All right, welcome to the afternoon sessions of Citi's Virtual Oncology Leadership Summit. My name is Geoff Meacham. I'm the Senior Biopharma Analyst here at Citi, and I have Jarwei Fang from my team with me as well. We're thrilled today to have Jean-Charles Soria from Amgen, who is the Senior VP, Global Development in Oncology. We did this session last year. A lot of really good meat on the bone, also Casey Capparelli from the IR team. So guys, welcome. Thanks for joining us. Thank you so much for the invitation. I am happy, yeah. Yeah. So I guess, Jean-Charles, we'll just kick it off with, you know, kind of the high-level questions on Amgen's kind of oncology approach. Maybe just talk through kind of the, you know, as you see them, the top priorities within oncology for Amgen on the R&D side. Maybe what are the bigger opportunities? Are you guys good with the technologies you have in place, and now it's just a matter of moving the products through clinical development at a high level? Just want to get some perspectives from you. Yeah, thank you for that question, Geoffrey. Well, you know, we have a framework that allows us to see how oncology, our investments, will be delivering. We believe that we are committing to bringing differentiated and transformative therapies. We don't want marginal benefit. That's one of the big rules. The other rule is that we want to see, to play both in hard-to-treat solid tumors, as well as selected hematological malignancies. The third one is that we have at least two clear pillars in our modalities, one being the T- cell engagers, and the other one being the precision therapies with our small molecules. I would say on the T-cell engager front, we have invested for decades, and we are the only company with the T-cell engager approved both in hematological malignancy and solid tumor, and there is more to come there. The frontier of bringing T-cell engagers in frequent solid tumors is a very important one for us. On the small molecule front, we, our strong chemistry teams have been able, you know, to get to very tough targets such as KRAS or PERI and PRMT5. That being said, we are also looking at diversifying our modalities, among which, we believe ADCs can play a role. But, you know, we're very selective in when, where do we choose to play, because it needs to be leveraging our own strengths. We are a biologics company with good chemistry understanding that makes, for instance, the choosing other modalities not the ideal fit for us. So that's the global framework. Yeah. Yeah, and it's interesting, Amgen's one of the companies that can really add value along the entire way of the value chain. I think it's going back to, the deCODE data, right on the discovery side, straight through to technology using BiTE and other platforms. I think that's somewhat unique. I mean, there's not necessarily a need to do a deal to bring in new technologies, nothing that you guys don't already have in-house in a dramatic way, right? Yeah, thank you for that comment, Geoffrey. I think resilience is an underrated virtue in pharma. Like, we have stuck with T-cell engagers for a very, very long time, and, you know, it's a little bit the north face of the Annapurna to bring them to solid tumors without HLA restriction and in frequent ones. We are very glad for the patients that are on IMDELLTRA. It's bringing transformative benefits in small cell lung cancer, and we are very hopeful to see xaluritamig potentially doing that in prostate cancer, a tumor type where immunotherapy is basically totally inactive. But we monitor the external environment, and we are convinced we don't have the monopoly of the best science, but we will do selective investments where we see it's complementary to our priorities, to our own pipeline, and it's truly transformational. Yep. Well, you mentioned IMDELLTRA, so let's get into the market of product portfolio, and that's a good place to start. So, full approval, extensions, extensive-stage small cell lung cancer, but many other tumor types, you know, that it could go into. Maybe just help us with kind of the commercial backdrop here. How do you see, you know, kind of the next 12-18 months roll out on a geographic basis? And maybe help us with, or remind us of, the other datasets to come that could further expand the label for this exciting medicine. Yeah, Geoff, why don't I jump in on the, just the commercial aspects, and then Jean-Charles, I'll turn it to you to highlight, maybe just reflections that you've heard clinically from the approved indication, which is second-line or later small cell lung cancer, but also, you know, maybe a few words on the development program. So as I mentioned, Geoff, you know, approved in second-line or later small cell lung cancer, that's full approval, received last year in 2025. And in addition, NCCN guidelines have been updated, to reflect IMDELLTRA's benefit in that setting. And so we feel like we have a lot of momentum commercially, in reaching patients with IMDELLTRA. In fact, you know, over 1,600 sites in the U.S. now administer IMDELLTRA, and the majority of our doses are provided in the community setting. That was an open question, that we had, in our ability to really reach patients that are treated with small cell lung cancer in the community setting. And based upon what we've learned from BLINCYTO, we've really been able to do that in a fairly rapid fashion with IMDELLTRA. We have approval in Japan, pending approvals in other geographies based upon the phase III study that generated full approval in, in the U.S. I mean, we're