indications have the potential to generate over $10 billion of sales for Teva going forward. Now, for any company, that would be significant. But for a company of Teva's size, I think this really creates an opportunity to create a biopharma company that has a growth trajectory for many years to come and create real shareholder value. I'd also like to point out that two of the assets on this chart, duvakitug anti-TL1A and anti-IL-15, are products where we have multiple indications, so often referred to as a pipeline in a product. We've clearly shown this is possible with the two new indications that were announced earlier this year for duvakitug, and now we have the second data for anti-IL-15 on celiac backing up the data we gave you a quarter ago with vitiligo. So lots to be excited about. Five submissions in five years of assets that all have the potential to achieve over $1 billion in peak sales and some considerably more. So it's a really exciting time for Teva to continue on this growth trajectory, both on top and bottom line. But I know you want to get into the data, so without further ado, I'm going to hand you over to Dr. Eric Hughes, head of R&D and head of our CMO. Over to you, Eric. Thank you, Richard. It's great to be here and have the chance to talk about some new data in our pipeline. I'm really excited to be here and talk about this next step in our IL-15 program. Just to start off first, celiac disease, it's a very important disease. 1% of the population in the U.S. and EU are affected, and that's up to 5.1 million people. But most importantly, 50% of these people, even if they can strictly adhere to a gluten-free diet, still have symptoms. There's currently no therapies for these folks. So this is a very important disease, and I think it's unmet medical need, and it's something that is highly overlooked, I think, and underserved at this point. We'll talk a lot about a normal gut villi that you see here on the right of the slide, where you have nice normal villi, where there's a high surface area to absorb nutrients. But in celiac disease, this architecture is highly blunted in the gut, and this is the basic pathophysiology of the disease. Moving on, give you a little bit more flavor to understand the data we'll talk about today. As I mentioned, there's normal gut villi with these finger-like projections. The basic pathology in the disease process is the exposure to gluten, which causes a stress response in the epithelium of the gut lining. This leads to a release of IL-15, a key cytokine in the pathogenesis of the disease. That release drives the migration and proliferation of pathogenic intraepithelial lymphocytes. These are the cells that rush into the gut lining and cause the inflammation, and ultimately the destruction of the villi. You can see on the right-hand side, again, a gut epithelium that's blunted with its villi, lower surface area, poor ability to absorb nutrients, and infiltrated with many different lymphocytes. That's the basic pathology, and I think it's a very important aspect to remember, because one of the things I'll harp on today is that these anti-IL-15 therapies, including ours, are really driving at a disease modification. We are, by definition, changing the course of the disease with these treatments. Moving on to the first slide of our data. I just want to start from the beginning. This again, as Richard mentioned, a homegrown antibody from the labs of Teva. Just like our duvakitug program, it's the same scientists who do a great job at designing these antibodies. Just like duvakitug, we're focusing on the fundamentals of drug development throughout the process. We start with our antibody. How does it compare to other antibodies we've created in our labs based on the IP of other competitors? You can see here that we're more potent by two different assays, considerably up to 50 times more potent when you look at different assays. On the bottom, in a transgenic IL-15 mouse, we can suppress IL-15 in a greater extent in a directional comparison to these other antibodies. Again, the fundamentals of the antibody is higher affinity, better suppression, pre-clinically. Teva also did something completely unique in the field right now. Years ago, we took a population of macaques, non-human primates, and about 1% of macaques actually spontaneously develop celiac disease. That was a great opportunity in a non-human primate pre-clinical model to see what effect does anti-IL-15 therapies do. You can see here quite clearly on the left, there's some histology of the gut on monkeys that were challenged with gluten and either treated with placebo or TEV-408. You can see quite clearly that the normal architecture that you see on the lower part is dysregulated and disturbed on the top. You can see in a quantitative fashion that that villous height to crypt depth, that actual measure of the blunting of the histology in the monkeys really showed a strong effect. We also showed that the intraepithelial lymphocytes were in a statistical fashion also decreased. In the monkeys, you also actually saw a decrease in the serology of the anti-gluten antibodies and transglutaminase antibodies. A really strong pre-clinical signal that in fact, anti-IL-15 really is a disease-modifying antibody. Now, moving on to some human data. When we started our phase I program, which is pretty extensive, you can see that we looked at a nice PK profile from low to high doses. We observe a half-life of approximately 38 days, which really extends the capability of the molecule to be in a more broad schedule, out to three months. You can also see on the right-hand side, when you look at the two top doses, we suppress the free IL-15 considerably, almost below, well, essentially