Amgen Inc. (AMGN) Earnings Call Transcript & Summary

Great. I think that's quarter past. Good morning, everyone. My name is Trung Huynh, I'm the large-cap pharma, biopharma analyst here at UBS. It's my great pleasure to welcome team Amgen. We've got Peter Griffith here, CFO of the company. We're also joined by Narimon Honarpour, hopefully, I've pronounced that correctly, Senior Vice President of Global Development; and Justin, who everyone here knows and loves from IR. So team, thank you very much for making that short trip over. I do have 1 point of admin. [Operator Instructions] But with that said, perhaps, Peter, why don't you start with some opening remarks and we can go from there.

Sure. And thank you very much. We are so glad to be here today. And innovation continues to move at speed and scale at Amgen. And I'll -- Narimon and I will address in a moment, the research note that was published yesterday. But before that, let's talk about Amgen broadly. Four therapeutic areas, all doing very, very well, maybe starting in that with our rare disease portfolio, up to $1.2 billion in revenue in the third quarter, up about 21% year-over-year, led by 4 products in rare disease that are early in their life cycle doing really well. TEPEZZA, KRYSTEXXA, TAVNEOS and UPLIZNA. And UPLIZNA is doing really well in the pipeline, too. I'm sure we'll visit today about UPLIZNA and IgG4-related disease and our data there and also our data that was -- we talked about, myasthenia gravis. So let's move over to the general medicine. In general medicine, Repatha, our LDL, bad cholesterol drug, if you will, up 40% in the quarter, doing really, really well. Also, TEZSPIRE -- excuse me, in general medicine, also doing well with Prolia and EVENITY in the bone franchise. EVENITY up to almost $400 million in the quarter, up about 30% year-over-year. The bone franchise continues to be just a great for patients, women, postmenopausal women with osteoporosis disease. So general medicine doing really, really well. And then going to inflammation and immunology. I almost jumped the gun there on TEZSPIRE, which is easy to do, medicine for severe asthma, up 67% in the quarter. And certainly, we're all looking forward to, as we announced the COPD Phase III work in -- that we announced in TEZSPIRE. Moving over to oncology, lots of great news there. The oncology innovative portfolio was up 17% year-over-year in the quarter. And so we're really, really pleased with that, led by BLINCYTO, acute lymphoblastic leukemia medicine that you may want to ask Narimon about and that was up 49% year-over-year in the quarter. So onc doing really, really well. And the pipeline in [indiscernible] xaluritamig, another bispecific T cell engager and a common solid tumor along the same modality as IMDELLTRA, which during the quarter generated $36 million as a bispecific T-cell engager against small cell lung cancer. So we're really excited about what's happening in oncology, both in the end market portfolio and in the pipeline. And back to general medicine, in the pipeline, we have olpasiran, which enrolled over 7,000 patients, as fast as any enrollment we've had in an outcomes trial for investigating Lp(a). And of course, we'll talk about MariTide and we look forward to that. Our conviction in the promise of MariTide to address significant global public health crisis hasn't been stronger. So we're excited about that. So that's the 4 therapeutic areas. We continue to be laser-focused on a Phase III development program for MariTide. So I'd like to just talk a little bit about investing in our business. Our first capital allocation being investing in the best innovation, internal and external, then we invest in our business. So we continue to prepare for a broad Phase III program in that and that includes our process development, the science and manufacturing that our team is so good at. We think we have one of the strongest engineering teams in the world working on construction around the world on our plants and also our manufacturing continues to operate at the highest levels. And then I would just suggest, from a volume-driven growth standpoint, Trung, volume was up 29% in the quarter, driving 23% revenue growth. As an example of that, 43 million units in 2024, we expect to deliver to 11 million patients for Prolia and Repatha. So the strength of what we do in terms of volume, we're prepared to keep that up and delivering to patients. And then finally and then I'll visit in a moment about Narimon and turn it over to him. Research and development. Research and development, Trung, in the quarter was up 35% year-over-year. So we're driving innovation and that's so important for us to allocate capital to it. We've now guided to over 25% growth in research and development year-over-year, 2024 over '23. So we continue to be focused as a company on innovation and driving it at speed and scale. So now let me flip over to this research note that was published yesterday. We weren't contacted ahead of time. A number of other analysts have pointed out the limitations in the research note. We're glad to have the opportunity today to correct this for investors and have invited our Senior Vice President of Global Development, as you introduced him, Dr. Narimon Honarpour to join us to give a few comments on that. So let me ask Narimon to give a few comments on that situation.

