Hello all and welcome to Arcus Biosciences' first quarter 2024 earnings call. My name is Lydia and I'll be your operator today. If you'd like to ask a question during the Q&A, you can do so by pressing Star followed by 1 on your telephone keypad. I'll now hand you over to Pia Eaves, Vice President of Investor Relations and Strategy. Hello everyone, and thank you for joining us on today's conference call to discuss Arcus's first quarter 2024 financial results and pipeline updates. 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 annual report on Form 10-K and quarterly report on Form 10-Q, which have been filed with the SEC. We strongly encourage you to review our filings. Today you'll hear from our CEO Terry Rosen, COO Jennifer Jarrett, and CFO Bob Goeltz. We'll also be joined by our CMO Dimitry Nuyten and President Juan Jaen for questions after the prepared remarks. For ease of listening, we will be referring to abbreviations of our molecule names: Domvanalimab as Dom, Zimberelimab as Zym, Casdatifan as Cas, Quemliclustat as Quemli, and Etrumadenant as Etruma. During today's call, we'll refer to slides in our corporate deck which can be found on the investors section of our website. With that, I'll turn the call over to our CEO Terry Rosen. Thanks very much, Pia, and thanks to all of you on the call for listening in today. As you know, 2024 is shaping up to be an incredibly catalyst-rich year for Arcus. By the end of this year, we'll have data to support all four of our later-stage clinical programs: Dom, Zym, and lung and upper GI cancers; Cas and clear-cell RCC; Quemli and pancreatic cancer; and Etruma and colorectal cancer. We'll spend most of the call today setting the stage for these upcoming data events. With over $1 billion of cash on hand, runway into 2027, partnerships with Gilead, AstraZeneca, Taiho, others, along with a very diversified pipeline, we're extremely well-positioned to capitalize on these data sets and advance our potential first and also best-of-class treatments towards approval and commercialization quickly and efficiently. Let me start with ASCO. ASCO is less than a month away, so we're almost there. We're thrilled and honored to have two oral presentations, both of which will provide strong support for our efforts and programs in the GI cancer field. Importantly, both data sets are in settings where there's limited competition and huge unmet need. These are genuine opportunities to make a meaningful difference for patients. So first off, on Saturday, June 1st, we'll have updated data from cohort A1 of the phase II Edge Gastric study evaluating Dom+Zym+Chemo in first-line gastric cancer. As you're aware, Dom is the only Fc-silent anti-TIGIT antibody in late-stage clinical development, and we believe that the data presented to date indicate that Dom may potentially have an improved safety profile when combined with chemotherapy relative to that of the Fc-enabled anti-TIGIT antibodies when they're combined with chemotherapy. As a reminder, we presented initial data from this cohort of Edge Gastric at the ASCO virtual plenary session in November of last year. At the time, median PFS was immature. However, we did present mature landmark 6-month PFS numbers, which you can see on slide 16 of our corporate deck. What you can see is that 6-month landmark PFS was 77% for the overall population and 93% for the PD-L1 high population. So given that the median PFS for standard care in this setting ranges from 7-8 months, these data were obviously very, very encouraging. At ASCO, we're very excited to be presenting mature median PFS data. We expect the updated data will further support the potential for Dom+Zym to provide clinically meaningful benefit relative to the standard of care in gastric cancer. Importantly, Edge Gastric evaluated the same setting and similar patient population as our ongoing phase III study STAR221. So therefore, we expect these data to foreshadow what we are seeing or our confidence in our STAR221 study. In that context, enrollment in STAR221 is expected to complete by mid-year. The incredibly rapid enrollment of the study is indicative of the lack of competition in the gastric cancer market and the immense need for new therapeutic options, particularly with overall survival in this patient population ranging from only 13-14 months in studies with anti-PD-1 antibodies and chemotherapy. We also felt that we actually achieved some tailwinds with our data presentation at the end of last year. Putting this all together, you can infer that there's a line of sight to data and that domvanalimab will have a very substantial head start over potential competitors given there are no other anti-TIGIT antibodies in phase III development for this setting. We think we're going to