below the level of detection out to 80 or 90 days. Again, the fundamentals of the antibody are strong. Long half-life and clear target engagement out to 80 or 90 days in healthy volunteers. Also note something that the team did extraordinarily well, and that's the follow-up. We have a follow-up out to two years in our phase I program. Again, the antibody itself is strong, the pre-clinical data has been unique and strong, and the phase I data is probably the most extensive I've ever seen in a program at this stage. Now moving on to our first celiac. Remember, we actually are going to be talking about data from our second celiac challenge, but our first one showed some very encouraging data. It was a safety study in celiac patients. We also looked at a number of biomarkers, and I thought one of the most interesting biomarkers that we looked at, and we've talked about before, was this FABP, this fatty acid binding protein. What you can see here quite clearly is that patients who received placebo and then were challenged with gluten showed a bump in the free acid binding protein. The free acid binding protein is a marker of gut inflammation and health. When you see a release of that, you're inferring that there's inflammation going on. So those people who received placebo had a bump, but then the patients who received TEV-408, you can see that not only they didn't get a bump, but if you overread the data, you can actually see an improvement over time, and it goes below their baseline. This is very encouraging. Obviously, we're protecting the gut according to this biomarker from the challenge of the gluten. But also, the curious possibility here is that we're actually treating smoldering disease that was at the baseline of the patients to begin with. That was another bit of data that we are very excited about in our first celiac patient challenge study. What we learned from that study, we actually rejiggered, and the team did a great job in executing this next study, this phase II-A study, challenging celiac patients again. This was in 50 patients, randomized one to one to placebo or active. Again, we gave a single dose on day one, and two weeks later started a six weeks challenge. I want to emphasize that. Remember, everything you see today is a single dose of TEV-408. That's all we gave in this study that was a challenge of eight weeks. We'll be following these folks up out to week 80. But the important thing in this study that was differentiated from the first study is we did a six week challenge, and this study has biopsies in it. The first one was just a safety and biomarker study. This one has biopsies. As I mentioned, it is 50 patients, 3 g per day for six weeks. The primary endpoint is the villous height to crypt depth ratio, which is important when we think about phase II and phase III. We also looked at intraepithelial lymphocytes and a number of other biomarkers. Now getting onto the actual data today. We were super encouraged. The joke I wanted to make today that the study was so well run that even the statisticians were happy. Everything went in the right direction on this study. Here, I am just going to be talking about the primary and key secondary endpoints. When it comes to the primary endpoint, its villous height to crypt depth, we had a very robust study design. We protected the gut. When you look at the placebo drop to 0.88 on the ratio when compared to the TEV, you can see it only went down to 0.43. The important point here is that the delta is 0.45, and that is a numerically very high reported result in one of these challenge studies. That villous height to crypt depth actually showing a protection of the damage to the gut epithelium is key. I would then point you to the right-hand side, where we are looking at the count of the intraepithelial lymphocytes. The count of these pathogenic cells per every 100 enterocytes. This is one of the basic ways of measuring celiac disease. Here again, you can see basically the TEV-408 did not move at all. The placebo went down by a remarkable. The number of cells went up by a remarkable 27.6 with a delta of 27.23. That is an extremely robust, again, statistically significant effect. I would also mention that the primary endpoint was not only statistically significant, but the threshold of 0.4 was met, which is clinically meaningful. These are in such a relatively small study, remarkable results showing a very robust response. The last thing I would just highlight on this slide, too, was we have seen trends in the symptoms, actually, in the study. We looked at the Celiac Disease Symptom Diary, which is the standard PRO, and we see a clear trend towards protection from symptoms. When it comes to actually thinking about what a patient will experience, that is important as well. These are the key aspects of how we are going to move forward in phase II and phase III. Again, it was very well-tolerated treatment. Overall, you will see in the future of presentations of the data that it is a very favorable safety profile. How does that compare to other proof of concept studies and gluten challenges out there? Right now, we think that we are looking very favorable. Remember, with a single dose, saw statistically and clinically meaningful change on the villous height to crypt depth with this challenge. You see here other compounds in development, slightly smaller studies without necessarily a statistical change on this endpoint. We are very pleased with the results. Again, the power of a single dose over three months is another evidence that the compound based on its fundamentals, its potency, its PK, its target engagement, is doing what we expect it to do. When you think about celiac disease and what it represents, there are 1.6 million people already diagnosed out there. There's no options for therapy for these patients. The peak sales and the possibilities here are high. There's no pharmacotherapy out there. I challenge people to say that a gluten-free diet is good enough for these patients out there. 