Good morning, everyone, and welcome. I'm Bill Szablewski, Head of Capital Markets for Viatris. It's a pleasure to have you all here today for our Viatris R&D event. Before we begin, there will be a brief forward-looking statement. During today's discussion, we may make forward-looking statements on a number of matters, including our pipeline and strategic initiatives. These statements are subject to risks and uncertainties. Please refer to today's slides and our SEC filings for more information. With that, turning to today's agenda. With us today from Viatris is our CEO, Scott Smith, who'll be providing a strategic overview. Following Scott will be our President, Rajiv Malik, who'll be talking about our durable and high-margin organic pipeline. Following Rajiv will be Philippe Martin, our Chief R&D Officer, who's gonna be discussing the Idorsia collaboration, our two phase III assets of selatogrel and cenerimod. And with Philippe today, are two distinguished key opinion leaders. Following Philippe will be our CFO, Doretta Mistras, who will be talking about the structuring of the Idorsia collaboration, the commercial overview, and the opportunities that we see with these assets. And lastly, following today's presentation, we will have a question-and-answer session, so we please ask that you hold your questions to the end. And with that, I'd like to hand it over to our CEO, Scott Smith. Thank you, Bill. Let me see. So, good morning, everybody, and welcome to our event. I'm very excited about where we are as a company and about our new partnership with Idorsia, and the potential it has to broaden our reach and our pipeline. Before we get into the bulk of the presentation, I just wanna let everybody know how personally excited I am about the two assets we're gonna talk about, the two new assets in selatogrel and cenerimod. I believe they both have the potential to not only be blockbuster assets, but to be significant advances in terms of unmet medical need in acute MI and in SLE. As you will see today, I believe Viatris is well-positioned not only to complete, but to accelerate the development and commercialization of these two important assets. So for those of you who are new to the story, here's just a little snapshot of Viatris. We are an extraordinarily strong and diverse company. We operate in 165 countries, about over 30,000 employees worldwide. In 2023, we did over $15 billion in revenue, over $5 billion in adjusted EBITDA, and approximately $2.4 billion in free cash flow. As we increase the innovation across our pipeline, as we're doing with this deal and will do with future deals, and more deals as we do them, patient impact and value we can deliver will only continue to increase. You know, whenever I see this slide, the one thing that sort of gets really is important to me is that on a yearly basis, Viatris over 1 billion patients take Viatris medication during the course of a year worldwide, which is just an astounding number when you think about it. What an opportunity for us, and what a platform for us and for me to be able to affect human healthcare in a positive direction. So, you know, very, very exciting for us, the breadth and the scope that we have as a company globally. As I stated before, I'm extremely excited about where we are today as a company, and I'm even more excited about our future. We have sign of w e have s orry, a sign light, sorry. We have a line of sight to our gross leverage target of approximately 3x, and we expect to deliver over $2.3 billion in free cash flow on a yearly basis going forward. Our plan is to return approximately 50% of our free cash flow to shareholders through quarterly dividends and share repurchases. This year alone, we've already bought back $250 million in shares and have increased our authorization for repurchase to $2 billion. With the other 50%, we plan on investing in assets and businesses that will drive future revenue growth. The four main areas that we're looking to invest in, we're gonna continue to invest in the base business to fuel organic growth. We're continuing to invest regionally in country-specific opportunities to leverage our strong global operations. We wanna invest to develop our three core therapeutic areas that we've talked about before: ophthalmology, GI, and dermatology. And importantly, as we've done here with Idorsia, we wanna be opportunistic in seeking out opportunities that fit our company and can help drive future revenue growth. Now, specifically to the Idorsia collaboration, it's a great example of our disciplined capital allocation strategy. We are bringing in two late-stage potential blockbuster assets, both with long dated patent protection and major lifecycle management and indication expansion potential. We are connecting Idorsia's proven, highly productive drug development engine and innovation engine with our strong global infrastructure and experience. I do believe that both selatogrel and cenerimod can become meaningful components of the Viatris business over the long term and will help us deliver on our goal of building more durable, predictable, sustainable portfolio going forward. So I'm excited to get into the, into the bulk of the presentation. I'm very excited to talk about the, the Idorsia deal and the assets that we're gonna talk about. But before we do that, it's very important for us, to talk about the base business. The base business is in great shape, as a company, very strong. We're seeing revenue growth on a quarterly basis moving forward, and we have delivered in the past and will continue to deliver $450 million-$550 million in new product revenues every year. And so it's very important for us to take a moment and to turn it over to Rajiv, and he's gonna discuss, and you're gonna understand why my confidence in the future starts with the strong base business that Rajiv and his team have built over the many years at Viatris. So with that, Rajiv, please come up and talk about the base business, and then we'll get into the Idorsia assets a little bit after. Thanks, Scott. Thank you. Good morning, everyone. Pleased to have you all over here. While most of today's discussion is going to be centered around the two new innovative assets, we wanted to take a few minutes to walk you through and reiterate the strong foundation these two assets are walking into and will be able to leverage. So going up the value chain for us has been a strategy for the last decade, more than a decade, and Idorsia is perhaps the next logical step in that direction. We have spent maybe number of years to build this platform, create this deep and broad pipeline, which gives us the confidence and forms the basis of this new launch revenue, which we have been talking about. And we have also, as a part of this journey, we have created a strong track record of delivering this new launch revenue year after year. So in the next few minutes, I'm going to focus into the three buckets. I'm gonna walk you briefly the in-house capabilities, the deep capabilities we have put together. I'm gonna walk you through the diversity, the depth and the breadth, the richness of the pipeline with few examples, and I'm gonna walk you through the proven track record we have over the few years. And also, I think it's equally important as I walk you through this, is to reflect upon the, our ability to manage the collaboration, the collaborative science, because that's very important when you look into the example which we are going to walk you through, like Idorsia. So let's just look into the capabilities and what do we have to execute. Strong team of 3,700 people across the globe, nine different centers. Some of the centers, some of these development sites are just focused on key technologies, and where they basically excel in is, I think there is no doubt about what they bring to the table from the development capabilities, formulation development capabilities, the characterization, the basic table stakes, you need to have that. But I think more importantly, moving into the device engineering, because that's where the lot of complexity comes into, a lot of clinical, medical, clinical strategy, medical, you know, clinical trials, medical affairs team across therapeutic medical areas, but more importantly to me, the proven regulatory, legal, IP skills which you need, because you need to bring this all together to bring a product to the finish line. So fine, you brought a product to the finish line, and I think where we have excelled is we have never missed an opportunity to bring that product to the market. It's one thing to bring the product to approval, but we have always executed on get it approved and get it to the market as quickly as possible. Where we, again, little bit differentiate ourselves, it's not what you have got to work with, what can you get out of this? What can you extract out of this platform? And I think on the right side, if you look into the slide, complexity of these technologies, whether novel products, complex injectables, respiratory, but that's how our focus also has been moving. We have been moving more from traditional generics to, into more complex products, more complex technologies, and now we have the, you know, those technologies as an asset to us, which we can continue to deploy as we move on and look for more and more opportunities. And one good example, you know, and let me give you about diversity of the pipeline first, and then I'll give you that example. This is not one market-centric pipeline. This is a global pipeline. We are not dependent upon one market. Yes, U.S. plays a big role in building up this pipeline, but we have a dedicated pipeline for China, for Japan, for rest of the world markets, for Europe, because as this all comes together to make that, the new launch target we talk about, whether it's $450-$550 for this year and similarly for the next following years. So we have for USA, more than 200 products with an IQVIA value of more close to $250 billion, which we are targeting. And key contributor of this pipeline, if you see value perspective, is multiple products from complex and novel products. And yes, of course, traditional generics like lenalidomide are also there, where we have the first to market opportunities. But if you take other end, China, this pipeline caters to the strengths of that market, commercial strengths, what we have in that market. We have a very