Well, good morning once again. We're delighted to have Bristol Myers Squibb here at the Cowen 44th Annual Health Care Conference. Representing the company is Roland Chen, who is Senior Vice President and Head of Immunology, Cardiology, or Cardiovascular and Neuroscience Development. So thank you so much for making the effort to be with us. Thanks, Steve. You're in charge of three critical areas to the outlook for Bristol Myers Squibb. Just tell us in very brief fashion, what is the central objective in each of these three areas, say, for the next three to five years? Yeah. So thanks for that question, Steve. It's a pleasure to be here. I think if I just think about the three areas, I mean, let me start with cardiovascular. I think where we are focused is in cardiomyopathies and heart failure, and thrombosis. And so if you think about the next three to five years, we are highly focused on CAMZYOS, our first-in-class cardiac myosin inhibitor, now approved for obstructive HCM, as well as milvexian, which is deep into phase III as a next-generation oral Factor XIa inhibitor in the antithrombotic space. And so those are two pillars that we continue to be focused on in the cardiovascular area. Now, with respect to neuroscience, this is an exciting area. Bristol was in neuroscience. This was in the past decade. We exited. But we are reemerging in the neuroscience space. We are looking to build a diverse portfolio of agents with a focus on conditions of high unmet need. That is, in conditions which are neurodegenerative in nature, neuroinflammatory, and neuromuscular, areas of high unmet need where the technology and the science are really starting and really just at the cusp, I think, of seeing really great innovation and products there. Of course, we're excited about our pending acquisition of Karuna and what KarXT does in terms of accelerating our entry into neuropsychiatry. And then finally, in immunology, of course, we've been long in immunology with Orencia. We continue to have a focus and development in the rheumatologic space, of course, with the ongoing development of Sotyktu. We also continue on with programs in the GI space. We're very excited about pulmonary. And so with our LPA-1 antagonist, which is now in phase III for IPF and PPF. Those are some of the areas of focus, Steve. OK, great. I should have mentioned at the outset, should you have questions anywhere along the line, please ask, and we'll get your questions answered. So lots to dig into here. So much going on. Let's start out with milvexian. So the last time I think we got a full update was perhaps at your analyst meeting back in September. Give us an update on the three major studies: stroke, ACS, and AFib. Where do they stand? How is enrollment going? And when should we look for data? Yeah. So thanks for that question. As I mentioned already, we're very excited about milvexian. Milvexian is a new approach in the antithrombotic space. And it really is trying to address an unmet need that continues to persist. In spite of the advances represented by Factor Xa inhibition, there still remains unmet need, particularly with respect to bleeding, the inability to use Factor Xas in certain clinical conditions, and to combine with certain agents. That is what we are trying to achieve with milvexian. That is to bring forward a molecule with efficacy that is at least as good and hopefully better than Eliquis, but with a better bleeding profile. We continue to be very confident based on, again, the number of lines of evidence that support Factor XIa as a target, genetic, epidemiologic, preclinical, but I think most importantly, our phase II clinical data, which was a comprehensive program in two very different treatment constructs that gave us the confidence as we move forward into phase III. I think, Steve, you asked about phase III and where we are. We are well underway in phase III. We're very pleased by the way in which our programs have been received by the investigator community, of course, our academic leadership. We are progressing well. We have received fast-track designation in all three of these indications that we're pursuing. We're looking forward to bringing data in-house around the 2026 time frame for ACS and SSP, and in 2027 for AF. Of course, we're looking to do everything we can to accelerate that with our partners at Johnson & Johnson. Maybe you can talk about this unmet need. Eliquis is a very good drug, huge success. So where are all these patients that will be helped by milvexian that aren't by Eliquis? What do those patients look like? Yeah. So thanks for that question. It's an important question because, again, it goes right to the heart of where the unmet need is. It's been estimated that upwards of 40% of patients don't receive a Factor Xa or are underdosed with a Factor Xa when indicated for that. The types of patients that one might associate with this could be those who are elderly, those who have certain comorbidities, such as, say, renal disease, and other factors, as well as intangible factors that lead to this situation, where patients are unable to receive a Factor Xa inhibitor. I would add one other thing, Steve, to your question is that it is a challenge to combine Factor Xa inhibitors with certain