50% of these patients don't respond to a gluten-free diet anyway. We saw clinically significant, clinically meaningful results today with a single dose. This builds upon what we've already shown earlier this year. I was very pleased with the results in vitiligo. That again, was a two dose study over 24 weeks. I just remind you of the results we saw on two representative patients here who saw themselves or experienced much improved skin. That's remarkable. Another clinical study that shows we have activity. Just to summarize about how much data we're accumulating at this point, we've had, as I mentioned before, a very robust phase I study, including 115 patients, that went out to two years. We had our first celiac challenge study in phase I-B, where we learned and saw encouraging biomarkers. Today, we talked about very robust challenge data with biopsy data endpoints that are key for our development into phase II and then phase III that we'll build upon. Then we also had the vitiligo data. All of these have been accumulating our confidence in the target, our confidence in the safety. It's been very well-tolerated to date, and no concerning signals have been identified. We're moving forward as quickly as possible and very excited by the program. That reminds me, where do we go from here? Right now, we are working very diligently on getting our vitiligo study initiated this year, our phase II/III seamless design. We will also be next focusing on bringing this exciting data we had today to FDA and other regulatory authorities to design the next step for celiac disease. That's going to be our next focus. But in the future, we can imagine parallel work with other targets. There's a natural progression in thinking about alopecia areata, eosinophilic esophagitis, and even potentially atopic dermatitis in the future, which we have pre-clinical data to support. Again, we've shown another clinical efficacy point today that really builds this as a pipeline and a product as a key site kind of in multiple different indications. Finally, I'll just wrap up by saying, again, this program, like duvakitug, is a homegrown antibody from the labs at Teva. We build upon fundamentals. Developing very potent antibodies that have favorable PK, that can be used and shown in strong pre-clinical data, now in celiac and vitiligo, that we have a very safe and potentially highly effective molecule that's convenient for patients to take once every quarter. We have fast track designation in celiac disease. We'll move into phase II as quickly as possible when we take this data to FDA. We've already engaged with FDA on vitiligo and have a seamless design moving very quickly to start this year. In the future, we'll look at expanding indications, as I mentioned. But the data today highly support moving forward in celiac disease. I appreciate your attention. I think now I can hand it over to Chris, and we'll probably take some questions. Thanks, Eric. Before I hand it over to Sammy to start the Q&A session, I just want to remind people to please keep their questions as brief as possible, one question and then one follow-up if need be. If they have any further questions, you are more than welcome to get back into the call. Also, I want to remind people that Eli, Richard, and Eric are all joining for the Q&A session now for your questions. With that, Sammy, please go ahead. Thank you very much. To ask a question, please press star followed by one on your telephone keypad now. If you change your mind, please press star followed by two. Once [inaudible] asks your question, please ensure your device is unmuted locally, and please do remember to pick up your handset before asking a question. Our first question comes from David Amsellem from Piper Sandler. Your line is open. Please go ahead. Hey. Thank you. Two quick ones from me. I wanted to better contextualize the change in villous height to crypt depth here. You had a six week gluten challenge, so I guess my question here is, can you talk about the magnitude of that gluten challenge in terms of how much gluten you are introducing, and duration of gluten exposure, and how that ties into worsening of villous height to crypt depth over time? The reason I am asking is because we did see data for other agents, such as the Forte Biosciences agent. I believe that was a two week gluten challenge. It looked like they had stabilization on villous height to crypt depth. I am just wondering here is how you would contextualize this slowing of, I guess, for lack of a better term, disease progression here. That is number one. Number two, also a question for Eric, is how should we think about the kind of symptomatic assessments that you may look at in future studies, be it phase II-B or registration quality studies, and help us better understand what you are going to be looking for, both in terms of GI symptoms and non-GI symptoms? It might be early to answer that, but I figured I would ask anyway. Thank you. Great. Thank you, David, for the questions. Let me take them one by one here. The villous height to crypt depth measurement and the amount of gluten challenge, both the dose and the duration. This is a little bit of the art and the science of these gluten challenge studies. There is no one absolute answer. When it comes to Teva, we learned. We did a 14-day challenge the first time with 3 g, and we did a six week challenge the second time. The important thing here is you want to have a strong enough