excited about the potential to continue to reach patients, with this second-line or later setting in the currently approved indication. But there's a lot more going on with IMDELLTRA, even beyond, you know, the current approved settings. And Jean-Charles, maybe I'll turn it to you to talk a little bit more about that. Yeah. Thank you, Casey, for that context setting. We, with IMDELLTRA, you know, saw such a compelling activity on the basis of the phase I and II, that we launched multiple phase III trials. And we have, on top of the already disclosed positive second-line phase III trial, three other ongoing phase III trials. One, in the first-line metastatic setting, in the maintenance setting, that's trial 305, which is fully enrolled. We have another first-line metastatic trial, which is trial 312, that is enrolling, and that gives IMDELLTRA in combination with chemo and PD-L1 upfront. And then we have another phase III trial ongoing in limited stage small cell lung cancer. So we really want to bring the value of this modality to the whole spectrum of the disease. Just given the modality of this with it being a DLL3, Jean-Charles, maybe help us with kind of the any other tumor types that you think, you know, could be suited here. I know obviously, the most of the focus is on small cell lung cancer, but, you know, are there reasonable opportunities looking broadly across the lung or other tumor types? Yeah, certainly, Geoff, thank you for that. Beyond IMDELLTRA and other tumor types, we are also doing a lot of efforts to make this more convenient and friendly for the patients and the healthcare providers. We are testing BLINCYTO subcutaneously. That will alleviate a lot of the pressure on the beds. We are doing alternating testing, so not only q2 weeks, but also q3weeks, q4 weeks. Those trials are ongoing. We are prospectively testing whether the monitoring can be reduced to shorter time frames, like six to eight hours or even shorter. All of these will facilitate the uptake of this therapy in community-based hospitals and beyond. But your question more specifically is, are there other tumor types in which these DLL3 T-cell engager could potentially play? And the answer is yes. We have reported data on the activity of our T-cell engager in neuroendocrine prostate cancer. That's a different type of neuroendocrine tumor versus small cell lung cancer. That's a neuroendocrine differentiation under therapeutic pressure. It happens when you have people with prostate cancer that had multiple lines of therapies, and then you have a transformation towards a neuroendocrine form. The same way you can have EGFR mutant adenocarcinoma of the lung, that develops small cell lung cancer transformation under therapeutic pressure. Those are areas where potentially this asset could be developed. Right. Okay, that makes sense. And moving down the pipeline to, I would say, more recently marketed product, like LUMAKRAS, same thing there in terms of expanding the opportunity beyond lung into colon cancer. I know you guys have done some work on this over the past couple of years. Maybe give us a status update of where the phase IIIs are going. I know you are still enrolling first-line lung and colorectal, but are there any other, you know, kind of line extensions that make you more excited as you look at LUMAKRAS as a brand that's still growing and impactful to Amgen? Thank you for the question. I mean, LUMAKRAS is currently available in both second-line non-small cell lung cancer and third-line colorectal cancer, in combination with our own Vectibix. Longer-term, growth of LUMAKRAS will probably be driven by it's moving into earlier lines. So let's discuss lung and then colorectal. In non-small cell lung cancer, we have seen that the combination of LUMAKRAS with chemotherapy did lead to durable responses with a very good manageable safety profile. And this was notably in treatment-naive patients with KRAS G12C mutation. So this is why we launched the CodeBreaK 202 phase III trial that is testing the combination of chemotherapy with LUMAKRAS versus chemotherapy and pembrolizumab that in KRAS G12C patients who are PD-L1 negative. For the colorectal tumor types, the triplet combination of LUMAKRAS, Vectibix, and FOLFIRI show very compelling objective response rate of around 55%, with the disease control rate north of 90%. The responses were observed regardless of the number of prior lines of therapy, including progression or irinotecan, and this is why we launch a first-line colorectal cancer that is currently enrolling and hopefully will bring this therapy into that earlier mindset. Okay, that's, that's helpful. Well, I think Jarwei from the team had a couple, we wanted to, to stick with market of products with BLINCYTO, but then obviously, that has a pretty deep pipeline behind it. Jarwei, go ahead. Yeah, definitely. You know, so on BLINCYTO, you have a number of phase III studies that are currently enrolling, you know, one of which is, I believe it's the Golden Gate study for older patients with leukemia. I guess, just thinking about the opportunity and also just the bar for efficacy that you need to see there, you know, how do you think that represents another leg of growth for BLINCYTO going forward? Thank you for that question, Jarwei. I I would say what we have come to realize with BLINCYTO is that as we move this asset to earlier lines of therapy, we see higher efficacy, better tolerability, and that's an important trend. And in fact, it's a blueprint that we are using for the development of IMDELLTRA. Referring