regimens that are already in place for very important indications. So the challenge of combining Factor Xa inhibitors with, say, dual antiplatelet therapy has been a challenge. It's not a challenge on the efficacy side, we think, based on data that came out in the ACS space, but really a challenge with respect to safety. And that's really impeded the ability to use Factor Xa inhibitors in conditions such as acute coronary syndrome or secondary stroke prevention. So those are the kinds of populations and the kinds of patients that we're really trying to study with milvexian to see if we can make a difference for those patient populations. Questions from the audience? So one of your competitors in an AFib trial had an issue. Our independent KOLs believe that Bristol's trial design was just more thoughtful and better plans. So maybe that could be one reason why the competitor had an issue, and Bristol has not. But does Bristol believe it's out of the woods with respect to the AFib trial and having a similar issue? Are we far enough along? Have we seen enough patients to be reasonably confident we're not going to have a similar issue? Yeah. So thanks for the question. I might touch first on the first part of your question and what you mentioned. It's part of why BMS continues to have confidence LIBREXIA AF. And it is founded on the data that we accrued in phase II, specifically, and most particularly in our TKR study, where milvexian was studied as monotherapy in patients undergoing total knee replacement. We had the chance, and this was also across our other study, to evaluate milvexian across a very broad dose range. This was a 16-fold dose range across both studies. And in both studies, we saw proof of concept, and efficacy, and safety. In TKR, and this was the model, the phase II model that was used actually to help develop Eliquis moving forward into the Aristotle program, is that in that study, we were able to show a dose response for efficacy as well as no major bleeding. And so that allowed us to really select a dose that we thought would be able to compete with Eliquis in LIBREXIA AF. Specifically, with 100 milligrams BID in our phase II study, we were able to show superiority versus enoxaparin, which is the standard of care. And we showed superiority to an extent, of course, with the caveats in cross-trial comparisons that we think will give us the opportunity to compete on an efficacy front and/or perhaps even be better than Eliquis. We'll have to wait for that data. But also, I think with that, we were able in our phase II program, by studying in two populations, to tailor the dose in our phase III program. So if you think about the dosing strategy that we took for LIBREXIA AF, it's a dose 4x that we're using in ACS and SSP. And that is important because I think we know that we're going to have to take a higher dose in the AF program because we had an active comparator and a really good product in Eliquis to go up against. In terms of your question about how we think about readout, we're not going to get into specifics on interim analyses. We do have a DSMB that is monitoring all three studies and all programs. There are regular intervals at which the DSMB, I would say, actually evaluates these data. Of course, as more time passes, we continue to gain reassurance with the program. But we continue to read forward. We are well underway with the programs. Things are going well with recruitment. Great. Can I ask if the competitor's trial hit futility relatively early? Presumably, that would give one pause about the idea that a higher dose would ameliorate any issues on the efficacy front. Do you consider that a fair statement? And with your interim analyses, are you beyond where they were at their futility analysis? So, actually, there isn't a lot of detail as to exactly why the study OCEANIC-AF was terminated. We have word from the press release, actually, that it was terminated based on the DSMB recommendation. We don't know the details. We don't have a sense of the details. I think, though, when you think about our program, if you can go back to our phase II study, we've selected doses based on efficacy against standard comparators, as well as our knowledge of Eliquis and our modeling data that we think can give efficacy that is on a par with Eliquis in LIBREXIA AF. So it's hard to comment exactly the reasons or how far along they are. We would just be speculating at this point in time. But we continue to gain confidence as we move forward in the milvexian program. So let's move on to other assets within the Bristol portfolio. Maybe we'll move to CAMZYOS. So we're awaiting the HFpEF data, phase II-A readout later this year. What's your level of confidence? Or what should investor confidence be in this readout being positive? Yeah. So we're very excited about cardiac myosin inhibition broadly with respect to heart failure with preserved ejection fraction and with CAMZYOS in particular. And I'll also touch on MYK-224, our next generation CMI in HFpEF. With CAMZYOS, our confidence is borne really, if you think about our phase II study, the MAVERICK study in nHCM, where we saw really strong decreases in NT-proBNP and troponin, as well as other markers and indices in a condition that shares