Thanks for joining us at the next session. I'm Graham Parry from Citi, and it's a pleasure to be able to introduce Sanofi, and in particular to introduce Paul Hudson, the CEO. It's great to have you here in Miami, Paul. I'm sure it's nothing to do with the sand and the sea that interests you here. It's purely the investment community. Perhaps if I can get you to kick off with some high-level sort of opening remarks just to talk about where you think Sanofi is at the moment. And I guess the thing that's on a lot of investors' minds still is how Sanofi is planning to navigate an LOE in 2031, and the sort of what does Sanofi look like post that date? So a few things. You know, we've come a long way. Just to give you some headlines, we were, I don't know, EUR 33 billion in revenue when I joined, around, EUR 45 billion now. We were 118,000 people in 2019, we're around about 72,000 now. We had, I forget how many, but upwards of 70 sites in manufacturing, we're now 38. We've really tried to modernize the company. We exited consumer. We've tried to turn ourselves into an R&D-led pharma company 'cause we felt we were structurally gonna be behind our peers. We had to do a lot and invest a lot in our own pipeline, and we even recommitted our vows to that in 2023 when we took quite a hit saying that we needed to do this. And we needed to do it partly because that's the future revenue generator of the industry, but also with DUPIXENT ahead of us. You know, we have U.S. at 2031 and Europe at 2033. Some external watchers have us at around 2033 in the U.S. We have a lot of patents. We have some good ideas that we haven't shared yet. We'll share those in time when we feel comfortable, without giving too much away. But in essence, we have to get the medicines launched. And what I learned over the last year is we're a really good commercial organization. I mean, we're really nailing it. We're growing close to double digit. DUPIXENT, despite the threats and the wonderful people in this room that predicted our demise with lebrikizumab and everybody else coming, we grew 26% in Q3. You know, this is the real deal. We know how to commercialize. And what that brought home to me over the last few years was, we do need to get those drugs over the line out of R&D. If we can get tolebrutinib approved, if we can get amlitelimab phase II as a positive readout, if we can get lunsekimig into phase III, we really know what to do. And it's been a bumpy ride. It's. I should have perhaps signposted it more that it might be a bit bumpy. It's not my natural style, but I'm really happy where we are right now. We have a lot to do, but I think I'm really happy with how we're set up with what we have, plus the acquisition of Blueprint to come through the Dupi LOE. Should we underwrite that a bit? Should we add some things? Maybe that's part of the conversation. Probably. Yeah. Yeah. Okay. I was gonna ask that. So if when you look at your mix now between internal pipeline and M&A or BD, how do you see that going forward relative, you know, if you look at the strength of what you've got internally at the moment, and the need to do additional deals perhaps to continue to fill out the pipeline? I think we, if I look at the number of preclinical phase ones versus our peers, I think we're light. I think we're not where we need to be. We might be somewhere between five and 15 programs short, high-quality programs. I think short. We brought in our new head of R&D a couple of years ago because he has reflexes in that area, perhaps even more so in the earlier space. We're looking at a lot of things we'd like to add. I think we need to because if we turn the mid-late-stage pipeline into what we expect, we'll have enough confidence to ride through Dupi, grow EPS. But then the question will be, "Well, we're not so sure about your growth story, 33 to 40." We're like, "Well, actually, you can be more confident because these assets are now in phase II, III, as we get through the end of the decade," and I think that work is also for those that follow us, which is making sure that we, we've spent all this time and effort becoming R&D-led real pharma, that we don't leave ourselves with a gap. Mm-hmm. Longer term. So we can do much more there. On the sort of mid-late stage, if everything that we have, not everything, out of the 12 drugs that we have, if four or five are wins, we have enough to cover and to grow EPS. If we get three or four failures out of the next ups, then we're gonna have to think more creatively about what we get from outside. So you shouldn't see the emphasis in preclinical phase I. You should see it as opportunistic in later stage. The Blueprint deal was really about underwriting the top-line growth all the way through to the early 30s. Mm-hmm. By saying, "Look, we're gonna give you top decile performance on growth. As we turn the cards over and you get more confidence in the pipeline, you'll start to feel