Good afternoon. Thank you for attending today's Arcus Biosciences Third Quarter 2024 Earnings Call. My name is Tamia, and I will be your moderator for today's call. All lines will be muted during the presentation portion of the call with an opportunity for Q&A at the end. If you would like to ask a question, please press star one on your telephone keypad. I will now pass the conference over to your host, Pia Eaves, Vice President of Investor Relations. You may proceed. Hello, everyone, and thank you for joining us on today's conference call to discuss Arcus's Third Quarter 2024 Financial Results and Pipeline Updates, including our upcoming presentation of ARC-10 data at SITC. I'd like to remind you that on this call, management will make forward-looking statements, including statements about our cash runway and our expected clinical development milestones and timelines. All statements, other than historical facts, reflect the current beliefs and expectations of management and involve risks and uncertainties that may cause our actual results to differ from those expressed. Those risks and uncertainties are described in our most recent quarterly report on Form 10-Q that has been filed with the SEC. Today, you'll hear from our CEO, Terry Rosen; CMO, Dimitry Nuyten; COO, Jennifer Jarrett; and CFO, Bob Goeltz. We'll also be joined by our President, Juan Jaen, for questions after the prepared remarks. With that, I'll turn the call over to Terry. Thank you very much, Pia, and thank you all for joining us today. As we head into 2025, our highest priority is to launch our late-stage development program for our HIF-2alpha inhibitor, casdatifan. As you know, just two weeks ago, we presented initial data from our ARC-20 study evaluating casdatifan in late-line clear cell RCC in an oral plenary session at the ENA meeting. These data clearly validate our conviction that casdatifan will be a best-in-class HIF-2alpha inhibitor, demonstrating improvement in every key efficacy measure that we analyze versus belzutifan. As you know, belzutifan is the only HIF-2alpha inhibitor on the market today. So let's go to slide five, and I'll recap the highlights from our data set. First off, the rate of primary progression in the 100-milligram daily expansion cohort was only 19%, and it was similarly low in the 50-milligram daily expansion cohort. In fact, the rate of primary progression for the combined 60 patients in the 50-milligram and 100-milligram expansion cohorts was approximately half of what was observed in LITESPARK-005. Keep in mind that the primary progression rate and disease control rate, DCR, are the only data points that are fully mature and will not change. So this is really a huge difference for the molecule. Second, we reported a 34% ORR and 25% confirmed ORR for the 100-milligram cohort, with two of the three unconfirmed responses pending confirmation, and also multiple stable disease patients still on therapy. As of the data cutoff, every responder across both cohorts remained on treatment, with the exception of that one patient whose response did not confirm. The belzutifan data actually provide good precedent for the kinetics of response with HIF-2alpha inhibition. So this is important. Approximately 60% of responses occurred within six months of treatment, and an additional 20% occurred in each of the ensuing six-month periods, so that goes out to 18 months. These data illustrate why our ORR could, and in reality, more likely should, further improve across both cohorts. Keep in mind those follow-up times are eight months and 11 months, respectively, for 50 and 100 milligrams. The ARC-20 data also demonstrated that the activity of casdatifan is extremely durable. As of the data cutoff, a median PFS had not been reached, even with that 11-month median follow-up. Recall that belzutifan was approved based upon its PFS of 5.6 months, and our median PFS, which we expect to report in early 2025, should easily exceed that benchmark. Given that PFS is the registrational endpoint, this will be another important source of differentiation. Our spider plots show multiple patients either past or approaching the 52-week duration of treatment, and you also see deepening of responses with time. I want to emphasize that these data were generated in a heavily pretreated patient population relative to that of LITESPARK-005. Specifically, approximately 25% of the patients enrolled in ARC-20 wouldn't have been eligible for LITESPARK-005. For the 50-milligram cohort, despite only eight months' median follow-up at the data cutoff, we reported a 14% primary progression rate, a 25% ORR, and just over 21% confirmed ORR, with the one unconfirmed responder pending confirmation, and a very impressive, almost remarkable DCR of 86%. One of the confirmed responders was a complete response. Beyond the responders, and again, another important point, nearly 40% of patients still continued on therapy with stable disease, including a few who are extremely close already to the 30% response threshold. You can see that in the spider plots. While this data set is still evolving and will continue to improve, we now have two different cohorts that are demonstrating clear efficacy differentiation relative to that of belzutifan. There's a lot more data to come. On slide six, we show the data that we expect to share from ARC-20 throughout 2025. We plan to present additional data from the 100-milligram and 50-milligram cohorts of ARC-20, including more mature ORR and median PFS. That'll be early next year. Later in the year, we plan to present initial data from the 150-milligram and the 100-milligram once-daily tablet expansion cohorts. So that's another 60 patients' worth of data. We also plan to present initial safety data from our Cas plus cabo expansion cohort. To date, the safety data from this cohort, which we already shared with the FDA as part of our pre-phase 3 meeting, are consistent with the profiles