Healthcare conference. It's the first one at TD Cowen. I'm Yaron Werber from the biotech team. It's a great pleasure to moderate the next fireside chat with Mike Morrissey, our President and CEO of Exelixis. We have Chris and Susan here as well. Mike, always good to see you. Yeah, you too. Thanks for joining. Yeah. Appreciate it. Great to be here live again. Lots to talk about. CABOMETYX continues to grow annually. The pipeline is coming now into late-stage development, early-stage development, multiple different new platforms coming through. Right. Let's maybe talk first on CABOMETYX because it's still very much the growth driver. You gave guidance of growth about 13%-20%. year-over-year. What's driving that? Is that still share gains? Is it durability? I don't know how much you can comment between renal and liver as well. Yeah, for sure. Well, again, great to be here. Congrats on the meeting, having it live again. It's great to see the, you know, the hallways buzzing again, so. Yeah. Congrats there. Yeah, for sure. I'll be making forward-looking statements today, so please see our SEC filings for a description of the risks that we face in our business. Yeah, CABOMETYX growth has been strong the last couple of years. you know, overall, we've seen a double in net product revenue since the end of, well, since 2020. That's been nice. Obviously, the CheckMate 9ER data is, was strong, continues to be strong. You know, we had the 44 month median follow-up data at ASCO GU. About a month ago, that was the hit of the meeting. You know, the maturing survival data there looks impressive. You know, median of about 50 months now. Really challenging a lot of the dogma around expectations for survival with an IO TKI. You know, best in class molecule in terms of RCC, top TKI for RCC in terms of a combination with an IO, and then top in the 1st line setting and then top 2nd line drug as well. We're pleased with all that. In terms of growth, again, we've seen strong growth since the 9ER approval, right? If you look at that, over the last 8 quarters, first 2 quarters, we grew about 5 share points, and then we've been growing a single share point since then, over the last 6 quarters. That's again, a single share point may not seem like a lot, but when you look at what that's worth to us in terms of top line revenue, that's a big number. To see that consistent growing, and that's due to both very solid NPS growth. We're starting a lot of new patients in the front line setting, and then the fact that we have long duration of therapy with the PFS in the 16-17 month range from the 9ER study, seeing this compound stacking of patients year-over-year helps too. In terms of 23, the growth is a mix of both, certainly more NPS, more and more, more new patients start as well as that continued compounding. 2 years in, have a lot of patients who are on study and are on drug and doing well, in their frontline setting. We're excited about that. Not certainly gonna rest there in terms of, being content with that data, but we're, very aggressively marketing the drug per label and, hoping to see that continue to grow in the years ahead. Is most of the growth from first line renal? Yes. from new adds Yes. Is it from durability? It's a combination. Combination of both. Yeah. Yeah. For sure. What's going on with share in second line? I assume you're gaining in first, and second is sort of stabilizing or maybe. Yeah. If you look at the brand impact data, which is, you know, probably the most concurrent publicly available data where they look at SharePoint, and you can argue about the methodology, but it's a good, I would say benchmark. You know, front line, we're in the, you know, 20%-25% range consistently. Second line, we're in the 40% range overall. That's a very strong place to be in terms of having a majority of impact on patients in those first two lines of therapy for RCC. How are the trends? 40% sounds like it's been fairly stable. Is the growth really just capturing share in first line, or you're seeing a little bit of a shift? Yeah, no, it's really growth, capturing the first line setting. Yeah. Keeping the second line constant. Yeah. Okay. For sure. Let's talk about maybe COSMIC-313. You know, you've hit on PFS survival. Obviously, it's been a little too early. We're about 20 months so far. In terms of follow-up, the activity, you know, was overall, but there was obviously a better activity driven by intermediate risk than poor risk. You're still waiting for an update on survival, I believe this year. Right. What are you expecting to see? I don't know if you can share with us. What do you think you need to see to get a label? Yeah, it's a good question. Obviously, we've had a lot of discussions internally and with the FDA on that topic, I don't wanna provide too much oversight on that right now. I think what's safe to say is that the mature data is the most important thing, as we accrue more events, and we have the second interim coming up in the second half of this year. We'll see how that data looks. If it's, if it's appropriate, we'll talk to the agency about that. If not, we'll go to the final analysis and then see how that goes. Obviously, you know, bar is pretty high here. PFS has historically been enough for approval. I