like now we're worth a re-rate. We've waited a while, right?" And it is, it is what it is. But, I like the way that's come together. The Blueprint deal was a little bit above what we were planning, but we were disciplined. And I think to pick a baby kit, which will be a blockbuster next year, and then a little bit of pipeline behind it turned out to be a good deal. Good news. Okay. I guess the other thing that's been a focus for investors is margin progression. You were a bit clearer on Q3 about how you see 2026 panning out. Yeah. But I think the 2027 commentary's a little bit more cautious. So, and this is, but the extent to which, if we can just clarify the extent to which that's just around the Regeneron R&D offset going away. Yeah. Look, it's been a big deal, and it's you know, in the high hundreds of millions EUR. Of course, the AMVUTTRA royalty is coming up fast. And while they're not like for like, the gap will close. I don't know what you have as consensus for AMVUTTRA in 2027, but it's a big number. Yeah. Yes, and you know, we're looking at 30% of that. So I think we feel quite well placed for bridging that. Plus, we moved towards a more specialty care-led portfolio, which has a mixed benefit. We're becoming more efficient in general as a business, you know. You should look back. If you look at Q3, we were 8.8% growth on the top line. We were 9.7% growth in BOI. We were 12.4% growth in EPS, and minus the buyback, 10.2%. We like the shape of that. I'm not saying the numbers will be the same when we guide for 2026. We won't guide for 2027. You should see us driving numbers that show our efficiency and our ability to execute and show an attractive P&L at the same time as growing the top line and investing in R&D. That's the job, right? Mm-hmm. But I feel we at Q2, we were not clear enough about our desire to run a leveraged P&L, and we went to great lengths at Q3 to make sure there was no misunderstanding. Mm-hmm. A company where we're at still with a sort of could do better in R&D, then we must deliver the financials. And as is the case, not only not everything hit through the course of the year. So to what extent was the ability to grow BOI next year, margin next year, down to perhaps a lowered R&D budget, or does the R&D commitment stay there and you just refunnel it into earlier stage projects if you're not running quite so many phase III? I think some stuff graduates. You know, some of the OCEANA, the amlitelimab program graduates, like, leaves us a bit of capacity. I, you know, I know people love to say, "Well, you know, if nothing hits, we will redirect the resources." Things not hitting is more of an issue than the R&D spend. Yeah. You know, that would force us out to trying to buy things that would come with R&D spend most likely. I think, I think we are in the sort of eight and change R&D region for R&D. I think that we should try and manage within that. Mm-hmm. You know, should we do something opportunistic, maybe add a little bit. I don't think we should get ahead of ourselves. If for a decade plus, we were around EUR 5 billion, it was never gonna be enough to replenish what we had ever. Mm-hmm. We made the tough decision to add more and take the hit back in 2023. We shouldn't blink now, particularly as we have an approval ahead of us, the second phase III pivotal on amlitelimab, lunsekimig phase II. I think we have enough going on to say, "Just stick with us. We'll do that." The phase ones, we can add them. We can add them a little bit later in the year even. We don't have to see a big rise in R&D spend. We've kept G&A roughly flat the entire time we've been in the company. Where we've pushed the sales piece, we've had it back in top-line growth. Mm-hmm. You know, I think we're doing things right. The question is, is the total R&D investment getting the return? And I think there's still a question mark. When I look at some of the bumpiness of this year, it's often attributed in sentiment-wise to just can Sanofi really just get out of their own way and do some R&D. But, you know, we had a standout win on itepekimab study one, and study two a fail. Roche had two underwhelming study readouts. AZ failed a phase II, and, we'll go to phase III in my opinion, without a recognized subpopulation. And so, you know, we're all finding some of these things quite difficult. Mm-hmm. It's not just us. We've chosen a difficult area, but we've chosen an area that's high reward as well. Right. Because we know this, and I spent some time. Some of you in the room have heard me mention this today already. You know, there is something special about immunology. While it may be harder, and there may be some risk, when you do get approved, a company like ours that can execute, you have a multi-billion dollar drug literally by just being not the other things. That's the function of highly heterogeneous, highly symptomatic patients that are never happy with their treatment. And