of the individual drugs, and the dose intensity of 100 milligrams of casdatifan and 60 milligrams of cabozantinib has been maintained. Given the importance of the ARC-20 data, and that's important to us, it's important to you, it's important to investigators, the ongoing evolution of the data sets and the multiple cohorts that we've enrolled, we're considering additional opportunities to provide updates from this study in the more near term. We remain full steam ahead towards the initiation of our first phase 2 study, PEAK-1. The investigator enthusiasm for this study is incredibly high, which we believe will support rapid enrollment. Now, let me switch gears to domvanilimab, our Fc-silent anti-TIGIT antibody. Just yesterday, the SITC abstract was released with data from part one of our ARC-10 study, which evaluated dom plus zimberelimab, that's our anti-PD-1 antibody, versus Zim versus chemotherapy in first-line PD-L1 high non-small cell lung cancer. As a reminder, we terminated the study for strategic reasons to focus on STAR-121, our chemo combination study. But the early termination gave us both an opportunity to generate and now present a data set from a study that was conducted under phase three conditions. On slide 27, we summarize the abstract. We show that dom plus Zim exceeded Zim monotherapy on ORR, PFS, and OS. For both PFS and OS, we achieved a hazard ratio below 0.65, which is far better than the threshold considered clinically meaningful in this setting. With median PFS of 11.5 months and median OS not reached for dom Zim, these results are meaningfully above contemporary benchmark studies for anti-PD-1 monotherapy. Dimitry is going to discuss these data in detail, but I want to make two important points. First off, these data reaffirm the growing recognition that Fc-silent anti-TIGIT antibodies have a differentiated safety profile relative to that of Fc-enabled antibodies. There are only two Fc-silent TIGIT antibodies in late-stage clinical development today: dom and AstraZeneca's anti-PD-1 anti-TIGIT bispecific antibody. In the last few months, AstraZeneca presented two data sets for their antibody in first-line non-small cell lung cancer and first-line gastric cancer. Interestingly, both data sets looked very similar to our own, specifically similar efficacy as well as AE rates that are in line with anti-PD-1 therapy alone. That's an important component of the profile. In contrast, for the Fc-enabled anti-TIGIT antibodies, we continue to see reports of higher rates of immune-related adverse events and treatment-related discontinuations. Combining the Fc-enabled antibodies with chemotherapy absolutely seems to exacerbate these issues. The second point that I want to make is that with this ARC-10 data set, which will be presented in more detail at SITC, the ARC-7 results in PD-L1 high non-small cell lung cancer that we shared last year, and the EDGE-Gastric data that we presented earlier in this year at ASCO, we now have three compelling data sets supporting the potential of dom Zim in both lung and gastric cancers. For our EDGE-Gastric study, we showed a median PFS of 13 months for dom Zim in first-line gastric cancer, which meaningfully surpassed the PFS of seven to eight months seen in benchmark studies. And in the first half of next year, we expect to present mature overall survival from the study. Meanwhile, we continue to execute on our three phase 3 trials for dom Zim. In first-line gastric cancer, with our STAR-221 study, we have the potential to be first to market with an anti-TIGIT antibody in this setting. With this study fully enrolled, we're actively preparing for readout and potential submission to health authorities. We believe this setting alone is a $3 billion-plus opportunity. In lung cancer, with our STAR-121 and PACIFIC-8 studies, the latter in partnership with AstraZeneca, we have a potentially differentiated anti-TIGIT combination in the two settings we're pursuing: first-line and stage III non-small cell lung cancer. We continue to evaluate our statistical analysis plans for all our dom Zim studies to ensure that they're optimized for probability of success, but also while addressing the largest number of patients. We also continue to advance the other programs in our pipeline. We've initiated PRISM-1, our phase three study evaluating quemliclustat plus chemo. That's quemliclustat is our CD73 inhibitor in first-line metastatic pancreatic cancer. And with Taiho opted into this program, they're executing the study in Japan. We believe this could be a transformative first-line therapy in a disease you're aware with dismal outcomes for patients. Early next year, we expect to advance AB801, a highly selective Axl inhibitor, into expansion cohorts in non-small cell lung cancer. Our relationships with Gilead, AstraZeneca, and Taiho are strong, and they've enabled us to aggressively advance all of our programs in a highly resource-efficient manner. With $1.1 billion in cash and investment and runway into mid-2027, we're comfortably funded for multiple clinical readouts. Before we go to the ARC-10 results, I'd like to turn it over to Jen to discuss our development plans and the market opportunity for casdatifan. Thanks, Terry. Starting with PEAK-1, our first phase 3 trial for casdatifan and clear cell RCC, we expect to begin this study in the first half of next year. The design is shown on slide 23 of our deck. The study will enroll approximately 700 patients and will compare casdatifan plus cabozantinib to cabo monotherapy and IO-experienced clear cell RCC. Cabo is the standard of care in this setting, so clinicians are extremely comfortable administering cabo and adjusting its dosing to optimize both cabo's efficacy and safety. We believe that the vast majority of the second-line patient population, approximately 80%, will be eligible for PEAK-1, given this study only includes patients who received prior treatment with cabo in the