Hello and welcome to the duvakitug anti-TL1A positive phase II-B topline results conference call. My name is Elliot, and I'll be coordinating your call today. If you would like to register a question during today's events, please press star one on your telephone keypad. I'll now hand it over to Chris Stevo, Senior Vice President of Investor Relations. Please go ahead. Thank you, Elliot. Good morning, good afternoon, everyone. Thank you for joining us on such short notice. I'd like to remind you that during today's call, we'll be making forward-looking statements, and we undertake no obligation to update those statements after today's call. And if you need more information on our forward-looking statements and other risk factors, please see our SEC filings under Forms 10-Q and 10-K. And with that, I will turn the call over to Richard. Thanks very much, Chris. So, welcome, everybody. Good morning, good afternoon, and really pleased you could join us here on this exciting day for Teva and our partner, Sanofi. Now, before I start this call, I want to make sure I get in the thank yous. So I'd like to thank my colleagues within Teva, particularly within Eric Hughes' team, my R&D colleagues. Also, I'd like to thank the investigators and the patients who have allowed us to be in the position today to present this very important and impressive result. Without them, their help, their dedication, none of this would have been possible. So next slide. Now, in May 2023, we laid out our Pivot to Growth strategy. We shared the plan with you, what we wanted to do, how we wanted to do it, even when we wanted to do it. Now I'm extremely pleased to say we have another example of us at Teva delivering to this plan. This is further evidence of the great team Eric has put together and our ability, particularly on pillar two, to Step Up Innovation. I've always said a company is all about its people, their hard work, their commitment to their success, but also their commitment to executing this strategy. And I think you've seen over the last 18 months, Teva has consistently delivered on all of these pillars. But today, it's all about pillar two, Step Up Innovation. Next slide. Now, as you can see, our top line results for duvakitug in the IBD trial are transformative. These positive results show that duvakitug is potentially best in class and, might I add, best by design. Now, Eric will talk a bit more about this later, but we have always been convinced that we have potentially the best in class TL1A. Now, to remind everybody, the IBD market is expected to be around about $31 billion by 2030. And an approval in these two indications will open up duvakitug to this large market opportunity and allow us to serve the significant patient population with such a large unmet need. Now, this is a major step and a major milestone for Teva because we are a global pharmaceutical company, a company with a world-class generics business, but also a world-class innovative business. Now, with that, I know you're desperate to hear more, so I'd like to hand over to Eric Hughes, who will walk you through some of our exciting details of these results in more detail. Thank you, Eric, and over to you. Thank you, Richard. This is truly a great day for the innovative R&D team at Teva and for our partners at Sanofi. It is rare to bring a new medicine to this stage successfully, but even more rare in two indications on the same day. But first, it is important to remember this program begins and ends with a patient as our motivation. Over 40 million people suffer from inflammatory bowel disease. Less than 50% of these patients achieve a clinical remission, and these responsiveness can be lost over time. But most importantly, 20% of ulcerative colitis patients and 75% of patients with Crohn's disease still require surgery. So we have a long way to go to treat this illness. Now, TL1A is a key mediator of this inflammatory response on multiple different levels in multiple different pathways in the immune system. It also has a potential to directly impact fibrosis. These qualities make it possible that this target could be key to many different disease areas in the future. So we're excited by that potential. Now, the duvakitug program is a great example of the expertise, the capabilities, and the rigor of our R&D team at Teva and what they bring to the drug development engine here. These same scientists and physicians work on other programs such as our anti-IL-15, our anti-PD-1-IL-2, and other programs in the preclinical space. Their better-by-design thinking really differentiates our innovative teams. Now, why do I talk about differentiation and this better-by-design? Our duvakitug program has been specifically designed to be selective for the DR3 signaling pathway. The DR3 signaling pathway is the bad inflammatory signal that we need to block. But we designed the antibody to also allow continued binding to the decoy receptor. This allows for the binding and clearance of the biologically active trimer of TL1A and therefore removes the exuberant response of this cytokine in the inflammatory bowel disease space. Now, on this next slide, you can see we have created other antibodies from publicly available information that are in development and compared them to our duvakitug antibody. And what you can see on the left, we can show that we have 60-84 greater potency in the inhibition assay in vitro. In addition, as I mentioned, we are more selective. You can see that we have a 117-fold more selectivity on the right-hand graph over DR3 versus the decoy receptor of DcR3. This is 40 times more selective than other programs. We have also differentiated ourselves by looking at