Arcus Biosciences, Inc. (RCUS) Earnings Call Transcript & Summary

Great. Good morning. Thanks for joining us, everybody. I'm Terence Flynn, Morgan Stanley's U.S. Biopharma Analyst. I'm very pleased to be hosting Arcus this morning. Joining us from the company, we have Jennifer Jarrett, the company's COO and Richard Markus, the company's CMO. Thank you both so much for being here. Really looking forward to catching up. Before we get started, 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. With that, I thought maybe, Jen, just give us kind of an overview of strategic priorities for the company as we head into 2026 here, and what you and the team have been focused on and then we'll dive into the pipeline.

Sure. Well, thank you, Terrence. So first of all, I'd just start with a very, very high-level overview of Arcus, and then I'll get into what our top priorities are right now. So Arcus is very unique for a smallish biotech company. So we have 3 different programs and 5 Phase III studies, all targeting very, very large tumor types, including gastric, lung, pancreatic cancer and renal cell carcinoma. One of the reasons -- probably primary reason we've been able to pursue so many different Phase III studies in parallel is because of the funding that we've received from our partners, specifically Gilead, AstraZeneca and Taiho. And in fact, we're only having to operationalize 2 of those 5 Phase III studies. So that gives us a huge advantage from operationalization perspective. From a priority standpoint, probably priority #1, 2 and 3 right now is execution of the global Phase III program for casdatifan. Casdatifan is what we believe is a best-in-class HIF-2 alpha inhibitor there's only one HIF-2 alpha inhibitor that's approved and in development today, other than ours. That's Merck's belzutifan, which has had a very, very successful launch so far in RCC. Today, it is only approved in late-line RCC for our first 2 Phase III studies, we are going to be targeting earlier line settings, so specifically the second-line setting or IO-experienced RCC; and then first-line RCC in collaboration with AstraZeneca. We've now presented data from about 90 patients for CAS monotherapy, which showed clear differentiation relative to belzutifan in every efficacy measure that we reported on. So that was primary progressive disease, ORR and PFS. We have data coming in October that we'll be presenting at an investor event on 120 patients where we'll have about 8 months more follow-up versus the last data presentation at ASCO GU. We've now started our first 2 Phase III studies, as I mentioned earlier. The first is a study called PEAK-1 that is evaluating CAS plus cabo and IO-experienced RCC. That's about a $2 billion market opportunity, in G7 countries alone. And then the second Phase III program, which we're running in collaboration with AstraZeneca is actually set up as a Phase Ib Phase III study. So we've just started the Phase Ib portion with them, and that is evaluating CAS with AstraZeneca's type anti-PD-1 CTLA-4 bispecific antibody in first-line clear cell RCC, and that's a $3 billion-plus market. So we think these two settings alone can be about $5 billion in G7 countries. So that is priority #1, 2 and 3, as I said. Our next fourth priority is getting to the Phase III readout from our two most advanced Phase III studies. The first, is a study called STAR-221, which is evaluating domvanalimab, our Fc-silent anti-TIGIT antibody in combination with anti-PD-1 in chemo, in first-line gastric cancer. We are running that study in collaboration with Gilead. That readout is expected in 2026. That's about 1,000-patient study. And then the other study where we could get to Phase III data as soon as late next year, is our PRISM-1 study, where we're evaluating quemli, our small molecule CD73 inhibitor in combination with chemo in first-line pancreatic cancer. That's about a 600-patient study. So one really important thing to mention with both those studies. Those are 2 Phase III studies, both of which are completed enrollment, the first STAR-221. We completed enrollment on in only 18 months and even more impressively for PRISM-1, we completed an enrollment in just 9 months. So that's shown as we're going into PEAK-1 our first Phase III study for casdatifan that we've been able to execute on two very large global Phase III studies in oncology. So very different than a lot of biotechs, which out of the gates are having to run a big global Phase III study for the first time. So we have a lot of experience already. The next priority that I want to mention is we have some really active discovery efforts in inflam. We've now been working on these for almost 3 years. So we're not just re-purposing some oncology molecules, we have been working on for inflam. These are all best-in-class and/or first-in-class opportunities. We'll have the first disclosure on these programs at our investor event in October. And then the last thing that I want to mention from a priority standpoint is we are very, very focused on capital preservation. We're very fortunate today to have over $900 million in cash from our balance sheet as of the last quarter. And we want to make sure that, that capital lasts as long as possible. So we've paused a few things that felt a little bit less strategic and important and we're really focused on conserving capital anyway we can as a company.

