Great. Thanks for joining us, everybody. I'm Terence Flynn, Morgan Stanley's U.S. Biopharma Analyst. Very pleased to be hosting Eli Lilly today. From the company, we have Jake Van Naarden, who is President, Lilly Oncology, and David Hyman, who is Chief Medical Officer. Thank you both for joining us. For important disclosures, please see the Morgan Stanley Research Disclosure website at www.morganstanley.com/researchdisclosures. If you have any questions, please reach out to your Morgan Stanley sales representative. I thought maybe we'd start with just for you, Jake, if you could remind us of the company's overarching strategy in oncology here. I know you did a little bit of a reboot a couple of years ago, and you hosted a session at ASCO where you talked about this. Maybe just level set us in terms of where you stand now in terms of the overall strategy.
Yeah, happy to do that. Thanks again for having us here at the conference this year. As you mentioned, a couple of years back, we took on a task of really rebooting the R&D strategy in oncology at Lilly to try and create a more durable productivity within the organization. I f you rewind the clock of Lilly's history in oncology, there's been a number of really important medicines that the company has invented and marketed, from chemotherapies to naked antibodies to small molecules. They've happened somewhat sporadically over a long period of time and without as much consistency as I would like, we would like. The goal was really, how do we form a strategy combined with a technology toolkit that can discover, develop, and ultimately market great medicines that are more consistent over time? We've really honed in on, I would say, a twofold strategy.
One is going after common cancer vulnerabilities. We have a number of programs that exemplify that now, things like olomorasib, the G12C inhibitor, KRAS G12C, 13% of lung cancer. It's basically tied for the most common genomic event in lung cancer. That's a medicine that just received breakthrough therapy designation from FDA in a phase III program. Our PI3Kα program, 40% of ER-positive breast cancer, the most common genomic alteration there. Our FGFR3 program, 15%- 20% of bladder cancer. You get the theme. We've been able to identify tumor types that have these genomic alterations that you can build, for the most part, oral small molecules against either alone or in combination with standard of care hope to advance care for patients. That's one category of the activities that we do and I think a lot of our programs exemplify.
The other is really thinking about treatment resistance and, in particular, some of the tumor types that haven't seen as many advances in care over the past 20 years. I think when you take a step back and you look at particularly what PD-1, that's a class of medicines, has done for improving outcomes, it's been phenomenal, and y et there are some major solid tumors that have really not benefited from that innovation at all. Whether it's treatment resistance in the sense that we have great medicines, but tumors evolve and we need to be able to keep patients alive for longer with good quality of life, or those cancer types that have, as we like to call it, been left behind by the innovation of the past two decades, we're doing a lot of work there. That, for the most part, looks like different technology than the oral small molecules.
We're doing that work predominantly with antibody-drug conjugates and increasingly moving beyond even chemotherapy and the emerging radioligand work that we're doing. Having built up a toolkit to be able to make all these different medicines, occasionally we opportunistically see ideas for medicines that actually don't fit neatly into either of these buckets. As an example, our folate receptor alpha antibody-drug conjugate, which does utilize chemotherapy, probably doesn't quite fit into either of these buckets. Once we learned how to make these types of medicines, you have the ability to spot opportunities to do new things for patients. That was one of the reasons we pursued that opportunity going into phase III soon. That's what we've been doing. I think we're starting to put some points on the board now of momentum behind the strategy with a bunch of phase III starts ongoing, some pivotal studies reading out, new launches.
I think we're seeing some green shoots of the strategy we set in place a few years ago paying off. Of course, ultimately the currency of the realm is new approved medicines. Hopefully we have a bunch more of those in the coming years as well.
Maybe just the last one here on the strategy side is where does immuno-oncology fit into this? A t Lilly, yo u had some fits and starts here in the past. What's the current interest or appetite on the IO side?
One of the things you didn't hear me say in the overview of our strategy is anything really about axis of biology. I think we're pretty agnostic, whether it's a cancer metabolism target or a cell signaling target or something that harnesses the immune system. We're open to all of these things. It's really about where we think that we can build something differentiated and where we think that we can understand what the medicine might do preclinically that makes us smarter before we go into the clinic. I think the challenge with so much of the "next PD-1" efforts that the industry has attempted and even Lilly flirted with a little bit is that the preclinical models are not terribly predictive, and even early signs of clinical efficacy aren't particularly predictive.