signal with the amount of gluten you use, but you have to do it in a way that people can finish the study. If you have known anyone who has a gluten intolerance or celiac disease, 3 g is what we gave. That is essentially a slice of normal bread. Some people, that is almost impossible to tolerate. It is very challenging. You have to be able to have a patient population that is sensitive but tolerable to that dose, and then you have to choose a duration dose that people can tolerate. From our learnings and our experience, the team did an excellent job at executing this study. Getting the people to the end of the six weeks and then getting the biopsy at that time is really kind of threading the needle here. My answer is there is no one defined way in which you do this, but it is the way in which you execute. The team's excellence and their ability to really learn and pivot and design and execute the study is really the key here. You can see from our data that the 3 g for six weeks, and then making sure we finished the study well, gave a great signal-to-noise ratio. I think the team hit it right on the head. Again, other people do it different ways. It is all about execution at this point. My final thing on this is, these are challenge studies. These are somewhat atypical in the dose that we give because we want to get a signal and show the potential of the compound. When you go into phase II and III, if you do what we call a sig study, which is a simulated inadvertent gluten exposure study, those are probably going to be lower doses, so that it is more physiologic and inadvertent exposures in the real world. This is a well-designed study showing the signal and the power of the compound, and that is why we chose 3 g per day for six weeks. Your other question, the symptoms. I think the symptoms are super important because that is what the patient will experience. I think the FDA appreciates that symptoms are important in the patient experience and the fact that we should change and improve the gut histology of the patients. That is why both of those will be included in phase II and phase III as moving forward. We use the Celiac Disease Symptom Diary, which I believe is pretty much becoming the standard at this point for how we measure that. That is a measure that includes abdominal pain, diarrhea, nausea, bloating, and fatigue. Fatigue is usually separated differently from the quantitative components of the measurement. But those are the symptoms that are most important for people with celiac disease. Certainly the people I know, those are the critical ones. We will talk about our symptoms in the future presentations, but we do see a very nice trend in how we protect people from those symptomatologies that they experience. Thank you for your question. Thanks, David. Next question, please, Sammy. Our next question comes from Louise Chen from Scotiabank. Louise, your line is open. Please go ahead. Hey, this is Corey Rosenb aum on for Louise. Thank you for taking my questions, and congrats on the data. Can you just discuss how the positive celiac disease and vitiligo data from earlier in the summer inform your confidence in TEV-408's potential across other IL-15 mediated diseases? Secondly, I know the study enrolled adults with celiac disease. How are you thinking about development in pediatric and adolescent populations, and what would need to happen before expanding into those groups? Thank you. Thanks, Corey. Your first question is, how does this add to our confidence in the program in general, was the first question? In other potential indications. Oh, yes. I am sorry. IL-15, you can see, is pretty much a key driver of a lot of these surface diseases. You will see programs across the landscape now developing across the dermatology and GI space. I think there is a lot of pull through from vitiligo, celiac disease to alopecia areata. I think most people would assume that there is going to be a strong pull through to that. I believe as I mentioned before, eosinophilic esophagitis will be important. It is encouraging to see other companies going to atopic dermatitis and even lichen planus, which are other surface indications, topological dermatologic indications that are important. Obviously, atopic dermatitis is very big, and I have mentioned that before. Lichen planus is an underappreciated disease that has no therapies as well. There is the world of indications for anti-IL-15 therapy as the safety continues to be strong, keeps opening up. I think that this is another inflammatory program that has a long way to go in multiple different indications. A very important question about pediatrics. That is a great question. Certainly, people with celiac disease start developing it frequently early in their life. In fact, it is frequently underdiagnosed early in life. For these programs at this point, we will have to continue to develop the safety, prove the efficacy in the adult population, and most certainly will be developing along the way pediatric programs as the FDA requires. That would be probably a future indication that we certainly look forward to. Thank you for the question, Corey. Our next question comes from Dennis Ding from Jefferies. Your line is open, Dennis. Please go ahead. Hi, this is Anthea on for Dennis. Thanks for taking our question, and congrats on the great data. Could you talk a little bit more about the regulatory path for celiac and your initial thoughts around that, and how you are thinking about mucosal damage prevention versus mucosal healing? Secondly, how are you thinking about developing this yourselves versus partnering out to a pharma company to co-develop similar to the anti-TL1A? Thank you. Eric, maybe you want to take the first two and then- I