specifically to the Golden Gate phase III study, this is a study in older adult patients, mostly 55 years and above, with newly diagnosed B-ALL. That is an indication where we have, you know, chemotherapy-sparing regimens that are very important for those patients who have less tolerability. So that will bring a new perspective for BLINCYTO. We're also advancing subcutaneous blinatumomab, which has the potential to improve convenience, tolerability, and efficacy, and we believe this is gonna be very important also for this asset. We have had the phase I-B data suggesting better efficacy as CIV, and we have other trials that are gonna be exploring this in a more registrational manner. And so for the subcutaneous formulation of BLINCYTO, do you expect certain indications or certain age groups to see faster uptake? Or could you see a scenario where subcutaneous formulation kind of supplants the current route of administration fully? Well, we will be driven by the data, correct? And what the data tells us in a very limited phase I-B setting was that this potentially will bring more convenience and even higher activity. But you imagine the effort and number of trials it took for BLINCYTO to be validated in later lines, relapsed, refractory earlier. Now, the first-line setting, you will need to do that movement for subcu at the same time. So, let's see how the initial readouts pan out, but yes, that could be potentially a framework. Casey, anything to add on that? No, I think you covered it. I would just quickly mention, Jarwei, I know we're focused on oncology, but we're also exploring blinatumomab in the, in the space of autoimmune disease, where, where B-cell depletion has been shown to be important in a variety of autoimmune settings. We have a couple of phase II studies underway exploring blinatumomab, both in, in the SLE, with and without nephritis setting, as well as in refractory rheumatoid arthritis. And, and so, you know, potential to even move beyond oncology with, with a B-cell depleter like BLINCYTO. Thanks. I would add to that, Jarwei, that it makes complete sense mechanistically, correct? Because, CD19 is a B-cell antigen, and B-cells produce antibodies, and if you suffer of an autoimmune disease because you have autoantibodies, depleting the B-cells that produce those autoantibodies is rationally very logical, and thus the path that Casey has highlighted for our own BLINCYTO in that setting. Gotcha. Makes sense. Maybe just one more, shifting back to IMDELLTRA real quick, since we had talked about BLINCYTO and the subcu formulation. You know, ease of access for patients and also reducing bed burden is definitely top of mind for community centers. Could we see later on, as IMDELLTRA becomes more mature in its product cycle, that subcu might one day be explored as well? Or do you have to see BLINCYTO data first as the gating factor for the BiTE program? For BiTE platform, rather. Yeah. Thank you. Well, in fact, we are exploring IMDELLTRA in a phase I-B trial that is ongoing because we are completely cognizant of the barriers of, you know, patients being treated in community-based hospital need to overcome and, you know, not competing for the beds, being able to provide subcu, being able to do q4 dosing versus q2 dosing, or being able to have less of a follow-up after administration, are some of the levers we're very actively trying to pull through with prospective data and therefore making IMDELLTRA more available. Makes sense. I think, Geoff, I think you have a few questions on prostate. Maybe we can move to that. Yeah. Yeah, Yeah, yeah. Yeah, let's switch gears, Jean-Charles, to xaluritamig, which is a super exciting, you know, product in prostate and in Ewing sarcoma. But there's a lot of investments you guys have made in prostate. Maybe just at a high level, you know, talk through how you think the differentiation could play out. This is obviously a pretty crowded market, but so far, you've had some pretty compelling, you know, kind of mid-stage data. Maybe what makes you exciting as you prepare to turn the card over on larger scale phase III's and then move to market? Yeah, thank you for that question. You know, what is really exciting for us with xaluritamig in prostate cancer is that it leverages a mechanism of action that has currently no approval. There are no PD-1s, PD-1 or CTLA-4s approved in prostate cancer. Patients with that disease are very well aware of that and really would like to see an immune-related asset that could bring sustained responses, and that's number one. And the second one is that we have seen very clear signs of efficacy, both in PSA90, PSA50, but more importantly, in objective response rate, for this asset. And therefore, we are gonna do many things, we are doing many things in our phase III trials to differentiate ourselves in a very competitive landscape, as you rightly highlighted. First, we want to lead with the gold standard of survival evidence, especially versus highly active chemotherapy comparators. We are designing our pivotal programs to generate overall survival in both the post-taxane and the pre-taxane setting. That's a bold bar in prostate cancer, but we are confident, and we really want to make sure that we are having the right comparators with the right endpoint. The second element is for us to speak to market. We have prioritized monotherapy development in the post-taxane setting because that's an area with very high unmet medical need, and we want to reach the patients very, very quickly. The third element, I would say, is we want to be differentiated