Okay. Great. I know we're going to dig into a lot of these. But maybe first, just another high level one. Obviously, there's been a lot of focus on kind of some of the changes at the FDA, et cetera. I know you guys mentioned you've a lot of upcoming pivotal programs, ongoing pivotal programs. What's been your view on kind of interactions with the agency? Is it steady state? Are there any changes? Any slowdowns, acceleration? How would you frame that for investors?

Yes. I think the change in the FDA really hasn't had any effect on us. We've had good communication with them, clear communication with them and being in the oncology space is really still, I'd say, steady as it was -- as it goes. And our study designs, also, I don't think are controversial in any way being randomized, double-blind type studies, et cetera. So I think we're very comfortable and confident still in what we've put in place and the reception it should get at the health authorities.

Yes. Okay. Great. Maybe moving on to cash, just given Jen, this 1, 2 and 3, as you said in terms of priority, I know you mentioned you have 90 patients and you are going to get another 30 patients. It sounds like in this next update and longer follow-up. So maybe remind us kind of what the data was that we saw already as we look ahead to this next set of data, and then the Welireg or Belzutifan, the Merck program, just remind us of kind of the relevant benchmarks as we look for this next data update from the fuller data set here in October?

Yes. So this next data set, as you pointed out, there will be 120 patients. So all 4 of the monotherapy cohorts that we're evaluating casdatifan and late-line clear cell RCC. These are all patients that received at least 1 anti-PD-1 therapy and one TKI. So a very advanced patient population. It is -- look at the data. We'll have about 8 months more follow-up versus the last data presentation so its quiet a bit more follow-up. As a result, we'll be able to provide a lot more PFS information relative to what we provided the last time around at ASCO GU in February. So what you should expect to see is updated safety and ORR data, further the 120 patients. And then whatever we can share on PFS. So the last time we presented data in February, we only had 1 median PFS [indiscernible]. That was for the 50 mg BID cohort. That was the first cohort to complete enrollment. So it's this next look, we may not still be a median PFS for some of these cohorts. This is obviously a very good thing, but we'll show the Kaplan-Meier curve, so we'll start to get people a sense for where the PFS' could come out for these other cohorts. The other thing that I think will be very interesting for people to see is that first cohort to enroll the 50 mg BID cohort. We now have a lot of patients that have been on therapy nearly 2 years. So you'll really start to see the tail of that we'd expect to see with HIF-2 alpha in addition. And you can see the percentage of patients that have now been on treatment close to 2 years. And obviously, that translates into very, very meaningful clinical benefit for patients as well a very large revenue opportunity for us as you think about the time on treatment. To your question on the benchmarks, so belzutifan across all of their studies. So this isn't just Phase III study. They've shown an ORR in the range of 18% to 22%. Looking at a similar patient population, actually, in a lot of cases, a little bit of a less advanced patient population than what we're looking at. As a reminder, at the last data presentation for the 100 mg QD cohort, which is our going-forward dose and formulation. We showed a 30 -- oh sorry 33% confirmed ORR and we showed a higher ORR all 3 monotherapy cohorts relative to that belzutifan benchmark. The other two efficacy measures that we reported on were primary progressive disease in PFS. For primary progressive disease in LITESPARK-005, the Phase III study for belzutifan. They saw about a 35% primary progressive disease rate. So these are patients that are progressing on or before the first scan, so patients that never even get a chance to benefit. So far, we've been showing a primary progressive disease rate in the teens, so about half of what's been showed for belzutifan. And then for PFS, Merck reported a 5.7 month PFS in LITESPARK-005. They also had another smaller data set that was just presented earlier in the year, similar patient population for belzutifan, and they showed almost exact same PFS so about 5.6 months. In contrast, when we presented the data in February, we showed a 9.7-month PFS for that 50 mg BID cohort. And then we also showed the 50 mg QD cohort and you can see that clearly, like we were going to be beyond 9.7 months PFS for that cohort. So we're significantly beating all of the efficacy benchmark data for belzutifan.