different play to in China, and where, that's where we are building up a pipeline around cardiovascular, combination products around cardiovasculars. Not the generic products, but 505(b)(2)s over there, but more importantly, also respiratory being a big area for focus out in China, we have been getting to launch the products like Yupelri, Dymista, Perforomist, and also generics like Symbicort, which are pretty complex to bring to that market. So every market has its different needs. Europe, if you see, is more European generics are very different from the even analog perspective. They are not six months play. They are once you launch them, they are there for you to leverage them for five, six years. So we continue to add some of those generics and complex generics in Europe. Japan is mostly around the life cycle management of some of the brands we have. Take, for example, Effexor or Creon. We are trying to work around the life cycle management of many of those brands while adding on more generics also. So every market has a different need, and that's being. You know, this pipeline is catering to or building up to cater to the needs of those market. The second aspect of this pipeline is just complexity, the richness in terms of, you know, when we call high value, durable value, high gross margin, that's where it comes to. These are a bunch of difficult-to-make products, difficult to develop. They are not easily. You know, you can't easily commoditize them. You will have one, two, three players show up over a period of time, but they are not going to be 10, 15 different players right away. So these products, once you launch, they are there for 5, 6 years for you. Wixela is a good example. We launched in 2019, and it's still a meaningful product for us in our portfolio. So, over here, this example is the complex injectables, where we have put together these technologies, whether it's the microspheres, the liposomes, the peptides, you know, and you can call some of the iron complexes and also oligonucleotides. Many of these technologies are, you know, just not difficult to develop, difficult to work its way through the regulatory channels, difficult to scale up, and there's no dedicated, you know So you need to build some dedicated facilities to do that, and can give you a very exciting opportunities. Take, for example, over here, the portfolio of GLP-1s. And, you know, the starting with Victoza, which we'll be launching this year, and putting together opportunities like first to market, potential opportunities on 9 of these products, including products like Ozempic, Wegovy. Adding to this now, we are very excited to add products like Mounjaro. So this is, you know, this is just one example of that complexity when we talk about 57 products in this category, 9 potentially first to market positions secured, and we continue to add to this portfolio as we go along. Other aspect of when we say now products 505(b)(2) is repurposing of some of the existing molecules. This can be a new dosage form, new indication, new route of administration, for a route of or a new dosage strength. And there are several examples. So GA once monthly, which we are working, you know, hard with the FDA to bring it to the market, is just replacing those 12 injections by one injections in a month for a MS patient. Xulane low dose, a different dosage strength, where the market desperately was looking for a low-dose estrogen product. So that's an example of, you know, bringing the, you know, having an unmet need being met. And take, for example, a Mounjaro or a GLP-1 like Ozempic, from once a week to a once a month or a once a three months sort of approach. So there are many of these technologies which I walked you through can be deployed to this approach, and we have some of these things already embedded, like a Xulane low dose. Botox is in this category because it's a challenge of its own from the complexity point of view. We talked about, you know, an extra indication, additional indication for Effexor, venlafaxine, for generalized anxiety disorder. So we keep on looking for some of these opportunities, and this just adds to that, the richness of that pipeline and the numbers which I talked to you, and this speaks to the quality of that pipeline. Third piece, which is very exciting, is the eye care portfolio and pipeline, which we acquired as a part of Alcon and Famy Life Sciences, and we have been executing it over the last one year, making steady progress. One very exciting opportunity, you know, after, you know, was this gene therapy product, MR-146, which is neurotrophic keratopathy. Now, we are into IND-enabling studies. Very soon, we'll be able to share a little bit more with you. But, phase three program for presbyopia is moving steadily. Second dry eye program for telvornamab is in a second phase three study has been initiated. Blepharitis, phase three is getting initiated next month. And, phase three for the dim light product is already underway. So many of these products will hit the market by 2026, 2027, and these are not just a U.S.-centric program; these are the global programs. So we plan to take all the science to not one market, but every market where we have a global presence. So equally important for us, which gives us confidence that we have done it in the past and we can do it, our confidence to deliver consistently the new launch revenue basically comes from some of this proven track record. Over a number of years, we have consistently driven more than $450 million of new launch revenue year after year, while getting many complex products to the market first, you know, ahead of our competitors, whether it was three, biosimilars, which we have, you know, not divested, but now partnering differently with Biocon. The first interchangeable insulin, the first Herceptin biosimilar, first Neulasta biosimilar, but also more importantly, products like Rexulti, a generic to Symbicort called Breyna. And, you know, of course, Copaxone 40 milligram, which we were the first to get to the market. So there are many such examples, and we have perhaps, one of the most effective and productive R&D machines I can say, spending about 4%-4.5%, 4 to 4.5, 4, 4.5% of our total sales to generate these sort of consistent cash flows. So to sum it all up, deep in-house capabilities coupled with deep and solid pipeline, you know, the depth and the breadth of the pipeline speaks for itself, as well as a proven track record. We feel very confident to continue to deliver a new launch revenue of, for example, for this year, we said $450 million-$550 million, as well as potentially in the coming years, this pipeline continue to deliver similar numbers. As you can see, not only do we have strong existing pipeline, we also have strong science capabilities, a track record, meaningful track record. So this all robust foundation will serve Viatris well as we continue to add capabilities and move further up the value chain with more innovative assets like what Philippe is going to walk you through. So, Philippe, please come over. Thank you very much, guys. Thanks, Rajiv. Bye. Thank you. Okay, good morning, everyone. So we are very excited to talk to you about the next two assets, selatogrel and cenerimod. And before I cover the asset, no one better than our next speaker to talk to you about myocardial infarction and selatogrel. Let me introduce Dr. Bhatt, which is a top expert in cardiovascular medicine, interventional cardiology, and is the director of the Mount Sinai Heart. Dr. Bhatt? Thank you. Thank you. Well, it's really great to be here with all of you. It's an exciting day, I know, and I'm gonna speak about acute myocardial infarction. I'm sure sometimes the audience is a little mixed in their background. That refers really to heart attacks, and selatogrel is an antiplatelet agent. That is one that prevents blood from clotting. So selatogrel is being investigated for self-administered emergency treatment for current acute myocardial infarction, that is, repeat heart attacks. You'll hear in a little bit about the trial, SOS-AMI. I'm the study chair of that trial, and in that role, do receive research funding from Idorsia that goes to my, well, my prior institution, Mass General Brigham, and now my current institution. So just to make sure everyone's on the same page, here's a little bit about the epidemiology of acute myocardial infarctions or heart attacks. They occur pretty much in anybody. Everybody's at risk. Everyone in this room is at risk. There had been some sort of misconceptions, I suppose, that it was a disease of the old, but that's not true. In fact, in the U.S. in particular, heart attack rates in young people are going up quite a bit. That's not entirely understood why, but that is pretty clear from the epidemiology, occurs in all races and ethnicities. For many years in the past, it was thought really to be more a disease of men than women. But it's quite clear that women, especially as they get older, are also at great risk for eventually developing coronary artery disease, heart attacks. About a third of deaths in the industrialized countries can be attributed to heart attacks. So that's a pretty sobering statistic. It really If you look at cardiovascular disease as a whole, it remains the leading killer in the U.S. and worldwide, and then specifically, heart attacks or acute myocardial infarction are a part of that cardiovascular disease and remain a really, a big part of that. The average age at first heart attack, you can see some of the numbers there for men and women, 66 and 72 years, respectively. Eighty percent of the deaths that are caused by cardiovascular disease are due to heart attack and stroke. So, as I mentioned, a big chunk of that cardiovascular disease, which is the leading cause of death, ultimately are due to heart attacks and also strokes. Patients that have a history of a heart attack, seems intuitive, I hope that makes sense, are at higher risk of a repeat heart attack. So So if you've already had one and you survived it, many don't survive it, but if you survive it, then you're at higher risk of having another one. In terms of some numbers, about two million or so people are living in the U.S. and European Union that are having a heart attack each year, so large numbers. About 9-10 million or so in the U.S. and EU have a history of a heart attack within the past 10 years. Lots of patients