so, getting approved and then putting it in our commercial hands is really the meat and potatoes now for us. Got it, and then the other sweetener, I guess, on the margin has been the capital gains. So you've done about EUR 0.5 billion a year. Yeah. That's been pretty consistent. Not quite sure where you find all the products from. So how long can you keep finding products? I think, you know, the history of this company, there's no short supply of products. Fail. One of the interesting things when I joined in 2019, I went around the world, and everybody that presented to me had a different portfolio. So, you know, we've managed. One of the reasons we dropped the number of sites. You know, we were, I think, 340,000 SKUs. I think we're around about 200,000 now. All of these are the efficiency gains. We will make around about EUR 500 million in capital gains. We'll drop about EUR 200 million in revenue. Mm-hmm. That we'll have to make up for those divestments, but that's good business, good pruning. I should have said this earlier, and I didn't when you asked about R&D spend, but we're also pruning some of the R&D. So what you don't see is a little bonsai work that's going on where perhaps we're trying to get beyond indication one and two with some of the immunology drugs 'cause you can. I think we've sat back and reflected and said, "Well, we could go after some smaller indications." 80%-90% of the value was on indication one and two. Why don't we just do that and remove the opportunity cost on doing the other indications that may have washed their face, but that money's better for us deployed elsewhere in R&D? You don't see all that pruning. Mm-hmm. But that's going on regularly. Got it. Just moving to pipeline, actually, so you've touched on a few of the things. There's been, as you say, some hits, some misses. Go back to the R&D day 2023. There was a sort of basket of products you put in the EUR 2 billion-EUR 5 billion peak sales range and then some at EUR 5 billion plus. Mm-hmm. So if you assess your scorecard on that, how happy are you with where you've got to today? and would you reorder those two to fives and five pluses at? It's probably better you tell me because, we, you know, if I look at where we are, where we could be with the next ups, I have amlitelimab squarely in the 5+. And I'm actually more confident now than I've ever been. Again, when we released the COAST-1 data, we crushed primary and secondary endpoints. The market, I think, was a bit underwhelmed because of the effect size comparison to DUPIXENT because everybody sees it as a direct comparator. DUPIXENT grows till its end. Stop worrying about that. We have a plan for that. The question is, can amli, amlitelimab, be EUR 5 billion on its own? Does it stand on its own? Think of it as sitting in another company. We were blown away by the fact we could start patients and have success on a Q12 regimen. You know, it's the same group of people that asked me, "Paul, are you interested in this company with a long-acting IL-13?" And I say, "Not really." And then I say, "Well, I have a long-acting OX40 ligand. It's almost like the same person can't think about the same thing, twice." And we, if we're really Q12, you know how it will work. For biologic naives, the physician will tell people for the first time, "You're gonna have to go on an injectable treatment." The patient will say, "How often?" The physician will say, "Every two weeks, maybe every four weeks," or there's one every 12 weeks. They won't even ask what it is. And we love Dupi, Dupi grows. Mm-hmm. A group of patients just don't want to do it and would rather do a Q12. That is a major percentage of naives. With amlitelimab on top, there's a chance of drug-free, disease-free remission for a small population, but the promise of it at initiation is enough to inspire people that amlitelimab is certainly worth a third of new patients at initiation. That's why we go beyond five. There'll be a debate about how quickly the efficacy is onset. So I think we should not try and appear as the first choice for a patient that is what I call the hot patient who comes in highly symptomatic and needs something quickly. Mm-hmm. I think for the 91%, we should be looking at taking a third. So I'm very happy with the number. Yeah. Okay, and you said, as you point out, so the effect size numerically when you compared it to DUPIXENT was low, and it actually looked more like the Amgen rocatinlimab data, both of which had looked higher effect size in phase II. Yeah. So just talk us through what your thoughts are on why you saw a drop-off in or a numerically lower effect size in phase III versus phase II? I think, I mean, just take one step back. Look at the consensus for the other drugs. We could pick NEMLUVIO for a moment. We know that up to 50% of patients drop out at six months 'cause their AD is no better. Consensus is around EUR 3 billion. The effect size is lower than