And just remind us the Phase III dose that you're using here because, again, you've had 4 doses we're going to see and what's the right one to look at for the Phase IIIs?

Right, so 100 mg QD tablet is the going-forward dose in formulation. So the 4 cohorts that you'll be seeing are, first of all, that 50 mg BID-cohort, that was the first cohort to enroll. We only had capsules -- 10 mg capsules at that point in time. So that's why we had to split it up into BID. So patients are really taking 5 large capsules per dose. And then we had 2 dose optimization cohorts, so a 50 mg QD and 150 mg QD. So we've been able to check the box on the dose optimization requirement and then last with that 100 mg QD tablet dose in formulation, which is the going-forward dose in formulation for our Phase III studies.

And you still feel good about that choice of dose given the more maturing data that you're seeing?

100%. Yes. I think when people see the data, I think they will feel very, very good about the 100 mg QD. I think what's also important because the 50 QD, also looks very, very good. There are going to be patients that get dose reductions because of anemia and hypoxia, which were the 2 on-target toxicities that you see with HIF-2 alpha inhibition if you look at the belzutifan studies, they have about 30% dose reductions due to these on-target AEs. If you do have to dose reduce from 100 mg to 50 mg, patients are clearly getting a very, very efficacious dose of CAS, which is different than belzutifan and if patients have to go from 120 to 80, which as I said, about 1/3 of the patients seem to do, they're definitely losing efficacy. So we think this is another big advantage for us.

Okay. And that's built into the protocol already in Phase III, the dose reduction?

Yes. We have very strict guidelines.

Okay. Great. All right. And then I guess the other opportunities that you're doing, the combination with cabo, you had some data at ASCO. Maybe there, just talk about it? I know you did a lot of work on dose selection there. Maybe just give us an update on kind of what the key findings were for that study because I know that informed your PEAK-1 Phase III program.

Yes. So that was evaluating 100 mgs of CAS, same dose of CAS with 60 mgs of cabo, which is the approved dose of cabo. So very importantly, from the data set that we presented at ASCO, we showed that you can safely combine those two drugs. The safety profile looks very good. Only two patients had to discontinue, one therapy, no patients discontinued both therapies, which is very important because at all points in time, patients were getting at least one treatment, and then we reported a 46% confirmed ORR, even though it was an early look. That compares to a 31% confirmed ORR that was reported in a similarly designed study for belzutifan plus cabo.

Okay. And then on PEAK-1, again, I know you mentioned here the design is IO-experience population. You're going combo versus cabo mono. Again, any more details in terms of powering assumptions that you can share on the trial?

Yes. So the CAS cabo study versus cabo alone is the key registration study. It's randomized placebo controlled, and the key endpoint is PFS. So that's accepted endpoints in this population globally. So we are on good grounds there. And it also, of course, moved the time line in significant amount by looking at PFS versus OS. But that said, we do have OS data being collected. It's a prespecified secondary endpoint, so it will satisfy all the health authorities requirements when we look at the OS data that's available, but the PFS is the registration endpoint. And I think that's also in our favor.

And what kind of effect size are you guys looking for in the study?

So we can say that cabo alone generally will have a PFS in the kind of 9- or 10-month range would be the assumption. We expect to be significantly and clinically greater than that.

I mean it's 20%, the minimum bar usually in oncology that...

