Amgen Inc. (AMGN) Earnings Call Transcript & Summary

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 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. We also have Casey Capparelli from the IR team. So guys, welcome. Thanks for joining us.

Thank you so much for the invitation

Yes. So I guess, Jean-Charles, we'll just kick it off with kind of the high-level questions on Amgen's kind of oncology approach. Maybe just talk through kind of as you see then 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 wanted to get some perspective from you.

Yes. Thank you for that question, Geoffrey. Well, we have a framework that allow us to see how oncology or investments we'll 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. So there's one rule that we want to steal, 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 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 are strong chemistry -- teams have been able to get to very tough targets such as KRAS or PRMT5. That being said, we are also looking at diversifying our modalities, among which we believe ADCs as can play a role. But we're very selective in where do we choose to play because it needs to be leveraging our own strengths and we're a biologics company with good chemistry understanding that makes, for instance, choosing other modalities, not the ideal fit for us. So that's the global framework.

Yes. Yes. And it's interesting, Amgen is one of the companies that can really add value along the entire way of the value chain. I think 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 to do a deal to bring in new technologies, nothing that you guys don't already have, in-house, in a dramatic way, right?

Yes. Thank you for that comment, Geoffrey. I think resilience is an underrated virtue in pharma, like we have stick with T-cell engagers for a very, very long time. It's a little bit North Face or 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 is 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.

Yes. 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, extensive stage small cell lung cancer, but many other tumor types that it could go into. Maybe just help us with kind of the commercial backdrop here. How do you see kind of the next 12 to 18 months roll out on a geographic basis? And maybe help us with -- remind us of the other data sets to come that could further expand the label for this exciting medicine.

Yes, 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 maybe a few words on the development program. So as I mentioned, Geoff, 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, 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, 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 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 the current approved settings. And Jean-Charles, maybe I'll turn it to you to talk a little bit more about that.

Yes. Thank you, Casey, for that context setting. We fit IMDELLTRA, we saw such a compelling activity on the basis of the Phase I, 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 we -- that gives IMDELLTRA 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 being a DLL3. Jean-Charles, maybe help us with kind of the -- any other tumor types that you think could be suited here? I know obviously, the -- mostly the focus is on small cell lung cancer, but are there reasonable opportunities looking broadly across the lung or other tumor types?

Yes, certainly, Geoff. Thank you for that. Beyond I expand on other tumor types, we are also doing a lot of efforts to make this more convenient and friendly for the patients and health care providers. We are testing BLINCYTO subcutaneously that will alleviate a lot of the pressure on the beds. We are doing alternative testing, so not only Q2 weeks, but also Q3, Q4 weeks, those trials are ongoing, we are prospectively testing whether the monitoring can be reduced to shorter timeframes like 6 to 8 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 and that's a different type of neuroendocrine tumor versus small cell lung cancer. That's neuroendocrine differentiation on the therapeutic pressure. It happens when you have people with prostate cancer that had multiple lines of therapies and then you have a transformations to a standard endocrine form at the same way you can have EGFR mutant adenocarcinoma, the lung that develops small cell lung cancer transformation on the therapeutic pressure. Those are areas where potentially this asset could be developed.

Right. Okay. That makes sense. And then moving down the pipeline to, I would say, more recently marketed products 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 in colorectal, but are there any other 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. LUMAKRAS is currently available in both second-line non-small lung cancer and third-line colorectal cancer in combination with our on 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 led 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 triple combination of LUMAKRAS, Vectibix and FOLFIRI, show very compelling objective response rate of around 55% with the disease control rate north of the 90%. And the responses were observed, regardless of the number of prior lines of therapy including progression [indiscernible]. And this is why we launched a first-line colorectal cancer that is currently enrolling and hopefully, will bring this therapy into that earlier line setting.

Okay. That's helpful. I think Jarwei from the team had a couple, we wanted to stick with marketed products with BLINCYTO, but then obviously, that has a pretty deep pipeline behind it. Jarwei, go ahead.

Yes, definitely, on BLINCYTO, you have a number of Phase III studies that are currently enrolling. 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, how do you think that represents the -- another leg of growth for BLINCYTO going forward?

Thanks for that question, Jarwei. 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 in older adult patients, mostly 55 years and above with newly diagnostic B-ALL. And that is an indication where we have 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 who has the potential to improve convenience tolerability and efficacy. And we believe this is going to be very important also for this asset. We have had Phase Ib data suggesting better efficacy at CIV. And we have other trials that are going to be -- we 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 told us in a very limited Phase Ib setting was that this potentially will bring more convenience and even higher activity. But you imagine the efferent 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 space of autoimmune disease 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 the SLE with and without nephritis setting as well as in refractory rheumatoid arthritis. And so potential to even move beyond oncology with the B-cell depleter like BLINCYTO.

