All right. Good morning, everybody. Thanks for joining us. I'm Terence Flynn, the US Biopharma analyst here at Morgan Stanley. Very pleased to be hosting Eli Lilly this morning. I'm hosting Jake Van Naarden, who is President of Lilly Oncology. Jake, thanks so much for being here. Really appreciate you taking the time. Thanks for having me. For important disclosures, please see the Morgan Stanley Research Disclosure website at www.morganstanley.com/researchdisclosures. Again, Jake, thanks so much for the time. Really appreciate it. I know we had a chance to catch up at ASCO. This year, you guys had a pretty big presence as you kind of, you know, rebooting Lilly Oncology. Maybe you could just talk about some of the steps you and the team have taken here as you kind of revamp the pipeline, and then talk about, you know, the rationale and some of the examples that, you know, you've implemented, since your time in the role. Yeah. So, you know, a little bit of a retrospective on what we've been up to the past couple of years. A couple of years ago, we took a look at the pipeline of programs that we had in oncology and the technologies that we had in-house to make new medicines. And it was sort of increasingly clear to me and others on our team that we just really weren't sort of set up for where the future was headed with making new medicines to treat cancer. And so we took a pretty ambitious step of terminating most things in the pipeline at the time, with the exception of a few, and making a bet that between internal discovery efforts and business development, we could sort of put our heads down, hunker down for a few years, and build back to a pipeline that of similar size, but with more relevance and sort of an overall higher likelihood of delivering medicines, really based on the back of biology conviction. So putting our programs through the lens of: Do we like this target? If we drug it in the right way, do we think it's highly likely to work based on everything we know pre-clinically, such that we can put it into the clinic and really expect to see tumors shrinking on CAT scans? That tells you a lot about a medicine that tends not to happen on its own, and that, that kind of risk reduction allows you to put more capital into a program and, and have a higher confidence that you're taking it forward. You know, I've seen a lot of other strategies deployed across, frankly, historical Lilly and other companies, either, you know, tied around an axis of biology, like immuno-oncology or targeted therapy, you name it, or tied around tumor type, so we're only going to do lung cancer and prostate cancer, as an example. You know, my observation is just that making new medicines against cancer specifically is so unbelievably challenging that, like, getting yourself wrapped up in, like, other artificial rules that only narrow the opportunity set, was not something we wanted to hold us back. So we've kept a wide aperture and said, "If we think that there's a good target biology idea, and if we think we can make the medicine, we'll do that, and if it's gonna make a difference." That sort of dovetails with the making of the medicine piece, which is that, you know, we really needed to modernize just the toolkit of technologies that we actually had at our disposal. We, at the time, really could only make a small molecule and a naked antibody. And I think, you know, we all know just from seeing the kinds of innovations that, frankly, many others have advanced, that, like, that's not enough to be a relevant player going forward. And so we've invested in antibody drug conjugate technologies, we've invested in T cell engagers. We're in the process of building a radioligand platform. And so I think now in 2024 and going forward, we really have the ability to make medicines with, I think, almost every modality that is validated today, and some that, frankly, aren't even quite validated yet. So that is great. That's exciting, and, you know, this year is a particularly productive year for new clinical starts. I think we're gonna put somewhere between five and eight new medicines into the clinic this year in oncology. Next year will be pretty productive, too, I imagine. We're putting those plans together right now. You know, that clustering, of course, isn't a surprise. Like, we hit the reboot button a few years ago. That's sort of how long it takes to make new medicines, and now we're sort of seeing the output of that effort come through. These are not all gonna work. They're not all gonna end up being approved medicines. That's just not the way it works. But I think that as a portfolio, the probability of success there is higher than what it was in the past, and more diverse. So, you know, we now have a, just to give some examples, a portfolio of ADCs in the clinic, two Nectin-4 ADCs, one folate receptor ADC. We have one radioligand in the clinic, more to come. We have three oral small molecules in a KRAS portfolio. We have a G12C inhibitor, G12D inhibitor, a pan KRAS inhibitor. So, you