You need to be running randomized trials just to know what you have. That's a pretty expensive and time-consuming way to conduct clinical research. We don't tend to do that in almost any therapeutic area at Lilly . We've thought about other ways of harnessing new innovation there, whether through business development or otherwise, and we're totally open to that. I think there's another idea, which is a bit of an offshoot to "immunotherapy," which is T cell redirecting bispecific antibodies, which of course is different than a naked antibody akin to a PD-1 antibody. We're doing CD3-based bispecifics. We're putting our first one into the clinic actually right now. We'll do more and more of that work.
Of course, those are much more tumor-specific ideas because you have to choose a tumor antigen to then bring the T cell over to, which is different than just a broad, put the gas on the immune system or take the brakes off the immune system approach.
Can you tell us what target you're going after with your CD3 bispecific?
Yeah, it's a BAFF-R CD3 bispecific for B- cell malignancies. This is a pretty interesting target that's not CD19 or CD20, but has pretty high and broad levels of expression even in patients who have relapsed on either the bispecific or cellular therapy versions of medicines targeting CD19 or 20. Back to my earlier point about treatment resistance, this is an idea that fits in that realm. T hose medicines have advanced care for patients with, for the most part, aggressive lymphomas. We're starting to see a lot of relapses from those medicines. We think this mechanism could play an important role there. We'll see. We're starting phase I here very soon.
What is your thought on the PD-1/ VEGF target? I know there's a lot of debate about that amongst investors and companies. What's the latest from Lilly ?
Timely question in light of the World Lung Meeting this past weekend. I think a very provocative set of data that I think we've all seen as a field in lung cancer. Yet some pretty important questions, I think, still remain outstanding, some of which maybe we're starting to get answers on this past weekend. I think one question is the translatability from China-only data sets to global data sets. I think we saw a hint of that over the weekend from the ivannesimab data that are somewhat in the eye of the beholder, probably, depending on which side of this debate you were on to begin with. There's the question of overall survival. Do these studies, the global studies that are currently ongoing, need to win on overall survival? Do they just need to trend on overall survival? I don't know the answer to that, actually.
I think you hear different things from different clinicians. I'm sure that different regulatory bodies around the world will have different things to say about that. Obviously, you can imagine like we and everyone else are following that target area pretty closely. A decent number of unanswered questions still.
Okay. Maybe, David, over to you for one here. The company is going to have two important presentations at EASD coming up this week. Maybe you could just give us an overview of t hose two presentations and then w e'll dig in a little bit deeper to some of the data.
Yeah, thanks again for having us. It's been a busy couple of months in the past and also looking forward in the incretin business. Obviously, we've had a lot of major readouts. You're referring, obviously, to the Orforglipron readouts. We've had two major studies read out recently there, the ATTAIN- 1 and 2. Those are the obesity/overweight study in non-diabetics and then diabetics. You've seen the top line data from those disclosures. The other major disclosure in the portfolio, obviously, is our outcome study, our largest and longest outcome study of Tirzepatide in patients with diabetes. That study showed not only an 8% improvement in the traditional MACE3 outcome, but major improvements on all secondary endpoints, including really provocatively all-cause mortality. You'll have more to say about that in the disclosure. I think the scientific community wants to see all the details of this disclosure.
I think in many ways, though, like you've seen the top line numbers. What we've shown with the Orforglipron program overall is a medicine that really does, in a non-peptide small molecule pill, convenient once-daily medicine, no cold chain, a medicine that we can scale really to meet global needs, is a medicine that recapitulates the efficacy and safety profile of a GLP-1 monoagonist. That was really the thesis coming out of the program. I think that's what we've seen in the clinical studies. The drug, I think, like we've gotten great feedback on the profile of the medicine. There's a ton of interest in the patient and physician community for an oral, convenient, small molecule medicine that can scale like an Orforglipron.
Great. It sounds basically we shouldn't expect any surprises at EASD, is kind of what you're saying.
No, I think we try to avoid surprises at medical meetings. I think we've been very forthright about the data to the limits of what we can in the press release. I think, obviously, people are interested in the texture and fine details. I think just taking the data at face value that's already been disclosed, you really already understand the profile of the medicine. Obviously, there's been a lot of discussion over the profile of the medicine. We're extremely happy with it. I think it's really very on thesis for us.