have a clear first-to-market advantage. This creates an exciting opportunity for us to be first in this setting with an addressable patient population of over 25,000 patients in the U.S. alone and 100,000 patients in the G7 countries. This equates to the potential worldwide market of over $3 billion. Now moving on to our second presentation at ASCO. On Sunday, June 2nd, we'll be presenting data from our Arc9 study in third-line colorectal cancer. This will be the first presentation on this study. The data will be from cohort B, which is evaluating Etrumadenant in combination with Zimberelimab, FOLFOX, and BEV versus Regorafenib, one of the standard-of-care treatments for third-line colorectal cancer. On slide 41 of our corporate deck, you can see the study design and the inclusion criteria for this portion of the study. Patients in this cohort must have received BEV, unless contraindicated, a prior oxaliplatin-based regimen and an anti-PD-1-based regimen. These are the current standard-of-care therapies for first- and second-line CRC. 105 patients were enrolled who were randomized 2 to 1 between the Etrumadenant arm and the Regorafenib arm. So this is a relatively large data set. ARC-9 also included two additional randomized cohorts which evaluated Etrumadenant plus Zimberelimab plus FOLFOX and BEV versus FOLFOX and BEV in second-line colorectal cancer. These data are not yet mature and will be presented at a later time. Second-line setting, as you know, has a substantially longer OS. The ASCO presentation will include mature PFS and OS data with a median follow-up of over 20 months. Our data will include patients with and without liver mets. This is important since patients with liver mets tend to have a poor prognosis and they're not always included in late-line CRC trials. As many of you know, there are very limited options in third-line plus colorectal cancer. Patients are typically treated with regorafenib and more recently with a combination of Lonsurf and BEV based on the Sunlight study, which showed a PFS of 5.6 months and OS of 10.8 months in the third-line patient population. While acknowledging the limitations of cross-trial comparisons, but we all do it based on our data, which will be shared with you next month, we believe the Etrumadenant-based combination regimen may represent a very substantial improvement over current options for patients in the third-line setting. I also want to point out a small data set of 35 patients that was just presented in a poster at AACR, which actually captured quite a bit of interest and further supports our hypothesis that adenosine blockade enhances the immune-activating benefits of chemotherapy. These data were from the Morpheus PDAC study, a randomized phase 1b/2 trial operationalized by Roche that evaluated our molecule Etrumadenant plus Roche's anti-PD-L1 and gemcitabine and nab-paclitaxel versus chemotherapy alone in first-line metastatic pancreatic cancer. We've highlighted the design on slide 37. On slide 38, we've shown the spider plots for both the control arm and the Etrumadenant-based regimen, which showed durable responses. In this trial, the Etrumadenant-containing arm demonstrated a meaningful improvement in both PFS and OS, and we've shown these data on slides 39 and 40 of the corporate deck. Specifically, the PFS hazard ratio was 0.48 and the OS hazard ratio was 0.67, with the Etrumadenant-based regimen yielding an absolute improvement in median overall survival of 4.4 months over chemotherapy alone. The median OS for the Etrumadenant-containing arm was 16.5 months, very similar to what we saw in Arc8. Before we leave Etrumadenant, I want to highlight that now, with the Arc9 data presentation, we'll have three data sets presented in a very short period of time for our two molecules that inhibit the ATP adenosine pathway, quemliclustat and Etrumadenant. Between ARC-8, which evaluated quemliclustat in combination with chemotherapy in first-line pancreatic cancer. Morpheus PDAC, very similar, which evaluated etrumadenant with chemo in first-line pancreatic cancer. And now, ARC-9, we have three independent but similar data sets which together provide compelling evidence demonstrating that mitigating the immunosuppressive action of adenosine, combined with immunogenic chemotherapy, may prolong survival relative to that associated with chemotherapy alone. For those of you who've been following us for a long time, keep in mind this was the original hypothesis which drove us to the adenosine axis in the first place. So we're getting to the point where the data are matching the hypothesis. Importantly, two of these studies showed meaningful improvement in OS versus the standard-of-care control, and all three showed substantial improvement above historical