in terms of practicability, meaning we don't need a biomarker gate, and our breadth of addressable patients is extremely broad. In the prostate cancer space, we don't need enrichment through PSMA or through PET or through a mutation or anything else. That's another element. And finally, the chemo-free regimen for the pre-taxane setting is another pillar of differentiation. We are positioning ourselves as a potential non-chemotherapy option with survival advantage versus chemotherapy. That's bold twice because you're putting OS as an endpoint and because you want to show that you can beat chemo without being combined with chemo. So those elements are very, very clear, and we believe in these combinations in that setting. Finally, we want to remove a lot of the friction that comes from implementing a new modality with a new mechanism of action and new tolerability challenges for the clinicians. As we are enrolling in our phase III trials, we are working very much hand in hand with investigators to clarify the type of adverse events and how do we learn and modulate them, and what is the, you know, optimal management of this therapy. Prostate cancer is a world where you have multiple players, whether it is urologists, nuclear medicine doctors, or medical oncologists. Those will be the key differentiator drivers. Yeah. Yeah, I wanted to ask you on a couple of the comments as a follow-on to your response. When you think about, you know, prostate overall, it's a lot of different markets, and so I was wondering if, you know, there is a way to maybe take advantage of some of the differentiation. You know, would there be a regulatory incentive, for example, to, you know, to maybe pursue accelerated approval for, you know, post-taxane, just given the unmet need or, you know, chemo or hormone-free, doing a head-to-head? And would, could you take advantage of faster regulatory pathways through that? I'm just trying to think of ways to maximize the novelty from a clinical development perspective with regard to the mechanism. Thank you for that. We haven't shared any details of any of our statistical analysis, so I'm not gonna reveal anything here, but I would reply to your question by saying that we are so convinced of the importance of this therapy that we are bringing it, and it's completely under the regarded by many investors, to earlier lines. We have three ongoing phase I-B's, one in the neoadjuvant setting, so before surgery. We have one in biochemical recurrence, and we have one in hormone-sensitive prostate cancer. So we already changed the narrative. We are not waiting for our phase III's to read out positive in castration-resistant prostate cancer, post hormonal therapy, post-taxane. We are already testing it in the phase I-A setting in the earlier sites of prostate cancer, so we hope that will generate data that will help us then move to that setting in registrational trials. And Geoff, I wanted just to build on what Jean-Charles is saying. You know, one of the things that provides us confidence to do, as Jean-Charles described, is what we've observed with both BLINCYTO as well as IMDELLTRA, and that is when you move a T-cell engager earlier in the treatment paradigm into settings of lower tumor burden, you really see impressive inflections in survival. We saw that with BLINCYTO. We're seeing evidence of that with IMDELLTRA, and that furthers our hypothesis and the rationale to, you know, pursue xaluritamig in the early stages of prostate cancer as well. We'll have to see what the data teach us, but, you know, that underpins some of the thinking that Jean-Charles just described. Okay, that's helpful. Thanks, Casey. Makes sense. And maybe, just sticking on xaluritamig for a little bit longer, you know, we often get questions on prostate cancer, but Ewing sarcoma is, is certainly one that, you know, isn't really brought up very often. And, you know, given you have phase I-B study and a pretty broad population going on in relapsed and refractory, you know, maybe tell us a little bit more about xaluritamig's opportunity there and why, you know, STEAP1 would be a good target for that type of indication. Jean-Charles, I think you're on mute. I am on mute. Thank you for letting me know. So in drug development, we always navigate this tension of what can we do for rare indications? But when you have an asset like xaluritamig, where the development plan in a common indication is there and is clear and is compelling, going to Ewing sarcoma is something that was justified by the biology of the disease, the extremely high levels of expression of the target, and the true unmet need. Because if you fail the frontline therapy in Ewing sarcoma, and this is both for young adults and pediatric cases, it's not a good prognosis. So we are very excited to bring this innovation in that setting. And the trial is open, and we are eager to see what it will bring, but, you know, the biology makes sense, the unmet need is there, and it. It's a rare disease, but we can justify doing it because we have already made early investment in the common tumor type. Jean-Charles, let's switch gears to maybe the earlier to mid-stage pipeline. So AMG 193 in development for MTAP- null solid tumors. Talk a little bit about, you know, kind of what insights that Amgen has gained here, given this, the mechanism. I think it does showcase kind of Amgen's more discovery, you know, kind of angle here to bring a unique asset like this. But talk about, you know, the next. What What tumor types do you think could this work for the best? Based on