I would like to add, Jarwei, that it makes complete sense mechanistically, correct? Because CD19 is B-cell antigen and B-cells produce antibodies. And if you suffer an autoimmune disease because you have auto antibodies, depleting the B-cells that produce those autoantibodies is rationalisticy very logical those -- the pad that Casey has highlighted for our own BLINCYTO in that setting. .

Got you. Makes sense. And maybe just one more, shifting back to IMDELLTRA real quick since we talked about BLINCYTO and the subcu formulation. 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 a gating factor for the BiTE program, for BiTE platform rather?

Yes. Thank you. Well, in fact, we are exploring IMDELLTRA in a subcu Phase Ib trial that is ongoing because we are completely cognition of the barriers of patients being treated in community base hospital need to overcome and 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 are very actively trying to pull through with prospective data and therefore, making IMDELLTRA more available.

Makes sense. And I think, Geoff, I think you have a few questions on prostate. Maybe we can move to that.

Yes, yes. Let's switch gears, Jean-Charles to xaluritamig, which is a super exciting product in prostate and Ewing Sarcoma, but there's a lot of investments you guys have made in prostate. Maybe just at a high level, talk through how you think the differentiation could play out. That's obviously a pretty crowded market, but so far, you've had some pretty compelling kind of mid-stage data. Maybe what makes you exciting as you turn the card -- prepare to turn the card over on larger-scale Phase IIIs and then move to market. .

Yes. Thank you for that question. What is really exciting for us with xaluritamig in prostate cancer is that it levers a mechanism of action that has currently no approval. There are no PD-1s, PD-L1 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, that's number one. And the second one is that we have seen very clear signs of efficacy, both in PSA 19 and PSA 50 but more importantly, in objective response rate for this asset. And therefore, we are going to 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 prospect 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 both twice because you're putting OS as an endpoint 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 this combination, in that setting. Finally, we want to remove a lot of the friction that comes from implementing a new modality with a new mechanism exception and new tolerability challenges for the clinicians. So as we are enrolling on our Phase II trials, we are working very much hand in hand with investigators to clarify the type of adverse events and how do we learn and moderate them and what is the optimal management of this therapy. Prostate cancer is a world where you have multiple players, whether it is Urology, the Nuclear Medicine doctors or Medical Oncologies. Those would be the key differentiator drivers.

Yes. Yes. I wanted to ask you on a couple of the comments as a follow-on to your response. When you think about prostate overall, it's a lot of different markets. And so I was wondering if there is a way to maybe take advantage of some of the differentiation. Would there be a regulatory incentive, for example, to maybe pursue accelerated approval for post-taxane just given the unmet need or chemo or hormone-free doing a head-to-head. 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 going to 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 in and this is completely under -- regarded by many investors to earlier lines. We are -- we have 3 ongoing Phase Ibs, 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 now waiting for our Phase IIIs to read out positive in castration-resistant prostate cancer, post-hormonal therapy, post-taxane. We are already testing it in the Phase Ib sitting in the earlier sites of prostate cancer. So we hope that we'll generate data that will help us then move to that setting in a registrational trial.

I mean, Geoff, I want -- just to build on what Jean-Charles is saying. 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 the T-cell engager earlier in the treatment paradigm into settings of lower tumor burden you really see impressive inflections in survival. And we saw that with BLINCYTO, we're seeing evidence of that with IMDELLTRA and that furthers our hypothesis and the rationale to pursue xaluritamig in the early stages of prostate cancer as well. We'll have to see what the data teach us, but 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. We often get questions on prostate cancer, but Ewing sarcoma is certainly one that isn't really brought up very often. And given you have a Phase Ib study and a pretty broad population going on in relapsed/refractory. Maybe tell us a little bit more about xaluritamig's opportunity there and why 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 its clearing 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 the biology makes sense, the unmet need is there, and it's a rare disease, but we can justify doing it because we have already made an 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 mTAT solid tumors. Talk a little bit about kind of what insights at Amgen has gained here given this -- the mechanism. I think it does showcase kind of Amgen's more discovery kind of angle here to bring a unique asset like this. But talk about the next -- what tumor types do you think is -- 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 to the path of where the science could go in terms of other tumor types.