benchmarks when adenosine blockade was combined with immunogenic chemotherapy. Now that we've covered what we'll be sharing at ASCO, I'd like to turn it over to Jen to discuss expectations for our HIF-2 alpha inhibitor program later this year. Thanks, Terry. I'll now turn to our data events for the second half of 2024 and specifically for Cas, our HIF-2 alpha inhibitor, which we are developing in clear-cell renal cell carcinoma, or ccRCC. As a reminder, HIF-2 alpha is a validated mechanism, with belzutifan recently approved as monotherapy for late-line clear-cell RCC patients. Cas has PK and PD advantages over Belz, which should enable it to hit the target harder with the goal of achieving greater clinical efficacy than that of belzutifan. As we talked about on our last earnings call, there are multiple opportunities to improve upon the profile of belzutifan: a lower rate of primary progressive disease, a higher overall response rate, and more prolonged responses, any of which could translate into a higher PFS and ultimately longer OS for Cas relative to that of belzutifan. Our phase 1b study for Cas, Arc20, now has enrolled over 80 patients. That's 80. It was designed to answer numerous questions, so I want to spend a minute describing the various components of this multi-cohort study, which is summarized on slide 27 of our corporate deck. First, for the dose escalation. As of our last earnings call in February, we had completed enrollment of the 20 mg, 50 mg, and 100 mg dose cohorts with no dose-limiting toxicities observed. We have now completed enrollment of the 150 mg cohort, and again, we did not observe any DLTs, and we just cleared that dose. Additionally, we continue to see linear dose-proportional PK for Cas even at the 150 mg dose. The dose expansion portion of Arc20 was designed to serve a few purposes. First and foremost, to generate data for our proposed phase 3 dose of 100 mg of Cas. These data will be used to support initiation of our first phase III study, which is in the advanced stages of planning for casdatifan. The monotherapy dose expansion portion is enrolling patients that have received at least one prior anti-PD-1 therapy and at least one TKI. In the 100 mg dose cohort, approximately one-third of patients had received four or more prior lines of therapy, so these patients were relatively advanced. On our last earnings call, we disclosed that while the majority of patients in this cohort had only received one or two scans, we were already seeing a response rate, including responses pending confirmation, in line with LIGHTSPARK-005, the phase III study for belzutifan. We also mentioned that we observed a lower rate of primary progressive disease, where the percent of patients that progressed prior to their first scan then was reported for LIGHTSPARK-005. This is important, as one weakness in the LIGHTSPARK-005 data set, as we've heard consistently from clinicians, is the high rate of primary progressive disease. Bringing this rate down should result in more patients benefiting from treatment and prolonged PFS and survival. We are very excited to present detailed data from this cohort at a medical conference in the second half of this year. We also designed the dose expansion portion to satisfy the dose optimization work required for regulatory submissions. Specifically, we included two additional monotherapy cohorts in Arc20, which are evaluating a 50 mg dose and a 150 mg dose. We have now completed enrollment of the 50 mg cohort, and we just initiated enrollment of the 150 mg cohort. In addition to enabling us to complete the dose optimization work required for Project Optimus, these cohorts will also generate a lot of additional data that will further elucidate the clinical profile of Cas. In addition to the three monotherapy expansion cohorts in Arc20, we are about to initiate enrollment of a cohort to evaluate Cas in combination with CABO, the most commonly used TKI, and clear-cell RCC. Data generated from this cohort, in addition to the data generated from STELLAR-009, our phase II study being operationalized by Exelixis, will be used to support the planned initiation of at least one phase III study for Cas in combination with the TKI. Given the enthusiasm for Cas and the rapid enrollment of Arc20, we expect our 100 mg dose expansion cohort data presentation later this year to be followed quickly by data from the various other cohorts. We are aggressively advancing Cas towards the initiation of our first phase III trial early next year. Importantly, we are taking a strategic approach to our development plan to maximize the value of what we believe is a best-in-class HIF-2 alpha inhibitor. For example, the STELLAR-009 study is evaluating Cas with a next-generation and potentially