Yes, we haven't really come out with where the study design is on -- but I'd say it's a well-powered study for clinically meaningful benefits.

Yes. Okay. And what maybe just talk through like how site activation is going, enrollment? I mean, Jen, you kind of alluded to some of this in your prepared remarks. But maybe just any update there. And then I think the competitive study that some people are focused on is the Welireg study in terms of time line. So how are you stacking up in terms of time lines relative to that study?

Yes. I mean I'll talk to the start up and PEAK-1, and you can just talk about the other if you'd like. But in active start-ups globally, it's going well. I think the study design is quite readily understood and available from a health authority perspective, no real pushbacks from the health authorities around the world for that study. So I also think from a patient and investigator perspective, this is a really desired study design and combination. And by the way, it's 2:1 randomization as well for the CAS cabo group. So that also is in favor, I think, to facilitate enrollment. So I do think the start-up should go well. And as Jen said earlier, we've done this before. and beat most normal time lines, I'd say in this. So we're hoping to replicate that a third time, but I think the start-up should go well and the patient recruitment obviously should go well given the study design.

And just the fact that we've now had 3 medical conference presentations for casdatifan has really driven awareness of the program in the clinic community even in the patient community, you go can to these patient chat rooms. There's a lot of discussion around casdatifan, and one of the reasons why we did want to get this data out in October versus sit on it for 4 months, is that we have people lined up and running. And eVOLVE is now up and running and just to create even more awareness around the opportunity with casdatifan. And then to your second question, the study that most people are focused on that's somewhat competitive, what we're doing with CAS is a study called LITESPARK-011, that Merck is running where they're combining belzutifan with their TKI, which is lenvatinib. We think that we have a better combination and development strategy for a whole bunch of reasons and just to get through a few of those. With their study, they are, as I said, combining Belz with Lenva, but they're using cabo in the control arm. So they're using a different TKI in the experimental arm and the control arm, which definitely made things more complicated. We actually think cabo is a better TKI, both from a tolerability and an efficacy standpoint. If that's true, it's really going to work against the Belz plus Lenva arm. Belz is actually, a lot of people don't realize. It's not really used today as a monotherapy. It's used in combination with Everolimus. So it's a little bit unclear exactly how Lenva mono performs relative to Cabo mono. Some of the other key difference between what they're doing and what we're doing is not just one primary endpoint of PFS. Our understanding is that they have PFS and OS as dual primaries. So they did some interim analysis probably looking or will do looking at PFS, but they've had to split out their alpha because of that versus because we have one full primary endpoint of PFS, we've been able to put all of our alpha on that endpoint. And because we think there's potentially now waiting on OS, that allows us to close the gap in time lines because we had that PFS endpoint. So we definitely think we have a better strategy, a better combination partner, and we're really able to close the time lines.

I know historically, like and everyone's focused on PFS going all the way back. So why do you think they took that strategic decision to use OS as a co-primary?

So, OS can be helpful with reimbursement in Europe, which may have been one reason which is why we have it as a key secondary endpoint for our study, which we think is more than sufficient. Maybe it's also just because HIF-2 alpha inhibition is very much like IO where you have this long tail effect, and you do tend to see benefit in survival. So they may have thought maybe at the time like that may have been a safer endpoint for them. I think they probably would think differently now. And in fact, in second line RCC it's been very difficult to hit an OS endpoint. There's only one second line RCC study that's hit an OS end point, which is METEOR. But because these patients tend to go on so many subsequent therapies, it tends to be a bit harder to use OS as an endpoint in second-line disease.

And you would anticipate you'd have data before them, I guess, given that you have a PFS endpoint?