with existing heart attacks and a lot more accruing heart attacks as the years go by. What causes heart attacks? That's an hour-long lecture. Lots of different pathways involved, but there is a major role formed or founded on the concept that there's plaque in an artery, and that's usually from cholesterol and fat and other bad stuff that builds up in the artery, plaque. And then that plaque can get inflamed. A variety of things can do that. That inflammation can cause the plaque to rupture, exposing the inner contents to flowing blood, and then a blood clot forms. That's what ultimately causes a heart attack, because a blood clot obstructs the artery, blood can't get to the heart muscle delivering oxygen. And an important part of that blood clot forming is the platelet, and therefore, agents that antagonize platelets or antiplatelet agents have an important role in cardiovascular disease, including in prevention as well as treatment of heart attacks. So in that paradigm then of plaques rupturing, blood clots forming, time is muscle. So the longer that that artery is blocked up or occluded, the more heart muscle is dying. And these slides, hopefully, they project pretty well. I don't have a laser pointer here to walk you through it, but the concepts, again, are hopefully intuitive. There's a period of time in which if you act, you can minimize the damage caused by that blockage of that artery and the amount of heart muscle that are dead. But the longer you wait, the less likely there's gonna be any salvage of the heart muscle or myocardium, as it's called. In those first few hours after a heart attack, that's when it's really possible to make an impact, and some will even talk about the first hour, that golden hour. That's a concept actually stolen from the trauma literature, but then brought to heart attack and stroke. If you can act within that golden hour, many times you can actually abort that heart attack, such that there's virtually no damage that occurs. That relies on a lot of things happening right now. You can think in New York, it depends on the patient calling 911, the ambulance coming, traffic and whatever it is, getting to the hospital, getting treated. So there's always a certain delay that happens. But at least, in theory, if you could get right to the patient and treat them in that first hour, you could minimize the damage from a heart attack and potentially even just abort that heart attack. And this graphic essentially gets to that point. And a related point that is a sobering fact, that of the people that are having deaths from heart attack, about 30% occur prior to admission to the hospital, about 10% during that hospital admission. So even if you've got a great hospital, a great healthcare system, and there are a lot of holes in our healthcare system in the U.S. and worldwide, but even if it were perfectly optimized, the majority of deaths from heart attack are occurring before that patient gets to the hospital. And that points to the importance of pre-hospital care, but very difficult, many times, delivering care, say, in an ambulance. There are all sorts of rules and regulations that vary from place to place. But if we could get to the patient before they have that fatal event outside the hospital, imagine the sort of impact we could have. And it's really with this concept that we have been exploring selatogrel, and you'll hear again, a little bit later about the design of the SOS-AMI trial. But the reason we thought it would be good to study an antiplatelet agent early on in heart attacks is exactly to try to abort the heart attacks and prevent the bad things that happen, especially early on, once a heart artery is occluded. So there are other antiplatelet agents out there, and in the universe of antiplatelet agents, there are P2Y12 inhibitors. That's a particular type of antiplatelet agent, refers to a receptor on the platelets, the P2Y12 receptor, the ADP receptor, and a number of them are approved. Clopidogrel, probably everybody knows that one. Very common, the trade name is Plavix, though of course, it's generic now. Very commonly used drug for patients with a variety of different things: heart attacks, strokes, peripheral artery disease, that is, blockages in leg arteries. Prasugrel is basically a, the more powerful version of clopidogrel. Ticagrelor, similarly, more powerful than clopidogrel. Cangrelor is an intravenous agent, very useful in the cath lab. Actually, I co-chaired the phase III program for that, along with Bob Harrington. And, these are all terrific agents. They're all in clinical use. They have limitations like every drug. Clopidogrel and Prasugrel, for example, are irreversible antiplatelet agents. What that means is once they or their active metabolites bind to the ADP P2Y12 receptor, they're there for the lifespan of that platelet, usually about 7-10 days or so. And, that can be a bit of a problem, say, if a patient needs urgent surgery because the drugs are on board. So there's some subtle differences between those different agents I mentioned, but the one really that I'm focusing on today is selatogrel, and that is a subcutaneous agent, so different from everything else that's listed here on this table. It's reversible. That's also true of Ticagrelor and Cangrelor. It doesn't require metabolism, so it doesn't, it's not a prodrug, unlike Clopidogrel and prasugrel. And it's the only one that is available for subcutaneous injection. The time to peak effect is about 15-30 minutes or so, about 24 hours for offset of effect. And so altogether, that's a really favorable profile for the sort of indication that we're discussing, patients that are having a heart attack, and we're hoping to abort that, or at least minimize it. There's already some data out there. I alluded to the ongoing phase III trial, SOS-AMI, but there are some ongoing, there's some already completed trials from the phase II program in acute coronary syndromes and acute myocardial infarction. Again, various flavors of chest pain and heart attack. What is already known about this agent is that it's got a robust and rapid effect, greater than 80% inhibition of platelet aggregation within about 15 minutes or so. It's got a height of IPA, as it's called, effect. That's, again, the amount of platelets that are inhibited, that's extended over about 8 hours, with platelet recovery in about 24 hours, as I mentioned on the last slide. IPA was faster, more pronounced, and more consistent with the 16 milligram versus the 8 milligram dose that was studied, and therefore, that seemed to be the dose to go with. And the effect was obtained on top of background, so-called dual antiplatelet therapy, meaning aspirin and an oral P2Y12 inhibitor. Some of the data are shown on the right-hand panel there, with purple and placebo. selatogrel, 8 mg is in blue, but really the one of interest is selatogrel 16 milligrams in black. This is showing PRU values. It's just another way of looking at inhibiting platelets and the profound and sustained effect thereafter that single sub-Q injection. So already we know significant effects on platelet inhibition, ones that we would expect to be clinically quite meaningful. Every drug has the potential to affect multiple other receptors, and you know, that's true of the ADP or P2Y12 receptors studied to date. But unlike the case with those agents, with selatogrel, there doesn't seem to be any sort of off-target biological activity going on in terms of revving up the inflammatory system, for example. That's what is summarized in the table there, just to translate it to lay terms. As well, what's been seen to date, in terms of preclinical work, such as this work on rats, was that there was less blood loss with selatogrel than an oral P2Y12 inhibitor, ticagrelor, with an equivalent efficacy. So at least in that rat model, it didn't seem like selatogrel was causing a bunch of bleeding, which theoretically might have been a concern with a novel agent. Shown here is the overall safety profile from the data that accumulated to date. Of course, we have much more data accumulating in the large ongoing phase III trial, but in terms of what's there right now, this table summarizes treatment-emergent AEs, or adverse events. What you can see here is, for the 8, 16 milligram in placebo arms, respectively, a pretty good safety profile, even if we're looking at things like, patients with, one or more bleeding events. That's the, final two rows in the blue box. For the 16 milligram selatogrel, you can see that there were five events, and in the placebo arm, 8 events. So no, real, signal that the selatogrel 16 milligrams is causing some large increase in major bleeding events. Very reassuring phase II data. So that's really what leads us, to conduct the phase III trial that's, ongoing, and, I'm gonna just summarize before that presentation some take-home points as far as selatogrel goes. It's a potent, reversible, and highly selective P2Y12 receptor antagonist. There's reduced off-target interference, of hemostasis compared to other P2Y12 inhibitors in preclinical testing, at least. It has a rapid uptake and fast onset of action, and in the phase II testing, greater than 90% of participants had greater than 80% inhibition of platelet aggregation 15 minutes after dosing. That sounds like what you would want in a drug you were giving to a patient who was having a heart attack. It has a relatively short duration of action, with IPA effect lasting about six-8 hours or so, with platelet recovery by 24 hours. So seems to be really potent and on when you need it in the early hours after a heart attack, and then after that, goes away. It seems to, at least, this far, in testing, have a suitable safety profile with no difference in major bleeds compared to placebo on top of standard care in a phase two trial. Obviously, need much more data that is being accrued in the phase three testing. To me, it's really interesting. I, I've done a lot of, trials with, cardiovascular drugs. I've done a lot of trials with cardiovascular devices, but here is a marriage of a, a drug and a device. selatogrel, it's administered in an auto injector. Like I said, it's subcutaneous, and that's designed for emergency use. It's safe, it's easy to carry, and store. It's stored at room temperature, which is, quite useful. And, the data to date, and it's accruing, I think, will provide really great insight into