first-line setting. You can see on slide 24 that this study targets an approximately 11,000 patient population in the U.S. Assuming a treatment time in excess of 15 months, this is a $2 billion plus market opportunity in the G7 countries alone. We are also excited to move into the IO naive setting with our collaboration with AstraZeneca to combine casdatifan with their anti-PD-1 CTLA-4 bispecific, volrustomig. The anti-CTLA-4 PD-1 combination Opdivo currently has about one-third market share in the first-line setting, and that share is growing, given the preferable safety and tolerability profile of IO-based regimens relative to those of TKIs. By combining casdatifan with volrustomig, we have the potential to develop a first and best-in-class TKI-sparing regimen. This represents a patient population of approximately 12,000 in the U.S. alone. And assuming a potential median treatment duration of 20 months, the total addressable market would exceed $3 billion across the G7 countries. Additionally, we are working to further expand the development program of casdatifan into other RCC subpopulations. And you'll see us add additional cohorts to ARC-20 in the coming months. We remain confident in casdatifan's ability to play a very meaningful role in the RCC market. Today, patients cycle through different treatment options for years, receiving multiple different TKIs with seven different TKIs on the market. But today, in the HIF-2alpha field, it is just casdatifan and belzutifan. I'd now like to turn the call over to Dimitry to discuss our newly released data for dom Zim in lung cancer. Thanks, Jen. Our abstract for ARC- 10 was released yesterday morning, and data will be presented in a late-breaker poster session this Friday at SITC. ARC- 10 was originally a global phase three study evaluating dom and Zim versus Zim versus chemotherapy in patients with PD-L1 high non-small cell lung cancer. This is important since the trial conducted with the same rigor as would be expected from a registrational phase three. Though ARC- 10 was discontinued for strategic reasons, we continue to follow patients, and now, with over two years of median follow-up, we are presenting our first overall survival data for dom and Zim in any setting. As you will see, the results are supportive of dom's ability to meaningfully extend survival in patients. Starting with the design on slide 30, the trial was randomized two to two to one, so there were 38 patients in the dom and Zim arm, 40 patients in the Zim monotherapy arm, and 17 patients in the chemotherapy arm. Baseline characteristics were generally well-balanced across the arms, with some prognostic imbalances favoring the chemotherapy arm. The data cutoff for this analysis was May 17, 2024, and the median follow-up was 24.5 months. On slide 31, we showed a Kaplan-Meier curve for overall survival. These results are quite impressive. In fact, even with two years of median follow-up, a median OS has not been reached for dom and Zim. The hazard ratio for overall survival was 0.64, a result that is very clinically meaningful. Additionally, the Zim control arm performed right in line with the benchmark studies of pembrolizumab in this setting, with a median overall survival of 24.4 months. When compared to chemotherapy, Zim demonstrated a hazard ratio of 0.63 for overall survival. Again, this is right in line with KEYNOTE-042 and other benchmark studies. The poster presentation will also highlight additional data, including progression-free survival and overall response rates, which also showed a clear benefit for dom and Zim over Zim and put Zim performance in line with the benchmark studies for pembrolizumab. The safety profile was also consistent with prior observations for dom and Zim. Immune-mediated adverse events were similar for dom and Zim relative to those for Zim alone, at 23.7% and 20% respectively. These results are substantially different from data reported from studies with the Fc-enabled anti-TIGIT antibodies, where immune-mediated adverse events and treatment interruptions and discontinuations have been meaningfully higher than the anti-PD-1 or PD-L1 alone arm. In fact, it has been cited as the cause of trial failures. The compelling data from ARC-10, both for efficacy and safety, increases our confidence that combining dom and Zim with chemotherapy in STAR-121 will further improve outcome and provide lung cancer patients with the best chance of success in their first-line treatment. Now I'd like to turn the call over to Bob to cover our financials. Thanks, Dimitry. Our cash as of the end of the third quarter was $1.1 billion as compared to $1 billion as of the end of the second quarter. Our cash position was bolstered by a $100 million collaboration continuation payment from Gilead. Turning to our P&L, we recognized GAAP revenue for the third quarter of $48 million, which compares to $39 million for the second quarter of this year. Our revenue is primarily driven by collaborations with Gilead and Taiho, and in the third quarter, included $15 million resulting from the Taiho opt-in for quemliclustat in July. We continue to expect to recognize GAAP revenue of approximately $30 million for the fourth quarter of 2024. Our R&D expenses for the third quarter are stated net of reimbursements from Gilead and were $123 million as compared to $115 million in the second quarter of this year. We continue to expect modest increases in R&D expenses for the fourth quarter of 2024. G&A expenses were $30 million for the third quarter and were flat compared to the second quarter of this year. We expect G&A expenses to remain stable for the fourth quarter. Finally, we expect our cash and investments balance at the end of 2024 to be between $950 and $985 million as compared to our prior guidance of $885 to $925 million. We expect these resources to fund operations into mid-2027. Our guidance excludes additional potential opt-in payments and milestones