the data that you have today, I know you have phase Is in lung, but maybe lead us down the path of where the science could go in terms of other tumor types. Yeah. Thank you. Thank you for that. We presented our data at ESMO in a presidential session and show activity across multiple tumor types, but we have focused the development more on lung and gastrointestinal solid tumors. In lung cancer, we have phase I-B combining AMG 193 with different standards of care to see the combinability, that's an important one. In lung, we also are doing the randomized dose optimization to define what will be the recommended dose for registration on trials, and that one is ongoing. And it makes sense because it's a very big tumor type, where the prevalence is significant. I mean, not significant, but at least good enough that you have enough patients. We are also combining AMG 193 with other standards of care in the setting of gastrointestinal tumors. I would just refer also to a trial in which we are combining AMG 193 with the Revolution Medicines RAS inhibitor in pancreatic cancer. This is to tell you, we are following the science and the biology and combining with what makes sense as the standards of care in different tumor types or standards of care to be common in the case of Rev Med. Yeah. Jean-Charles, are there lessons to be learned in the case of the mechanism here from resistance? In other words, can you find, you know, other dual mechanisms as you try to think about a combination sphere that could help, you know, mitigate the risk of that and maybe maximize the anti-tumor activity? Yeah. That's a very good question. In fact, the biology of PRMT5 inhibition in the setting of, you know, MTAP deletion is a new one, it's a new frontier. We had the first-generation inhibitors that were not really active, that had a lot of high toxicity, but second-generation inhibitors that are MTA-cooperative are a new reality. And what we are discovering is that the biology of how the tumor responds to that therapeutic pressure is pretty unique. We have not only objective response rates, but we have stable disease that become, with time, objective responses. That's not common in oncology to have that transformation. So it's an area where further investment in understanding the science is yet needed, and more to come as we unfold the results. Yeah. Yeah, and I guess just as a follow-on to that, when you look at the tools that Amgen has in place, you know, I mentioned the deCODE, but also the utilization of more AI-driven, you know, talk a little bit about how that, you know, how technology has played a bigger role in the maybe discovery, but also just trying to maximize the earlier phase I data that you get, that can maybe de-risk a drug or give you a window into maybe other tumor types. Yeah, that's, that's a very good question. You know, we completely recognize how important the pace of change through technology and AI and machine learning is changing the world, the world of biology, the world of drug development, but the world as a whole. You know, at Amgen, we are really leveraging these tools from target identification and molecule design, and generation of target antibodies to translational insights and better understanding our own clinical data. The tools will help us enhance our ability to analyze complex data sets. You need to understand the complexity of putting those data sets in Excel file is beyond human understanding when you have very rich omics and radiomics and clinical data points. That's an area where, you know, pattern recognition will be heavily expedited through AI. Our goal is not just speed, it's also precision in improving the quality of our hypotheses and how we prioritize things and how we execute. You can imagine, for instance, how important it is to have an AI protocol authoring tool that will help you get protocols that are sharper, with zero inconsistencies, where we'll integrate, you know, amendments in an easier manner. Those are obvious ways. We view AI as an amplifier of our human expertise. These technologies really augment what our science and our drug developers can generate in terms of creativity, in terms of experience, in terms of analysis. But we need to maintain extremely high standards. We are a regulated environment, so this needs to be done within defined guardrails. We are embedding AI and advanced analytics in most of our research engines, and we are already seeing a shortening of the timelines as well as enhanced decision-making, and I'm very optimistic of what this will bring. It's accelerating quarter by quarter. It's getting better and better. So maybe sticking on to the AI theme, you know, given this, the potential of your BiTE platform, you know, how are you leveraging AI and maybe looking at other targets that you could look at? Maybe, you know, your research into what other solid or liquid tumors that you maybe could target. Maybe give us a sense of, you know, the types of work you're doing to expand that platform and just make it even more fulsome than what we've already seen. Yeah, thank you for the question. Obviously, creating new white space for our T-cell engagers, but other modalities, too, is extremely important, correct? We suffer in our industry from sometimes all going against the same targets. We were, you know, quite unique with DLL3 as a T-cell engager. There are many other modalities now. So creating white space is very important, and it comes frequently through the very unique conversions of biology, technology, and compute power, and I will give you a very