was saying the same thing. I will do the first two and I will probably pass the partnering out to Richard. Anthea, thanks for the question. The regulatory path, I am not going to give too much clear detail right now because we are going to be going to the FDA with this new data soon, and that will be a negotiation. I think that in general, when it comes to celiac development, I have mentioned many times before that it is going to be a component of these biopsy readouts and the symptoms. I think that regulators see the value in both because you want to make sure that you are disease modifying the basic pathology of the disease, like I believe anti-IL-15 can do. But more importantly, you want to make sure the patients feel and experience a better quality of life. I think that that's why I highlighted the symptoms today trending in the right direction, which is very encouraging. So those two things will be used. I think that, when you think about different study designs in the future, I think that one of the things that's becoming more commonplace is this idea of low-level, inadvertent, planned exposures to low levels of gluten. I think that's probably the best way to move forward. That's something we need to still discuss with regulators at this point. The question of prevention versus healing, that's a more broad question. I think that's something we also have to be discussing about how far can we drive a label. I personally have an aspiration that this should be all comers, people who want to be able to have a normal diet. Beyond just the people who don't respond to gluten-free diets, I think there's a great value in being able to travel and live your life the way you want it to be. So those are the discussions we have to have with regulators and make sure that how we design the phase II and III studies achieve those goals. Why don't you pass off the last question about partnering to Richard? Hi. Yeah. Thanks for the question, and thanks to Eric. As you've seen over the last few years, Teva has developed an excellence in commercial execution across a number of therapy areas. Based on that capability, based on understanding these disease areas through the work we're doing in clinical development, we have no plans to partner these products. As you saw by some of the partnering we did on financing with Royalty Pharma, we're in a position to develop these on multiple indications all the way through to launch. Thank you for the question. Excellent. Our next question comes from Melanie Fong from Bank of America. Your line is open. Please go ahead. Hey, this is Jason on for Melanie. Eric, can you talk a little bit about what you want to learn from phase II? Do you want to explore another dose, or are you looking for evaluating the impact of the drug with longer gluten challenge and longer treatment exposure? Just trying to get a rough sense of what we can learn incremental in phase II. When I look at the placebo effect to your gluten challenge, -0.9 on the measure, it looks like historically it was like -0.2 to -0.6, so your gluten challenge seems to be maybe having more of an impact on patients. I assume all the patients in this phase II were able to stick it out in this trial. As you think about longer trials, I'm just wondering how you employ gluten challenge with the goal of keeping patients in the study. Great. Thanks, Jason. What do we want to do in phase II? Again, we need to take the data we have right now and have this discussion with the regulators. Certainly, my goals are, I'll fall back on the fundamentals. We want to make sure that we recapitulate and show symptom improvements and biopsy results. That is why this study today was so important. We have a very good idea what we can do with regards to those endpoints. We will want to make sure we push the duration more and more because we have to start building up the safety database and the duration of therapy, and follow-up, so that we can have the safety database for the submission. We will do more than one dose because we have to do dose ranging to fulfill our commitments with regulators and understand the modeling and simulation on dose. Those are the fundamentals, and dose is the most important thing when it comes to a submission success. So those are my goals in phase II. Then we will recapitulate those in phase III. You do not want to change too much along the way because we want to make sure that you are going to succeed. So that will be our next steps with our discussions with the health authority. Now, back to your question about the gluten and the robustness of the study design. As I mentioned before, in these studies where it is a pretty strong dose of gluten, you want to balance your signal to the ability to complete the study so that you really have a good comparison. This study was run very well. The majority of subjects got all the way to the end, and we had a good comparison. It was balanced between placebo and active. So that is why we are confident in the numbers we were able to generate today. When we talk about the phase II and the phase III, and this thing I keep talking about, this simulated inadvertent gluten exposure, getting that dose right that it is tolerable over a very long duration of time, but also give you the signal you need is going to be the important next step. We are already in discussions with our experts, and we will have that discussion with the regulators next. Thanks for the question, Jason. Our next question comes from Matt Dellatorre from Goldman Sachs. Your line is open. Please go ahead. Great. Good morning, guys, and congrats on the positive results. Maybe just on the multi-dose phase II that you're going to start shortly. What's a reasonable base case for timelines for that