know, I think you look across sort of the buckets of what we've focused on, and I think in a couple of years, hopefully, we'll have a bunch of clinical data sets we can point to, to say, "Okay, like, this has actually worked in delivering new medicines, not just new INDs. Yep. No, that's a great, great way to start and frame the conversation. I guess the one follow-up I had is just as you look at the platforms you guys have already kind of, you know, built out through business development internally, any others that are on your radar screen that you think you still, you know, would like to enter into, or is this pretty much steady state now? You have what you need, and you're like, to your point, you're just focused more on now processing, you know, getting clinical trials underway, generating the data. Yeah, I think, you know, so a couple of things. First is, like, as it relates to things like the engineered biologics, like T-cell redirectors, bispecific antibodies, antibody drug conjugates, that there's actually a lot of innovation, even within any one given category there, that we can and will continue to tweak. So when I say we're invested in those areas, I'm sort of forward-looking and including the additional engineering choices that we'll make for next generation products, whether it's linker design, payload design, antigen choices for the antibodies, masking technologies. I mean, there's a lot of flavors within there. There are also things that, at least to date, we've not done or chosen not to do. We don't have anything going on in cell therapy as it relates to cancer treatment. That's a decision. That's not something we've sort of not assessed. We've, of course, looked at that. We see those products out there, and we continue to monitor that space. I think, you know, for us, getting into that, getting into cell therapy would, of course, be another step change, in the, much in the way that getting into radioligand is sort of a step change for us. We're open to it, but I think we'd have to. We'd have to get confidence that we can deliver, like, a scaled pharmaceutical product. I think a lot of those products sort of are not quite sort of scaled pharmaceutical products. But that's, at Lilly, that's what we're good at doing. And so if something like that emerges, I think we'd be open to it, but I think that's probably the one last sort of modality class we've not yet ventured into. Okay, great. Maybe just before we get into some of the products and pipeline, just a high level one on IRA, you know, maybe two parts. So the first is just, you know, some companies have kind of adapted their strategy to, you know, evolve in this post-IRA world. Anything you're doing from a forward-looking perspective as you think about, you know, navigating it in Lilly Oncology? And then number two, does the Part D redesign impact rebating dynamics meaningfully, you know, for, let's say, Verzenio, for next year, other products, or is it again, kind of steady state? So kind of two parts on the IRA implications. Yeah. So on the first one, the answer is, of course, yes. You know, we, from the minute IRA was enacted into law, we started reassessing sort of how we're doing things. I think, first of all, the diversification away in part from small molecules and towards biologics was, in part, a reaction to wanting to diversify our pipeline modalities, as I mentioned earlier, but in part, a reaction to the IRA dynamics and an incentive structure that exists today. I don't think it is, frankly, a good incentive structure for, like, the healthcare system or for patients, but it is what exists, and we'll see if it ever changes. I hope it does. But for now, small molecules are being penalized, and so, you know, we have to react to that. I think the other thing that is probably a little bit more substantive, actually, is just thinking through our development programs through the lens of when the IRA clock starts and, you know, what does that really mean? It means, frankly, just putting the gas accelerator on our development programs in more aggressive ways than we would have historically. So as an example, you know, in the... Just to sort of provide a compare and contrast, in the Verzenio program, this, of course, is pre-IRA, you know, we waited to start the monarchE adjuvant study until we had the first PFS data in the metastatic setting. That was like a few years went by, and the result of that, of course, because the adjuvant study took so much longer, a much bigger study, longer to enroll, longer to read out, there was a pretty big time gap between when Verzenio launched in metastatic and when Verzenio launched in adjuvant. Okay, that was. We did that through the lens of sort of careful risk reduction, like, you don't want to invest until you know you really have something. I think that's, in many ways, the way our industry has operated for a long time. The IRA has forced us to think a little bit differently than that, and, you know, I think if you look at, as an example, olomorasib, our KRAS