free TL1A in the body in our studies. In this prior study in asthma, you can see that we have a rapid, profound, and sustained suppression of free TL1A levels. This is a key biomarker in our program that will help define and guide our dose selections in the future. This study also showed continued safety and tolerability of the compound and also showed less than 10% anti-drug antibodies. These all give us great hope that our program is truly differentiated. Now, on to the study that we're talking about today, our duvakitug phase II study in ulcerative colitis and Crohn's disease. As a reminder, this was a robust 240-person study evenly divided between ulcerative colitis and Crohn's disease. There were two doses, a high and a low dose compared to placebo. The primary endpoint and the data we're talking about today in this induction study is at week 14. It's important to remember this is the first Crohn's disease study in a randomized controlled fashion for this MOA. Our primary endpoint, as a reminder, for ulcerative colitis is clinical remission, the Modified Mayo Score, and for Crohn's disease, it's the endoscopic response. Now, on to the exciting part and the results that we're talking about today. You can see here the primary endpoint on the left for ulcerative colitis, and you can see on the right the primary endpoint for Crohn's disease. I'm very happy to say that we've shown statistically significant and clinically meaningful responses in both. We were very happy with the delta of 27.4 on the clinical remission for ulcerative colitis, and we were very happy with a 34.8% response delta change from placebo for the Crohn's disease. Very convincing and clear results with a dose response. All very happy. All these things make me very happy that we can really model and simulate in our dose estimations in the future based on this robust data set. So with that, I want to remind everyone of why we believe this is certainly a potential best-in-class compound. We have high potency. We have high selectivity. We have shown low anti-drug antibodies. We've demonstrated a rapid, profound, and prolonged suppression of free TL1A. We've shown a consistent and favorable safety and tolerability profile to date, which leads us to believe that we are best in class potential with significantly meaningful clinical responses in both ulcerative colitis and Crohn's disease. This is something I just want to say thank you to all the people at Teva who worked so hard to bring this compound from our labs in the early days all the way through these clinical results. I want to thank Sanofi as our partner in this endeavor, but most importantly, I want to thank our investigators and particularly the patients who participated in the study and made this all possible, and with that, I want to pass it off to Eli Kalif. Thank you, Eric, and good morning and good afternoon, everyone. I will discuss financial considerations related to this very exciting development in our innovative pipeline, which demonstrates flawless execution and focused capital allocation strategy driving our Pivot to Growth. As many of you know, in October 2023, Teva entered an exclusive collaboration with Sanofi to develop and commercialize Teva's anti-TL1A asset duvakitug. This collaboration allows us to leverage each partner's strengths, accelerate development, and share costs. Not only do we maintain significant upside through a 50/50 worldwide profit share, but since Sanofi adds significant value, we believe this unlocks significantly more value to Teva than what we will have achieved on a standalone basis. As part of this agreement, Teva received an upfront payment of $500 million in the fourth quarter of 2023, which was recognized as a license agreement revenue. As Richard mentioned earlier, with the positive phase II top line results that we are announcing today, Sanofi and Teva are now planning to initiate phase III development in IBD, pending regulatory discussions. To remind everyone, Sanofi will be leading the phase III clinical trials for duvakitug, and Teva will contribute 50% of the R&D costs. As per the agreement, Teva expects to receive approximately $500 million in total development milestone payments upon UC and CD phase III initiations, i.e., $250 million each for both indications. These payments, when received, will be recognized as a revenue consistent with the fourth quarter of 2023. However, it's our policy that we don't include milestone payments in our guidance until they are earned. Therefore, when we provide 2025 guidance with our Q4 earnings goal next month, we will not include these expected payments in our guidance. As we continue to execute this next phase of our Pivot to Growth strategy, we expect our improving portfolio mix, ongoing cost optimization efforts, and our disciplined capital allocation to support potential higher R&D spend related to the phase III development of this program. Moving to the next slide. We established a very comprehensive capital allocation strategy last year in order to make sure that we are able to fuel our growth and innovation, improve margin, and at the same time meet our financial commitments. We remain committed to following this approach in order to keep deleveraging to make sure we are reducing down our debt towards our goal to be investment grade, keep investing in our growth engine AUSTEDO, AJOVY, and UZEDY, and keep investing in R&D with the right prioritization and focus on innovation as well as thoughtful business development. Turning to the next slide. We remain on track to achieve our 2027 financial target. On revenue, we have already shown a solid execution with the seven consecutive quarters of growth. We