Probably still after, but we think not long after yes. So we feel like very good about like our combination, our strategy. The other thing is I think just going on top of cabo versus lenva gives us that big advantage. As I said, a lot of people think cabo is a better tolerated and better overall TKI relative to Lenva. If you look at cabo use versus Lenva use in the U.S., about 2.5:1 outside the U.S. and some of the major European countries it's as much as 10:1. So clinicians have a lot more experience with cabo. The other thing that we like about cabo relative to Lenva, especially since we're combining it with another anticancer agent is cabo is much more easy to dose. It's only available in 3 dosages, is 20, 40, 60. You typically start with 60, each dose reduces toxicities. In the case of Lenva, the dosages are from 4 all the way to 22 or 24 mg a lot of clinicians claim that they're not even sure exactly how to dose Lenva in every Phase III study, they've used a slightly different dose. So we think there's a lot of advantages to us going with cabo versus a different TKI.

Okay. Great. The other combination you mentioned was with the Astra PD-1 CTLA-4 here. So maybe just talk to us like why was that an interesting combination to pursue? And then what are the data shown? And I know this is your first line kind of approach.

Yes. So I think we're quite excited about this study, especially it's a frontline study now. And the real concept here is to be TKI-free in the front line and push to the TKI associated toxicities towards later lines. So Volru, like you said, a bispecific CTLA-4 PD-1. And the study design, again, is a Phase Ib/III design. So it's seamless to go from a Phase Ib to III on a global scale. The Phase Ib part is looking at our CAS 100 mg our standard go-forward dose daily with 2 different doses of Volru, just as mostly a safety run in, think of it that way and pick the Volru dose that best combines with CAS. And then we go straight into the Phase III, which is Volru plus CAS compared to ipi/nivo as the primary comparison for registration, which again ipi/nivo now is probably the dominant first-line and preferred first-line therapy, again, because it's TKI free. So that's covering about 30% of the front line and growing as opposed to going the other direction. So like using cabo in the second line, which is a dominant second-line current therapy. This is a dominant first-line therapy, and we're adding tests. So that's really the Phase III registration design. There is a third arm of Volru alone, but that's just for competition of components. The main statistical comparison is CAS plus Volru compared to ipi/nivo.

Yes. And remind us how large and how long is that run-in or lead-in phase going to be? And then what triggers the Phase III -- move to Phase III I guess.

Yes. The -- we said we have data probably second half of next year from the run-in part or safety parts. And meanwhile, the Phase III is being prepped globally, so we'll be able to just go straight into that -- take the dose.

Okay. And is it more -- I mean, I'm assuming you're going to collect efficacy data, but is it more of a safety check the box and you'll see pretty limited -- you'll see some ORR data or something like that?

Yes. It's mostly a safety check. Just two different doses of Volru. We expect the CAS to be able to combine well with Volru. We don't expect any overlapping toxicities, but it is still a safety check.

Okay. And does that have a dose reduction as well for CAS? Can you go from 100 to 50 if needed?

Yes, we'll have the same kind of concepts available for patient management, especially because we expect patients to be on therapy for a long time, like years. So we do have safety management.

Okay. Great. And then I guess, just as you think about the asset, Jen, you kind of framed out the commercial opportunity here in various lines based on the 2 studies that you're pursuing right now. What's the latest thought on kind of partnership? I know you guys have -- are taking this forward solo right now, but how are you thinking about that, especially as you think about like that first-line investment?

Yes. So what I think is really nice about how we're running eVOLVE is that AstraZeneca is actually the one running eVOLVE. So it is part of the clinical collaboration with AstraZeneca, which is really, really attractive for us. They're actually operationalizing the study, so that obviously saves us a lot of resources are paying for about 50% of the study. So it's a really, really capital and resource efficient way for us to pursue the frontline and they've been a great partner, we know them well. So it's been a great collaboration so far. So in some ways it's like a partnership. What's nice is we retain all of the economic and commercial rights. So that makes a huge difference if you think about it from an NPV perspective, if you're paying half of the steady cost that retain all of the upside. So I think for now, we're probably more interested in doing those types of things, but there's interest for sure in the asset, and we'll see how things play out over time. I think for now, PEAK-1 is kind of well underway. We've got a good strategy for front line. So we feel very good about where we sit today, but you don't see what happens longer term. So what is nice in RCC is we see with like [indiscernible], I mean they've been a great case study for us. And -- they have made cabo -- talk about the dominant TKI in the RCC market and I think it proves a biotech can very effectively go after that market, and do it on their own if they want to.