every drug you've mentioned. So let's take it on both levels. What are we really talking about? We're talking about new mechanisms with long interval with an increasing efficacy 'cause we were only 24 weeks in that study. Mm-hmm. So we feel very good about the class. We feel very good about the ligand. It's not really an issue. I think what is materializing. You've seen it with some drugs: IL-17s that have surprisingly failed or IL-5s that have failed in certain diseases. Where you choose to do your study and who you choose to include is more important than it's ever been. When DUPIXENT was first out of the blocks and everybody was naive, the effect size is massive. Everybody's excited. It's a miracle. I've been there before when we launched REMICADE a thousand years ago. If you were to do the DUPIXENT studies now, I think as amazing as this medicine is, you may find it middle of the pack, not because it deserves to be, but the patient selection is getting more demanding. And I think we're gonna find, by the way, a more complex set of results from biologics in autoimmune disease over the next half decade until people iron that out. Many drugs are already in flight. So it's getting very specific and very important to know your biologic experience versus naives in your sites and not just look at the total and make sure the screening is perfect. So I, I don't worry about that. I know that if you can give somebody incredible benefit over a 12-weekly regime with an efficacy that keeps improving with a chance of remission, you are a major player in atopic dermatitis. That's all I really care about. Again, we know how to commercialize things. That's not really the issue. That profile, but I spoke to our commercial leaders after COAST-1. They're like, "Can we go now?" That's they know what they have. Yeah. I said, "Well, we should really wait till we're approved. Yeah. So we'll get COAST-2, and then we'll deal with it after that. But that's the sentiment 'cause we know, well, you guys like your cross-c, your cross-trial comparisons. We like the fact that patients who need a great medicine with the right profile will get it and will go fight that. Mm-hmm. I think in the past you've alluded to or talked about the fact that, you know, in immunology, patients cycle through therapy. If you look at psoriasis, multi-class drove a lot of penetration, etc. Mm-hmm. Do you think that is how ultimately the AD class will develop? 100%. So therefore, do you see that if the AQUA results are positive that in the DUPIXENT-experienced patients, that is also a sizable part of the EUR 5 billion that you talked about? I think DUPIXENT is gonna grow till the end. We gave some ideas around EUR 22 billion, I think it was, in 2030. You know, people laughed when we gave EUR 10 billion in 2019. Nobody's really laughing at the EUR 22 billion. So DUPIXENT is so well understood and so many indications and so trusted. Its profile is without question. I think what's gonna happen is there's gonna be an absolute mirror replay of psoriasis, and I find it a bit surprising sometimes that people haven't sat back and said, "How can four IL-17s be successful in psoriasis and HS?", and how many advanced therapies are there? 10? Is it all blockbusters? One oral's not gonna get to blockbuster status, but everything else that's injectable is a blockbuster. And when we look at head-to-heads and we do effect size comparisons, don't forget that most patients, and I think you touched on this, will have two to three or more biologics in their life with the disease. Everybody is moving all of the time. These patients whose lives were horribly impacted, they go on a great medicine, they get 95% clear, and they're pissed about the last 5%. A few years later, they say, "I need something else." It's normal. Expectations get raised. We've seen it play out carbon copy in psoriasis. In 2023, when we did the R&D day, we used psoriasis as the example. We said, "You go from the first drugs, which are not normally as good as DUPIXENT, but come in like a HUMIRA or REMICADE or ENBREL. In fact, then you become more selective and more efficacious." Well, DUPIXENT sets some of that bar, but there's still room. And then you go to interval, and then you go to oral. And all of these things take the patient pool. And we know. We absolutely know for sure that the reason DUPIXENT grew 26% in Q3 despite two or three new entrants is because biologic penetration is less than 15%. So 85% of the patients that should be on DUPIXENT are not on DUPIXENT, which means that every time there's a new entrant, all boats rise and we're the market leader. It's going to be the same. Mm-hmm. Exactly the same. That's why I find it a bit perplexing when people don't study psoriasis and say, "Let's apply that to AD." Hey, and let's apply that a bit to asthma. Slightly higher penetration, but what happens if it plays out the same? It's going to play out the