think the winds are shifting a little bit in terms of expectations, and the overall risk-benefit here. Survival is an important part of that equation, and we'll get more mature data and see how that looks. Right. I mean, the hazard ratio was already 0.7 on PFS, right? Yeah. That's unlikely to change at this point, right? Yeah, exactly. It's a question of, I know you haven't commented a lot. The second analysis usually sort of 50% of the events. Is that even in the? I would say a bit more. Bit more? Yeah. Yeah. Okay. The final sort of in the seventies, would be? Well, final would be 100%. You have to wait all the way to the end, okay. If we have to go that far. Again, I don't wanna project too far. Let's get the next interim done and see how that looks. Yeah. The next one should definitely be maybe more than 50, probably even. Yeah. Yeah. Yeah. Yeah. Okay. Got it. I mean, survival, if I remember correctly, in this setting is, well, the data's been sort of maturing, right? It was almost 40 months in first line when you look at some of the competitors. Am I, am I off? It really depends. The question is, say, with Ipi/Nivo, you're looking at intermediate poor with the TKI/IO combos, you're looking at all three, with favorables, obviously, will right shift. Yeah. the complement pretty dramatically. It's all, you know, trial dependent and situationally dependent in terms of what you're looking at and, you know, the ratios and those kinds of things between the two. Yeah. three different risks Is there a chance, and I know I'm jumping ahead here, but is there a chance to get a broad label or you might still be driven by the intermediate risk cohort? You know, I wouldn't wanna speculate on that right now. That's. Yeah. A discussion for us and the agency at the appropriate time. Look, we're looking to enhance the opportunity for patients to access CABOMETYX as a single agent, as a doublet, and potentially a triplet. I think we'll get the data that we need. We'll work with the regulatory bodies to figure out what makes the most sense there and then move forward appropriately. Okay. Right. In principle, this was a study in essentially both cohorts, right? It wasn't really. Cutting into a sub-segment is not probably where you wanna go. Ideally, the bigger population's better, but that's gonna come down to the data and, you know, how the various stakeholders view that data relative to standard of care and risk benefit. Okay. If there's any questions in the audience, just, yeah, by all means, let me know. Let's talk about CONTACT-02 in, you know, metastatic castration-resistant prostate cancer. I think we're expecting an update later on this year. Yeah. Just given the historical data, right? About 18% response rate, what, you know, from the prior cohort, I'm talking about COSMIC-021. Right. What are you expecting from this? you know, how much of an important indication is it for CABOMETYX at this point? Well, it's certainly a large population, even considering the subset of patients that we're looking at with measurable disease by RECIST 1.1, either visceral mets or extra pelvic, lymph node mets. It's an important opportunity here. Obviously, we have a lot of history with prostate cancer, with the Cabo molecule going back- Yeah. To the, you know, early days in 2011 with the bone scans and. The COMET trial. In the beginning. yeah, it's been a long, a long story. again, the primary endpoint for CONTACT-02 is progression-free survival. We're going against a second NHT, which, and I think is a relatively low bar. we'll see how it looks, right? From the standpoint of how PFS for the CABOMETYX/atezolizumab doublet compares to a second NHT, in this relatively defined population of patients with measurable disease. It's the cleanest experiment we could run to be able to really answer the question of the impact of that doublet on disease progression in that population. If it works, you know, we have lots of opportunity with XL092 relative to how we might play that zanzalintinib, how we might play that going forward. We'll talk more about that later, I'm sure. You know, prostate cancer is an important opportunity. We've all seen some failed trials that are recently looking at IOs by themselves or in combination with various chemotherapies. It's a, it's an area that really needs new therapies, new approaches, and we think this is an important one to test, and looking forward to having those results later in the year. What's considered clinically meaningful in this? Is it sort of six months is the bar, or you wanna see kind of a three months difference from Control? Yeah. I'll just take the P value. Yeah. frame it the right way, and we'll navigate the rest. Yeah. Okay. great. let's talk about zanzalintinib. I mean, you naturally alluded to that already. Before we go on, though, let's talk about CONTACT-03 real fast. Okay. second line renal trial. I wanna just. It was a trial that read out last week. It's an interesting dynamic and certainly opportunity for us. You know, we ran that trial for a couple reasons. Well, it was a very clean way to ask the question, does sequencing one checkpoint inhibitor after a patient's failed a first or second checkpoint inhibitor, does that actually add value in terms of risk benefit