from our partners. For more details regarding our financial results, please refer to our earnings press release from earlier today in our 10-Q. I'll now turn it back to Terry for concluding remarks. So thank you all again for joining us this afternoon. As I mentioned earlier on the call, we have a lot coming, and that starts with our SITC presentation for dom Zim on Friday, followed by additional presentations from ARC-20 and the initiation of our first phase three study for casdatifan over the coming months. As we head into 2025, we'll be approaching our first phase 3 data set for STAR-221 in first-line gastric cancer. We appreciate your interest and support of Arcus, and I'll now open the call for questions. Thank you. We will now begin the Q&A session. If you would like to ask a question, please press star followed by one on your telephone keypad. If for any reason at all you would like to remove that question, please press star followed by two. Again, to ask a question, please press star one. As a reminder, if you're using a speakerphone, please remember to pick up your handset before asking your question. The first comes from Yigal Nochomovitz with Citi. You may proceed. Hi, Terry and team. Thanks for taking the question. I'm getting a lot of interest in Cas, and people are asking about the potential for Gilead's opt-in. Can you provide any more color there as far as whether there's specified windows? Obviously, you mentioned that you need a qualifying data package. Does that mean it could be the monotherapy, or is Gilead interested in seeing some of the combo data with volrustomig or the initial combo data with Cas plus Cabo coming up coming up soon? That's the first question. Thanks. Yeah, so we have aligned with Gilead on what data is needed for the qualifying data package. We're very close to meeting that data requirement, so we will be delivering a package to them relatively soon. And as we've been saying, we expect a decision to be made either late this year or early next year. Okay. Thank you. And then I'm just curious. Was there any preclinical work done with volrustomig and Cas to sort of just do a quick validation of the combo safety in in in NHPs or something before going into this collaboration with AZ? No. There was no preclinical work done. It was a very typical sort of situation where you have two molecules, well-defined profiles that we're simply taking into those studies initially in human. Okay. And then our last one is I'm curious about about etrumadenant. Obviously, you had the data, I believe, at ASCO for the ARC-9. What what are you thinking there in terms of the later development? There is the other cohort, which is the second-line cohort, cohort A. Is that what you're waiting for before you decide with a registrational study, given the obviously very, very strong OS that you saw in the in the third line? No. To be honest, it's just a matter of us moving. So we're extremely excited about the data set, and we're just working through with Gilead. You can see, obviously, we're starting a number of later-stage trials, and we still have the full portfolio going. So we're working through what our next steps will be, and we'll share them once they're defined together with Gilead. Okay. Thank you, Terry. Thanks to you, Yigal. Appreciate it. Thank you. The next question comes from Li Watsek with Cantor Fitzgerald. You may proceed. Hey, guys. Thank you very much for taking my questions. I guess, one, in the IO naive renal cell cancer setting, I understand AZ is running the study, but I guess what can you say about what the next step might be and the timing of a potential pivotal trial? Yeah. So so I'll comment there. We've agreed with AstraZeneca to not comment anything further than those initial plans, and we'll say more once the study shows up on clinicaltrials.gov. Okay. Understood. And I know you mentioned on the call, it sounds like you're looking to optimize the step plan for the phase three non-small cell lung for dom. Can you expand a little bit on that? What does that entail? Yeah. So my comment was more general than that. We make that point for all of our studies that we're continuously looking at the step plans for all of our programs. Obviously, in the anti-TIGIT field, there's been changes made by others. There's been some comments or statements put forward from the ODAC with the FDA. So at this point, we're not making any changes, but we just wanted to acknowledge that we're always considering that possibility. Okay. Got it. And maybe just the last question. I wonder if you can talk a little bit about the clinical benefits that you're seeing for stable disease patients from the Cas study, and it seems like you got a decent number of them still on study. So I guess how clinically relevant is disease control for these patients? Yeah. So just to be clear, I'll take the question. So it's very, very relevant for patients. Just imagine RECIST was determined based on large data sets, mostly for chemotherapy. There had been an effort to standardize assessments of treatment, and based on reproducibility, inter-observer variability, a threshold of 30% was set. I think everybody would agree whether or not you're at 25% or 35%, depending on the tumor volume. That is not really relevant. Having tumor that doesn't grow and that has gone down in tumor volume is very important. And then the other point that is more, let's say, from a regulatory perspective, response rate is never, ever a registrational endpoint beyond accelerated approval. In this case, in kidney cancer, progression-free survival is the relevant endpoint, and everybody who does not progress contributes to that. And in a Kaplan-Meier estimate, the longer you are free of progression, meaning the longer your response is lasting or the longer your stable disease is lasting, contributes equally for each patient to the Kaplan-Meier estimate for progression-free survival. So both from