a lot of similarity with heart failure with preserved ejection fraction. So that was the genesis of the EMBARC study. We are looking forward to data coming out this year in-house that we'll have to evaluate with the EMBARC study. And so we're very excited about that. We're also excited about the fact that we've initiated a phase II study in heart failure with preserved ejection fraction with our follow-on cardiac myosin inhibitor, MYK-224. This is a molecule that we're very excited about. We've been studying it in patients with obstructive HCM, a condition that we know a lot about and helps us to accelerate our own understanding of MYK-224 as we move forward. We're excited that that study has kicked off. We are looking forward to data coming out of our phase II program with MYK-224 in 2025. I think this highlights as well the flexibility, Steve, that we have in having more than one cardiac myosin inhibitor. By having a portfolio, if you will, of CMIs, we can tailor how we develop our programs accordingly. So we're excited about data readouts in both. So if EMBARC hits its phase II- A endpoint later this year, do you move to phase III? And what does phase III look like? So I think we're going to have to wait and look to see what the data are in EMBARC. I'll say that we are really, though, focused in HFpEF with MYK-224, our follow-on compound. And so I think we'll also be able to take a look at the data from EMBARC when it's available and also use that to apply learnings as we think about our cardiac myosin inhibitor portfolio overall. OK. Another asset you have in development is danicamtiv. And we're awaiting data here too, also phase II data. What's your level of confidence in that? Maybe you could also say a word about primary dilated cardiomyopathy and what the level of unmet need is, and so forth. Yeah. So I think with danicamtiv, that's our cardiac myosin activator. It is currently in study in patients with genetic dilated cardiomyopathies, a a condition of high unmet need. Look, at this stage, we're looking at various options on how we could develop danicamtiv and how we'll actually move forward with that asset, especially when we have data in-house and the complete data picture. But I think we've been focused, I will say, on our cardiac myosin inhibitor portfolio right now. That said, we'll continue to look forward as to how we might move forward with various options with danicamtiv. Questions from the audience? Sticking with cardiology, Bristol had a relaxin program for years and years and years. We don't see it in the pipeline any longer. Other companies are starting to work in the area. What's going on at Bristol with relaxin? Or is it a target that you're not focused on at this point? Yeah. So we did discontinue our relaxin program a few years back. It was because it didn't meet the high bar that we set for development products in general, as we think about how we prioritize in our development space. That said, relaxin is an interesting target. And along with all other targets in cardiovascular, one that we monitor, we'll continue to look at as we move forward. But we discontinued our program a few years back. OK. Let's move to KarXT. So what should investor expectations be for the phase III readout in adjunctive schizophrenia that we'll get next year? Yeah. So with the adjunctive readout, first of all, I think if you step back with KarXT, there's a high degree of excitement founded on the EMERGENT data that is EMERGENT-1, EMERGENT-2, EMERGENT-3, and then the data that's forthcoming in the long term. I mean, this is an innovative approach to schizophrenia, an area where there really hasn't been innovation in decades, literally. And I think with that and that data with an efficacy and safety profile that differentiate from standard of care, there's a lot of excitement here. I think when you think about adjunctive schizophrenia, the realization is that a number of patients who receive atypical antipsychotics, as much of an advance as that was, patients don't necessarily respond. There is a fraction of patients that don't respond and certainly a fraction that respond incompletely. I think that is compounded by the fact that there are tolerability challenges with atypical antipsychotics. With KarXT having a complementary mechanism of action that is M1/M4 agonism, that is, we believe, complementary to the atypical mechanisms, that there's an opportunity to show benefit in an adjunctive indication. I think the target is data around 25 in-house for the ARISE program. Again, an exciting program if you think about the data that have come forward thus far. You touched on this a moment ago. But compliance is an issue with schizophrenia drugs. Is there any reason to think KarXT will be better or worse in that regard? The compliance, we'd be very excited about the potential for KarXT to be different based on its profile. If you step back with the atypical antipsychotics with compliance, there are challenges with, if you think about metabolic impact and adverse effects, weight gain, and other issues with the atypicals, as well as factors that relate to, say, movement disorders and other side effects. Because KarXT works through a different path, a different mechanism, again, through M1/M4 