for the patient? Secondly, it was really asking the question, for single agent cabo, can we actually benchmark what that would do in the context of a patient who has progressed on a checkpoint inhibitor? The important biology here is that, you know, it's, you know, CD8-positive T cells live a long time, even after you stop dosing with a checkpoint inhibitor. It really asked the question in a very broad sense, you know, can you, can you magnify the activity of that relative to adding on a compound like cabo? It was a very interesting experiment. Trial didn't work in terms of showing a differentiation between the doublet cabo/atezo versus cabo. There's been a lot of chatter around, "Well, you guys used the wrong checkpoint inhibitor. Atezo isn't that good, blah, blah. I think the reality is, in our hands, in the couple of cohorts from COSMIC-021, we were able to actually show that CABOMETYX plus atezolizumab, either at the 40 milligram dose or the 60 milligram dose of CABOMETYX, actually had very similar activity in terms of response rate and PFS to what we saw with CABOMETYX and nivolumab and that combination. Response rates in the 50%-60% range, PFS in the 15-20 month range. We feel like it was the right checkpoint to use. The question is, what does the biology tell us about what's happening there? We'll talk about the actual data when it comes out this summer. It's really interesting to note that CABOMETYX by itself performed really, really well. In fact, single agent CABOMETYX in the control arm actually met all of our hopes and aspirations for what the doublet would do from a duration of therapy point of view. Okay? Interesting. It wasn't so much that, you know, Cabo/Atezo didn't work, but that Cabo by itself worked really well, and that's probably because all these patients have activated CD8-positive T cells already in place. They don't need to be activated further by a checkpoint inhibitor. It's already happening, right? Data coming out shortly, but I'm really proud that we and the investigators, you know, did the right study, asked the right question. It's gonna be really important for, I think, the community, 'cause a lot of patients are sequentially treated, you know, with one checkpoint after another. In this case, I think it really shows, at least for renal, that that's probably not the best way to go. Okay. There's still sort of a win here for CABOMETYX alone. Well, Yeah, from a duration point of view, you know, if we're seeing in this population the duration with CABOMETYX that we were hoping for with the doublet, then yeah, CABOMETYX does well there too. Okay. let's now move to non-clear cell RCC. You know, some moving on to zanza. Obviously, the STELLAR three or four studies, zanza plus Opdivo head-to-head against Sutent. Maybe, you know, put that also in context of the prior COSMIC-021 data. With CABOMETYX TECENTRIQ. Sort of, you know, I'm trying to... You know, CABOMETYX Tecentriq is obviously not approved for NCC... Right. Moving on with the next generation. Maybe just kinda set for us where, what do you wanna see from a bar? How much CABOMETYX is actually used right now in NCC? Yeah. The latter question I'm gonna answer first. It's hard to actually break that out. We don't have real good analytics on the breakdown from a commercial point of view between clear cell and non-clear cell or different types of, all different types of non-clear cell. You know, historically, it's a 15%-20% mix of the overall population. I would assume that kind of tracks the same. The label for CABOMETYX is broad enough to cover all forms of RCC. That's not really even off label per se. It's just part of the overall experience. There's very little randomized data in that setting. Again, from the standpoint of pushing the wave of zanza pivotal trials forward, we thought that made a lot of sense as the lowest hanging fruit in RCC. We have a lot of interest in looking at novel triplets in RCC, with both, you know, zanza plus a doublet of IOs versus zanza plus an IO plus other modalities. More on that as those trials evolve and get started. Again, I think this is a great place to start and to kinda reinforce our interest in the franchise of kidney cancer and then to build out the zanza pipeline within RCC as well as other tumor types in GU and GI and thoracic and beyond. With zanza, again, you're sort of going back old school and doing this study with Opdivo and now with Tecentriq. Right. Why is that? You're just trying to build on what you already approved? Yeah. I think the, I think the overall approach is to be somewhat agnostic in terms of the checkpoint that we use. We've got nivolumab with 304 in non-clear cell RCC. We're using atezolizumab in 303 in the third line CRC, and we have plans to use other checkpoints in future pivotal trials that we'll announce this year. It's really a catch-all from the standpoint that we view those as all more or less the same, more or less interchangeable. It's just kind of, you know, mixing and matching based upon the different situations and opportunities. 