a clinical perspective for patients and from a regulatory registrational perspective, they're very important. And from a registrational perspective, it is equally important as a response. Okay. Thank you. We'd like to be able to get to everybody. So if you have more than a couple of questions, can you please hop off and join the queue at a later point? That would be great. Thank you. Thank you. Our next question comes from Jonathan Miller with Evercore ISI. You may proceed. Hi, guys. Thanks for taking my question and reminding us to limit our questions just before I got my chance in the queue. Appreciate that. Can I start with some questions about HIF2, please? I noticed in your prepared remarks, you talk about two unconfirmed PRs that could still confirm. I'd really like to get some detailed color on that. We hear reports. There have been, there have been papers written that suggest that one of, I think one of those two, based on how I'm counting, had a subsequent scan of stable disease. So can you comment, of those two unconfirmed partial responses that you're talking about, how many of those have not had a follow-up scan yet or or or might be expected to confirm based on one additional follow-up scan? Then maybe building off of that, given that a lot of the differentiation you're talking about compared to belzutifan is in the PD rate, i.e., at the first scan here, how well or early in the course, how well do you anticipate that to translate to a better profile versus belzutifan in a combo setting, especially combos with drugs like TKIs, which give their benefits rapidly at those first couple of scans? Go ahead, Jen. Yeah. So the first question kind of takes you to there's a lot of different questions in there, but maybe just to jump to the back part of your question as far as who has not had a follow-up scan yet that was a responder. There was one patient in the 100-mg cohort that had not had a follow-up scan yet and one patient in the 50-mg cohort. Their last scans show them as being responders for the first time, and they are waiting for their confirmatory scans now. And then, as we said, for the 100-mg, there is one patient that did not confirm so far, only one patient. And in fact, as we mentioned in the script, out of all of the responders, every responder is still on treatment with the exception of that one patient that did not have a confirmed response in the 100-mg cohort. Did that answer your question? And we can go to the second part. Yeah. I was thinking specifically of that 100-mg cohort. I'm just trying to count UPRs and try to get a sense for where the ORR could realistically get to at the end of the day. And in that 100-mg cohort specifically. Yeah. So 33+% was the ORR. We said that one patient will not confirm. So that means the maximum confirmed ORR that we can get to based on the current responders. So that's excluding stable disease patients that have also seen significant tumor reduction. So there could be other stable disease patients that also contribute to the ORR. But based on the current responders, the maximum confirmed response rate we can get to is 31%. And then if just one of those pending responders confirms, then that would take the ORR to 28.3%. Great. Got it. Yeah. Great. Got it. Yeah. Great. Got it. Yeah. I can take the second part, second part of the question about stable disease in the combination. So a few things. So of course, in the combination, we are going against Cabo, and we're building up on top of Cabo. So everybody in the control arm would get Cabo, and we are doing the combination. If you think what the combination can do, it can actually help patients in different ways. On casdatifan, we see both early responders. We have more than a few patients responding at the first scan at six weeks. We've also disclosed two patients now that responded respectively at 12 and 14 months. So that's something that goes on top of the TKI response rate. The primary progression response rate for cabozantinib is about 20% or a little bit less, and we hope to catch more patients from that 20% with a different mechanism for the combination. So of course, we can speculate what it would be, but let's say we would expect it to also improve on top of a TKI. Sure. I guess, but I'm asking specifically about the comparison to the other HIF-2 here, to belzutifan. If your differentiation from them is in PD rate, or at least a lot of it is in PD rate, how well would you be able to observe that differentiation in a combo setting where you have the TKI to pick up the slack on the first scan a little bit? So so, I'll comment there. I mean, again, you're purely speculating, but as you know, greater than 90% of those patients have some sort of HIF-2-driven component. And so there's absolutely still room to reduce the rate of primary progression. It puts more people into the queue, if you will. And I think that the place where you'll see that number of patients then leads into every other efficacy measure, whether it's on ORR, PFS. I have to say there's no reason to not start to think about why you may not see advantages in OS, even though that's not the approvable endpoint at this stage. There's nothing intrinsic about Clear cell RCC that should suggest that you couldn't start to prolong OS as well. Thank you. Thanks, John. Thank you. The next question comes from Peter Lawson with Barclays. You may proceed. Great. Thank you. Just a couple of follow-ups on the opt-in. Kind of what drives that decision for Gilead between this year and next year? Is it something from your side, their side, or is there a different data cut? And then if Gilead doesn't opt-in, what are the next steps? Yeah. So I'll take that. First of all, there's nothing specifically driving it other than how long they take to make a decision. It happens to be that because of when we're delivering it, it's relatively near the end of the year. They have a certain amount of time that