Thanks, Peter and thanks for having us, Trung. So first and foremost, it's important for me to share that we remain very confident in the promise of MariTide for patients with obesity, type 2 diabetes and obesity-related conditions. And we're looking forward to sharing with the broader audience, the upcoming Phase II study results later this year. As we previously stated, going all the way back to December 2022, we have not at Amgen seen an association between administration of MariTide and bone mineral density changes or safety signals for bone. Our Phase I data, I think, we're pretty conclusive in showing that and we had published on that. Importantly, there is nothing in the Phase I data that more broadly suggests a specific safety concern that's, of course, inclusive of bone health. And we had prosecuted this question further with our colleagues at deCODE Genetics, looking at a variety of GIP receptor variants that had reduced activity associated with them. And from that study of over 1 million different patients with variants, there was no signal identified that had an association with bone disease or bone mineral density reduction. So we feel pretty confident about that observation. Now getting to the Phase I study specifically, it's important to lay some initial principles about that trial. This was our first clinical experience with MariTide. It followed a range of single administrations and multiple administrations up to 3. And the intent of that Phase I study, that first-in-human study was to provide us with an initial assessment of MariTide attributes, pharmacology attributes, general safety and tolerability attributes, pharmacodynamic effects like weight reduction. It is a limited study in size. And when you look at certain parameters, particularly biomarker parameters that have intrinsic variability into them, drawing significant inferences or conclusions from limited data sizes with variable parameters are simply very difficult to infer. There is a large variability associated with them, those types of results. And this type of variability was something that was not mentioned or contextualized in that research report that Peter was mentioning earlier. So we, again, to underscore, have seen no difference, clinically significant difference, statistically significant difference on bone mineral density with any MariTide administration from that Phase I trial. We do believe that the research note had suggested an inappropriate inference of the data, given its limitations and it utilized unfinalized data tables and charts that we had inadvertently included in supplemental materials that the journal, Nature Metabolism, had requested us to provide. And as these data tables and charts were not subject to our standard institutional review nor were they subject to the peer review in the way that they ended up being in those materials inadvertently, we have asked Nature Metabolism to put a correction in and put that final data available into the supplemental materials and we'll keep track of that, obviously. So that's all I was really planning to say about that. We feel very comfortable and confident about MariTide and bone mineral density, we'll have more to say on the Phase II later this year.

Okay. Very clear. If you have a look at that data, it looked like 4 out of the 8 patients on the 420 mg completed the study. It looks like 1 patient in particular, drove the effect like perhaps a 10x bigger effect for 1 patient only. Is that right to say?

Well, I think we have to acknowledge the significant variability in that readout for 1 patient. When you have a measurement done, all of us have experienced this, when you go to your doctor's office, sometimes the numbers or the assessment that you get, it's not exactly the accurate assessment. We acknowledge this in the way that we design our clinical trials by increasing the sample size. We have to acknowledge that there is a randomness to errors that occur. And to offset that, we increase the end -- the sample size. With the Phase I study and with this particular Phase I study, the limitations of the data were pretty clear and there's not much that we can read into a single measurement for 1 patient. If one were to look at a statistically analyzed result on the chart that you are looking at, what you would observe are large margins of error that overlap across all of those doses and including placebo. And in fact, when we had done that assessment ourselves, that's what led us to the conclusion that we've not seen any association.

Understood. And it looked like you were seriously digging into GIP antagonism and how that would impact bone health. We also got some data from AMG 598 that's the GIP antagonism monotherapy. Can you perhaps talk about any of the data we saw there?

Well, maybe what I can allude to first and foremost is that we have disclosed results from that study. It's posted on clinicaltrials.gov. We will have more to say about 598 in due course. We haven't planned any additional studies with 598 at this time and we have completed our experience there. So that's all we have to say about 598 right now.

Okay. Excellent. Well, I think -- for me, the story from yesterday, it felt a bit -- a lot less about the data but really the share price reaction to it. I mean, ultimately, it was a Phase I trial that was uncovered, it was in a few patients. Just how comfortable are you with what appears to be a quite big disconnect between the fundamentals and the data, the actual MariTide event that's going to happen. We'll obviously discuss other things that are going on in your pipeline but the market seems super hyper focused on this MariTide readout. So just are you worried about the intrinsic value of your stock being just overshadowed by this 1 event?