I'll just add, I think that there's a temptation, especially with a program that's this large, to look at every individual study readout of some new event or new piece of information. Yet, given what the stated goal of the program was to begin with and how much we know actually about GLP-1 agonism vis-à-vis semaglutide, I'm actually not sure how much we're learning incrementally with every new study other than the fact that there's important evidence generation. Many of these studies are required for regulatory authorities or health assessment bodies outside the U.S. There's an interesting dichotomy there where we're running these studies, we're spending money against them, they're important, they matter for the overall long-term trajectory of the medicine. Yet I think we know already today, basically, qualitatively, everything there is to know about the medicine.
We just have to do the work to now bring it to market and get it out there to patients globally.
One area I think people still press a little bit on is the tolerability profile of an oral versus an injectable. Maybe you just elaborate on h ow Lilly has seen that data evolve. Because again, to your point, Jake, I mean, there are multiple studies here. It's not just a single study. As you now have several studies in hand, how do you think that tolerability profile stands up relative to, let's say, not a GIP like Tirzepatide, but a GLP-1 monoagonist?
I think that's a key point, actually. I think we've shown clearly in head-to-head studies against GLP-1 monoagonist with Tirzepatide that the GIP mechanism is important not only in driving efficacy, but does have a safety component to it. We see lower rates of vomiting. That said, with Orforglipron, and again, speaking to the totality of data, not any one specific study, and we're talking about a program now that's treated thousands of patients for over a year, we see a tolerability profile that really closely matches what you expect from GLP-1 monoagonism. Full stop. I don't think there's really any further qualification required for that. I think you'll see that again in the presentations.
I know there's been some investor focus on the overall rate of treatment discontinuations in these clinical trials, as if it's some read-through on real-world persistence of these medicines or adherence. I think that's the wrong conclusion to be drawn. Across all of these studies, you see very, very similar rates of treatment discontinuation within the clinical trial. There's a whole host of reasons that that happens. That's normal. In fact, the data that we put in press release form for the recent Orforglipron studies to this respect are not actually outliers at all. Yet, in the real world, we don't see persistence or adherence challenges so long as patients are benefiting from the medicine, most are, and so long as their insurance or out-of-pocket cost situation allows them to stay on the medicine financially. It's just worth clarifying.
I think that was sort of a little bit of a misfire on the reaction side. We've gotten a lot of questions about it. I don't think that's a real issue.
Okay. Maybe one more before you go back to oncology is just, you know, the next study coming up is ACHIEVE 3. Now this is the head-to-head versus Novo's Rybelsus, the low-dose Rybelsus 7 or 14 mg. Maybe just level set us in terms of what you guys are hoping to achieve with that study.
Yeah, I guess I'd go a little bit back. Jake set me up nicely for this one. I think you've seen the profile of this medicine. This is a medicine that we are submitting to regulators this year. We've already indicated that we have all the data package necessary for a chronic weight management clinician. There's a lot of studies that we do, including the one that you mentioned, that are either directly required for regulators or are part of what we need to get reimbursement abroad for these medicines. I don't think they actually change or really meaningfully inform the profile of the medicine. Obviously, we expect to be superior to Rybelsus, or we wouldn't have run the study. I don't think it really will meaningfully educate us or the world on the profile of the medicine.
Okay. Maybe Jake, back to you. You had another phase III readout here for Jaypirca this morning. Congratulations on that data. We were talking about this before that I think last year you had some data for ondansetron. You're setting a precedent here in terms of disclosing some.
Breaking news at the Morgan Stanley conference.
Exactly, we'll take it. Maybe you could just remind us the purpose of this study versus the 314 study that read out a couple of months ago. How does this inform how you're thinking about where this therapy might be positioned in the market over the medium- to long- term?
Yeah, so just for level setting, we're talking about Jaypirca, pirtobrutinib. This is our non-covalent BTK inhibitor currently approved in certain settings of CLL and mantle cell lymphoma. We recently read out two big phase III studies that we've put out positive top- line press releases with. The data actually will be presented, we hope, later this year. Maybe I'll just walk through both of those studies because they're different. Both in CLL, one is a head-to-head study of Jaypirca versus Imbruvica or ibrutinib in a population of patients who've never seen a BTK inhibitor. Some of those patients in the study had seen other prior therapies, so we call them relapsed refractory CLL. Importantly, this study included a fairly sizable cohort of true treatment-naive patients. The design of that study for the primary endpoint compared Jaypirca with Imbruvica on a response rate endpoint.