G12C inhibitor in lung cancer, we're taking a very different approach. Like, we're gonna launch every study for where that medicine could eventually land, all probably within a 12-month period of time. Now, there's more risk inherent in that approach, I think, and we're doing this across the entire portfolio. We will experience more clinical failure, I'm convinced, as a result of this, but I think it's an adaptation we have to pursue. Fortunately, for Lilly, and I think this is one of the things that puts Lilly in a unique position as a company, like, the company is doing fairly well overall. We have the income statement capacity to be able to do this kind of stuff. I think if we didn't, it would make for a much, much more challenging dynamic. Yeah. No, it makes sense, yeah, for some of the smaller companies that don't have that balance sheet. Yeah, it can be tougher to make those decisions. Yeah, or you just end up in a world where, you know, you've rushed your great new cancer medicine to market for the sake of patients in a late line setting. You've started your IRA clock, your sort of bigger impact and bigger market indications don't come on until you're five, six years into your clock, and now you don't have a ton of time left. So we're trying to pursue strategies that just inoculate us from some of that. We're not gonna be able to do it entirely, because even if you started a first-line study and an adjuvant study on the same day, the adjuvant study is reading out many years later. Right. Is there any momentum in D.C. to change that small molecule biologic delta from nine-13 years to minimize that, that you guys have heard or not? I mean, not that I see, but, you know- Okay. There's an election coming up. Right, yeah. and this... I mean, look, this would have to be new law. Yeah. So betting on new law in D.C. these days, I think, is tough. Yeah, yeah. But, we'll keep at it because it, I think they just made a straight-up mistake here. Yeah. Okay. Okay, great. Maybe we'll move on. You know, your anchor product as you alluded to is Verzenio. You know, as we think about, you know, there were kind of the two phases of launch, metastatic and now the adjuvant side. I think at ASCO, you said you had, you know, in the high-risk, early-stage patients, you had about 60% penetration. So, you know, how much more headroom is there to grow that here? And then kind of the second derivative question is just, you know, how do you think about entry of potential competition from Novartis' Kisqali at some point? Yeah. So, we're actually probably closer to 70% now. Okay. You know, this launch has gone pretty well. We're only a couple of years into the label expansion for Verzenio in high-risk adjuvant breast cancer, and we're like 70% of eligible patients are receiving the medicine. That's fantastic. Of course, the flip side is that 30% aren't, and we're talking about a curative setting of cancer. So that is like, forget about the business impact, that's just bad for humanity. So we continue to work to change that. Of course, if you look at like oncology analogs, even like the best medicines, there tends to be sort of an asymptote of like 80% is sort of the maximum of like new medical practice adoption within a reasonable timeframe. We'll see if we can change that. I think this is an area in which new competition actually could help. You know, maybe having another company talk about the importance of treating early breast cancer with CDK4/6 inhibitors could actually expand the pie, so to speak, and, and sort of raise that 80% ceiling. We'll see. Look, there's a lot of unknowns, I think, still in what Kisqali will do to this marketplace. I remain completely convinced that in a data side by side, in a regimen side by side, Verzenio will remain the standard of care. I think ASCO guidelines have already spoken. There was an op-ed just yesterday in the Annals of Oncology that talked about this even further. I think that for the patients we studied in monarchE, two years of Verzenio will remain the standard of care. Will there be patients for whom three years of ribociclib is more appropriate? Perhaps. I think it's gonna be, at least in the high-risk EBC, my prediction is that it'll be a minority. And then, of course, there's the high-risk, node-negative population that they've talked a lot about. It's not really our business. I have sort of intellectual medical curiosity about what's gonna happen there, but it's not a place where Verzenio is used today. We're not indicated, we don't talk about it. It doesn't really impact us. It's sort of for them to figure out whether or not there's a real risk-benefit proposition for those patients. Yeah. Okay. Maybe just to kind of other question that segues into the next topic, is just first-line metastatic for CDKs. How is that market evolving right now? And then we can transition. I know you guys have a, you know, a pipeline drug that could potentially, you know, address that opportunity as well. But how do you see that kind of first-line