best-in-class TKI, zanzalintinib. We believe that both Zanza and CABO could have advantages over belzutifan's TKI partner, Lenvima, with a better tolerated AE profile. And therefore, we expect our Cas-TKI combination could be differentiated from both an efficacy and safety and tolerability perspective relative to belzutifan plus Lenvima. I'd like to end by spending a few moments on the RCC market, of which approximately 80% of patients, 80% of patients, have the clear-cell histology. The annual addressable patient population for first-line clear-cell RCC includes over 12,000 incident patients in the U.S. and approximately 30,000 in the G7 countries. Around two-thirds of these patients progress on first-line treatment and are addressable in the second line, resulting in more than 8,000 patients in the U.S. and approximately 20,000 across the G7 countries. The ccRCC market is fragmented, but CABO is the most frequently used TKI. CABO sales in 2023 in the U.S. alone were over $1.6 billion, driven almost entirely by RCC, and with only 25% market share in first-line and under 50% market share in the second-line setting. In terms of the treatment paradigm for first-line RCC, patients are typically treated with anti-PD-1 plus a TKI or a combination of nivolumab plus ipilimumab. When patients experience tumor progression on front-line therapy, they cycle through different TKIs frequently for a few years or more. With few options beyond TKIs, the clinician community has been eagerly waiting for the introduction of HIF-2 alpha inhibitors, particularly given the relatively benign safety profile relative to TKIs. And so not surprisingly, the positive Phase III data for belzutifan resulted in an immediate and steep inflection in script trajectory. Monthly scripts are now at twofold since top-line data for Belz and clear-cell RCC was released in August 2023, and up 50% in just the first four months after belzutifan's approval in this setting. Based on just March scripts, belzutifan is now at an approximately $400 million run rate in the U.S. alone and growing. As we've discussed, we believe that Cas may improve clinical outcomes relative to belzutifan, and we plan on developing Cas in differentiated combinations, all of which support a very meaningful market opportunity for Cas, which we believe is north of $2 billion. Before we conclude, I'll now turn the call over to Bob to review our quarterly financials. Thanks, Jen. Arcus continues to be in a strong financial position. Our cash as of March 31st, 2024, was $1.1 billion as compared to $866 million as of December 31st, 2023. Turning to our P&L, we recognize GAAP revenue for the first quarter of $145 million, which compares to $31 million in the fourth quarter of 2023. Our revenue is primarily driven by our collaborations with Gilead and Taiho, and in the first quarter, included cumulative catch-up of $107 million resulting from the Gilead amendment we executed in January. We expect to recognize GAAP revenue of approximately $30 million per quarter for the remainder of 2024. Our R&D expenses for the first quarter are stated net of reimbursements from Gilead, and were $109 million as compared to $93 million in the fourth quarter of 2023. In the first quarter, non-cash stock compensation represented $10 million of our R&D expenses. The increase in the first quarter was related to higher clinical manufacturing, clinical trial, and headcount-related costs associated with our late-stage programs. We continue to expect modest increases in R&D expenses as our phase III studies mature and spend will fluctuate primarily based on the timing of clinical manufacturing activities and the purchase of standard-of-care therapeutics for our clinical trials. G&A expenses were $32 million for the first quarter compared to $29 million in the fourth quarter of 2023. Non-cash stock compensation represented $10 million of our G&A expenses for the first quarter, and we expect G&A to remain stable for 2024. Total operating expenses in the first quarter were impacted by a $20 million non-cash impairment charge resulting from the intended sublease of a portion of our office space. Finally, we continue to expect our cash balance at the end of 2024 to be between $870 and $920 million and to fund operations into 2027. This guidance includes a $100 million partnership continuation payment from Gilead in the third quarter and excludes potential opt-in payments and approval milestones from our partners. For more details regarding our financial results, please refer to our earnings release from earlier today and our 10-Q. I'll now turn it back over to Terry for concluding remarks. Thanks, Bob. As you've heard from us today, we are genuinely at a significant inflection in the evolution markets. With completion