Of course, we'll look at time-to-event endpoints like progression-free survival and eventually overall survival. What we put in the press release is the study was successful on the response rate endpoint. We tested it for non-inferiority, although it was actually nominally statistically significant for superiority, with trends in the right direction on progression-free survival in favor of pirtobrutinib over Imbruvica, particularly in the treatment-naive subsegment of the study, which, as I mentioned, is not small. It's a decent amount of the study, actually. O ther medicines that have run similar studies, actually, in CLL. I think the most comparable one is a study that was run with Brukinsa or zanubrutinib called Alpine, which had an extremely similar design, head-to-head versus Imbruvica. That study did not have any treatment-naive patients in it. That study's gotten a lot of attention over time, but i t's also generated some questions.
I think as folks sort of think about our study heading into the data disclosure, it's probably just worth maybe saying, one of the things that I think has led to a lot of debate among physicians about Alpine was that the Imbruvica arm of that clinical trial did not perform as well as people thought it would. Then they said, 'Okay, Brukinsa beat it, but the control arm seemed to underperform what we thought Imbruvica should do." We didn't really see that in the study that we run. You'll see the actual detailed data when we present them. I 'm hopeful that when these data are digested by the clinical community, they sort of look at them and say, "Okay, clean study that I can actually interpret without a lot of questions." That's the first one.
The second one that we press released just this morning is exclusively in treatment-naive CLL, and it's Jaypirca monotherapy versus a chemoimmunotherapy doublet of bendamustine/rituximab, which is admittedly an older standard of care, but still one that is used in a variety of places around the world. Again, a study design that others have run before. I'll use another Brukinsa example because that's the most recent one. They ran a study called Sequoia, very, very similar study design to the one we ran. Heading into this study, we said, "Okay, we know where the benchmark is because there's this Sequoia study out there, " admittedly with a covalent BTK inhibitor, not a non-covalent one.
When we unblinded the data, we were just fairly surprised in a positive way by the effect size that we observed on both certainly progression-free survival, which is the primary endpoint where the study was successful, but even some of the early data on overall survival. Really interested to get reactions from the community on that one. Both of these studies, as packaged together, will form the basis of regulatory submissions around the world for label expansions into first-line CLL. I think, and you and I have talked about this a little bit over time, one of the questions for this medicine over time will be what is its most appropriate placement in the treatment algorithm. Unlike the covalent BTK inhibitors, so that's Imbruvica, Calquence, and Brukinsa, those three medicines were b uilt for treatment-naive CLL, and that's the ground they compete on.
Jaypirca works really, really well on patients that have relapsed on those medicines, whereas you can't recycle them after each other. For a disease that physicians manage over the course of sometimes decades for any given patient, it's all about the total amount of disease control over the life of that patient that you can get by sequencing different effective regimens one after another. I think one of the things that we'll have to figure out as we position the medicine coming out of these data is just how physicians, hematologists, oncologists are thinking about that. Do they like the idea of giving Jaypirca as the first medicine, or would they rather reserve it as the second medicine? I think for Lilly, for the business, for how we think about this medicine, we can make this a really big and important product either way.
We just want to do the thing that I think is falling downhill the easiest. As we present these data publicly, it'll be really important to get reactions as to how folks are thinking about that.
Great. T he other nuance here is there's these fixed duration regimens in the first-line setting. How does that impact how you think about first-line versus second-line and where are we going on the treatment duration side?
It's actually interesting. It adds to what Jake was just saying about we have a unique opportunity with Jaypirca to have this medicine be an important medicine for a subset of patients that are treatment-naive, as well as patients that have had prior therapy. I think if you look at the overall trends of these time-limited therapies, and these typically almost always include a medicine called venetoclax, a BCL-2 inhibitor, what I think we're actually seeing is not that the size of the BTK market is shrinking, but actually more duration of therapy is shifting from first-line to the relapse refractory setting. I think in some ways, Jaypirca is skating to where the puck is going as a field. We're also running a study with a German CLL group, which has venetoclax-containing arms in it, including in combination with pirtobrutinib. That'll generate Jaypirca.
That'll generate data on time-limited therapy in first-line and a large international study as well.