could, in fact, creep into next year. It doesn't necessarily creep into next year. So that's that's the only component why we introduced that ambiguity in laying out a timeframe. As you know, they could opt-in yesterday if they wanted. So it sort of defines a latest point of when they can opt-in. The second question. Right. If they don't opt-in, there's not necessarily anything that we would do immediately, but it could be any of the three things that you might think of. We're very comfortable continuing with this one on our own. We love the program. I think it's a, it's a great opportunity. Secondarily, we've already had plenty of inbound interest from others who recognize that there is an opt-in decision. I think most other companies have expressed the thought that they think Gilead would opt-in, but we could consider partnership with another company as well. Just on the economics, Peter, so it's a $150 million opt-in fee should they decide to opt-in, and then we share costs 50/50 on the program going forward. And then I don't know if you were getting at this with your question, but obviously, if Gilead were to opt-in, then we'd work through the details of any additional studies we might want to add to our clinical development plan together. Great. Thank you so much. Thank you. Thank you. The next question comes from Asthika Goonewardene with Truist. You may proceed. Hey, guys. Thanks for taking my question. And I'm going to repeat what John did and ask a multi-part single question here. So on on cabozantinib plus casdatifan, when you think ahead as the right comp for maybe some sort of a pivotal study down the line, what do you think the right comp is? And I ask because nivo + IPI makes it the most logical comp, but obviously a very high bar. And related, the durable CR rate with nivo + IPI is something that is quite attractive about that combination in RCC. But how important is it for you to kind of replicate that or beat that specific endpoint adjacent to the regular primary endpoints that you would consider? Yeah. So just to make sure I can take the question, so the relevant benchmark would be the CheckMate 214 study, although, of course, that is now somewhat outdated. But I think with the mature follow-up, the data has held up very well. We are building up on the bispecific, meaning the data for volrustomig has been presented last year at ESMO in kidney cancer. And I think most people objectively would agree it looks at least as good or perhaps a little bit better than ipi-nivo. Some of the toxicity is a little bit better. So we don't expect, let's say, to have to beat ipi-nivo with Cas alone. We know we have a solid CTLA-4 PD-1 backbone and then build on top of that. The CR rate, indeed, the durable, or you say the durable response rate is important. Obviously, we don't completely know, but I think it's reasonable to hypothesize that, let's say, one of the things for ipi-nivo is the primary PD rate. Investigators typically will not use ipi-nivo in the setting where they really need a fast response for a patient. So that's something we might be able to change. We might be able to get a lower primary PD rate when we, when we build upon it. And every other benchmark, we expect to be able to deepen or lengthen, meaning longer duration of response because we add a mechanism that really helps out in the long term, longer progression-free survival, and hopefully longer overall survival as well. Yeah. And I think just to hit on the primary PD point, that was, I think, what got AstraZeneca very interested, is that you do have 25% of patients that just flow right through Imfinzi. And so by adding a drug that seems to have a relatively low primary PD, we think we can especially improve that front end of the PFS curve. Yeah. And then lastly, to add on top of that, also the safety profile for HIF2 targeting specifically casdatifan would be far more favorable than adding a TKI on top of that regimen. So that's what we refer to the TKI sparing approach because first-line patients can be on treatment for a very long time, which is cumbersome and, let's say, a burden on patients if they have to stay on a TKI for a long time. Great. Thanks so much, guys. Thank you. Thank you. The next question comes from Daina Graybosch with Leerink Partners. You may proceed. Hi. I'm going to follow up right along with what Asthika just asked about the trial conduct for both PEAK-1, the combo with Cabo, and the combo with the CTLA-4 bispecific. And that we've seen in RCC that keeping patients on studies seems to be really important, that if you have any toxicities, then managing those discontinuations can really drive the primary efficacy endpoints. Can you talk through your strategy in both of those trials to manage treatment exposure, particularly as you started with the 60-mg dose of Cabo, and they haven't always done that in their combination studies? And then also what you're doing with Astra to manage tox with a pretty toxic anti-CTLA-4 as well. Yeah. So I'll start with the Cas combination. So good points. I see it as a benefit that we would be starting with 60. The trials where the TKI, in this case Cabo, wasn't started at full dose was based on toxicities identified with a combination. And therefore, you give up on some early higher exposure for an active agent like Cabo. So I think it's important for people to be able to start at full dose. That's the safety data we are generating right now. We already have generated a lot of experience with Cas by itself and how investigators manage the toxicity. I think the data that we've shown is very convincing that we have virtually no one discontinuing the drug for toxicity. We have some interruptions, and people are able to manage the toxicities and then stay on. So that's the experience we'll also use for the combination. The other thing that makes it a little bit easier in giving guidance is the specific profiles for toxicity for both Cas