of enrollment of STAR221 first-line gastric cancer expected by mid-year, we're turning our attention to our first phase 3 readout. Behind this, we'll have phase 3 data from our second registration study for domvanalimab, STAR121, and first-line non-small cell lung cancer, with enrollment for this trial also expected to complete this year. In addition, we'll be starting at least two additional phase 3 trials by early next year for casdatifan and clear-cell RCC and quemliclustat in first-line pancreatic cancer. As we talked about today, we have several important near-term data sets which may provide further validation and meaningful de-risking of several of our programs. This will all kick off shortly at ASCO with two oral presentations for Domvanalimab and Etrumadenant-zimberelimab, and together, they'll showcase our emerging GI cancer franchise. We're, of course, looking forward to sharing much more on our HIF-2 alpha program later this year from the dose expansion cohorts of Arc20. I want to highlight how unusual it is for an early-stage company to be executing multiple phase 3 studies for several different molecules, all targeting massive opportunities and doing so in parallel. This is obviously all enabled by our current cash position and our partners that include Gilead, AstraZeneca, Exelixis, and Taiho. These partnerships have and will continue to provide a combination of development funding through the receipt of opt-in fees, milestones, and cost sharing to reduce our overall development expenses. I want to conclude by thanking all of you for your continued and ongoing support of Arcus and our mission to bring innovative therapies to patients in need. We'll now open the call for questions. Thank you. Please press star followed by the number one if you'd like to ask a question, and ensure your device is unmuted locally when it's your turn to speak. Our first question comes from Kaveri Pohlman of BTIG. Your line is open. Please go ahead. Yeah. Good evening. Thanks for taking my question. For HIF-2 alpha, some of the literature suggests that HIF-2 alpha is upstream of VEGF, and it leads to its production. So they're basically in the same pathway. Do you think that could make CABO-responsive patients more sensitive to 521? And because of the same biology, do you expect to see any overlapping toxicities with zanza, which also targets VEGF? Yeah. So they are in the same pathway. We do believe that HIF-2, on the other hand, though, since it controls probably 100 genes, there are other effects ongoing in cancer. We don't really expect, and in fact, we know what the side effect and AE profiles are. So we do not expect that you would see overlapping toxicities. And I would just say that with HIF-2 alpha, those toxicities and AEs have already been well-defined by belzutifan. What you primarily see is very manageable anemia. We've seen similar. And even though we believe in knowing, in fact, that we're hitting the target harder, essentially, nature's built in a break because only so much HIF-2-mediated EPO expression is happening in the kidney, and there's other sources of EPO. And we've seen a safety profile that continues to look very similar to what has been reported for belzutifan. As Jen noted, we've actually even completed a 150-milligram cohort. And again, you have not seen any DLTs to date. Got it. That's helpful. And maybe a quick one regarding STAR121 trial for first-line non-small cell lung cancer. It has primary endpoints of PFS and OS. Do you have to win on both? And what are the expectations from the arms? How much variation from the control arm and/or TIGIT arm is acceptable? Thank you. Dimitry, do you want to handle that question? Sure, Terry. So the first question is relatively simple. So statistically speaking, the way it's set up, it's a dual primary endpoint, meaning that either PFS or OS, if either one of those is statistically significant, it would be a positive trial. I think we've been very clear in previous calls as well in lots of interactions that are in the public domain that from a regulatory perspective, OS is really the registrational endpoint. PFS is supportive. And your second question, can you repeat it, please? I didn't get the entire question. Sure. I just wanted to get some so the PFS and OS are really comparing arm A and B. B is, I believe, Keytruda combination, but there is an arm C for Zim. I was just wondering how much variation from that arm versus control arm, Keytruda arm, or TIGIT arm is acceptable. Yeah. That's a hard question as the FDA would say it's a review issue. That arm, I think, is clear from, let's say, the public domain. It's a 4:1 randomization. So a very limited number of patients is going on to Zim and chemotherapy to establish contribution of components. Based