Trung, The most important observation for all of us now is to wait for the data. It's coming by the end of the year. Let's get the data in. We're going to get it out. We look forward to presenting our analysts and our investors with the top line data from the Phase II, which Narimon, I believe, is 592 patients or so.

Yes. That's right.

Okay. And how do you think your expectations are on that data relative to what the market's expectations are for that data?

As we've said when we started today and as Narimon said too, we remain confident in the promise of MariTide for patients with obesity, obesity-related conditions and type 2 diabetes. And we're looking forward to sharing the data. And I think that's what we want to get to and we'll expect to share that by the end of the year.

Understood. And on that data disclosure, have you thought about what you're willing to present because there's 11 arms in this study. We saw what happened yesterday. If you present 1 data -- 1 arm that worked, perhaps, then everyone's going to question the rest of the arms. But then if you present all of the arms, you're going to have maybe an overinterpretation of the results. You're a in a bit of a kind of...

Look, I understand why that -- you ask that question and others might ask that question. I think the most important thing to remember is, we need to get the data. We need to allow our scientists. We need to allow Narimon. We need to allow Dr. Bradner and others to look through this and really interrogate it, make sure we know this as well as we always want to know the data because #1 is patients. And we're going to look through that with patients in mind. And we will present to investors and analysts that data and we look forward to doing that by the end of the year. And we continue, again, to have conviction in the promise of MariTide for the global public health crisis.

Understood. And on the timing of that data, perhaps, have you booked up a Christmas holiday, Narimon or Peter?

I've got -- I always -- I look forward to the holidays. I've got 4 children, 5 grandchildren. It's a great time but boy, is this is a great opportunity. And I am an Amgen because I want to enable Dr. Honarpour to discover and develop these diseases. And this is on my list right now, it's #1. So anything I can do to help him and the team enable the top line data and putting it together for investors and analysts before the end of the year, that's what I'm focused on.

Okay. Understood. And Narimon it's not the -- I don't often get the opportunity to talk to someone like you. So perhaps can you comment on the Phase II study and the 11 arms that are running? Just the rationale between the different dose titration, the different approaches for the Phase II, different dosing intervals, just some thoughts behind this?

Yes, I'd be happy to double-click on the principles by which we put the Phase II study together. It's important to acknowledge that we put forth a very rigorous Phase II study design. We want to understand the full attributes of MariTide across a variety of doses. We're talking about different dose doses in terms of the level. We're talking about different frequency of administration. We even added and amended a second part to the Phase II to see what else we could learn in terms of a maintenance paradigm. These are all important questions, we believe that have value to patients. They have value to the healthcare ecosystem. And we want to be in a position to inform our Phase III experience with the most robust dose-ranging experience we have in our Phase II. So when we speak about things like 592 patients, 11 arms, different dosing frequencies. It's not because we believe that all of that is going to end up in Phase III. We want to have a rich dataset to pick the best opportunity, what we believe will render the highest value for patients with obesity, obesity-related conditions into Phase III. It would be shameful if we didn't because we see so much opportunity with MariTide. So we really want to open it up and explore the variety of different circumstances with dosing for MariTide and that is why we ended up with, for example, 11 dosing arms and including patients with diabetes in this case, into 1 Phase II.

Understood. And is there anything you can say to make people a bit more comfortable with the idea of dose titration, minimizing the tolerability effects while keeping the efficacy.

Well, I will say -- what I can say is the Phase II data will speak for itself. So as Peter was referring, later in this year, we expect to have that information available. That was informed by our Phase I experience generally. So we believe that it was important to assess that and we'll see the data when it comes in by the end of the year. I'm looking -- actually, I'm looking forward to it.

Excellent. And then maybe final one on this topic. Is there anything related to AMG 513 you can talk about? Is it an integrin-based approach?

We can't speak much to 513. It is an obesity product we have put into Phase I. But we'll have more to say about that in due course.

Okay. Let's switch gears then. Let's talk about immunology. We've had some great data, UPLIZNA, you showed in MG. Perhaps can you, for people in the room, just give us a brief overview of what you took out from this study? And have you had any feedback from physicians on this data?