And just remind us, like from a commercial footprint perspective in the U.S., that'd be like 100, 150 reps roughly?

Yes probably not even 100, probably a little bit less than that. It's a pretty concentrated market as geo-oncologist. So as we think about a partner, what could be interesting is as we think about further expanding the development program for CAS, even though we're going after like sort of the lion's share of the market, there are some other things that we could do, especially other tumor types we may want to pursue. And so partner could potentially be helpful there.

Okay. And last, just remind us of the IP, like how far out you guys go on CAS?

I want to say it's 2041, 2040. So this is homegrown, molecule and so lots of IP life left.

Okay. Great. Maybe just pivoting over to dom here. I know there's been a lot of ups and downs in the TIGIT space over the last, I mean, 18 months, 2 years or so. And so you spoke to some of this in terms of the differential on Fc regions. Just remind us kind of why you're still confident here in the program because I think from an investor side, I'd say that people are probably a little bit more skeptical would be my guess right now.

Yes. So the key difference from -- of our antibody compared to the prior 18 months, as you said, ours is Fc-silent as opposed to Fc-active. So what that functionally does in addition to hitting the TIGIT receptor and blocking that is ours will not deplete the T-cell. T-effector and T-regs while an Fc-active will. And so if you do deplete those, especially like T-regs, you could get more immune-mediated adverse events, but then these two patient discontinuation from therapy, which obviously then doesn't allow the therapy to work, as well as depleting T-effector cells. So by being Fc-silent, we don't have those two detriments to the therapy. And our data has been quite consistent so far. We have it in gastric and in lung, both with consistent results. And interestingly, AstraZeneca still has a very robust program also with an Fc-silent antibody, and their results are also very consistent with ours, are happy to say ours will read out before theirs, but that also adds to the confidence seeing that it's not just a onetime, one study aspect that we've seen our results.

And you mentioned, again, gastric, lung, kind of 2 focal indications here. I know you'll have some updated gastric data from Phase II at ESMO next month. And so maybe just help frame for kind of the prior data we've seen a similar question as before with CAS like what's going to be incremental in terms of either patients, follow-up, et cetera?

Yes, big data. So we've had EDGE-Gastric data before. And by the way, the EDGE-Gastric population here is really the same population as our STAR-221 that's going to be reading out for the Phase III registration. Before we've had PFS data and the PFS data is, in essence, overlapped with what was otherwise OS data for comparators, and we'll be coming out with our OS data now, and that's the biggest new reveal, let's say, at ESMO would be the OS data, which hopefully will show what we can do in the STAR-221 study.

Yes. And I think just looking at my notes, PFS, I think you're at 12.9 months in the intent-to-treat population, 13.8 in the PD-L1 high population. And then so maybe just remind us like what the PD-1 chemo typically does? I think it's somewhere in that same range?

It's on the same kind of 13, maybe 14 months range. That's right.

For OS.

For OS, sorry, right.

So you would expect your OS data to...

Exactly be greater than our PFS data. That's exactly right.

Okay. Understood. And then anything else that you think is going to be notable? Or is OS going to be the key thing this presentation or anything else that's going to be -- that we should think about?

I think the biggest part will be the OS I think everyone wants to see is what is the efficacy of this therapy and how will it compare or has it compared to otherwise with the control arm equivalent in the standard of care.

Okay. And then maybe just on STAR-221 is the pivotal trial. You mentioned very similar population to EDGE-Gastric. Just remind us, the design here and then timing of data?