injectors in the use in acute coronary syndrome patients. Of course, there's already a vast history of use of injectors in other settings. I know all my kids have an EpiPen, for example, but to really bring this to a patient who's had a heart attack, so they have a good sense of what it's like, but now think they're having a repeat heart attack And being able to then self-administer a rapid, safe sort of therapy to bust up the blood clot, hopefully abort the heart attack, is potentially an enormous paradigm shift in the way we treat heart attack patients. So I'm really excited about the SOS-AMI trial. I think there's a good scientific basis for why it's being conducted, and I'll turn things back over to Philippe Martin to talk about exactly what the SOS-AMI trial is. Thank you, Dr. Bhatt. Thank you. Thank you, Dr. Bhatt. Thank you so much. We certainly share your enthusiasm for selatogrel. Based on this robust phase II data, we decided to initiate a large phase III study. That study is called SOS-AMI. So I'm gonna go over the design of the study. It is a simple study design, and that was done on purpose to maximize operational success. This is a typical randomized, double-blind, placebo-controlled study on top of a standard of care. The patients are randomized 1:1 to either selatogrel or placebo, with selatogrel 16 mg, which is the dose that was identified in phase II. There's multiple phases to the design. The first one is the screening phase, where we train patients to recognize symptoms of a heart attack. These patients already had a heart attack. That's one of the requirement. So they are familiar with the symptom. That being said, we are training them just to remind them of what to look for. We're also training them to use the auto-injector. That will be quite important that the patient is able to self-inject, when needed. Once the patients are randomized, they enter an observation phase. So when they recognize a symptom of a heart attack, they are to self-inject and seek medical care immediately. So they have to take themselves to the hospital and get proper diagnosis and potential treatment at that point. During the observation phase, as I said, it's pretty simple. are phone calls that are being made to the patient to remind them of the study requirement, to check on them, and to make sure that they remember their training. If they don't, they have the opportunity to be retrained. Importantly, this study was designed in collaboration with various health authorities around the world, in particular, FDA, for which we have a SPA agreement in place. It was also designed with the medical community and experts, such as Dr. Bhatt. FDA also granted fast track designation for this study, which really speaks to the high level of unmet need that selatogrel may be able to fulfill. Now, it is a large study, simple study, but quite large. We are planning on initiating 500 sites around the world across 37 countries. Our current assumption, based on prior enrollment and based on Viatris' knowledge of what can be done to accelerate enrollment, we think we'll be able to enroll this study in 2026. Now, let me cover the primary endpoint of this or the main endpoints of the study. So the primary endpoint is the occurrence of death from any cause and a non-fatal AMI for up to a seven day post self-administration. For the secondary endpoint, if you recall, time is muscle, so it is a similar endpoint as the primary endpoint, but we've added hospitalization due to heart failure within 30 days of self-administration. So that should be able to show that we are stopping damage from occurring within 30 days. And then from a primary safety endpoint, we'll be looking at the treatment type three to five, grade three to five, treatment emergent adverse event of bleeding, using the BARC definition. So all these adverse events are adjudicated by an independent committee. Now, it is an event-driven study, and we have an assumption. Key assumption is we anticipate a minimum of a relative risk reduction of 20%. The type one error is set at 5%, so we believe that we'll need approximately 4,500 events for this study. A reminder, an event is defined as a patient treating themselves, so either with selatogrel or placebo. So we think that that translates into having to randomize approximately 20,000 patients ± 5,000 patients. We also have a, as part of the protocol, a blinded sample size recalculation that is allowed, and, we'll be looking at that as, the data, progresses. Now, as I mentioned, there's an important phase at the beginning of the study, which is the training of the patients. We've put a significant, training in place, to ensure that these patients that are already familiar with heart attack, with the symptom of a heart attack, which is, which is, often just, chest pain or chest discomfort, can recognize the symptoms, self-inject, and, take themselves to the hospital to get a proper, diagnosis. Now, we're also training them at the site for the use of the auto-injector. They can use demo devices to train, and then when they feel comfortable, they have to inject themselves with placebo. So we really think that there's really no, virtually no downside for a patient that already had a heart attack, identify a symptom to self-inject, based on the data that we've seen so far in phase II. Now, the study is ongoing. We've randomized approximately 6,000 patients to date and, you know, we've observed a number of things that look promising for this study. One is that the patients are generally comfortable with the concept of injecting themselves upon recognition of a symptom. But importantly, we find that these patients are injecting early, and they're injecting for the right reasons. There's no safety signal identified to date. We have an unblinded independent data monitoring committee that looks at the data on a regular basis. They've met a few times so far, and each time they've recommended to continue the study unchanged. So in summary, despite the recent advancement in management of MI, a significant need remains for a treatment that can be given at the crucial time between the onset and the time a patient can get medical attention. As Dr. Bhatt covered, the P2Y12 have well established, they're approved for the treatment of MI, they are well understood mechanism of action, but they have limitations. They have PK limitations, they have mode of administration limitations that do not allow them to be used as an early treatment. There's currently no approved antithrombotic for early, MI, treatment. So time is muscle. Early treatment is key, and so we believe that, selatogrel is the right treatment, for the right patient, administered at the right time. With that, we will now switch to, cenerimod, and it's my great pleasure to introduce our next speaker, Dr. Anca Askanase. She's the founder and clinical director of Columbia University Lupus Center, and the director of Rheumatology Clinical Trials. She's an internationally renowned clinician and researcher with more than 1five years specializing in complex SLE. Thank you. It is a pleasure and a privilege to be here, and it feels really stressful at this moment to come after heart attacks, 'cause heart attacks affect the world, and lupus is a smaller disease, so bear with me. I'll try to explain why that's important. cenerimod is being investigated for the treatment of systemic lupus, and we're gonna talk a little more about this. Now, you'll see the butterfly is the symbol of lupus. It's about the butterfly rash on the face of lupus patients, and purple is actually the color of lupus, so a nd May is the month of lupus, so all these things coming together to convince you lupus is important. Systemic lupus is a disease of a high unmet need. It affects about five million people worldwide, about 1.5 million Americans, and there are about 16,000 newly diagnosed patients in the U.S. every year. It is a disease of young women. The peak incidence is between 15 and 40, 9 women for every man affected. The main symptoms of lupus are rashes, arthritis, joint pains, and fatigue. However, lupus can range from mild to severe and life-threatening. And currently, there are limited treatment options. Whenever we're thinking about how to treat lupus and how to categorize lupus, we think about patients that have mild symptoms, moderate or severe and life-threatening disease. The drugs that are being developed right now, and cenerimod is being developed for moderate to severe lupus. Why do we need new treatments? Well, because the current treatments have a lot of limitations. Hydroxychloroquine became very famous during the COVID pandemic, but and it's been used for the treatment of lupus for over 50 years. However, its efficacy, it's modest at best, and it has side effects. We use a lot of steroids. I hope the audience is fully aware that steroids are amazing and extraordinary treatment tools, yet the side effects are devastating, and this has been the case for generations and thousands of people with lupus that have been treated with too much steroids over too long periods of time. About five decades ago, we started introducing immunosuppressants, broad-spectrum immunosuppressants, that we borrowed from chemotherapy and from organ transplant, but these are not targeted medications, and they have the risk of infections and malignancies. Over the past decade or so, we have started using biologics. Belimumab was the first FDA-approved biologic for the treatment of lupus. Rituxan is used off-label, and anifrolumab gained approval about two years ago. There are options in terms of biologics, but all of these have limited efficacy, and because of the intravenous administration for Rituxan, anifrolumab, and belimumab, these are a little more cumbersome to administer. There's always the risk of side effects, infections, and malignancies that have been at the background of all these treatment for systemic lupus. So now let's look at cenerimod as an opportunity to treat systemic lupus. Three main pillar in SLE pathogenesis that cenerimod works on: It inhibits the egress of autoreactive T and B cells, decreasing the autoantibodies. Lupus is a disease of anti-self antibodies. It reduces the main pro-inflammatory cytokine in lupus, which is interferon. It acts both on interferon alpha and interferon gamma, and it also decreases the migration of antigen-presenting cells. Antigen-presenting cells