same. Yep. Yep. And in the AQUA study, I think the patients enrolling are allowed to have failed a biologic or a JAK. But in the treatment paradigm, JAKs tend to get used later, unless they're sort of used for, you know, immediate flare resolution in the short term at the beginning. So in that study, will you be able to tease out the patients who have DUPIXENT or biologic failure, rather than from the JAK failure patients to get a clearly defined population? Yes, but the goal of the OCEANA program was, do we believe this drug can be one of the winners to go beyond 5 billion in asthma, of course, but importantly in AD? When we put the program together, we tried to understand what the physicians might want to see. Mm-hmm. It was less about competing with JAKs or DUPIXENT. It was more about saying, "Can you recapture a significant efficacy response in patients pretreated with advanced therapy?" It's more that. Mm-hmm. It's more on top of topical corticosteroids, in AQUA. It's more saying, "In your practice, in your office, who are you seeing? Can you have confidence to initiate for naive? Can you have confidence efficacy?" So COAST. "Do you have confidence that efficacy will continue and mature?" OCEANA. "Can you go on top of other things, AQUA or responders, SHORE rather, for TCS?" So that the physician feels extreme confidence in being able to say, "You know, I see the utility, at first advanced therapy or later. It's worth us trying. Mm-hmm. We just wanted to put the full data set together, so get COAST-2 and move from there. If I sort of understand it correctly though, from the way you talked about it initially, you talked about the frontline naive market. Yep. First and the potential for remission. So if you think about that five plus, for you, is that more weighted into the naive patients than it is into the post-DUPIXENT failure? I would. I know I read some of the notes and things, and the sort of overly simplified view sometimes of those that watch us is, "Well, if you're not as good, you're used afterwards." It's really the opposite. The question is, what are the things that drive penetration? It'll be interval in that case, chance of remission. And so if offered to naive patients, that's a huge amount of naive patients. So if that in that context, for me, and I have, you know, have the numbers close to hand, that would be half to two-thirds of the patients. And of course, just because you're not an IL-13 means you get used later. You just get used later. Again, if you're an IL-31 and one of the comments in the label is, "May make AD worse," the real thing is you're an IL-31. You're not an IL-13. And I think that's what gets physicians excited to try a different mechanistic approach. I have to say, I agree with that. I think that's the right thing. Mm-hmm. So we'll get a lot later, but we'll get more naïves than people realize. Most likely, again, needle burden, and for many who don't wanna ever do that themselves, four times a year is actually, "You know what? I may just get it done in the office." That's a tiny bit easier for everybody. And you don't have to meet a certain date. So maybe I'll do my labs and then go the following week. That level of flexibility is pretty extraordinary. Mm-hmm. I think we will get a lot more naive than people realize. I might switch to one of the other assets that's more imminent, I guess, as well, even as tolebrutinib had. So you have the PDUFA date coming 28th of December, which is delayed. Perhaps I don't know the extent you can talk about sort of what label you're aiming for or hoping for, from the, in the non-relapsing secondary progressive setting. You know, what we had in the study was no relapses in the last two years and still progressing. That's 25%-30% of the MS patients. I'm okay with that. If we get PERSEUS data that gives us a sniff at the primary progressive, could be another 5%-10% of the population. Mm-hmm. Overall, that's a big population for us to go for. More than enough to make it a multi-billion-dollar drug back to the, "Can it be five? Can it be more?" I think the reality for us is, we would just like to get approved. We used the voucher. We got earlier review, and then we lost the early because of the FDA taking more time. I don't begrudge them that. Unmet need, not a well understood part of the disease because there's never been any drugs. Also incumbent upon us to make sure the REMS is perfect. I said it to a few people today and yesterday, but I said it to the team. Launch uptake is not my concern. REMS uptake is my concern. Mm-hmm. Perfect REMS, perfect, perfect, perfect, so that if that means you take longer to have it end-to-end, nurse visits, your home, blood draw, physician sent labs, physician confirms receipt of labs, physician confirms reading. You know, it's like getting your, whatever it's called, you know, "Do you confirm your reservation for dinner?" and everybody scrambling to, you know, that is, that