and for Cabo are, let's say, Cabo, of course, very well known, and Cas relatively straightforward with anemia and hypoxia, no relevant overlapping toxicity. So giving guidance on potential dose reductions will be straightforward. And to make it as clean as possible, the trial is what we call an active comparator placebo-controlled trial. So people on the control arm will be getting Cabo plus a placebo to take out all bias from investigator and patients on the assessment of the AE profile. When it comes to AstraZeneca, we can't comment as much on that trial. Obviously, that's currently in startup and is led by AstraZeneca. Our colleagues at AstraZeneca have generated quite a bit of safety data. Some of that is in the public domain, as I referred to, from ESMO 2023. And there's a lot more data that's not in the public domain. And with that, and with that they've, let's say, generated a lot of experience in giving specific guidance. And the toxicities they are seeing, of course, are not new. Ipilimumab has been on the market for quite a while, and kidney cancer investigators are, let's say, very well aware and very experienced with the management of the toxicity profile of ipilimumab. And again, the lack of overlapping toxicities will make it easier to give specific guidance for each agent. Thank you. The following comes from Salveen Richter with Goldman Sachs. You may proceed. Hey, this is Mark on for Salveen. Thank you guys for taking our questions. We have a question on TIGIT and lung on the ARC-10 at SITC. It looks clear that TIGIT is adding a survival benefit, but why do you think the benefit on ORR is less clear? And also, how do you expect this data to translate to the STAR-121 study where it seems like OS benefit from the dom and zim is likely already above Keytruda chemo combo? When should we expect to see initial data from the STAR-121? Is it possible that we could see it in the second half of 2025? Thanks. So let me, let me start. I think that when your first question was about ORR, we think the ORR, there was quite reasonable improvement. Keep in mind, this is immunotherapy, and and it comes up time and time again. The place where you're really getting your benefit is enhancement of OS, and its durability, it's the tail. That's why it's a profound signal that we're seeing. ORR is better, but what you really should be focused on, the world uses ORR as a surrogate for PFS, as a surrogate for OS. The reason we're out at two-plus years and we have that OS data is that that's what you're really looking at. But nonetheless, we don't think there's anything, you know, unusual about the advantage on ORR. The second question that you asked was, how do you expect this data to translate to STAR-121? Oh, so so we think the translation, we've already seen in EDGE-Gastric an advantage on top of chemo. The thing that, and this is where we think we actually have a huge advantage. When we think about the STAR-121, while we stopped ARC-10 for strategic reasons, based just on an evolving market that physicians are moving more and more from just using Keytruda to using Keytruda plus chemo, even in high PD-L1, what's become very apparent is that the Fc-enabled anti-TIGIT have an issue with AEs in the context of chemo. So we feel like we're well-positioned to even have a stronger advantage relative to any of the competitors at this point in that population. Now, the second piece is just from a scientific standpoint, the underlying mechanism is that that anti-TIGIT is enhancing the activity of the anti-PD-1. Same phenomena that we demonstrated in the context of GI cancers on top of chemo. And we've shown the data from EDGE-Gastric, and we think that same thing will hold up there. And then the particular advantage is that when you add DOM on top of the anti-PD-1 chemo, what we're seeing consistently again is that we're not seeing any enhanced AEs. So you really get the full advantage of what the mechanism offers with the Fc-silent molecule. I think it's important stuff to realize there's enough data out there to just bucket into two categories, the Fc-enabled and the Fc-silent. So AstraZeneca and us, and all the other later-stage molecules are having issues consistently with those immune-associated adverse events. Oh, and then your next question was, when might we see? We haven't commented yet. The point that I would raise is that in the context of EDGE-Gastric, which was fully enrolled, I'm sorry, so our STAR-221, which is the phase 3 correlate to that, the OS for the standard of care is about 13 months. As you know, in non-small cell lung, there's going to be over 20 months. And so we'll give guidance on readout sometime next year. Sounds good. Thank you. Thank you. Thank you. The following comes from Jason Zemansky with Bank of America. You may proceed. Good evening. Thank you so much for taking our questions and congratulations on both the quarter and the recent presentations. Had a couple of quick follow-ups on the PEAK-1 study. You know, in terms of primary endpoint, you have PFS. Merck is advancing a number of similar studies with belzutifan, with lenvatinib, and a couple of different settings, including second line. Where the primary endpoint is PFS and OS, just curious on kind of the decision behind making the primary endpoint PFS. And then just kind of fundamentally, what do you think you need to do to distinguish yourself from Merck's combinations given their potential to kind of that first-mover advantage, particularly when if you look at, say, the first-line setting, there are a range of different studies, you know, that you might not have the same sort of efficacy, but but kind of that inertia there keeps them well-used. You know, example, KEYNOTE-426, looks like 17% still use it, even though it's maybe not as good. It said, you know, CheckMate 214 or CheckMate 9ER. Thanks. Yeah. So when it comes to treatment preferences, that's the last part of your question. There's