clear example. We announced a deal with a company called DISCO Pharmaceuticals because they were ahead of us on understanding the surfaceome. So the surfaceome is the reality of expression at the surface of a cancer cell of the different proteins, but people have a very simplistic view of how they are expressed. In fact, they create communities. They cluster together in certain ways. They have different densities. There are many new technological tools and, AI, tools that have helped tremendously accelerate the understanding of who is clustering with who and in which proportions. That all of a sudden gives you a wide space for new targets, that will be dependent on the co-expression of an existing target. You could choose to say, well, I want to know who's the best and closest partner of the other three in proximity in a surface, cancer cell" Well, we announced that deal with DISCO Pharmaceuticals because they found a very interesting, target in small cell lung cancer, and that's an example of bringing, in a very concrete way, what, you know, the advancement of biology, computing, and technology can do. Just as a follow-up to that, Jean-Charles, I know on bema, you guys aren't pursuing the gastric indication, but is FGF still an interesting target to you guys? Are there ways to go back to the drawing board using something like AI to maybe find some lessons learned here to try to redeploy into other tumor types? Just want to get your perspective on that. Yeah, sure. Casey, you want to start? Yeah, I'm happy to start. So for bemarituzumab, Geoff, as you mentioned, we've decided not to pursue regulatory submission in frontline gastric cancer. You know, we're currently determining, you know, what the best next steps are for that program and I think we'll have more to say beyond that. Jean-Charles, anything that you would add there? Yeah, you know, we follow the science, so we need to understand what happened in the phase III trial. So we are looking at elements from the biology that will explain some of the results, and we will share more down the line. But we follow the science in truly not only for developing our assets, but also for analyzing some of the outcomes. Okay, that's helpful. I guess in conjunction, you know, with use of AI and biomarkers, just help us with kind of how much emphasis does Amgen have on things like novel, you know, novel biomarkers, diagnostics, things of that nature? I wasn't sure, you know, if there is an approach to embed more kind of discovery or bells and whistles, if you will, in a phase one on, you know, more novel mechanism drugs, you know, like IMDELLTRA, like xaluritamig, that could help you down the road, right? More maximize treatment effect and minimize tolerability. It's a great question. Thank you. We, we have a precision medicine department that serves all the therapeutic areas that is trying to bring that value, the value of better predicting what's the best biomarker package of an asset that will enter phase I. Do we have molecular predictors of efficacy? But also the reverse translation of when you see an extreme responder or you see a emergence of resistance, what is driving that? So we, we really believe in the value of that, and we are investing. There are many frontiers, correct, in oncology, one of them being the availability of some of these markers in the blood versus the tissue. The tissue is the issue very frequently in oncology. Everyone wants the tissue, and people get very small biopsies. So that's a frontier where we have interest and we hope to advance radiomics and combining radiomics with our own omics from deCODE, and combining that with additional single-cell analysis or clinical data to create, if you want, a more comprehensive multidimensional dataset of clinical points is another one where we are investing. Yeah. And just the last question, just along those lines, Jean-Charles, and with regard to, say, cell and gene therapy, you know, that hasn't historically been a major focus from Amgen, but, is that a sort of modality or technology that I think over time Amgen could develop? Are you pretty comfortable with the, with the bispecific and T-cell engager and the ADC? You have a lot of tools right now in the, in the tool chest, so I guess that's the question: Do you add more or do you maximize kind of what you have? Thank you for that question. You know, our pillars on T-cell engagers and small molecules are not meant to be exclusive, so we will invest where it makes sense and leverage our strengths. I mean, ADCs is one area which could make sense because we are a very strong biologics company and have good chemistry. But on the cell therapy front, that's a completely different modality and quite competitive against our own T-cell engagers. Correct. We are happy to see our T-cell engagers bringing benefit for solid tumors patients. We have not seen cell therapy deliver that in solid tumor patients. So cell therapy comes with other complexities in terms of the production, the availability, the cost. So we are very pragmatic. We follow the data points, and that is the answer I will give it to you. We will follow the science but be very selective. Amgen is very disciplined in what it does, so we are not spreading and betting bets everywhere. We are selectively making certain bets. Makes sense. Okay. With that, we're out of time, so, so Jean-Charles, thank you so much, Casey as well. Yeah, appreciate the input, guys. Super helpful conversation. Yep. Thank you for inviting us. Yeah, thank you for having us today. Good to see both of you. You too.