Yes. Thank you. Thank you for that. We presented our data at ESMO presidential session and show activity across multiple tumor types, that we have focused the development more on long and gastrointestinal solid tumors. In lung cancer, we have a Phase Ib 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 registrational 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 at least good enough that you have enough patients. And we are also combining AMG 193 with other standards of care in the setting of gastrointestinal tumors. And we -- I would just refer also to a trial in which we are combining AMG 193. We did the revolution medicine 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 tarlatamab.

Jean-Charles, are there lessons to be learned in the case of the mechanism here from resistance. In other words, can you find other dual mechanisms as you try to think about a combination sphere that could help mitigate the risk of that and maybe maximize the antigen activity.

That's a very good question. In fact, the biology of PRMT5 inhibition in the setting of the pent-up deletion is a new one, is a new frontier. We had the first generation inhibitors that were not really active, that had a lot of hemtoxicity, but squeezed inhibitors that are MTA-comparative are a new reality. And -- what we are discovering is that the biology of how the tumor response 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 our understanding of science is yet needed and more to come as we unfold the results.

Yes. Yes. And I guess just as a follow-on to that, when you look at the tools that Amgen has in place, I mentioned the deCODE. Also the utilization of more AI driven. Talk a little bit about how that -- how technology has played a bigger role in maybe discovery, but also just trying to maximize the earlier Phase I data that you get that can maybe derisk a drug or give you a window into maybe other tumor types?

Yes, that's a very good question. 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 word of drug development, the world as a whole. And at Amgen, we are literally leveraging these tools from targeting 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 X5 is beyond human understanding, when you have very rich omics and radiomics and clinical data points. That's an area where patent recognition will be expedited through AI. Our goal is not just speed, it's also precision in improving the quality of our hypothesis and how we prioritize things and how we execute. You can imagine, for instance, how important it is to have an AI protocol uttering tool that will help you get protocols that are sharper with zero consistencies where we'll integrate amendments in an easier manner. Those are obvious ways. With you AI has an amplifier of human expertise. These technologies really augment with 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, 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 onto the AI theme. Given the potential of your BiTE platform, how are you leveraging AI and maybe looking at other targets that you could look at, maybe your research into what other solid or liquid tumors that you maybe could target. Maybe give us a sense of the types of work you're doing to expand that platform and just make it even more fulsome than what we've already seen.

Yes. Thank you for the question. Obviously, creating new white space for 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 quite unique with DLL3 T-cell engager. There are many other modalities. So creative 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 white space for new targets that would be dependent on the coexpression of an existing target. You can choose to say, what I want to know, who's the best and closest partner of DLL3 in proximity in a surface cancer cell. Well, we announced a 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 the advancement of biology computing and technology can't.

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? Is there -- 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.

Yes, sure. Casey, you want to start?

Happy to start. So for bemarituzumab, Geoff, as you mentioned, we've decided not to pursue regulatory submission in frontline gastric cancer. We're currently determining 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 in terms of...

Yes. We follow the science. So we need to understand what happened in the Phase III trials. 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 train, not only for developing of assets, but also for analyzing some of the outcomes.

Okay. That's helpful. I guess in conjunction with use of AI and biomarkers. Just help us with kind of how much emphasis does Amgen have on things like novel biomarkers, diagnostics, things of that nature. I wasn't sure if there is an approach to embed more kind of discovery or bells and whistles, if you will, in a Phase I on more novel mechanism drugs 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 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 emergence of resistance, what is driving that? So 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 old omics from deCODE and combining that with additional single cell analysis or clinical data to create if you want a more comprehensive multidimensional data set of clinical points is another one where we are investing.

Yes. And just the last question, just along those lines Jean-Charles. With regard to, say, cell and gene therapy, are you -- that hasn't historically been a major focus from Amgen, but is that a sort of modality or technology that I think, overtime, Amgen could develop? Or are you pretty comfortable with the bispecific and T-cell engager and pDC. You have a lot of tools right now in the tool chest. So I guess that's the question. Do you add more? Or do you maximize kind of working out?

Thank you for that question. 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. I mean, it's around T-cel engagers, correct. We are happy to see our T-cell engagers bringing benefit for solid tumor patients. We have not seen cell therapy deliver that in solid tumor patients. So cell therapy 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 making beds everywhere. We are selectively making certain beds.

Makes sense. Okay. With that, we're out of time. So Jean-Charles, thank you so much, Casey, as well. I appreciate the input guys. Super helpful conversation.

Thank you for inviting us.

Yes. Thank you for having us today. Good to see both of you.

You too.