304 is Bristol providing Opdivo? Okay. I assume Roche is providing TECENTRIQ for 303. Exactly, yeah. The commercial rights are just yours. They're all ours. For zanza. For Zanza. Yeah. Exactly. Exactly. Yeah. Yeah. This could be label enabling for the checkpoints as well, that study or no? Sure. It's, you know, it's the combination that is involved, right? So. Got it. Okay. Going back to STELLAR-303, right? Now you're talking about zanza and TECENTRIQ in third-line CRC. This, I assume you're building on TECENTRIQ from the prior study, and that's why you're doing TECENTRIQ. Really, it's more the CABOMETYX data that we had at ASCO GI in 2022. We had 2 different studies published where we showed a response rate in the 25%-50% range with 2 different checkpoints. Strong PFS data, you know, all the caveats of it being non-randomized, but strong PFS, strong survival. The unmet medical need there is very, very high. We feel like that's again, a relatively low hanging fruit that if we can win, it's a big move for patients and certainly a great start once we file and would, you know, get that approved and on the market. Okay. So far it sounds like you're going to, you know, colon, you're going to, NC, NCC, RCC. What's next for zanza? Yeah. That, that is to be defined this year. We've got at least a couple more trials that'll start this year, and then certainly more after that. You know, the overall framework here is to look at both existing CABOMETYX indications where we think we can design better trials, better combinations, better doublets and triplets, that would allow us to raise the bar in terms of standard of care for patients, as well as new indications where we have some activity, some historical activity with CABOMETYX, haven't pursued full development, so we can then engage there, with zanza plus, any combination partner which makes sense. Again, I'll just reinforce, we're not looking to just be as good as CABOMETYX, right? Yeah. We're looking to design better trials, better combinations. We have to improve standard of care, right? We have to be able to move the needle for patients 'cause that's the only way you're really gonna be able to make a difference from a pure marketing and overall commercial point of view. The days of having me two drugs sell are just over, right? Okay. It's all about bringing more value to patients, right? Data from STELLAR-002, that's the phase Ib testing, combination with zanza, with Opdivo. Of Opdivo and Yervoy or with Opdualag. Are we, and you're doing obviously dose escalation right now? Right. With all the cohorts. Right. Right. Any data released this year or sort of what's the next thing? We'll see. You know, it's all about execution this year. If we have the opportunity with mature data, then we'll certainly present that. It's, it's really important for us to launch pivotal trials, move compounds forward. That, that's the priority, right? But again, you mentioned this on the call and certainly, again today, the combination of zanzalintinib plus relatlimab plus Opdivo is a very attractive approach based upon some of the early melanoma data. Have a great relationship and history with BMS, so we're excited about that. If we can move that into, you know, multiple pivotal trials in the short term to, you know, to be defined across tumor types, that would be a great way to go, right? If you look at the some of the STELLAR-313 data, you know, ask some of the questions about where you can improve upon that just in general. Well, maybe swapping out IPI for relatlimab might be a better way to go, having ZANSA, you know, shorter half-life, maybe better tolerability for CABOMETYX, you know. Again, we're looking for winning combinations that we can then go against standard of care and improve outcomes for patients. Yeah. Okay. We're still around 2. It sounds like you're still in the dose finding, and at that point you'll do a whole bunch of escalations. COSMIC-021. Well, the question is, once we have a dose, what do we do, right? You know, we're not, say we're not shy about moving forward aggressively into pivotal trials if we have a dose, and we did that with CABOMETYX-nivolumab, CABOMETYX-nivolumab IPI, right? I would expect we will act in a similar fashion here. Yeah. Okay. Got it. Any questions from the audience? Let's talk about, you know, the one element I did not talk about is just litigation. The next trial has now gotten pushed from the spring to the fall, right? And. It's in October. Right. It's in October. I'm thinking the decision's probably more sort of next year, the way. Well, the last judge took, you know, 6, 7, 8 months to rule. I know you can't say a lot about that. The litigation with TAM essentially stayed pending the second case with MSN. Yeah, that's correct. Right? That's probably not gonna. I would imagine even, you know, pending a resolution with MSN or, and verdict, that's still gonna be whether that litigation starts right away or whether it waits for an appeal. Yeah. Again, wouldn't wanna speculate on what timing wise or what could happen. Yeah. Yeah. Okay. Sorry. I got you. You're right. The first case was a split decision. Second case, it is pending. We have a lot of confidence in the data and the depth of the IP, and certainly the team is, both internally and externally is first class. We're confident in what we've got and understand the value proposition. Off we go. Okay. Okay. Before we dive into the early pipeline, you know, you're sitting on a