study, and then timelines also for moving into phase III? As we think about the target profile for that next phase II and ultimately the phase III, would repeating this level of Vh:Cd ratio be viewed as success? In terms of benefit on symptoms and the Celiac Disease Symptom Diary score, could you quantify what kind of impact would you want to see there? Would that be a quantified number that you would share? Eric, you did also mention you want people to have a normal diet and be all comers. I just wanted to clarify, would patients who have gluten disease or celiac disease, after taking this therapy, would many of them actually be able to just live a normal life in terms of the diet? Thank you. Okay. Thanks, Matt. You got a lot of questions there, but I'll get them one by one. I'm going to first disappoint you on the first one. The duration of the phase II and the timelines of the phase II, that's going to be really dependent on the design we settle on with FDA. I can't really comment on how fast that is, and that would also trickle over to what I envision for the phase III. This is going to be a step-by-step process. We'll do phase II, then phase III. That's about all I know today. But we can update you in the future about how our discussions go. How I would generate or how I would measure success when it comes to the biopsy. In general, 0.4 change on the biopsy villous height to crypt depth is considered clinically meaningful. That's pretty much the answer I can give today, and I'd hope to see that in a study design in the future. It's a little bit more challenging when you do long-term, low-dose studies to get that amount of change. But that's certainly what our aspiration is. When it comes to the symptoms diary, the CDSD measurement, I'm looking for a statistically significant change in symptoms. That would be the simple goal there. The PROs will tell us whether their experience, their quality of life is improving. We'll probably add other PROs in the future to demonstrate the true value to people's lives. I think that gets to your last question about all comers. I speak sometimes a little bit too passionately about celiac disease because I think that certainly in my experience, in my training back in the 1990s, I was taught that this was all in the minds of the patient, which is obviously completely wrong. So when it comes to who should have access to a treatment like this, I think obviously people who do not respond to a gluten-free diet, which is 50% of the population right there, certainly deserve a treatment. But I believe the folks who have to change their entire life and think about this in every meal of the day deserve something that can free them up from that. I think that that is going to be the important discussions in the future when we talk about PROs with health authorities and make sure that we answer that question for health authorities about what the value is for all people who have celiac disease. Thanks, Matt. Our next question comes from Ash Verma from UBS. Ash, your line is open. Please go ahead. Great. Yeah, thanks for taking our question, and congrats on the progress here. Just trying to understand the next steps here. How much of dose finding work do you need to do in a phase II? Is it more sort of tinkering the level of gluten that you would give, or is it actually looking at different levels of the dose that you are providing for the drug? Then in the maintenance setting, could the dose be different compared to the induction data that you have shown today? Thanks. Great. Thanks, Ash. Great question. When we're talking about the phase II dose ranging, that is dose ranging of the drug. I can't get into too much specifics here because it will probably be highly dependent on how we have our discussion with regulators. But as you always do, you need to have dose ranging so that you have a strong understanding of your dose and response ratio. I would argue we have a very good dose response model already that has been developed with free IL-15 and other biomarkers across the program for a long duration. We're going into phase II with a lot of knowledge built on a lot of great fundamental science that the Teva team has already done. It would be most likely, or will be a dose ranging of the drug itself and not necessarily the gluten. Your second question, when it comes to maintenance, one of the things that I think differentiates our programs from others right now is we went right into it without a loading dose. We're planning on Q every three months. I don't think that has to change necessarily for maintenance. I want to make this as simple and as convenient for patients as possible, and we've started there. I wouldn't back up or regress in the convenience of the program at this point. I think that a simple shot every three months is what we'll focus on going forward. Thanks, Ash. Next question please, Sammy. Thank you very much. As a quick reminder, to ask a question, please do press star followed by one on your telephone keypad now. Our next question comes from Umer Raffat from Evercore ISI. Your line is open. Please go ahead. Hi guys. Thanks for taking my question. Hi guys thanks for taking my question. Can I ask- Of course, Umer. Touch up on two quick points. First, the sample size. 50 patients went in. How many patients are informing the analysis that's being shown? Secondly, the biopsy results that we're looking at, were they centrally read, and was the biopsy orientation perfectly vertical? Third, I understand the gluten background is 3 g a day. Other trials have as much as 8 g a day, which impacts how much placebo deteriorates. As we think about the effect size and the absolute numbers we're comparing, should we be comparing percentage