will continue to improve our operating margin towards our 30% targets for 2027. We continue to pay down our debt and progress towards the two times net debt to EBITDA ratio, and we'll, of course, need a strong cash-to-earnings in order to achieve all of these, and with that, I would like to turn it back to Richard for a summary. Thank you, Eli. Thank you, Eric. So I'd like to move on to the next slide. Now, to go back to the Pivot to Growth, it has all been about growing a sustainable, profitable, long-term business. And I think you've seen in the last 18 months, we've been all about delivering on this Pivot to Growth strategy. Now, we're about to start embarking on the second stage of it, which is accelerating growth. Now, there's a couple of things I'd like to remind you. Firstly, our innovative portfolio is still very young with a long runway to growth. And duvakitug and other late-stage pipeline assets such as olanzapine and ICS/SABA still have the potential to accelerate and grow the company. And then we have some early-stage assets which we are investing in and progressing through to the clinic, as Eric has mentioned, our IL-15 and our PD-1-IL-2, to name just two of them. All of these, to remind you, are curated by the same talented team led by Eric. Now, together, with us constantly focusing on driving our generics business forward and optimizing that and returning to that to growth, I think this puts Teva in a very strong position to deliver on its commitment to grow going forward. Next slide. So to conclude today's call, as I always do, I'd like to bring you back to the four pillars of our Pivot to Growth strategy and how you have seen us execute on this consistently for the last 18 to 20 months. And we commit to continue doing that going forward. I'd also like to once again thank Eric and his talented R&D team for the effort and the work they've put in, and to remind everybody, the work that the team did to accelerate this, so we were in a position to give you this data set today. I'd like to also thank our partner, Sanofi, for their help now and obviously their help going forward as we embark on this exciting journey into the phase III, and I'd like to reiterate these positive results underscore our ability at Teva to discover, develop, and accelerate access to innovative medicines, so with that, I'd like to thank you all for listening, and now I'd like to open up to a Q&A, so back to you, operator. Thank you. If you would like to ask a question, please press star followed by one on your telephone keypad. If you would like to withdraw your question, please press star followed by two. When preparing to ask your question, please ensure your device is unmuted locally. Today, we ask you limit yourself to one question and one follow-up. Our first question comes from Jason Gerberry with Bank of America Merrill Lynch. Your line is open. Please go ahead. Hey, good morning, guys, and thanks for taking my question and congrats on the update. So the question for me is just, can you speak to, you mentioned that the subgroups performed sort of equally well. Wondering if you can just speak to how well-represented biologic or refractory patients were in this study. And if you can offer any color just in terms of maybe what you'd attribute the relatively high placebo response in the trial versus some of the other UC trials that we've seen. Mindful that the placebo-adjusted responses look really good, but just kind of curious if you can put a little color on the placebo response you saw. Thanks. Thanks, Jason. Thanks for the question, and I'll hand that straight over to Eric. Yes, Jason, thanks for the question. So we were very excited to see that the placebo-adjusted rate for both ulcerative colitis and Crohn's disease was very clear and robust. So we reported here two numbers that are highest that have been reported for this MOA of 27.4 and 34.8. So that delta, as we mentioned in the press release, is consistent across all the subgroups. So we're very confident in the delta and the treatment effect that we've seen in both indications. It's also important to remember, and I think to answer your question, is that we have the normal distribution of subgroups in the study that you normally see in a study of moderate to severe patients. We have a certain amount of steroid-using patients. We have a nice spread of patients that have previous treatment with approved advanced therapies. The distribution across the world is typical of what you see in these studies. We've seen no change, and it's very consistent across all these subgroups in our analysis. I would focus on that delta, and that's consistent across everything. We're looking forward to presenting that at a conference in the first half of 2025 with a full data set. Today, unfortunately, I have to be limited to what we see in the press release. Understood. Thanks so much. Thanks, Jason. We now turn to Ash Verma with UBS. Great. Yeah, congrats from my side as well. Pretty impressive data. Just two quick questions. Can you elaborate on the dosing levels here? It seems like the safety is pretty clean. Does that. I think we lost him there. I only heard the beginning. We should still be on screen. Yeah, so while we kind of fix the audio. Yeah, maybe I would speak to should we go to the next question and come back to Ash, actually? Or can we go to the next one and then maybe come back to Ash, let him know when his line's up and running? Sure. You have the next question? So, Richard, while we're waiting for the next question to come up, I'll just answer that question that Ash had about safety. I think that that's a very important point. You saw from the press release