is what, how we want people to feel because if you're doing weekly for 90 days and the physician gets the labs and acknowledges reading them, if they're elevated, you stop them, and if they're not elevated, you continue. It's that simple. Mm-hmm. It's that simple. There's no burden. But if you mess that up, you know, you get a halo you don't need, and it stays around. Yeah. Given that it's unlikely we'll have a competitor for five, six, seven years at best, no need to rush that. No need to rush that. We have modest expectations for 2026, and we have more demanding expectations thereafter. Yep. And just going back to the label, so, do you, I guess the question is that the FDA's never actually approved a non-relapsing secondary progressive MS drug with that label or definition, and feels like the McDonald criteria shifting. So, is it a definition that you're discussing or? Are you coming back to active versus non-active? No, no. Just more about, is it gonna be an MS label defined population or, or wording of non-relapsing secondary progressive? 'Cause the physicians all recognize what that is, but FDA's never recognized that, so. Yeah. Well, that's right in front of us. That's, I mean, literally right in front of us now. Because, I think that's part of the challenge you go on. Sometimes the regulator, you, everybody agrees the study, everybody agrees who you're trying to treat. You do all the years of work, and then when it gets to it, it's like, "Oof, right now you're..." and there's a little bit, I think because of the elevated liver, I think there was a little bit of, you know, let's try and be really sensible about who's defined. Mm-hmm. Our position stays firmly. It's those that we studied. Yep. There is no point trying to re-characterize. Should, by the way, the MS definitions change completely? You know this, but the entire specialty says it's phases of disease. It's not different diseases. So you know, everybody's progressing, some more than others, and some are having relapses, some more than others. And it may change on their journey. So let's address, right. It's funny enough, it's one of the reasons why frexalimab will be in the, you know, top club because of its impact on innate and acquired immunity. It may be the one medicine that actually is standout, like best in class on efficacy and relapsing, but actually addressing disease progression at the same time. We thought for a while, should we do CD40 ligand frexalimab and tolebrutinib? Should we do combo? And I think we're gonna find out, does the data emerge with frexalimab that it addresses progression enough for it to be the one and done? Mm-hmm. That's gonna get interesting too, but the definitions are completely out of touch with reality. So what do we care about? Making sure that the population that will benefit is the population in the label and that we're not constrained for reasons that make no sense. Mm-hmm. And the delay happened just after the GEMINI data on disability progression were presented. So was that what was filed with FDA that led to the delay, and the major amendments? Was it specifically the disability progression data from the relapsing studies? Yeah. They, as we said, and they know the GEMINI population's not the secondary progressive population, HERCULES. So. Mm-hmm. So you don't learn a lot. I think they wanted to see all the data. We have over 4,300 patient years on tolebrutinib. And I think it's okay to ask for more data. If we were in a race to launch with somebody else, I'd be irritated. But the truth is we're not. So I'd like everything to be done, you know, it's painful for me. It's much easier to get approved. People take their overhang off, we move, the short termers disappear, and everything is happy. But in reality, a great label, perfect REMS are the only things that I care about because that's the long-term value creator. So we will see. A question I've been asked quite a bit since I've been here, in fact, is, well, will they ask to see the PERSEUS data? And, you know, if the PERSEUS data is great, I hope so. But there is a chance, and there's no indicator for this. Mm-hmm. But if the PERSEUS data comes while we're still talking about the label, what if they ask? And the answer is I don't know. And I've been telling people. Mm-hmm. You know, for the last few days, I really don't know. I worry less if it's great data than I do if it's not. Yeah. But I think if there'd been an extreme safety signal, we would know about it already. Mm-hmm. So maybe it's just more data. As it happens, we say we look forward to the PDUFA from December the 28th. We've given them everything that they could possibly want, and we take it from there. Got it. Fast forward to December the 30th. Yeah. If you assume you've got an approval with non-relapsing SPMS, how easy a population, identifiable population do you think that is for treated patients? 