Yes, absolutely. I'd be happy to share it. So just to level set. UPLIZNA is our CD19 monoclonal antibody. And so it targets B cells and plasmablasts, those things that go on to form antibodies. And the powerful point about UPLIZNA is by virtue of targeting and reducing that cell burden, in principle, it reduces the amount of autoimmunity that can happen because it's the B cells that are generating those pathogenic antibodies. So we have tested UPLIZNA in a variety of different autoimmune circumstances with rare disease, starting with NMOSD. We went on more recently to show a remarkable result of greater than 80% hazard ratio reduction in IgG4-related disease for patients that are having flares. And to go on later this year in generalized myasthenia gravis, this is a neurologic condition where your immune disease attacks the nerve cells ability to regulate your muscles. So patients feel extreme fatigue. They're not able to go about their activity of daily living. And when we had assessed the activity of daily living burden for those patients with generalized myasthenia gravis, we found that the burden was much reduced, statistically significant and also from a magnitude standpoint, magnitude and clinically significant level. What was also interesting from that study was we were able to recruit a sizable proportion of patients that are classically very difficult to treat within myasthenia. These are the so-called MuSk antibody patients, muscle-specific kinase and those patients had done as well with UPLIZNA as well. So we're very excited about this mechanism. We've gotten very positive feedback about the results. As a prior practitioner, for me, what is most heartwarming is these patients really have not had options. And if you look at the types of therapy that they have -- had been made available to them in the case of IgG4-related disease, a relatively newly characterized condition, there wasn't much at all. With myasthenia, there have been some options but there leaves a lot of wanting, if you will, for an improvement in the management of the patient and the patient symptoms. And we finally have a tool that can help in a very different way, those patients. And of course, we're very interested to understand what else UPLIZNA has the capacity to do. So we'll be looking at that further as well.

Excellent. And you touched upon there the various -- a few things within myasthenia gravis. How are you thinking about the positioning of this product based on that data you saw?

Well, ultimately, it's going to be the practice of care that dictates what the opportunity will be in terms of staging and order of utilization of this therapy. But what I think is compelling is UPLIZNA has fundamentally a different mechanism of action than the other therapies that have been approved for myasthenia gravis. I think the other compelling thing to consider for UPLIZNA unlike other therapies is you get initially 2 doses, approximately a couple of weeks apart from each other and then you're dosed every 6 months. As a patient, that's remarkable in terms of convenience and not having your medicine get in the way of you living your life. .

And there, Narimon, the point I might add as well is the steroid tapering feature of our trial. Maybe you want to touch on that for 1 second.

Very good. Yes. So the way that -- thank you for reminding me, Justin. So the way that Phase III study had been designed was, not only did we want to understand the impacts of UPLIZNA on these patients with the burden of disease that they had but these patients also oftentimes receive steroid background therapy. And we know steroids have been around for a long time. They have some modest efficacy, which is good for these patients but they're also associated with side effects. You don't want to be on steroids for a long period of time. They lead to a variety of other maladies themselves. So to really turn the screws and put the pressure on UPLIZNA's performance in this Phase III study, we actually had a forced steroid taper for the patients that came into the trial. So we not only wanted to see how well UPLIZNA did. We wanted to see how well it did in the presence of taking away something that patients had already been using for help, that we knew were associated with untoward side effects. And we found that the proportion of patients that were able to titrate their steroids successfully on UPLIZNA was also remarkably better and improved. So a lot of promise for this molecule and we have high hopes that it will be meaningful to these patients.

You touched upon this promise. You recently posted a clinical trial design for UPLIZNA and BLINCYTO in other autoimmune diseases. Perhaps can you talk about the opportunity of expanding beyond just myasthenia gravis?

Yes. This is something that a lot of us are very excited about in R&D at Amgen. So picking up on external data with CAR-T therapies that had shown their ability to modulate and help patients with the most severe forms of autoimmune diseases, awful lupus, awful scleroderma, awful other diseases, rheumatoid arthritis, we wanted to assess whether our B-cell modifying therapies, some of them which are quite mature, like UPLIZNA or even BLINCYTO used in oncology for ALL, as you heard Pete speak to earlier, if those could also be helpful in these patients. So we put together a novel and very nimble master Phase II protocol, where we're able to assess these therapeutics in 1 study and develop some proof-of-concept data to help us adjudicate and triage where else we can test these therapeutics inclusive of UPLIZNA. So we have started with lupus nephritis as our first indication. It won't be our only indication that we study in this paradigm. But we anticipate that we'll be learning a lot about the potential for UPLIZNA and other therapeutics in that master protocol.