that, in fact, we saw basically the same amount of treatment adverse events in both the placebo and the active arms. It was 50/50. So, stage of the development program in the safety and are not limited and have not seen those signals at this point. And I think Ash was also asking about the dose levels. We have both the high and the low dose here. We saw a clear dose response in both populations of both the ulcerative colitis and the Crohn's. This will help us greatly in our modeling and simulation as we update that model with both the top-line results, and then we'll get into the details of both the free TL1A and other biomarkers that we have in the study to really focus on the proper dose going forward in phase III. It's too early at this stage to define that, but that's something we'll be working with very closely with our Sanofi partners. Thanks, Eric. Can we get back to the operator now for the next question? Our next question comes from Balaji Prasad with Barclays. Your line is open. Please go ahead. Hey, Balaji, are you there? This is Shao for Balaji. Can you hear me? Yeah, we can hear you. Go ahead. Yes, we can hear you. First off, congrats on the data. So just want a little bit of color of your potential upcoming phase III study design. Given that a high delta was observed for both clinical remission for UC and endoscopic response for CD, wondering will you try for a once-monthly dosing interval for phase III? Thank you so much. So I'll take that, Richard. So thank you for the question. There's a lot of data to comb through at this point. We just had the top-line data revealed this last week. So it'll take a modeling and simulation effort to make sure that we're targeting the right position on the dose-response curve, and it will take some time to do that. And this will drive whether we use what dose and what schedule. So right now, I can't talk about which one we'll pick. I'll remind you that we used a two-week schedule in the induction study, in the phase II study, and we looked at and are running a Q4-week maintenance study. So with the combination of all that data, we'll work with Sanofi to choose how we design the phase III study. It's also important to remember that our phase II study was done all subcutaneously, and that helps us model and simulate our doses with greater accuracy since it will be delivered the same way in phase III. Thank you for the question. Thanks, Eric. Next question, please. Our next question comes from Ash Verma with UBS. Your line is open. Please go ahead. Hey, guys. Hopefully, [crosstalk] time. Hi, Ash. You're back. Yeah, that's great. So yeah, I wanted to go back to the anti-drug antibodies. So the 10% that you saw on that, just curious here, what are your thoughts on this, where it can go in the maintenance setting? As we know, that's a key shortcoming of the anti-TL1A. Thanks. Yeah, so. Thanks. [crosstalk] Yeah, thanks, Richard. That's a great question, and it's very important. In the programs I've worked on throughout my career, you want to make sure in a chronic illness like Crohn's disease and ulcerative colitis that you have a drug that is not only active but also durable. So low anti-drug antibodies are very important for that. We've made this using a human system in which the antibody is essentially as humanized as it can be. That will add to the low anti-drug antibodies, and that will help with the maintenance in the long run. So that's some data that we'll be sharing in the future. Remember, the follow-up and maintenance part of this study is 44 weeks, so it'll be some time before we see that full data set to share. But we're looking forward to that, and it'll help guide exactly how we do maintenance in the future. Thank you. Thanks, Eric. Thanks, Ash, for the question. A reminder, ladies and gentlemen, if you'd like to ask a question, please press star one on your telephone keypad now. We now return to David Amsellem with Piper Sandler. Your line is open. Please go ahead. Thanks. So just a couple for me. First, in talking with key opinion leaders in the gastroenterology space, there's a lot of interest in biomarkers here as it relates to the category. So I'm just wondering, and it might be too early to answer this, but how are you going to incorporate that into your pivotal studies? And maybe I'll ask it a different way. Are you going to test all comers, or are you going to look more specifically at patients with certain biomarkers? So that's number one. And then a broader question just about clinical development and how you're thinking about pipeline. With this event, how are you thinking about the potential acceleration of other early-stage programs just given the success today and just maybe holistically talk to overall strategy in terms of bringing early-stage molecules through development? Thanks. Thanks, David. Thanks for your question. I'll hand the first one over to Eric. Yes, thank you for the question. So first, with the question about biomarkers. So as I've said many times, we're including all the baseline biomarkers: proteomics, genomics, serum biomarkers, fecal biomarkers. But one of the things that differentiates us and makes us unique is we're also looking at this free TL1A levels. And we're on the third generation of the assay we've developed in-house. And the reason I talk about this so much is because this is a direct measure of target engagement. We've shown that we can actually suppress these trimers, these biologically active trimers in the human system very well, robust, and in a sustained way. I hope someday we'll have very clear baseline biomarkers to choose what patients to treat. But I would say that our data today really validates the all-comer