We're running a time-limited therapy with venetoclax study in second-line too. I think in broad strokes, what is the point of all of these clinical trials that we're running, both monotherapy, combination with venetoclax, first-line, second-line? It's really just cover the entire landscape. If we can get every possible realistic regimen and line of therapy in the label of this medicine globally, we can give doctors and patients a lot of different options about how to use a medicine that I think those who've used it already really like. It's well tolerated. It's easy to use. It works pretty well, particularly in the patients that we've studied it in. Our goal is just to allow as much prescribing flexibility with this great medicine as we can.
Big picture, when you wrap all this together, does the CLL market still keep growing as a result of on a dollar basis, new therapies, the duration cross-currents that we just talked about, or a re we at peak steady state right now when we look at it on a dollar basis for the CLL market?
It's a great question. I think it does keep growing in part because we are like, take a medicine like Jaypirca. If it's used in a later line population, that's a population that was not getting any effective therapy. They were probably going on clinical trials. If Jaypirca, let's say, can introduce another two years of disease control, that's two years of drug therapy that didn't exist prior to the introduction of the medicine. Now, this is a disease predominantly of older people. At some point, you start running up into these patients are dying of other non-CLL-related things that happen to them. There will be a natural asymptote to this where it's hard to imagine how any new class of medicine really intercalates to this treatment paradigm. I don't think we're there yet, but we're probably not that far away from that, actually.
Okay. Maybe going back to the incretin portfolio for a second here. You guys are going to present at EASD the t irzepatide SURPASS-CVOT data. Maybe just talk about the other study you're doing, SURMOUNT- MMO. What are the implications when we see this data for MMO, which is, again, an obesity setting? This is type 2 diabetes.
Yeah, in the SURPASS-CVOT , which is our type 2 diabetes outcome study, we did something the field had never done before, which is we actually said, let's run this against a really good medicine, Trulicity. An actively controlled clinical trial. We already know that GLP-1 plus drugs improve outcomes in patients with type 2 diabetes. Admittedly, a risky and a bold decision. I think it played out extremely nicely because we really have a contemporary comparator of an excellent medicine and demonstrated improvement in really across all the secondary outcomes measured. All-cause mortality, MACE4, kidney outcomes against the drug that already improves kidney outcomes. Extremely robust data package in that study. Really important.
I don't want to skip over that in answering the heart of your question about our outcome study in obesity because the data themselves really exceeded my expectations, what we could expect in an actively controlled study. When you actually look at the data in SURPASS-CVOT and you adjust it back to as if we had run the study against placebo, and we can do that because we ran the outcome study of Trulicity. We have the patient-level data from that. We have the patient-level data from our CVOT study. We actually pre-specified this analysis, which does matching for these patients. You generate point estimates for improved outcomes that are the best that the field has ever seen. Really remarkable improvements, like a nearly 40% improvement in all-cause mortality, 35% improvement in MACE outcomes.
These are huge numbers for the field in a medicine that also gives all other kinds of important wins, like on weight, on A1c , a massive win. Our SURMOUNT- MMO study is our equivalent, as I mentioned, in patients without diabetes, but with overweight or obesity. We're actually studying two populations in this study, the patients that are at risk for a cardiovascular event but have not had one, a so-called primary prevention group, and also patients that have had cardiovascular events already. That's the population that was enrolled in Novo's SELECT study. We have high hopes for that study. I think we would expect that the huge cardiovascular benefits that were described in the SURPASS study will come over to the MMO study.
I think also we'll be able to really answer the question for the first time about what tirzepatide/ Zepbound offers in patients that are at risk for cardiovascular disease but have not yet had an event. That's really where I think you want to be as a health care company and as a patient. You don't want to wait for your first heart attack to say, I should be treated for my overweight or obesity. You'd like to prevent that entirely. I think we have the opportunity to do that.
I think that's similar to what you did with the REWIND study for Trulicity back in the day a while ago. You did a primary and secondary, like a mixed population, right, if I remember correctly.
We generally, with many of our outcome studies, favor enrolling mixed populations of primary and secondary so that we can really answer questions not only about a segment of the patient population that are eligible to receive our medicine, but a much larger swath of them. I think actually the majority of people that are taking Zepbound today, thankfully, have not yet had a cardiovascular event. I think that, of course, they're taking it nowadays because of all the health care benefits that we've already defined for the medicine. It would be really nice if we had to also tell them about the outcome benefits that they're experiencing from the medicine.
Is it possible that we get that data next year, or is that more likely 2027?