are critical to the recognition of autoantibodies, further decreasing autoreactive T and B cells. So it acts on three areas, main areas of SLE pathogenesis, possibly supporting a higher benefit. We're looking here at comparisons between the mechanism of action for cenerimod versus the biologics that are currently in use for the treatment of lupus, and we note the same thing, that it acts at three levels of SLE pathogenesis: the T cells, the B cells, and the interferon, while the currently available biologics each act on just one of these targets. Additionally, cenerimod has a unique structure that allows it to be different from other S1P receptor modulators. Sphingosine-1-phosphate is a signaling molecule that acts through receptors. cenerimod is part of the class of receptor modulators. The pieces that are different about cenerimod, it is a very potent, selective S1P1 receptor modulator. It is oral once daily administration, and because of its attenuated calcium response, it is not associated with vasoconstriction, has minimal bronchoconstriction, and minimal cardiovascular events. What is the data to date? About 700 people have been treated with cenerimod to date. 200 healthy volunteers in the phase I study, 407 in phase II studies. There were one phase IIa study that had 67 patients, the CARE study that we'll talk some more about in a moment, that had 427 patients, and then 17 patients in a study in Japan. So altogether, 407 patients that have been exposed to cenerimod in phase II, and about 100 that are currently in the phase III study. So overall, enough data to give us the confidence both in the efficacy and the safety of the drug. These are sort of the This is the schematic of the phase II CARE study that had a primary objective to investigate decreasing disease activity. Lupus is a disease of the whole body, so when we're measuring disease activity, we use these complex disease activity measures. For those in the know, all of our disease activity measures have complexity that requires training for the investigator. So, the one that was used for the CARE study, it's called the SLE Disease Activity Index, SLEDAI, so you'll hear about it a couple of more times throughout this presentation. Four doses were evaluated: 0.5, 1, 2, and 4 mg, and those were evaluated in the treatment of patients with moderate to severe lupus, in addition to standard of care. Most therapeutic drug studies are against placebo, while in systemic lupus, all the studies are done in addition to standard of care, so it's placebo or drug in addition to standard of care. The dose that worked best was the four miligram dose. It is here in purple, and it is the dose that is currently investigated in the phase III study. The primary endpoint for the study was at six months. The study was continued for a total of 12 months to evaluate safety through 12 months. The study design was a little complex there because at six months, patients on the higher dose, the highest dose, the 4 milligram, were re-randomized to the lower dose of 2 mg or placebo. The concern was that there will be a lot of lymphopenia for patients with cenerimod 4 mg. That didn't turn out to be the case, but this was a study design mandated by the FDA. These are the baseline demographics and disease characteristics of the patients in the study. They were balanced well between the study groups. You will note the last two lines show a moderate disease activity measured by the SLEDAI. Part of the mechanism of action of cenerimod is to decrease peripheral lymphocytes. One of the measures in the SLEDAI is looking at the total white cell. Lymphocytes are white cells, so the measure was modified to exclude the lymphocytes, which are part of the mechanism of action. The last line looks at interferon, the big cytokine in systemic lupus. I already told you that cenerimod works on interferon. Yet, for the study, the number of people that had high interferon was disappointingly low. We'll see what that did for, you know, the study further. So these are the main study findings. cenerimod demonstrated clinically meaningful decrease in a modified SLEDAI score of 4 points, solid, robust, disease activity decrease compared to placebo, which was about 2.8. That had a p-value of 0.029. However, after adjusting for multiple comparisons, that became only nominally statistically significant. So, we then looked at a combination of disease activity measures. This is the traditional disease activity measure for phase III trials that the FDA is insisting on for phase III studies. It's called the SLE Responder Index. It is a combination of the SLE disease activity index, the SLEDAI, and an association with two others. I'm not going to bore you with, with details about those, but to make sure that while disease activity is decreasing based on the SLEDAI, for rare manifestations, there's no worsening in other organ systems. So in the overall population, the data on the SRI-4 is consistent with the, with the data on the modified SLEDAI. In patients treated with 4 mg, there was a higher percentage of those achieving SRI-4 response at six months compared to the placebo standard of care arm. Now, if we look at patients that have evidence of higher disease activity, as expressed by their high interferon signature, we note that. And that's to the left of the slide, I guess to your right there, sorry. To your right, you'll note that it's very. For this population that has higher disease activity and higher interferon, the difference between treatment and placebo was 24%. In evaluating interferon signature for the CARE study, about 51% of the patients had high interferon, compared to much higher percentages of patients with interferon-high signature from other phase III studies. Ergo, this resulted in a very bold study design for the phase III study, and Philippe is going to tell you some more about how that is taken into account in the design of the phase III study to enrich for patients with high disease activity and high interferon signature. We looked here at the efficacy of cenerimod across several characteristics that are associated with severity: high autoantibodies, high double-stranded DNA, low complement, higher levels of SLE disease activity, high steroid use, and a different measure of disease activity, the BILAG. These are the summary of the AEs and severe adverse events based on treatment group. I would like to draw your attention to the cenerimod 4 mg, which is further developed in the phase III, and that comparison with placebo. So overall, the number of adverse events balance between treatment and placebo. Adverse events leading to study drug discontinuation, a little higher in cenerimod. Serious adverse events balance between the groups. The part that is obvious is that there's more lymphopenia. It's part of the way the drug works. There's a little more hypertension as reported by the investigator, yet when we looked at the actual blood pressure reading at the visits, that was not really substantiated. Some headaches and abdominal pain. So, the safety profile is consistent with other medications in use for lupus, and there does not seem to be a major risk for serious adverse events. Furthermore, these are the adverse events of special interest. They are all mild and transient. There's no increase in the risk of infections, there's no increase in pulmonary-related adverse events, no increase in malignancies. There's always concern with the S1P receptor modulators, that there could be heart rate and heart rhythm abnormalities. There were no second-degree or higher AV blocks observed. There was no increase in medically relevant bradycardia or rhythm-related problems. There was also concern that there may be some macular edema. There was one patient where this was reported in the whole CARE study. However, upon review of the data by the Ophthalmology Safety Board, this was not substantiated. And, I will pass on the podium to Philippe to tell us about the CARE study. OPUS study. The OPUS study. Thank you so much. Thank you. Thank you very much. So as you can see, I think, we made the case that we've been able to, accumulate quite a bit of, data with cenerimod in healthy volunteers, but more importantly, in SLE patients. We have a large and consistent, dataset that gives us high confidence that, cenerimod, that, that, that the benefit-risk profile that's emerging for cenerimod, may be answering the, the, the current unmet need in SLE. Especially when you look at, the efficacy data, we're trying to put it in context here. In patients that are similar to the patients we intend to enroll in phase III, we see that the efficacy profile, the efficacy profile is, quite competitive, when compared to, to other clinical trials with a similar population. By the way, that population is a population of high interferon signature patient, about 80% of the patients. Now, in terms of the safety profile, as you just saw, we've seen an optimized S1P safety profile for cenerimod. We did not observe clinically meaningful effect for any of the adverse event of special interest that we typically look at for S1P inhibitors, such as first dose bradycardia, AV block, AV conduction issues, macular edema, liver enzyme elevation, and effect on pulmonary function and blood pressure. When you look at our safety profile compared to other SLE treatments, you see that cenerimod was not associated with an increased risk of SAEs, or infection, or malignancies. So that profile compares on top of a standard of care. That profile compares very well to other SLE treatment and can be given on top of other SLE treatment. So now moving to the phase III study. Based on this strong data, we've moved forward with a large pivotal program design. It is composed of two studies that are identical. The study design is a randomized, double-blind, placebo-controlled parallel group study, where we evaluate the safety, efficacy, and tolerability of cenerimod. So the patients, 420 patients per study, will be randomized 1:1 to either cenerimod 4 milligram or placebo. The primary endpoint is SRI-4 response at month 12 compared to baseline. Patients will be stratified by corticosteroid dose at baseline, by anti-dsDNA more or less than 10 at baseline, and interferon high versus low. Importantly, and this was not the case in the phase II study because of the actual design, we'll have a forced corticosteroid tapering that will be