approach. Both UC and Crohn's have shown very good deltas from placebo, and we'll move forward that way. But in the future, I hold out hope that an assay such as free TL1A could help direct therapies. That's something we have to work on and develop further. We'll always be testing for that in our program going forward. But someday we might have a baseline biomarker, but I have a lot more confidence in direct target engagement markers like the free TL1A assay. So we'll keep presenting that data, and if the data support it, that could be one way of delivering and guiding therapy. But right now, it's an all-comer program. The other question you had, I think, was, I believe, on indications for TL1A. Could you just clarify? Sure. Actually, it was a question more just on how you're thinking about accelerating other early-stage compounds just given today's success. And do you accelerate development and bring into the clinic other compounds? Do you look at R&D more aggressively just given the success to date on the TL1A? Thanks. Yeah, so the success today actually just confirms our strategy right now. At Teva, we have a late-stage portfolio that is what I would describe as higher than normal POS. We have the olanzapine LAI program in schizophrenia. We have the ICS/SABA, or dual-action rescue inhaler, in asthma. And now we have the TL1A program. These are all late-stage assets with higher probability as a result of today's readout. But in general, our strategy has been to focus and move those forward as quickly as possible. I get the question from Richard every day: how can we accelerate these programs? And you can see with TL1A, we accelerated it. With olanzapine LAI, we accelerated it. I'm running around the world right now trying to accelerate our asthma program, but it just gives us confidence in our innovative group that they can execute on these great molecules. So we'll apply the same logic and shoe leather to all of our programs throughout the development spectrum here. So it doesn't change anything. Just it makes us more confident in what we're doing. Yeah, and if I could add to that, Eric, to David. I mean, look, David, I appreciate the question, and I think it's a testament to the change in the view of Teva in the last two years that a question like that comes up, i.e., a question about, can you accelerate your innovative pipeline, and can you bring it into the clinic quicker? And I think it's also you ask it because of the success that Eric's team have had, excuse me, on olanzapine, accelerating that on TL1A, accelerating the phase II. So we're talking about it today. The fact that I think we'll be talking about IL-15, which is from the same team that created this duvakitug, as well as the PD-1 -IL-2, as well as emrusolmin that's in the clinic for MSA. So that's a change in narrative distinctly from what we had just under two years ago. And I think that reflects the confidence now people have in Teva and the innovative capability that Eric and his team have put together. So I welcome the question. But when we always go back to capital allocation, we go back to the Pivot to Growth strategy. What do we need to focus on? Where do we need to apply capital? And how do we need to execute? And that's pretty much what we've done and what we'll continue to do going forward: that ruthless allocation of capital and that pursuit of excellence, whether that's commercially, or whether that's in the clinic, or whether that's with our generics business. Thanks for the question, David. Next question. We now turn to Yifeng Liu with HSBC. Your line is open. Please go ahead. Thanks very much, and congratulations on the update. Just one quick follow-up question on the phase II. In the extension, are you going to still run three arms, or do you have your placebo arm switched to either lower dose or higher dose arm? And how long roughly would that part be running? Thanks. Thanks for the question. I'll hand it straight to Eric. Sorry, Richard. I keep speaking over you. I'm a little excited today, so yeah, so we're running a long-term extension after the study. Those folks who respond can go on to maintenance, and those folks who need a reinduction can get reinduced. So we're making sure that the drug is available, and we get that data for the long-term durability of the drug. That goes out for 44 weeks. We just finished this part of the study, so it'll be some time before we have a chance to present that data, and we'll be bringing that to you as quickly as possible, but right now, we're keeping the doses and the scheduling, other than the fact that it's four weeks, kind of quiet now. We'll present that at a congress when the data's ready. Thanks very much. Thanks, Eric. Thanks for the question. Next question, please. We now turn to Douglas Tsao with H.C. Wainwright. Your line is open. Please go ahead. Hi, good morning. And congrats and thanks for taking the questions. Just one thing that was very noticeable to me or sort of quite striking was the results in Crohn's disease, which historically has been viewed as more challenging than UC. And I'm just curious, do you attribute that to the sort of antifibrotic effect? And I guess the second part would be, does that influence how you think about development going forward and sort of the targeted indications? Thank you. Thanks, Doug. Thanks for that question. And yeah, you did spot something that I think has excited us as well. But over to you, Eric. Yes, thank you. This is actually a particularly interesting thing that caught my attention as well. And it leads me to only speculation at this point. But I want to dig into that endoscopic data. So just to remind everyone, in the Crohn's