How do you think about durability for your products versus something like a CAR-T?

Well, I think one of the important points, again, is to go back to the mechanism of action here. And when we're looking at therapeutics that are actually able to deplete or control the B cells, which are the pathogenic cause, if you will, of these autoimmune conditions, if you can reduce those to the point where the source of the disease is going away or attenuated, you should be able to appreciate a longer benefit. And that might be one conclusion one could draw from the every 6-month dosing, for example, that you get from UPLIZNA.

Okay. Let's switch gears. The bispecific T-cell engagers. It's surprising to me the lack of attention that I certainly get when talking about these things. So BLINCYTO, I know that you commented on it earlier, Peter. Just -- can you discuss the reception you've had for these products in oncology so far?

Well, the data have been remarkable. If you all have not yet had the opportunity to go through the papers that have been published on the responses that have been observed in acute lymphoblastic leukemia for BLINCYTO, or small cell lung cancer for IMDELLTRA, I would highly encourage you to do so. These are one of the cases where the figures and the data just speak for themselves. Just really remarkable results in diseases that at the time that I was practicing, to be honest with you, Trung, there were no great options for these patients. None. To see something like this, take evolution within my lifetime, I really view as being a once-in-a-generation opportunity. So it has been amazing to see these BiTEs take shape, not only from the research and development standpoint but from the integration into the health care landscape. And there has been a great reception from the utilization of BLINCYTO, as Pete can probably allude to as well, it hadn't taken very long for people to pick up on that data and incorporate it into practice. So the lag time from learning to practicing was very short for BLIN, it's been great reception there. Also equally great reception for tarlatamab or IMDELLTRA in small cell lung cancer, where we're seeing very durable results. And that's not where the BiTE story ends, obviously. We have a fantastic therapeutic in development for prostate cancer, xaluritamig, that's against the STEAP1. Pete knows the acronym spelled out really well. He knows it better than I do. I'm going to steal your thunder here.

We should maybe test, Justin.

I'm going to put a phone a friend on that one.

But in any case seven-transmembrane epithelial antigen...

Antigen of prostate 1, yes.

Yes. So this is the therapeutic that has shown some really promising early results in metastatic and androgen-resistant prostate cancer. And we have announced recently that we've transitioned to Phase III there. We have high hopes for this molecule as well. So reflecting back on our BiTE journey, it started with BLIN, a lot of us thought that maybe this was the extent of the opportunity in BiTE in looking at hematologic malignancies. But we took a very bold step in applying this really novel platform to solid tumors where a lot of people really had doubts that it was going to work. But we have found in the most recalcitrant difficult-to-treat cancers that, yes, BiTEs can be remarkably effective for patients. And we've also learned that the earlier you administer them, the less burden of disease there are, that the more durable those results and benefits can be. So a lot more to learn about the molecules that we have in development still.

Yes, that's an interesting point because that hopefully will give you ability to just move further up the treatment algorithm.

Yes.

Okay. Excellent. And then -- let's switch to CVD, Lp(a). So the Phase III OCEAN study, that's running, is going very well. It seems like you're running a quite smaller trial versus Novartis here, perhaps can you explain some of the reasons?

Yes, absolutely. And this is one where I wish I had a seatbelt on this chair because my background as a cardiologist makes me want to bust out of this and talk about Lp(a) all day. But you're quite right in that we have taken a different approach with our outcomes trial. This was designed as a 7,000-patient study. We had enrolled it actually in a record amount of time. We would have been satisfied, honestly, with 6,000 but we did not want to exclude patients that were really waiting and asking to be part of this trial. We had looked at and focused on cardiac events as part of this study. We have also selected patients with very high Lp(a) to be a part of this trial, this cardiovascular outcomes trial, which is event driven, which means the study doesn't end at a specific time point. Its ending date is predicated by the number of clinical events that accrue in the trial. So it's over when a sufficient number of deaths, cardiovascular events have occurred to inform the statistical analysis that has been predefined. Now what's really important, I think, for us to consider for Lp(a) are that in the way that we had utilized available data from our colleagues at deCODE published epidemiologic data, we understood that like LDL cholesterol, you would be able to maximize the observed benefit of the drug, the more total Lp(a) that you reduced, okay? So taking a very high Lp(a) level to a very low Lp(a) level is a large total reduction. And it turns out that the total reduction of Lp(a) that you have is proportional to the relative risk reduction in your cardiovascular events. It kind of makes sense. The more Lp(a) that you take out of the system, the better relative benefit that the patient will have on those subsequent cardiac events. So we designed the study to have a threshold of 200 nanomol per liter. That's a little bit different from how our competitors have been looking at the study and we focused on cardiac events because that is where we have seen the strongest signal correlated with Lp(a) reduction. So we're quite excited about this study result. It is informed by human genetic data. So I feel in some respects we're repeating Mother Nature's experiment here. But we have high hopes for this. And I am looking forward to not just our data but our competitor data as well because I think it will be a really informative and meaningful change for patient care.