metastatic market evolving once patients are treated with, with adjuvants? Is something where now that market is gonna shrink because docs don't want to retreat, or do they treat with a different CDK in the first-line setting? Like, any anecdotes? It's early days. I think that will take a pretty long time to play out, like long as measured in, like, these drugs may be IRA negotiated and/or generic by the time that has, like, material prescribing dynamics in the first-line. Just by the time patients go through their adjuvant course and then relapse, I mean, that you're talking about a pretty long period of time. So it's not really even happening at all yet. So I don't think that's sort of at play. I think there are other dynamics at play in first-line, ER-positive metastatic breast cancer, which is that, you know, there's a battle going on between Kisqali and Ibrance, and Kisqali is growing a lot of share, Ibrance is losing a lot of share. We've maintained basically constant for years. You know, there's like 30% of new patient starts in first-line MBC for whom Verzenio is the right choice. I think physicians have sort of spoken in that way. I don't. And that's maintained the same for a pretty long time. So I expect that to continue, is my guess. Okay. Okay, great. imlunestrant is your SERD, and there's, you know, a phase III trial going on. I think we're gonna get a readout from EMBER-3 later this year. And so I guess, you know, one of the investor debates is ultimately, you know, you've got the mutant and the wild type populations, these different populations. These drugs, again, you know, other drugs look more active in the ESR1 population. And so as you think about, maybe just remind us of kind of the rationale for your study, which I think has some different design features maybe versus some of the other studies, and then your confidence level, not just in the ESR1, but the broader population, which again, could be a differentiating feature. Yeah. So by way of context, we have two studies for Imlunestrant, our oral SERD. The first is EMBER-3, which is in second line, ER-positive metastatic breast cancer. This is a three-arm study of single-agent Imlunestrant, single-agent fulvestrant is another arm, and then Imlunestrant plus abemaciclib is the third arm. That. Let me come back to that because that's important. Verzenio, just for everyone. Yeah. Yeah. Yeah. Imlunestrant plus Verzenio- Yeah ... is the third arm. Yeah. That study, I'm actually excited to announce today, is a positive study. So disclosing that today for the first time. We'll present those data later this year. Excited to be able to share that, and, you know, you guys can react to that when you see it. So I've got to be careful what I say, but- I've got some follow-up questions. Please. Yeah. You know, I, so there's ESR1 versus wild type, but I think there's also the Verzenio combination, which is really building on the postMONARCH study that we presented earlier this year at ASCO, showing the continuation of CDK4/6 inhibitor therapy with an endocrine therapy switch. So postMONARCH was taking patients who had CDK4/6 plus an AI, and then in the second-line setting, switching to Abema, Verzenio plus Fulvestrant. We're sort of running a similar idea here, except instead of Fulvestrant, it's imlunestrant with Verzenio as that third arm. We've always thought that was not only like, a sort of unique idea, that of all the players in the oral SERD space, really only we could pursue, but I think, like, if you're gonna try and really move the needle for patients and extend durable disease control, do that with the best possible regimen you have, and you know, if you can deliver an all-oral regimen to patients in that way, that feels like a good thing to do, so that, to us, is a pretty important feature of this whole program and of that study. This other study we're running is Ember4, which is a study in the adjuvant setting, which you know is really like if you take a step back, it's really why this entire class of medicines, like, exists to begin with. You know, yeah, in the metastatic setting, I think no question, Fulvestrant is a suboptimal drug, and its delivery by way of painful intramuscular injection is a burden on patients and the system. They have to come into the office to get it. It's for sometimes for visits they otherwise wouldn't have had, and it is, like, physically painful to receive. So I think there's ways with an oral medicine that's well-tolerated, that you can improve on that. But in the adjuvant setting, you can't give Fulvestrant really at all. It's just too many visits over the course of many, many, many years. Remember, patients in the adjuvant setting get backbone endocrine therapy for five to 10 years. You can't have a patient coming into the office every month to get a painful injection. So fulvestrant's really never played there, despite, I think, a sort of well-accepted phenomenon, that SERDs, in this case, fulvestrant I'm talking about, is more effective than an aromatase inhibitor. And