a lot of things that go into it. I actually referred to that earlier on. Ipi-nivo, for example, is very well recognized for very durable responses and long-term survival benefit. The downside of the regimen is recognized as primary progression. So patients with bulky disease, patients who need a response immediately, they're typically not put on Ipi-nivo. And based on early readouts, patients with favorable risk were also not given the opportunity, but with longer-term follow-up, it's now very consistent that the IMDC risk categories are no longer considered to be predictive of Ipi-nivo benefit. So that's one of the reasons when it comes to differentiation, it's the question I answered previously. I think in this particular setting, Merck is not doing this trial. They don't have a TKI-free first-line trial, which from a physician-patient perspective, not having the TKI toxicity for the long duration of treatment in the first line by itself is already a very important differentiator. When it comes to the second-line differentiation, PEAK-1 versus LITESPARK-011, having a far more preferred TKI as combination partner, Cabo versus Lenvima, the logical choice because Merck owns Lenvima or part of it, for us is a major benefit. We consistently hear from physicians that Cabo is much easier to handle than Lenvima. The dosing complexity of multiple dose levels for Lenvima, the overall, let's say, less well-perceived toxicity profile is an important differentiator. The other differentiator we have is, even though Merck was earlier with the trial, that comes with the downside that their experience in post-adjuvant patients by definition will be very limited to almost non-existing. We will be able to capture those patients, so potentially we will get a broader label as well. And then the last part of your question about the dual primary endpoint, I cannot comment on why Merck is doing it. I can only speculate. The registrational endpoint is PFS. Whether or not OS is a well-powered secondary endpoint or a primary endpoint comes a little bit down to trial size efficiency. However, the only reason to do OS as co-primary or better saying dual primary endpoint is if you are not sure if you can hit PFS. So if you hit PFS as primary endpoint, all the alpha goes to the secondary endpoint, and you have an adequately powered overall survival analysis. And so, in my, let's say, let's say from my perspective, doing it as a dual primary endpoint unnecessarily makes the trial larger, but they might have done it because they didn't know what the trial readout would be. Obviously, we will have that advantage that the trial that they are doing will have read out before we get to our analysis. And in a rare case that we would have to make updates, we can do so. Got it. So if I'm hearing you correctly, you think between PEAK-1 and LITESPARK-011, you'll have a tolerability edge. Do you think you can also have an efficacy edge as well? Absolutely. If you, let's say, if I just start with the low bar, if you can stay on a TKI longer because it's better tolerated, you have more benefit. Then, of course, we are generating the casdatifan data that starts to look differentiated from belzutifan on efficacy, notably the primary PD rate, but also other benchmarks that start or other metrics that start to look better. So we are confident that both the combination partner, but also our HIF-2alpha inhibitor, both will be part of the story of a better efficacy and a better safety profile combined. Perfect. Thanks for the color. Thanks. Thank you. The next question comes from Eva Privitera with Wells Fargo Securities. You may proceed. Hi. Thanks for taking our question and congrats on the progress. A quick one from us. So for the domvanilimab and combo in the phase 2 EDGE-Gastric, you guided to OS data in 2025. So if I recall correctly, you've only shown data for one arm, but the study included more arms. I was wondering if you're going to share data from the other arms together in the same update or if this mitht come at a later time next year. Thanks. So the guidance indeed is correct. We have committed to the OS data for EDGE-Gastric that's maturing right now for 2025. I think we said it before, the enrollment in arm A1, that's the arm we presented, and then A2 is the contribution of component arm for regulatory purposes was not at the same time. They were done sequentially. The data, the data are maturing, and I would say it's unlikely we will present it all at the same time because these things don't mature at the same time. But at some point, we will present the data if it's mature. Thank you. Our final question comes from Yigal Nochomovitz with CITI. You may proceed. Yeah. Hi. Thanks for the follow-up. Just very quickly, I think, Terry, you mentioned in the prepared remarks that you may be in a position to provide updates in the more near term. Does that mean that you might, you might get some of this data that's referenced in the release this year? Just clarify what what what you meant there. Thank you. Yeah. We didn't want to get too specific, but let's recognize, look at all those studies we have ongoing. So we have our cohorts within the study. So we have a 150-milligram cohort. We have a 100-milligram tablet. We have the 50 and 100 that we've already talked about that are continuing to mature. And what we felt is for the transparency and the importance of these data, that when we see something meaningful, we're going to look to find a way to get it out there. But right now, we don't have any specific plans, but we recognize there's such a large volume of data. We see they're interesting. We want, we want to make sure to take opportunity to update whenever it might be meaningful. All right. Thank you. Got it. Thank you. There are currently no other questions in queue. This concludes today's conference call. Thank you for your participation. You may now disconnect your line. Thank you. Goodbye.