Yes. So the -- it's our dom and zim, our PD-1 plus chemo, basically compared to PD-1 and chemo with the standard of care of the control arm randomized study. And it's fully enrolled. It was enrolled by June of 2024. So we're now watching the study and counting the events because it's events driven, but you can do the math. We're more than a year out from when the last patient was enrolled already. And so it's a venture and so all we can really guide to is next year as far as when to expect data.

One other thing, just to remind people, so it's an OS primary endpoint. But we're looking at the both at the TAP greater than 5, which is essentially PD-L1 high and ITT separately. If you hit on one of those endpoints, you get to recycle the alpha into the other endpoint. It's kind of like a -- call it a two-ways to win site design. The other thing that we actually added later is if one of those hits -- sorry if it's TAP greater than 5 hits, there's a hierarchical analysis looking at TAP greater than 1. So we're really trying to fall for the broadest patient population possible with that design. And then one last thing to point out, some of you are familiar with the lung cancer market. In gastric, it's much more skewed towards high PD-L1. So in our STAR-221 study, actually, a little over 45% of the patients were TAP greater than 5 or -- and we think probably over 80% or so were PD-L1 positive or tap greater than 1. So TAP greater than 5 and TAP greater than 1 both capture a significant percentage of the gastric cancer patient population.

Okay. Got it. So you cover the landscape. And just remind us, you provided some numbers for CAS, but just as you look at that gastric opportunity, I mean, what's the size of the market, roughly?

TAP greater than 5 would be about $3 billion in G7 countries. So another very big sizable opportunity. In another market, like RCC, where there's just like very little competition, which is one of the reasons why we've been able to enroll STAR-221 so quickly. There was really no competitive studies out there, and so we think that's a real opportunity for the anti-TIGIT classes and works.

Okay. Great. And then dom STAR-121, which is the lung cancer trial. Just any update on enrollment progress in that study and how to think about the data timing?

Yes. STAR-121 is enrolling well, and we expect it to be fully enrolled by the end of this year. And then again, it will be a matter of time. It will be certainly beyond that of STAR-221 just looking at gastric versus lung cancer in addition to when the enrollment completes. But we can't really give guidance yet on to when the 121 readout would be, but it will be fully enrolled, or we expect it to be fully enrolled this year.

Yes. Okay. And so that's probably beyond '26? Right, if you look at timing of like what the control arm is, et cetera.

Fair. Yes, but it's hard to say like I said, it's been running for a long time for a while now, but it's lung cancer, so we'll see where we go.

Okay. Got it. as you think about -- I mean, lung cancer, to me, it seems like you have a lot of companies still pursuing kind of first-line options. Do you see this as potentially becoming the new standard of care is this the market that's going to get increasingly fragmented? Like how do you guys see that market playing out on the forward because I think there's still some uncertainty in terms of what it ultimately shapes up?

Yes. So we changed our primary endpoint from -- it was an ITT focus end point to greater than 1. So we're definitely positioning dom-zim for the PD-L1 greater than 1 or PD-1 positive patient population. Where we actually think there's a little bit less competition. I think the ADCs and like CTLA-4s tend to be more targeted at the PD-L1 low or negative patient population for KRAS, a lot of that patient population again, tends to overlap more with PD-L1 low. I think there's still some questions about whether or not KRAS can move in the frontline and how combinable it is both with anti-PD-1 and chemo. So even though there's a lot out there, which is why I would say, take a little bit longer to enroll, the study is positive. We actually feel very, very good about the potential for that molecule to take significant share of that PD-L1 greater than 1% patient population. There's obviously the anti-PD-1 DIGESTS out there. We'll see on that so far, we have not seen anything that would tell us that that's going to be a better combination versus anti-PD-1 data looks probably not quite as strong as ours based on the Phase III data that we presented. We haven't seen any -- they've been a slightly bigger patient population. So we'll see. And lung is so big. I mean that is $10 billion-plus market that there's also room for a few different players.

Okay. Well, great. Thanks so much, Jen and Richard, really appreciate the time and best of luck.

Thank you.

Thank you.