so oral SERDs, like Imlu, were developed to say, "Okay, well, here's a medicine that could be administered in the adjuvant setting because it's an outpatient oral medicine that could be better than an AI." So EMBER-4 is taking patients who've already received a few years of initial adjuvant therapy, with or without a CDK4/6 inhibitor, hopefully with, because that's what we think the right medical practice ought to be. And then physicians have the option of taking patients that they're worried about, and there's a set of eligibility criteria that delineate that, and either keeping them on the AI backbone that they were on or switching them to imlunestrant. That study is a 6,000 patient study, the largest trial we've ever run in oncology at Lilly. Accrual is going reasonably well. It'll take a while to read out, but you know, I think that that, like, in some ways, I think, is a like, underappreciated story within at least the Lilly oncology portfolio, only because if that study's positive, and it, it's still a pretty risky idea, but if that study's positive, you're talking about a medicine that patients are gonna be on for a long time, like three to eight years. You know, we'll see how that all plays out, but I think, and there are definitely learnings from EMBER-3 that I think you can look at when you see those data to help you feel better about the odds of EMBER-4 working. It's a different biology question we're asking in these two studies, so I think there's... In many ways, there's safety read-through, tolerability read-through, because a big part of the adjuvant idea is the ability for patients to stay on it. Yeah. Even AIs have real tolerability issues that patients have a hard time staying on. Right. But the efficacy question, admittedly, between EMBER-3 and EMBER-4, are sort of different ideas. Yeah. Okay, great. My two follow-ups, and again, not sure how much you can share, but on... You know, or as I mentioned, you've got the wild type and the ESR1, so can you tell us if you hit in both populations? And then the derivative is, obviously, you mentioned you have the monotherapy SERD, and then you have the combo with Verzenio. Was there any difference between those regimens and those populations? Meaning, did one do better in, you know, the wild type versus the other? Can you- Yeah. So let's just wait to show the data, and we can talk about it then. But I think that, like, what I-- Let me tell you what our expectations were going into this readout- Yeah ... and you can do whatever you want with that. Which is that, 'cause we've seen a lot of data from this class. I don't think that we went into this blind. Like, we have the EMERALD study of elacestrant, and we have data from AstraZeneca, the earlier phase II study. There's a lot of single-arm data and preclinical work. I mean, our expectation going in was that, like, the real effect size would be observed in ESR1 mutants. I think that's what most clinicians expect at this point, and, like, sort of we'll see what happens in the wild types. I think the other thing to consider is that, what is the value of a medicine in the non-mutant population? Even if, like... Take a draconian example, even if the efficacy is equivalent to Fulvestrant, and you have an orally delivered medicine instead of a painful intramuscular in-office injection. I think people need to think about that, and physicians need to think about that. And then sort of take it one step further, and sort of how do these dynamics change when you add Verzenio on top in that regimen? So those were the that was sort of the thought process we were going through going in. I think, you know, and then on the safety side, you know, there's been safety signals generated with these medicines over the course of time, that I think people have wondered, are they class-based or are they medicine-based? And so I think these data will be another set of evidence to look at that. I'm talking about ocular issues, cardiac events, and dyslipidemia. I think those are, like, the three things people have really kept their eye on as, like, watch-outs, that, like, if you look at the entire class of these medicines, from ours to Elacestrant, to the Roche and AstraZeneca programs, you sort of see different profiles with different medicines. I think a lot of people have wondered: "Is it the medicine? Is it the target?" This will be another data set that I think will help answer some of those questions. Can you tell us if you've seen a differentiated safety profile in your favor? I can say we saw a differentiated safety profile in the phase I experience, and we'll see if that replicated in the phase III. But, I'm excited about presenting these data. Okay, including the tolerability safety data? Yeah. Okay. And then maybe just to press on the Verzenio question, 'cause you kinda said your expectation going in, but you framed it as a question. So, like, what was your expectation for Verzenio going into the study in terms of if it would provide a benefit- If you- or not? You look at