disease endpoint, this endoscopic response, this is a truly objective measure here where we're taking biopsies of the gut and then sending them to a central lab and having them read in a blinded manner and scored based on the actual biopsy changes. So that's a very objective way of seeing down to the almost cellular level changes in the pathology of the gut. And your question is right on the money because is there something we can see in these histologic changes? Now, we'll look at these not only in the traditional way of looking at histology, but we'll do other more advanced ways of detecting and quantitating the changes in these biopsies. And the question gets right to the point that gets me excited, and it's that, are we affecting the fibrotic levels within the tissue itself? And that's one of the potential upside targets of anti-TL1A therapies where we do say that there is a direct receptor on fibrotic cells. And are we changing things on the level of the gut lining? That's a particularly interesting question. I think that it has potential great benefit for patients as we treat longer and longer. But at this point, it's just speculation. I do want to dig into that data very carefully and really make sure we can see what changes we're imparting at that tissue level. Thanks, Eric, and thanks for the question. Okay. And And just on the second part of my question, just does it? Go ahead. Go ahead. You can ask the second part. Yeah, I was just saying in terms of my second part, was just sort of does it influence how you think about other indications, or is that just maybe a little too soon? Thank you. No, that's a good point. So if TL1A treatments or targeted therapies can have a direct effect on fibrosis, yes, that does broaden your thinking about where you can take a drug like this. We always treat the inflammation to date, but we hope the treatment of the inflammation imparts an effect on the fibrosis. Here, we might be treating both the inflammation and potentially the fibrotic changes directly. So it does expand your thinking about what you can go into. There's a long list of indications you can name that would benefit from a drug that has a direct antifibrotic effect. Okay, great. That's very helpful, and congrats on the data. Thanks. Thank you. Thanks for your question. We now turn to Chris Schott with JP Morgan. Your line is open. Please go ahead. Great. Thanks. And congrats on the data. Just a couple of quick ones for me, maybe just on timing here. Just any guideposts you could provide in terms of assuming a 2025 start, when we could see phase III data and just how you think about the kind of timing, I guess, relative to competition for the program? And then maybe tied to that, I think just building on that comment about other settings that you'd explore the product, should we think about the company exploring some of those additional indications kind of in the near term or in parallel with these late indications, or would you really just focus on Crohn's and UC and think about those additional indications as longer-term opportunities once you run the phase IIIs on these first two? Thank you. Thanks, Chris. Appreciate the question. And before I hand over to Eric, I'll just make one quick comment. I'm excited that you and others are excited about how quickly we can not just get into phase III, but get the data from phase III. And what I'd also say, and I've been consistent saying, is it's never been where we are in this race to get to market. It's about what that actually looks like when the end of the race is complete and also the quality of the data. I think the quality of the data is really important. But with that set up, I'll hand it to Eric. Thanks, Richard. Yeah, so we're excited right now. We just got this data in. We'll build and work with Sanofi on building our model and do the simulations and be prepared for our health authority interactions to get phase III going in 2025. I can't say what date that will be yet, and I don't certainly know what the end date is of the study. But your question about other indications, we are not going to sit back with great data like this and not think of other things to do. We've already been working with our partner on choosing what are the highest probability indications we want to go into next. I don't want to divulge that today, but we've been working on it and excited by seeing the data today to engage on that in parallel. Thanks for the question, Chris. No further questions. So I'll hand back to Richard Francis for any final remarks. So thank you, and thank you, everybody, for the questions and the interest in Teva, as always. Appreciate it. And obviously, we're very proud and pleased with what we announced today. I think once again, it reinforces the excellent work the team are doing on executing on our Pivot to Growth strategy and the excellent work Eric and his team are doing on the pillar of step-up innovation. I think we've now consistently shown our ability to drive our innovative pipeline through some important milestones, and it's been a very important one for ourselves and our partner, Sanofi. So with that, I look forward to updating you at the start of the year with the rest of the team on the full year results for 2024 and obviously giving guidance for 2025. With that, I'd just like to wish everybody happy holidays. I know we're at the end of the year now, so I appreciate people taking the time to call in. I wish you all an enjoyable time with friends and family and look forward to connecting with you all next year. Ladies and gentlemen, today's call has now concluded. We'd like to thank you for your participation. You may now disconnect your lines.