lot of cash, and I get questions all the time. Does it make sense for you to do something bigger? It's something we've talked about for years anyway. Yeah. Sure. Sure. Valuations have come down, obviously. Valuations are fluctuating up and down all the time. Yeah. Yeah. Yeah. Why not go out and buy something in phase II? Yeah. Well, the issue isn't for us, it's not valuation. It's conviction in the asset, right? To be frank, there aren't really a lot of high conviction assets out there right now, right? I think that's not just our view, but that's the view of the general biopharma world because the number of big deals has been, you know, relatively small in oncology for the last few years, right? We're looking closely. We have a pretty short target list of, I would say, high value assets that we are pursuing. Those might work. They might not work. We'll see. The two option deals we did at the end of last year with Cybrexa and Sairopa, I think are a good example of how we can put the right amount of cash to work to be able to have access to clinical stage assets, and then essentially pay for success if that comes to fruition later. We're looking at later stage assets, those that are in, you know, late phase Ib, phase II, have reasonable to good data, and we'll see if we transact. Those would come at a bigger price tag. We think that's warranted based on our lens of what success could look like there. It's all about. You know, again, we're really informed by the Cabo experience. Again, Cabo is a drug that was, you know, returned to us twice, failed pivotal trials. We had a lens into the activity of that molecule that allowed us, with the data we had and the belief that we had in the, in the overall approach, to be successful commercially for a lot of patients, and generate a lot of revenue. I think that same lens is being applied to here. We're very disciplined. If we do transact on a bigger scale, then it'll be because we have the conviction, that it makes sense from a pure clinical commercial standpoint. Yeah. Let me actually, you know, one thing, I'll take a step back for a second and back here. You know what, one of the things that we don't have visibility on, and obviously of your planning internally that we don't have, we obviously don't have a view at this point what the IP is gonna be, right? Is it 26? Is it 28? Is it 30, 31? It's obviously four years that make a big difference, right? In terms of not just where the TAM and area under the curve, I'm talking about your ability to then replenish, right? Yeah. you're in phase III now in, you know, colon. Third line is interesting. That's not gonna be a CABOMETYX replacement, right? Where I'm going with this is that you know, over the next 12 months, you need to start moving into phase III. You can have data in about 2 years, launch, right, and be ready for the 2026-2028 timeframe. The worst case, 2028-2030 in the good case, right? How are you thinking about all that? The early pipeline is interesting, but it's just too risky and too far behind. Yeah. Yeah. you know, the clock never stops, and we talk about that a lot, you know, back in Alameda. You know, the temporal nature of what we're doing now internally, the value of speed in moving Zanza forward, XB002 forward, the early-stage pipeline that is, you know, will be in the IND-enabling phase right now. You know, the beautiful thing about oncology is that if you pick the right targets, you make the right molecules, and you do phase I the right way, you can get hints of activity early on and move quickly into phase III. That was the Cabo story to a large degree, right? Yeah. We feel like first of all, we're very confident in the 2030 window in terms of LOE for Cabo. We've got room to maneuver. We have a very deep pipeline of assets that we think can really generate the right level of data that we can then monetize appropriately if we move them into pivotal trials quickly. That's been our MOA years, right? There's a lot of companies, and no judgment here, but there's a lot of companies that almost avoid making that transition because it gets expensive fast. You gotta put all your chips on the table and say, "Okay, I'm gonna bet the farm on this approach." Well, we've done that, and we have the confidence in that and the conviction that we know what we're doing there relative to... You know, every trial is not gonna work, but we know how to play that game pretty well. All that being said, We don't feel any level of desperation to put money at work, take big bets. We have a sense of urgency and a sense of focus and a sense of energy in doing the right science, the right clinical science, asking the right questions. We have time and the luxury of having something like CABOMETYX that generates free cash every quarter. We can take these shots on goal, in the appropriate manner and really hedge our bets well with the internal pipeline, things that we can, you know, source externally and have a broad portfolio. It's all about the pipeline and playing that pipeline game. Yeah. as successfully. Let's talk about the early targets are super interesting, you know, the bigger question is just how fast, to your point, you can move them forward. With XB002, you're already differentiated, you know, you can