required between month 5 and 8 for all subjects that had a dose of baseline dose of corticosteroid of more than 10 mg per day. This design. This is a study that is a global study. The two studies are global studies. We intend to enroll 840 patients over 340 sites in 25 countries. We've had about, more than 100 patients enrolled to date, and we think, based on our preliminary assumption, that we'll be able to enroll the study by the end of 2025. This is an important slide, where we're comparing the study design from phase II to the current phase III study. As Dr. Askanase mentioned, we are enriching the study for the type of patient that responded better in the phase II study. These patients are patients with high interferon signature. We are targeting about 80, 80% of these patients to enter the study. As you saw, this is what is typically expected from a phase III population. However, should we see that we are far off the 80%, we can close one of the strata and ensure that we get to that 80% interferon high patient. We've modifying a number of other criteria to make sure that entry criteria, to make sure that we get these more severe patients. Of note, these are criteria that are typical in phase III, in other phase III studies, nothing out of the ordinary. We just didn't have those criteria in phase II. The primary endpoint is now at 12 months, which is what is to be expected for an SLE phase III study. That's quite important for cenerimod because it gives the drug full time to get to full effect. Importantly, it also allows for that, corticosteroid tapering strategy, which is typically seen in Phase III, and generally leads to a reduction in placebo rate of about 8%-10%. So delta in our treatment effect is expected, a higher delta based on the corticosteroid taper. If a patient is not able to taper, the patient is considered non-responder as part of the efficacy analysis. So, in summary, we think that there's a high unmet need, as you have heard, that remains for the treatment in SLE, especially for an oral therapy, that can be given on top of standard of care and prior to biologic treatment. We have seen robust data in phase II, across and consistent across the various phase II study we've done, and we believe that, the safety profile that is emerging is highly competitive, in SLE. We think that, cenerimod has the ability to become, the new standard of care, in the treatment of SLE, of moderate to severe SLE patients going forward. So with that, I think, I will give, the presentation to Doretta, and she will talk to you about the Idorsia transaction and the commercial overview. Doretta, thank you. Thanks, Philippe. Hello everyone, and welcome. I'm Doretta Mistras, the CFO of Viatris. It's been a exciting few months for me here at Viatris, and as I've had the opportunity to reflect on my 20-year career of helping companies across the healthcare industry drive shareholder returns, I have a strong appreciation for the unique position that Viatris is in today to create significant value for shareholders. This is as a result of our solid foundation and diversity of business, as we heard from both Scott and Rajiv, coupled with the stability of our cash flows. Which brings us to today, and I'm really looking forward to the opportunity to provide some additional color around the Idorsia collaboration, as well as provide a high-level overview of the commercial opportunity from this collaboration. The Idorsia collaboration is a great strategic fit, as it has the potential to enhance our growth profile by providing a portfolio of branded, patent-protected assets that are really targeting significant areas of unmet need. For both molecules, our unique history and organizational learnings have enabled us to have a real differentiated commercial and development insight, as well as give us the confidence that we are the right stewards for these assets. So we believe that both selatogrel and cenerimod can be foundational assets for Viatris, and this is due to their novel mechanisms of action, as we've heard, and their differentiation in areas of high unmet need. Given their long exclusivity runway, as well as the potential for life cycle opportunities, which we'll get into, they both will have a meaningful role in driving incremental long-term revenue and earnings growth. It was important to us to structure the collaboration in a disciplined manner, consistent with our balanced capital allocation strategy. The regulatory and commercial milestones are entirely success-based, and we believe the transaction offers an asymmetric risk-reward profile that has the potential to create significant value for shareholders. Regarding the P&L impact, I wanted to highlight just a few points. The deal structure leads to a prudent level of R&D spend. Both companies are expected to contribute to the development costs, with Idorsia up to $200 million. We expect our costs to be modestly higher and spread over multiple years. This allows us to effectively manage the near term and longer-term P&L impact, both from an R&D and earnings perspective. Though we haven't made any final conclusions, we currently expect to account for the transaction as a business combination, and as such, the $350 million upfront payment we expect to be capitalized. So now let's jump into both these assets. As we look at the commercial opportunity for selatogrel, there are three core elements that give us conviction in its blockbuster potential. First, as we see all the way on the left, on the right, is the market. This is a large global population consisting of post-AMI patients and annual new AMI cases, representing approximately 26 million patients worldwide. And as we heard earlier from the scientific presentations, this condition has devastating consequences for patients and results in significant costs for the global healthcare system. As many as four out of ten patients who suffer a heart attack die before receiving hospital care. Though there are many established treatment options for cardiovascular disease in both prevention and in-hospital acute care, currently, there are no approved treatments for the time of symptom onset, and with reoccurrence rates of 20%-25%, post-AMI survivors have a lifelong need for cardio protection. Second, is the science, and EU and US guidelines have identified early intervention as a critical factor for patients. selatogrel's innovative profile is well aligned to meet the significant unmet need and could deliver an important solution for these patients. Our global SOS-AMI study has the potential to demonstrate a compelling morbidity and mortality advantage, which we believe will be important factors to drive both adoption and value. Cardiovascular care over the decades has been shaped by numerous analogs, where cardiovascular-based outcome trial results drive paradigm shifts, disrupt markets, and rapidly advance patient care. Successfully registering selatogrel as the first and only patient-administered treatment would be a game-changing therapy in AMI care. And third is our capabilities. Viatris is well-positioned to commercialize selatogrel. Our extensive experience and track record with bringing access to patient-administered acute rescue medications is well aligned with the attractive commercial dynamics of selatogrel. Our experience, not only with patient education, but with services and patient advocacy, along with our extensive channel and distribution capabilities, will be critical to the access of an on-demand treatment for lifelong AMI patients. And so as we put this all together, as a result of all of these attributes, we see a large initial addressable market in this post-AMI setting. However, if successful in this setting, we see a natural pathway to be able to expand this addressable population through follow-on indications that could multiply selatogrel's market potential. So now let's turn to cenerimod. If we evaluate these same three core elements that we just talked about for selatogrel, the market, the science, and our capabilities, it just serves to underscore our confidence in cenerimod as a potential first-in-class S1P1 and SLE with blockbuster potential. As a chronic and progressive autoimmune disease, this is a well-established patient population. However, as we've just heard, there are limited treatment options for the five million people who suffer from lupus worldwide. As a result, there is a real need for treatment options that are tolerable and effective. Our highly innovative profile for cenerimod, which includes its unique mechanism of action, convenient oral administration, and our phase three evaluation, which is conducted in addition to standard background therapies, could deliver significant utility against these market needs. And third, listen, the unique dynamics of this autoimmune market are well known by Scott, by Philippe, and other leaders within Viatris, who possess deep commercial experience in rheumatic diseases. We believe the potential for delivering cenerimod, with its highly differentiated benefit-risk profile to a well-defined and succinct group of specialized prescribers, could provide an attractive value proposition in this serious disease setting. Listen, as we think about the broader potential here, cenerimod's unique mechanism of action and effects across multiple pathways has the potential for a broad lifecycle program. This includes diseases linked to lupus, rheumatic diseases, and other existing S1P1 autoimmune diseases. So just to summarize, I hope you've heard the excitement that we have, not only for this Idorsia transaction, but the steps we are taking to accelerate our growth and the outlook that we see for the company. So I know you guys are gonna have some questions for us, so let us take a few minutes to get situated, and then we'll transition over to Q&A. So thank you, everyone. Okay, now we're gonna proceed to our Q&A session. First question, we'd like to go to Jason Gerberry from Bank of America. Hey, guys, thanks for taking my question, and thanks for the presentation. Maybe just curious, you know, Rajiv, you outlined some complex injectable products, and some of those require presumably a lot of CapEx build to like the incretins or or the oligonucleotides. So just curious how you guys approach those sort of opportunities. Is it when you're getting to the finish line, so to speak, that you start to make those investments, or do you