Excellent. Well, we're entering the last 5 minutes here. Peter, I've not really given you a question. So I'm sorry. For 2025, obviously, you can't give guidance here but perhaps can you give us some levers we should think -- be thinking about the pushes and pulls for 2025?

Well, look, I think we covered them in the third quarter, Trung. We've got great momentum in all 4 therapeutic areas and in the in-market products. So I would continue to say we're focused in general medicine on Repatha. Super important medicine, up 40%, as I mentioned earlier in the quarter. So we want to continue the momentum with that. The bone franchise is working really well, EVENITY, again, up 30% year-over-year. We want to continue to get that out. 43 million units of Prolia and Repatha, to 11 million patients around the world. So when we look to the future, we want to continue that kind of momentum and volume-driven growth. When we think about research and development, so that's #1 capital allocation for us. It's our #1 guiding principle internally, is doing whatever we can, throughout the operations of Amgen to be able to reallocate capital back in innovation, both internal and external, the best innovation. And so we're going to continue to remain focused on that. We will continue to work on being laser-focused for a broad Phase III program for MariTide. But what I would say is, we're focused on our entire network optimization. We've got great volume growth. I think I mentioned 29% volume growth in the quarter, driving that 23% revenue growth. So we've been focused on volume growth for a long time. The new plant in Ohio, the new plant in North Carolina and working on that around the world. So in '25, we're gratefully going to be very busy, continuing to work innovation at speed and scale at Amgen in all 4 of the therapeutic areas. And we expect to be -- continue to serve millions of patients in 2025. And I think why we're coming to work every day and we're excited about that. So that's the way I think about '25.

Excellent. And you touched upon there, capital allocation. How should we think about share buybacks these days? It feels like it's certainly, over the last few years, taken a bit more of a backseat.

Well, we announced in December of 2022, when we announced the Horizon acquisition, we said that we expected share repurchases to be limited and to be primarily for -- to offsetting the dilution of share-based compensation. We have not acquired any shares through the -- since the first quarter of 2023 through the third quarter. But I would say in terms of our capital allocation priority of returning capital to shareholders that we've increased our dividend about 6% this year over last year. So growing dividends continues to be a priority now and we'll continue to stay focused on that. That's really important to our shareholders and we understand that. And we are looking forward to continuing to strengthen our balance sheet. As we indicated, we would, through the end of 2025, back to the pre-Horizon acquisition capital structure.

Excellent. And then we're entering the last couple of minutes here. One of the things that I've been asking people I've got up on stage is hopefully, you're going to come back next year. I want to get...

Well, if you have weather like this and dolphin pods that we saw off the coast this morning, we -- it's very inspiring.

It's very nice. What -- if you come back next year, this time next year, what are the 3 things you're going to hope to have achieved? What are the 3 key things Amgen is going to have done and I'll put you on the hook for it for next year.

Well, please do. I just go back to patients. So more innovation for patients. I mean how exciting is it to listen to Narimon on what's happening in innovation internally, more medicine to patients, right? In the third quarter, we delivered more medicine to patients all over the world than we've ever delivered before. So I hope I'll come back and tell you that again, Trung. And then finally, I hope I come back and say we've been laser-focused on moving forward with creating an Amgen that's fit for purpose for the coming long term. We want to drive innovation at speed and scale, totally focused on long-term growth that creates value for patients, for staff and for shareholders. So next year, I hope you test me on those 3 and I fully expect to pass with all my great colleagues at Amgen.

Excellent. Well, thank you, team coming. That was excellent. Thank you, everyone, for listening in.