'Cause, you know, who are already sitting on an anti-CD20 but haven't had a relapse for three, four years. It's easier than we would've imagined. It's, they're not identified, but they're known. Yeah. And what do we mean by that? And I met many neuroscientists at Mount Sinai not that long ago, where they're explaining to me they know exactly who the patient is, but right now they're not recorded as non-relapsing secondary progressive MS because if they are, their insurance company won't pay for OCREVUS, if they give them a definition that's not covered by the label, therefore the insurance. So they leave them on the old definition because they don't want to take their OCREVUS away. Mm-hmm. I think that's fair. While there may be no data to support it, and this is just anecdotal while we're here, I think it's quite important that the patient feels they're doing something, right? And OCREVUS is an excellent medicine. So, I think what we're, they're not identified, but they're known. Mm-hmm. And if we're gonna go slow and perfect on REMS, everybody has plenty of time to know who it'll be. I can tell you since the delay and the PDUFA, the number of emails and letters I've had from patients saying, "Hey, you know, you are gonna get this done, aren't you?" I'm like, "I got enough pressure from investors. I don't need your pressure." But we joined the industry. Mm-hmm. To do that. Yeah. That's what we're doing. And aside from that, do you think there's a community of patients or a pool of patients who've just dropped off therapy, or, or are they emerging patients on something? There may be. We've done lots of research. It's hard to tell because I think if you're an MS, if you're a secondary progressive patient and you're using a cane, and I'm oversimplifying, but the journey is towards a wheelchair. Mm-hmm. The data doesn't support it, but you feel like it might help, you don't really drop off. There'll be some, particularly in the constrained markets in Europe where they never use advanced therapies at that stage anyway, but by and large in America, I think it's not the case. Yeah. Okay, maybe shift gears onto itepekimab, so one hit, one miss. Maybe just run through the differences that might account for the differential results and then what your sort of steps forward from here will be. I was pissed because, you know, that sort of was our run into that part of the year where a home run would've been nice, get COAST- 1, get COAST- 2. It's hard for me to be pissed with the team because they did two studies perfectly. They just got different outcomes. Mm-hmm. That's the business we're in. I did tell you earlier or suggest that it's getting harder to take for granted studies in immunology. You've gotta be much more real-time. ARFI2, we believe, not 100% of the reason. So I won't, I'll deny it if you say I said that, but one of the leading reasons for ARFI2 was the legacy of COVID restrictions. Mm-hmm. Remember with COPD patients, we struggle a little bit. They struggle with infections that lead to exacerbations that lead to problems. That's the background expectation. Mm-hmm. And that was diminished because many patients that would've got an infection didn't go out or wore a mask. So we made it harder to get a Delta. And, it looked like, people were doing much better, on control than you ever imagined. Well, they weren't. They were just taking these incredible precautions. So we needed to have that sort of bias to understand. I said to the team, we shouldn't really do another phase III if we're not sure that if we have the same problems of success we had with the other two. We feel confident that a major contributor, so to say it like that, is COVID. Mm-hmm. That we can do something about that now. Again, don't forget, Roche struggled with both studies. AZ failed the phase II, and this is from recollection. So what that means is, whereas I would've hesitated if we were falling behind in order of entry, my real clock is ticking is can I get to market with itepekimab before I lose leverage of DUPIXENT rebate with payers? If I can get there before the end of the decade and if IP dates are right and we're through 2033. Mm-hmm. Then I have three, four years to deploy rebate to make us the preferred, the preferred IL-33. People say, "What about PBM reform? 