the postMONARCH results, and the benefit of Verzenio fulvestrant in that study, a pretty similar study, was really irrespective of, like, all baseline genomics. ESR1, PIK3CA, AKT, all these biomarkers that physicians are now testing for in second-line MBC, the, you know, Verzenio plus fulvestrant effect size was pretty consistent if you sort of stared down that forest plot. Meaning, like, you could theoretically think about a benefit of Verzenio plus Imlunestrant in a wild-type group? Yeah, I think that's an interesting thing to think through. Okay. Okay, understood. Is San Antonio the likely venue for these data? A reasonable yes. Okay. Okay, got it. All right, I'm just trying to think if I had any others. I mean, I guess the other one is, you know, Pfizer has kind of this strategy where they're looking at, you know, this next gen CDK, you know, and going back to your earlier comments, is that something that you could see Lilly pursuing as well? Or, you know, do these data now kinda change that dynamic? I mean, how do you think about, like, a more selective CDK? Yeah, you know, we've boiled the ocean on these next gen CDK ideas, both in-house as well as through business development, and there's sort of selective CDK4, CDK2, like, there's a bunch of these ideas. I think you're referring to the selective CDK4- Four, right - program- Yeah ... from Pfizer. You know, I don't really. It's hard to know what to do with that. In other words, like, abemaciclib Verzenio is a selective CDK4/6 inhibitor. It inhibits CDK4 more than it inhibits CDK6. So the Pfizer program sort of takes that ratio and makes it a little bit bigger. I think, like, if that was the first generation of these drugs ever made, maybe that was the right answer, but we're so far into this experience, and you have to run head-to-head efficacy studies that win on superiority. Either I don't... I wouldn't know how to develop that medicine and have confidence that those studies are actually gonna work, unless you just ignore modern medical practice and don't actually compare your drugs to CDK4/6 inhibitors, which, by the way, in part, they're doing. We have successful studies now in second-line MBC. I think they're running against monotherapy fulvestrant again. So how will the world react to, like, a answering a question that doesn't actually answer the question? I think in first line, that's gonna be way harder. Like, I think you're gonna have to run a head-to-head study. That is intense. Same thing in adjuvant at this point. So I, on one hand, if you could rewind the clock, maybe that's the best biology idea here originally. I don't know how you get there, though, at this point. Yeah. Okay, great. I'm gonna ask one obesity question, and then I'll come back to oncology, but just 'cause we only have a few minutes left. There's a fairly big announcement about the Zepbound vials in the US that came out of the earnings call, but then you launched it now in the US through Lilly Direct, and there were some details on pricing. So maybe just step back, again, I know it's not directly in your wheelhouse, but again, was told this is okay, a question to ask. Just give us the rationale here, and then how to think through, like, the, you know, commercial implications, both from, like, kind of volume pricing and- Mm-hmm ... and high level, what this means for the Zepbound strategy in the U.S. Yeah. So by the way, if you work at Lilly, it, tirzepatide is everyone's business. So it's fair game for- Fair ... for anyone carrying the Lilly brand. So maybe just take a step back, like, how did we get here, right? We, we launched tirzepatide, to really like, unprecedented demand, demand that put a lot of supply pressures on our system, and we are working, as you know, as we've made a lot of announcements, talked a lot about it, we are working furiously to bring online new nodes of supply as quickly as we can for the single-use auto-injector pen, as well as the multi-use KwikPen devices. These are devices that, you know, we invented because we think they're the best patient experience, and I think patients and physicians attest to that. They are the best patient experience, and our goal is always to bring the best patient experience forward as the main product presentation. In the face of that, a couple things happened. One is that we were facing supply challenges because of demand, and we launched the vial format outside the United States as sort of a test balloon to see what would happen, because we had never really done this before. And we learned that there was a lot of demand for the vial format when that was the only thing available in certain markets. So that was an interesting initial learning that made us start thinking, could we launch a vial in the U.S. as a way of increasing supply? And then a second thing happened, which is that a cottage industry of drug counterfeiters showed up and started making fakes of our product and distributing it in vials through online pharmacies, claiming it, that it's real tirzepatide. It