feel like you already have that investment already shored up so that it's not going to be a heavy lift from a CapEx standpoint? And then, you know, as you outline, you know, roughly 4.2% as an average R&D rate, as you kind of evolve from a hybrid generics brand company to more of an innovative company, I'm wondering directionally how that aligns. Like, what, what should we think about as sort of the peer group for, for spend, on a percentage of revenue? And then my last question is just with the AMI trial. I'm curious, are patients allowed to be on background antiplatelets? I'm wondering how to think about the data relative to sort of what you can get with antiplatelet therapy as a preventative measure, and would this sort of coexist with antiplatelets? Thanks. Thank you for the question. I think we have probably three different people to address your question, so I'll hand it to Rajiv to answer your first question relative to the complex generic- Yeah. portfolio. So, Jason, as you can appreciate, we would have been working for last 7, 8 years, 10 years, maybe, on these complex injectables. And as the science evolved, we have been investing, in fact, because even just to take these ANDA batches for many of these products, you have to go into a final facility to do those things. So we have been investing, in fact, and as we speak, a couple of plants are coming up, just from the capacity point of view. So I don't think there's a lot of CapEx going forward because we have already been working on it and spent it over the last few years. So that's, I think, as far as the R&D dollars Yeah, do you want to address the You want to talk about? Yeah, listen, I think from an R&D perspective, I think we've been open about listen, as we transition up the value chain, it is gonna require some incremental investment. I think what we've kind of said is, it's kind of we expect to generally increase in R&D spend generally in the 5%-6% range. But if you take a high level, just take a step back as we think about our profile in the kind of immediate term, you can think of the revenue growth that Rajiv has talked about in that kind of ±2% range. It will require some investment, so kind of flattish EBITDA growth and through our balanced capital allocation strategy, as we transition more to an EPS growth-driven story, you will see some EPS growth as well as we continue to bring on these kind of move up the value chain from a growth profile. Philippe? I will start on the MI, and I'll ask Dr. Bhatt maybe to add to what I'm saying. So phase III study and the phase II studies were on top of background P2Y12 inhibitor in combination with aspirin, so the dual antiplatelet therapy. So the reduction that you saw on one of the slides was on top of that background therapy. So when patients have MI, generally, they are still on background therapy, but the P2Y12 that they're taking at the time doesn't inhibit the platelet to the level that is required for the MI to stop, right? So that would be the difference. In phase III, we anticipate we'll have a portion of the patients that are on dual antiplatelet therapy. Sometime in some region of the world, they stop the dual antiplatelet therapy after a few months on treatment. In the U.S., they tend to continue, but so you'll have a mix of patients. But the data in phase II shows that the drug works on top of dual antiplatelet therapy. Dr. Bhatt, anything? I think it's a great question and a really thorough answer. I'll try to expand on points that were already made. So you're right. A lot of these patients at least should be on background antiplatelet therapy after their MI, and part will depend on how much time has elapsed since their prior MI. We're enrolling patients that had MI in the past month, but then, of course, we're following them over time. So let's say, you know, a month after an MI, I would expect the majority of patients would be on Aspirin and an oral P2Y12 inhibitor like clopidogrel or prasugrel or ticagrelor. Even in that situation, I would expect there would be incremental antiplatelet effect. In fact, that's already demonstrated. It's not an expectation. That's known. Just extrapolating, you know, from another trial that I was involved with, I alluded to some of the data for intravenous ADP receptor blockade with Cangrelor. Champion Phoenix was the trial, and there we showed an incremental benefit of Cangrelor over clopidogrel. That resulted in a reduction in ischemic events that resulted in the FDA approval of that compound for intravenous use in the context of stenting procedures. So I would think that selatogrel, with its ADP receptor antagonism, would be incremental to whatever background ADP receptor antagonist was on board and incremental to aspirin, which operates through a different pathway but is an antiplatelet. Both aspirin and the oral P2Y12 inhibitors are, you know, great drugs. They're, they're effective, but neither is super potent. They can't be because they're chronic oral therapy. You won't want a patient to have very, very high degrees of antiplatelet- Action every hour of every day, because then the bleeding risk would go up with chronic therapy. So for these patients that are even on aspirin and P2Y12 inhibitor, I'd expect the incremental ADP receptor antagonism to result in benefit. And as I mentioned, the further they get from their event, two things happen: one is that physicians de-escalate therapy, and they will often take patients off one of those two drugs some number of months after the event. And the second thing is patients often just, you know, take themselves off, not necessarily with their doctor's knowledge or permission. This is very common in heart attack patients, even though it shouldn't be, since they've had a heart attack, but it's true for, you know, aspirin, clopidogrel, statins. You know, a year after a heart attack, oftentimes registries show 50% of patients are off these drugs that they should be on. So I think there'll be an admixture of patients over the course of the trial with varying degrees of oral antiplatelet therapy on board. But I would expect that there would be incremental efficacy in all those cases. Thank you. Thank you, Dr. Bhatt. Next question. Glen, please. Yeah, thanks. Glenn Santangelo from Jefferies. Just a couple quick ones for me. First, Rajiv, on the $450 million-$550 million you know, you've talked about repeatedly. On your slides, you sort of put up a bunch of complex injectables and repurposing some existing molecules. I was wondering if you could just spend a minute talking about what you think are the biggest opportunities in 2024 and what we should be focused on. Yeah. This year, let's just take $450-$500, that range. 200, almost 50% of this is coming from the products which already we have either launched or got approvals and launching. So that's 250 already. You can say products like Breyna, because we, we take into consideration one full year of the launch period. So if we launch in August first, we have that period up to August of 2024. So that's 250, and then 250 comes from the several launches which are lined up across the globe, but key ones being Victoza, Sandostatin LAR. This year, we have in the second half, we, Venofer, which is another iron sucrose injection, and, you know, many more in this category. Again, these are the three big ones over there I will, you know, call out. Okay. Maybe just two quick ones for you, Scott. I was kind of curious if you could talk about the timeline for selatogrel. I think you said full enrollment, you expected in 2026. I'm just trying to gauge for how quickly you think that can be a contributor. And then secondly, for you, I think you said in your prepared remarks, you bought back $250 million worth of stock year to date. That was the number on the 4Q call, or is that the number as of today? That was done as of the Q4 call that happened in Q1. Yeah, that way it was, 250 had been done by then. I guess we would anticipate doing some more share buybacks as we go through this year, and look to accelerate that as we go into 2025 as well. The timeline on selatogrel? So the timelines, it's a little bit difficult when a study is actively enrolling to give an exact timeline. What I would say is likely to finish by the end of 2026, which could lead to commercialization if everything went well and everything positive. I would say the earliest would be second half of 2027, potentially into the first half of 2028. But in that timeframe, 2027, 2028, bridge, I think, would be the timeline for selatogrel. I think, just to add to Scott, it takes into account potential fast registration, fast review time for selatogrel based on the SPA and the fact that the FDA has been very engaged in the design of the study. Which I think is hugely complementary to the program. Yeah. People sometimes underestimate the value of fast-track designation and having a SPA in place for the program and other things, so it should lead to much faster regulatory reviews, and hopefully, the ability to get a life-changing, life-saving medication to patients earlier than you would otherwise, so. Thank you. Next question. We go to Nate, please. Thank you. Great. Thanks so much. Nathan Rich from Goldman Sachs. A few questions. I guess, Scott, in your opening remarks, you mentioned opportunities to maybe accelerate commercial development. Could you maybe just expand on maybe some of the specific opportunities there? And I guess, you know, as it relates to the P&L and, and as we think kind of the next five years out, maybe how OpEx as a% of revenue, you know, what you guys are thinking as, you know, you move into more of these novel products. And then a clarification on the Idorsia R&D split. I guess, how do you feel about line of sight on the R&D spend? And if there are variations, you know, how is that split between yourselves and Idorsia? Thank you. Yes. So, under the construct of the Idorsia deal, you know, we are, they are paying $200 million into the programs, and we're taking the rest. I think it's probably ending up relatively evenly split between the two companies from this point. I don't know, Philippe, if you- Yeah, I think, you know, it's going to be slightly higher for us than it is for Idorsia at this point, is the forecast, but not meaningfully different. You know, that's currently where we stand. The SG&A question, I think, I'll kick to Doretta to- Listen, I think it's a