25 years and waiting," you know, we may have a shot of making itepekimab the outright winner. Mm-hmm. In the 33s. If we leave it too late. Mm-hmm. It's more complicated. And so that's still the plan. So AstraZeneca's got phase III data on tozorakimab coming next year. They, their studies were post-COVID. So if you're right and it was COVID, they may not have that inhibition. It could be in the market earlier. So is there a risk they just steal, particularly the low eosinophil segment, which is kind of the obvious issue? It's very possible. Look, we'll take lunsekimi g again to COPD. Look, you know, we're back to what we said about psoriasis. People should not get hooked on winners and losers. They should get hooked on biologic eligibles and penetration. That's where you go to know if all boats will rise. I think it's better to have more mechanisms for patients. We take an IL-13 TSLP and we can get high T2s. Mm-hmm. Who knows? I wish everybody well. I want them all to do well because these patients are struggling. Again, they could be before us. I think one word of caution. I don't remember, you'll remember the study better than I do, that the, I think they're all comers. And we saw Roche do the same. You know, we focus on former smokers. We think the delta's bigger there. And so we will see how that plays out. Got it. Okay. Just actually mentioned lunsekimig. What was the rationale for taking lunsekimig into a phase III COPD before you've seen the phase II asthma? Did you just view them as totally unrelated and there's a mechanistic rationale in COPD, so go straight phase III? Yeah. Look, they're different diseases. And I, you know, and there's. I wish I could tell you there's a good reason to wait. I want it to work in both. Well, the question we have to ask is, would we stop the COPD work if we fail in asthma? And the answer is no. Mm-hmm. So why wait? And we know IL-13 and TSLP work extraordinarily well. We know IL-13 works well in AD, but not so well in asthma. We know TSLP works very well in asthma, but not so well in AD. But we know it may work not so well, but there is a 1 plus 1 equals 3. In May 2023 in DC at ATS, we saw a FeNO drop of 1 plus 1 equals 3. And so our bet is, for the high inflammatory burden COPD patient, if you're gonna get efficacy, it'll work. And same in asthma. Our hope is. Mm-hmm. That lunsekimig is the standard of care where efficacy is the lead consideration, in asthma. We'll find out. Okay. Just checking if there's any other questions. I mean, I might just throw one in on, you're taking on the pharma chair. What's top of mind in the agenda as you go into that role? I just, I would just, as I pivot into that, I would say what we didn't get to talk about is duvakitug, which I think is gonna turn out to be one of the best deals I ever did, the TL1A with Teva. I think it was smart for them. With us, I think it's smart for us. The data's telling us we may have best in class. We'll find out. We're already in the phase III with UC. And I would put that up there with the big medicines now 'cause it could be. The other one just to point it out because of the continuing the philosophy of markets growing, bimekizumab, the IL-17A/F in HS, it will be, we think it'll be a two-product race eventually, which puts us at a multi-billion-dollar drug. And so don't, again, everybody's looking at winners and losers. Do not think winners and only think winners and losers if you're 80% biologic penetrated. If you're 18% or less, whatever, everybody wins. It's degrees of win. Mm-hmm. Everybody is a $2 billion plus drug. Everybody. Some are five. That's where the differentiation and the commercial execution makes the ultimate difference. Mm-hmm. As for the pharma chair, you know, you get on the journey to that five years earlier. You run through each committee and you just assume you'll get there at some point. It's a big responsibility and honor, of course. I represent Europe at a time when that may be more important than people think in the room, in terms of medicines. 54% of medicines approved in Europe are not available to patients in Europe through reimbursement. I spoke to Chancellor Merz, Keir Starmer and his team, President Macron, and there's some sensitivity, the fact that with MFN, that medicines may not get approved in Europe because they'll be at U.S. prices. They'll get approved. They won't be reimbursed. They look at me like, "This is tough." I said, "You know, before Trump, 54% of medicines are not getting reimbursed. I think you've got some work to do long before that." And so, it could only get worse. I feel some responsibility for that. I didn't join the industry to drive further health inequity. So I don't like that. I would like to try and bring the President who wrote to 17 CEOs. He did not write to pharma. I'd like to get pharma back to be the convener. I'll try and play my part in that. I'd like to turn some attention to PBMs as tough as it is. And I would like to try and get a much more active debate on the fraud of 340B than duplicate discounting. So if I can do some things that capture the president's imagination, that are good for patients and good for us, I would like to stand for that. You wear two hats as pharma chair, your own company. Albert showed sometimes you have to make the company call. You know, I respect him for that. I hope to continue to wear two hats, through my tenure and do something good with it. Fantastic. We're up against time, so that's very interesting as always. Thanks, Paul. Great to be here. Thank you. Thanks. And, thanks everybody for listening in. Thank you. Thank you. Thank you.