Yeah, I'm not going to comment anything besides what's on CT Japerka. Obviously, these are event-driven clinical trials. We make our best estimates, but ultimately, we see how the events accumulate.
Okay. Maybe just one last one before I go back to oncology here is just you guys have a broad portfolio beyond even tirzepatide and orforglipron. You have retatrutide. You have eloralintide, the Amylin program. Maybe just how is the company thinking about the portfolio approach here and stratifying across maybe line of therapy or combinations? T here's so many different directions that you guys can go. Maybe just very high level, how do you see this all fitting together?
Yeah, obviously, we have the benefit of having a large portfolio of these medicines. I think if you just take a step back and you say, when you think about any chronic disease setting that even approaches the size of the overweight and obesity patient segment, there are a few chronic diseases actually that are that large. When you think of anything like in that stratum, you see some natural segmentation in the market because not all of patients' needs are going to be met by any one medicine, either on a supply or medical basis. Obviously, our foundational therapy now is tirzepatide. It's an amazing medicine. We talked about orforglipron, the ability to reach more patients with a medicine that's more than adequate for their medical needs.
Of course, there are going to be some patients whose needs are not met by either of those medicines, either by virtue of them needing more weight loss or being in the relatively small percentage of, call it 15% of patients of an otherwise very large number who don't tolerate these medicines. Where do these others fit in? Maybe I can take them in turns. Retatrutide is our tri-agonist. This adds in glucagon as the third mechanism of action. This is a medicine that we see delivering very high levels of weight loss. I should say that the program in which we're studying retatrutide in patients with overweight or obesity is called the TRIUMPH program. It has four core studies. Of course, to register any of these medicines globally, you need to conduct a prototype series of clinical trials.
Those are in patients with a broad range of overweight or obesity. We're running that program in this broad population because that's what you need to do to define benefit or risk of these medicines. That said, we actually think tirzepatide is a great medicine for patients with a lot of called class I, II, or sometimes even class III obesity. What you can expect us to look at very carefully in these studies is what is the benefit-risk of retatrutide in patients at the higher range of the obesity spectrum. It may be different. Retatrutide delivers a magnitude of weight loss and a repetitive weight loss that is not achieved with any of the medicines on the market today. You can imagine in a lower yet obese patient, that repetitive weight loss could be associated with some even undesirable side effects.
I think although we're running a broad series of studies, we actually are positioned to communicate these results in the higher end of the obesity spectrum so that we can understand and the world can understand the benefit-risk in different populations. Ultimately, you run these studies broadly and you see sort of where the medicine fits. We think ultimately, retatrutide will be a great medicine for patients at the upper range of obesity where even a great medicine like tirzepatide doesn't get them there. On eloralintide , this is our selective amylin agonist. It's just a little different than some of the other Amylin programs that you've seen out there, which have a dual mechanism of action of calcitonin and amylin. We really believe that the weight loss effects of these programs are driven by their amylin agonist, so w e matured a selective peptide agonist.
It's really the first medicine that is of a non-GLP-1 mechanism that can deliver GLP-1-like weight loss. Obviously, you could see that being used as an alternative therapy or an add-in therapy. In so many diseases, hypertension, dyslipidemias, you see patients starting on one foundational therapy and then if they need to escalate further, adding in another mechanism. I think that's generally how we've been thinking about an amylin agonist or, again, in patients that for whatever reason don't want to be on a GLP-1 agonist. I just had a lot of different things. Happy to dive into any of them. Obviously, a lot of opportunity within the portfolio. You'll be seeing a lot of updates from us and a lot of readouts. The first readout of retatrutide will be later this year.
I think one thing that just makes eloralintide and retatrutide, theoretically, you could both say are for a patient population that maybe needs more weight loss than what tirzepatide can deliver. I don't think you're going to combine retatrutide with tirzepatide because they have overlapping mechanisms of action; eloralintide , you would. I think they're going to play out differently, especially given the large base of patients who are currently on tirzepatide/s ema. I think eloralintide has a different contour of how it could be used relative to retatrutide over time.
I think in these large, that's really well said, in these large chronic disease spaces, I think there are some physicians and patients that really like the add-on approach. There are others that like switching. I think in either scenario, they can find their way to a Lilly medicine.
Great. I think we're up against time. Jake, David, thank you so much. Really appreciate it.
Thanks for having us.
Thank you.
Thank you.