little early, right, to be ultimately commenting as we commercialize, these assets. But listen, as if we see the same clinical benefit risk profile, we'll put the right commercial infrastructure in place at that time to commercialize those, those assets. And sorry, your first question was relative to my prepared remarks. I forgot the question. Oh, sorry. You had just alluded to maybe some opportunities to accelerate commercial development, so I just wanted you to expand on those comments. Yeah. So I think what I was saying there is we have an opportunity to accelerate both development and the commercial aspects of this, due to the funding that we can bring to the table, due to some of the logistic backgrounds we can bring. I think Idorsia was a little bit held back because of resource constraints and being able to really maximize some of the studies in terms of enrollment, in terms of moving things forward. I think, you know, not only can we add capital to really move that forward, open up more sites, get more patients into more sites, but we've got an operational network globally, which we can utilize to really help accelerate the study. So I would see us being able to do that much more quickly. We have in many countries very good cardiovascular commercial teams in place. You know, I would remind people something we forget sometimes is that we have $2.5 billion in cardiovascular revenue as a company globally, and so a lot of companies if the cardiovascular is their biggest therapeutic area. I think, you know, we, we've got that built in a number of places around the world. Combination of resources, logistics, and other things to accelerate on the clinical development side, and then on the commercial side, I think, you know, we've, we've got good, ready, strong infrastructure in place. Thank you, Scott. Next question. Ryan, right here, please. Hi, here for David Amsellem with Piper Sandler. For selatogrel, you'd essentially be introducing a new treatment paradigm as the potentially first self-administered treatment for AMI. So with that in mind, do you envision any commercial challenges or hurdles there? Well, again, you know, I'll kick it to Philippe and to Doretta to address. But, you know, I can't think of a company in the world which is better suited for a self-administered, life-saving medication than us. And again, there's that aspect of it, something we know very well, something we've executed very well. On one hand, on the other side, we do have, again, $2.5 billion in cardiovascular revenue worldwide, so I think we are very well-positioned to do so. Anytime you launch a new product, there are commercial challenges, there's obstacles in terms of reimbursement and other things. And so it's never an easy business to get a drug approved and then get the right kind of access to it for patients. But I think of any company in the world, we've got the best raw material to be able to do it in a really outstanding way, and we're really excited to be able to do it. You know, game-changing, life-changing medication to add to all the things that we already do, I think is really something special for us as a company, and we're very anxious to get the study done and going and get commercializing. I don't know if you two want to add? No, I think, you covered it. Thank you, Scott. Next question. Here in the second row, Kyle. Thank you. Katerina for Chris from JP Morgan. So two bigger picture questions, if I may. So first, just I guess on broader R&D priorities, which therapeutic categories are you most focused on at this point? Is derm, GI, and ophthalmology still kind of a big area for you, or should we be expecting kind of a broader R&D priorities going forward? And then I guess the second question is just, you know, what does the company's branded pipeline look like, you know, 5-10, 5-10 years from now? You know, how much of the pipeline do you think will be external versus internal? And, just kind of what does that look like? Yeah, so I think our strategy, I will say, has not changed at all, right? You know, over the last year, when I've had chances to present and talk to people and talk to investors and others, you know, we've always said we're still interested and focused in ophthalmology, where we've got a deep pipeline in place. As Rajiv said, we're interested in dermatology and where we have got active discussions. We're interested in GI, same thing, but we're also going to be opportunistic. And I think if you take a look at some of the really big medical innovations that have happened, particularly on the pharmaceutical side in this world, it's not that a company was looking for something very specific, it's that they realized an opportunity when they saw. So I think we're going to continue to be opportunistic. In terms of what the, you know, what the pipeline, you know, will look like, in five years, seven years, you know, we're commercializing something like 1,400 brands right now and 4,400 unique SKUs, and so it's and $15 billion in revenue. So it's a big, diverse company. The numbers, I think, will always be, with the, that side of the business that sort of exists today, what we call the strong base. But what we're trying to do is not move away from that strong base. What we're trying to do is add new, innovative products on top of that. If we took a look at 5, seven years from now, we would hopefully have, 4, 5, 6, 7, 8 branded commercialized products with long patent protection, during that time frame. So these are the first two new ones that were coming in. There'll be some from the eye care side, but you know, we're very interested in actively developing the pipeline. We think the company's in a strong place. The financial strength that we have gives us the ability to really give back to shareholders, as we're saying, have disciplined capital allocation, but also look for, you know, different manners to build the pipeline. We're looking at everything, right? We would look at M&A, we would look at licensing, we would look at partnerships, we'd look at research collaborations, we'd look at every way we could do it. We try and do it in a smart, you know, capital discipline, with capital allocation discipline way. But we're going to look at all manners to build out the portfolio for sure. You know, I think this type of deal is a good, you know, surrogate for us moving forward, where you're partnering. And the other side of this is, you know, we have a very, very strong global company, 165 countries. There's a lot, I get a lot of inbound. I get inbound every day. People with technologies, products, and things that are looking for a strong global company. They don't have the capital or the expertise to be able to commercialize globally. So there's a lot of those opportunities that come into me as well. They've got to be the right opportunities for us, and you know, for me, more importantly than which therapeutic area, although you do need focus, you can't do everything to everybody, is the idea: Can these really be impactful assets, and can we leverage this strong global infrastructure we have to make these assets better than they would be otherwise? Thank you. Next question? Hey there, thank you for hosting this. I'm Afsah Quadri from Barclays. I just wanted to see if you had any comments on the CRL you received on GA Depot about a week ago. We're just kind of wondering what that does to the timeline. I think you were saying it was gonna be 24 prior, and wondering if that has changed. The CRL we got, a couple of weeks back, is about certain characterization questions around CMC. Also, you know, the site audit has been pending because of facilities in Israel, and FDA has not been able to visit, and there are some questions about even the phase III study. So we have, we are seeking a meeting with the FDA to align on expectations. But having said that, even if this launch, you know, this launch will definitely get pushed out to maybe later in the year or early in the next year. But with even with that, we're very confident of delivering on our the new launch revenue expectation of $450 million-$550 million. Right. That's the key point, right? I think that, you know, we've built optionality into the pipeline. We're not dependent on what any one individual product at this point to deliver that new product number, and we're committed to delivering that $450-$550 this year and years going forward. Any additional questions from the audience? Wow! Okay, I think with that, Scott, we can conclude the Q&A, and it'd be great to hear a few final remarks. Well, I think we had a slide to tee up here for the end, which is not If we put that up just as a summary slide. And if not, I would just like to say to everybody, thank you for coming. I hope you can feel the excitement, the palpable excitement that we have to be where we are. And it's not just about the new assets, although we're very excited about them. It's about where we are, how strong we are as a company today, how diverse and broad we are, and then our ability to add new products to what we're doing and increase from 1 billion patients yearly to more is, I think, really important to us, and we feel very excited about where we are as a company and where we're going. We also feel very excited about this transaction, and I've said in my remarks, and everybody has said we think it's very complementary to what we do. These are really the potentially blockbuster assets. But more than that, right, more than the revenue, it's the ability to be able to go into areas of high and unmet medical need with either life-changing or life-saving medicine, expanding what we do as a company that we're very, very excited about. So a very bright future ahead for us. We had a great 2023. We're looking forward to having a great 2024. We're looking forward to bringing in more assets than we have and moving things forward. But, we're very, very excited about the place we are, the financial strength, our ability to generate GAAP free cash flows and be able to use those again to pay back to shareholders, dividends, and share buybacks and invest in new businesses going forward. So, thank you all for your attention and look forward to talking to people. I think we have a little bit of a social time after this, so any other questions people would like one-on-one, please feel free to ask any of us up here, and thank you again for your time and attention. Thank you.