numbers? Should we even be comparing versus trials which have much more gluten background per day? I'm just trying to put this all into perspective on the interpretability of this data set today. Great. Thanks, Umer. Let me go one by one. The first one, sample size. It's 50 patients in this study. The vast majority of the patients got through to the end, and they were balanced between placebo and active. The comparison and our confidence in the data are very high. The biopsy orientation, you're absolutely right. When you do the reads of the villous height to crypt depth, you always have to make sure, and the pathologist knows this, that what you measure has to be a slice through the entire length of a villus. You always have to make sure that you're seeing, they're always in different orientations when you slice the tissue, but you always have to make sure you have a clean slice from the very tip all the way through to the crypt of that villus. You have to have a clean measurement when you do this, and then obviously the intraepithelial lymphocytes is more straightforward where you count the number of IELs to enterocytes. That's a pretty standard way of doing it, and we make sure that our pathologist is well-versed in that. Then your final question is about the gluten. I'm not really sure exactly what you're asking. Was it the interpretability? I know that there's been a lot of questions about the dose in different challenge studies. If it was the interpretability, in these POC studies with these relatively high doses of gluten, I really do think it's a little bit of an art and science. You have to make sure that you have a dose and a population, people who are responsive but not intolerant of gluten, that you get the right people in, and that you have the right duration, and that you have the right support to get them through this study. That's the combination of why we settled on this population, 3 g per day for six weeks. Great. I think at the end of the day, it shows that the drug does the effect that we need for phase II and III. Thank you. Thanks, Umer. Our next question comes from Luisa Hector from Berenberg. Your line is open. Please go ahead. Hello. Thank you for taking my questions. I have a couple. Eric, I am curious what you would expect to see in the longer-term follow-up of the phase II-A. Would you expect a kind of waning when there is damage, or are the placebo patients sort of permanently worse off? Then a question on what the FDA might require. Do you have sort of a minimum number of patients that need to be on a maintenance dose for 12 months? What are the requirements there, and can you get to that without doing a gluten challenge all the way? Thanks. Great, Luisa. Thank you. Fantastic question. It is particularly interesting in the sense that we do have a long-term follow-up in this study. I expected this question from many others, but what is the actual long-term effect of this treatment? Our responsibility, my responsibility, is to make sure that we dose a compound based on the best data we have. We can clearly show that we can suppress IL-15 for 90 days, and that is why we are going to stick with a two, three-month dosing, a quarterly dosing. But the effect might be longer lasting than that. In fact, we do suppress these cells for a while after dosing, and we will continue to gain information like we have throughout the entire program about the recovery of the cells and the kinetics of this entire effect. So, there is a possibility it can last longer. I think that we have a very robust data set that tells us quarterly dosing will work now. But we will get more data in this follow-up to see how the patients do, what they are feeling long-term. And we will have more to talk about in that follow-up maintenance that you mentioned. But the possibility exists that since we are disease modifying, potentially, that effect might last longer than we even anticipated. So, great point. I think that just more data will determine what the true answer is. So the follow-up is important. Now, your question about what is required. The basics of any program is traditionally you have 300 patients at six months and 1,000 or 1,400 patients total in the safety database. Those are generalities for each program. Usually when you have a strong effect like this, statistically, you might be able to go smaller, but really safety will drive the long-term submission timelines. I hope that answers your question, Luisa. Thank you. Thank you. We currently have no further questions, so I would like to hand back to Richard for some closing remarks. Thank you. Thank you everybody who took the time to dial into the call today. Really appreciate your interest in Teva. I would remind you of some of the comments I made earlier in the presentation about 2026 being an exciting year as we progress on our Pivot to Growth strategy. We've had a number of readouts which we've had conference calls for, but just to remind you, we still have quite a few to come. Obviously, there'll be the completion of the DARI study in asthma. We will also have the futility analysis for emrusolmin, and we're fastly approaching the opportunity to be launching our long-acting olanzapine into the market in Q4. As well as now the exciting news that we have priority review for ecopipam and the ability to launch that early in 2027. So some great progress here at Teva on our innovative portfolio. Some great progress by Eric and his team, and I want to congratulate and thank him for that. I look forward to connecting with many of you over the next few months to highlight some more interesting milestones from Teva. Thank you. Goodbye. This concludes today's call. We thank everyone for joining. You may now disconnect your lines