agonism, the data that have come forth have shown a good tolerability profile that is different than from the atypical antipsychotics. I think that's part of the hope that that tolerability profile will drive a different compliance picture than we've seen with the atypical antipsychotics historically. Another indication you're pursuing for KarXT is Alzheimer's disease psychosis, about a year behind but also in phase III. What's your level of confidence here? Or maybe you could talk about that opportunity. Yeah. Another exciting opportunity is I mentioned BMS's interest in neuropsychiatry and, again, broadly, as we reenter into the neuroscience space. With KarXT, there's enthusiasm about its potential in AD psychosis because of the data that have come forward and because of the mechanism. So again, when you think about M1/ M4 agonism, these are places where we think that, of course, Karuna has thought that you could drive benefit. And this is borne out in part from data, proof of concept data that were generated from xanomeline. And so this was xanomeline alone prior to the construct that is KarXT with trospium. But xanomeline alone had been shown in patients with probable Alzheimer's disease to actually have benefits in Alzheimer's disease psychosis as well as agitation. When you look at a number of measures in that proof of concept study, that has driven some of the promise and the belief in this approach for that particular indication. I think, again, with data, we hope in 2026 with the ADEPT program, again, a very exciting program with KarXT and Alzheimer's disease psychosis. Across these indications, you may have competition from M4 selective compounds in the future. How important is the M1 pathway for all the various symptoms? Yeah. Thanks for the question. We think that the M1 pathway is important as well as the ability to have direct agonism at M1/ M4. I think if you think about the M1 pathway, that we think could be potentially important as you think about some of the cognitive benefits that might be associated with, say, M1/ M4 agonism, something that you would miss with, say, an M4 alone or an M4 PAM, for example. I think, of course, the data will bear out. But if you also think about the positive allosteric modulators, they rely on a sort of native level of acetylcholine for effect. Again, it differs from the way KarXT works with direct agonism at the level of the receptors. But when you think about it, that's part of the reason why we have belief in the KarXT approach. Of course, again, these will be studies that will run out over the coming years. Questions from the audience? You mentioned Alzheimer's disease. Bristol has a long-held focus in this area. Now you're working on an anti-Tau antibody. What should we know about that? Yeah. We're really excited about our anti-MTBR-Tau antibody. I don't need to spend time talking about the unmet need associated with Alzheimer's. I think that there is, as I mentioned or alluded to, some hope with recent approvals in that area. With our Tau program, we believe that we have a differentiated approach to how we're approaching Tau. I think a few things I would point out, Steve, is, I think, first, with Tau in general, Tau is a protein which seems to correlate better than, say, amyloid beta with respect to cognitive impairment. I think that's important as you think about attacking the sequelae of Alzheimer's disease specifically. But I think, secondly, with our approach, that is an antibody that attacks the MTBR region of Tau, there's a lot of data and data that continues to emerge that shows that the MTBR-Tau is actually very well correlated, perhaps best correlated with Tau accumulation through, say, Tau PET scanning, as well as cognitive impairment. So the approach of trying to attack Tau is one that differs from some of the other Tau approaches that have come before. And so we're very excited about this Tau program. I think that the preclinical as well as our clinical data thus far with our MTBR-Tau also give us belief in this target. And so we're looking forward to, in the near future, enrolling patients in our phase II study here. Great. We're down to about a minute left. You did mention at the outset immunology. Well, immunology is one of your areas of responsibility. But the pulmonary aspect of it. So maybe you could just update us on your program there. Yeah. We're very excited about our LPA-1 antagonist. We are well underway in both phase III studies in IPF and in PPF. Again, our belief born out of our phase II data, where we showed proof of concept and efficacy with over a 60% reduction in the progression of pulmonary decline by FVC with a good tolerability profile without GI tolerability issues and without hepatic issues. And so we're excited about this target. We had been excited about LPA-1 antagonism because this is actually a second-generation engineered molecule. But the first-generation molecule had also shown efficacy. That gives us confidence moving forward in the phase III. And so we're looking forward for data in-house in 2026 and 2028 in IPF and PPF, respectively. Great. With that, we are actually out of time. Is there one last question from the audience? OK. If not, Roland, thank you so much for a great rundown. Thank you.