mostly isn't. Advertising to patients online and, like, getting real volume and prescriptions of patients paying out-of-pocket cash for counterfeit medicine delivered in a vial. Number one, that is just completely unacceptable behavior that, like, the law needs to be actually enforced. But it was a learning for us that there was an opportunity, that there was real demand here. So let's be clear, like, we've deployed this strategy as a way of increasing supply of a medicine that there is a lot of demand for, that we're on a ramp to meeting that demand with the, what I think are the more patient-friendly devices. But in the meantime, this, you know, this is a way of getting more patients access to the medicine, and I think through a mechanism with LillyDirect that is very patient-friendly and, at price points that I think are competitive for this format. Okay, and the other thing is, I think it also from, you know, the Medicare side, maybe there's a- can you just elaborate on, like, that Medicare angle too? 'Cause I think that's something that maybe potentially could help- You talking about expanding coverage into the Medicare? No, just for this, I think, 'cause the way I understand it is Medicare, they can't get access to the co-pay assistance program, right, for auto injectors, so this would be another way to help that population, I think, get access. Yeah. Look, I think we're at a sort of moment in time right now with this whole story, that I think will be different in a few years. I sort of hope and predict. Yeah. So as it relates to Medicare, specifically, you know, you know, we've talked a lot about our strategy to increase the labeled indications for these medicines into diseases that Medicare has the ability to cover. That's coming pretty soon. Yeah. Starting with, you know, obstructive sleep apnea. I think, like, that is, like, a real moment-in-time phenomenon. In the meantime, the vial format is a completely self-pay idea. There really is no insurance path, Medicare or commercial, for accessing that format. You go on LillyDirect, you can literally do it right now, you'll see where that exists. There's no, like, co-pay buy-down card or anything like that. It's a cash price. Okay. Got it. The... And just the last one on this is, just remind us, like, was this included in the guidance for 2024? Yeah. We've been working on this for a while, so it was included. Okay. I think the uncertainty, and of course, there's always uncertainty when you give guidance, is just what kind of volume will this channel attract? And obviously, we just launched it, so we don't know. And I think that's a real uncertainty- Yeah ... because, you know, we just don't know. Yeah. Okay, last minute, just quick hit on your KRAS program. That's obviously another one that you've been excited about. Just remind us, kind of, differentiation versus the other KRAS inhibitors. Like, what are, you know, one or two key features we should keep in mind? Yeah. So specifically, we're talking about Olomorasib- Yeah ... the KRAS G12C inhibitor- Sorry, yep ... because we have others, too. Yeah. This is the medicine we're developing primarily in lung cancer. I think, you know, this class of medicines has been a little bit tarnished, I think, because the effect size as monotherapy in second-line lung cancer is pretty modest relative to even docetaxel. I think the sort of big impact lever for this class of medicines is getting it into the treatment paradigm in newly diagnosed lung cancer, and maybe even the adjuvant setting. In order to do that, starting with newly diagnosed first line, you need to combine with the relevant standards of care, which are either pembro monotherapy or pembro plus chemo. The existing agents have had a hard time doing that for tolerability and safety reasons. So, you know, our main idea out of the gate was: Can we develop a medicine that's combinable? And I think the answer to that is yes. So, we are in the throes of standing up a pretty big phase III program, starting with first line in both, the PD-L1 high population, where it's pembro plus or minus our agent, as well as in the PD-L1 all-comer population, which is the KEYNOTE-189 regimen, which is pembro and chemo plus minus Olomorasib, all being done under one big master protocol design that we're rolling out across the world right now. Okay. And then estimate for data, like, a couple of years? Yeah. I mean, we're just getting started with accrual. But, you know, over time, you'll see additional readouts from the program, from the phase I, because we still have a lot of patients ongoing there. So you'll see new safety experiences, new efficacy data. You know, we're continuing to generate data in other disease settings, like colon cancer. So there'll be other data updates on this program, but as far as, like, pivotal, randomized phase III data, that'll be a while. Okay. Well, I think we're up against time, but, thanks so much, Jake. Appreciate the breaking news and, you know, keeping it interesting. Thanks for having me. Thank you.