see an early look versus Tivdak. The question Tivdak in cervical is not gonna be big. Therapeutic window, and cervical is just not a big indication. Yeah. What's next? I know you got to figure out the dose still between 2 and 3 mgs per kg. You already got a differentiated profile early on. Yeah. Yeah. You know, you know, over and above cervical, what's the next tumor type that makes sense? We have. The dose expansion cohorts include 10 different histologies. We need to lock down the recommended phase II dose and, you know, all the Project Optimist machinations just complicate that to a certain degree, and we'll do that as part of dose range finding and then certainly in the dose expansions. To have 10 different tumor types, that really allows us to ask the question, including cervical, so we benchmark there. You know, are there tumor types, because XB002 has, you know, has a differentiated safety profile, has arguably better exposure, and a more potent toxin, right? Do we see tumor types that are insensitive or just modestly sensitive to TF actually have oversensitivity to XB002? That's the home run, where we can go from cervical plus indication XYZ versus just cervical by itself, right? That's either as a single agent or a combination. Project Optimist is, you know, look, it's spot on, but it complicates life, when you're looking at 10 different tumors, right? Is it that you need to find, Do you have to find the right dose in each tumor? Is it that you Well, I think you would use each or a subset of those tumor types to triangulate to the right dose for all of them. I think that's the issue, right? And it's- Again, and again, the question is when you do that and how you do that. Yeah. It's really hard to do that unless you have a sensitive tumor type. Yeah. 'Cause how else do you judge activity? You can judge safety and toxin tolerability, but if you can't judge activity, then it's really hard to do that, right? I guess cervical is a good starting point, right? There's an approved drug. Maybe. Yeah. Maybe. Yeah. Maybe. Yeah. Maybe. Yeah. I'm not convinced of that. You're not convinced of that. Okay. Yeah. No. Is 2 mgs per kg sort of the lower end or it's unclear? Could it potentially be even- I think it's the lower end right now, but we'll see. That was the data from last year, right? 2 mgs per kg at the exposure that we're getting is actually, you know, it packs a punch, right? Yeah. Relative to what Padcev has, right? you know, and I think a lot of companies, and we're asking everybody the same question, you know, you know, some companies have to contend with that when they're doing fairly rare, you know, tumor-agnostic approaches. It's not that easy to enroll. Yeah. you know, how do you determine the lowest effective dose in phase I, based on durability too? Probably can't do it in phase I. You probably have hints of that, but you really, really refine that later on when you have more patients, right? In phase II. Yeah. Yeah. It's more than a single dose. You gotta do a bigger phase II. Probably. The question is how, and what's the most efficient way to do that, right? Yeah. Yeah. That phase II is really phase Ib to a large degree. If you wanna define that window, that therapeutic window across cohorts, you can generate a lot of data across cohorts. You pick the winners, and you go to phase III, right? Yeah. I think that's the optimal. We did that with MTC, with RCC. We actually ran very few phase II trials with Cabo. You know, we were on kind of at the forefront there. That was Gisela's, God bless her. That was her kind of insight into, you know, how to play that game, and then she was spot on. So. In the novel world, this is we're talking about 20, 30 patients, multiple doses in phase II. About 30. Yeah. Yeah. It doesn't have to be statistically significant versus placebo at that level. Right. It's gotta be telling. Yeah. Yeah. You'll see activity when you see it. When you see it. Okay. At the right dose. Yeah. With about a minute left, let's talk about CDK7. What, you know, the big question is ultimately which indication? You know, obviously dosing, there's some competition here as well, but more what do you think the biology is most compelling? I think that's the issue. I think the big issue is it a target of interest, right? Because there's no clinical POC, no clinical concept here at all. We have the right probe. It's potent, it's selective, it's irreversible. To ask the question, does this molecule, does this approach of it, you know, basically irreversibly inhibiting CDK7 do anything? I think that's the first big question. But I, you know, I like the scientific part of that. We're asking a very fundamental, fundamentally important question around the biology of cell cycle and we're gonna get that, I think with this program. It may be, it may be good news, go into indication XYZ. It might be don't bother, and we'll find out, right? How do you tell that from phase I? I mean, the magic here is you wanna find it in phase I? Well, I think we'll find. Or- within phase Ib. Yeah, sure, because we have the right expansion cohorts to be able to feel good about that. Yeah. Yeah. Yeah. Okay. Great, Mike. Good to see you. Hey. As always. Thanks for the time. good to see you. Thank you. Excellent.