on FDA guidance, I can share that contribution of components mostly is established by looking at the response rate. And of course, in a randomized fashion, a time-to-event endpoint could also be assessed. There's no absolute guidance on what the variability can be. That's a review issue. I can summarize. I'm very confident with the data we've generated for Zim that a positive trial, meaning that Dom and Zim combined with chemotherapy clearly beat Keytruda, that the contribution of components, let's say, discussion is a modest part of the discussion. I'm confident that we will be able to achieve that successfully with the study design. That's very helpful. Thanks for taking my question. Thank you, Kaveri. The next question comes from Peter Lawson of Barclays. Your line is open. Great. Thanks so much. Thanks for taking the question. Just around HIF-2 alpha, for the second-half data, kind of what defines success for you from that data set? And could you remind us what Gilead or what the trigger points are for Gilead to potentially opt in? Thank you. Sure. Thanks, Peter. So on what defines success, as we've articulated, there's a number of variables and opportunities for differentiation from belzutifan. So starting with response rate, rate of primary progression, depth of response, even if we have PFS by that point. So we want to do better than belzutifan. I'll remind you, in thinking about our overall program, though, based upon what we've already seen, the data look good. And we're full speed ahead to registrational trial. And keep in mind that we are not going to be developing this, at least in the near term, as a monotherapy. And we also believe, as Jen was discussing, that we'll be combining with a better TKI than lenvatinib. So that'll give us another opportunity for differentiation. So there's multiple places when we think that we have an opportunity to beat belzutifan on more than one of those. In terms of the Gilead opt-in, that's something that we would expect. We've converged on what would define that opt-in, and we would expect a decision either towards the end of this year or early into next year. Great. Thanks so much. The next question comes from Yigal Nochomovitz of Citi. Please go ahead. Hi guys. This is Ashiq Mubarack on for Yigal. Thanks for taking my questions. I have a few on the Arcus gastric update at ASCO. Obviously, based on the data you've already shared, it looks like the Kaplan-Meier curves on PFS are trending well beyond the 7-8-month hurdle I think you cited, but naturally with a small N. So I'm just curious how much greater do you think the PFS benefit really needs to be to de-risk STAR221? And a more theoretical question, I guess, how well do you think PFS correlates with OS benefit in this setting given that's the primary endpoint in STAR221? So thanks for the question. You're right on the sample size. And I think you'll be able to make your own call on that. As you suggested, it's known. And actually, the data has been pretty tight. So in addition to CheckMate-649, there's been two other registrational studies with anti-PD-1 and chemo. And they've both come in in that roughly just under 7-8 months PFS. So that's a pretty firm number. We think our data will be quite meaningful. I think one other thing to keep in mind when you compare our data sets, interestingly enough, CheckMate-649 had 60/40 high PD-L1 to low PD-L1, and we're actually 40/60. So pretty substantial difference. And as you saw, even our numbers in the all-comer population look pretty good. So we're three weeks away. We're excited about the data. You'll make your own call on how much you think they've de-risked the site. Interestingly enough, as we also mentioned, we're on the cusp of that registrational study being completed. So you'll see those data in a couple of weeks. In terms of the correlation, as you know, in general, PFS and OS, particularly in the context of immunotherapy, are certainly qualitatively correlative. But I wouldn't necessarily think that you can plot a line for them. But given our data set, I think you'll clearly be able to form some speculation as to what might happen on the OS, just like you formed some speculation on the six-month landmark numbers, what might happen. I think those dots are going to connect, at least qualitatively, in a direction that will be confidence-enhancing. Yeah. If you look at the CheckMate 649 data set, I think you could say that the PFS and OS benefit was pretty correlative and pretty similar if you look at the hazard ratios. That's at least one data point that I think shows that the correlation should be pretty strong between PFS and OS in this disease. Got it. Got it. I have one more. Correct me if I'm wrong, but I think you said the Arcus gastric data at ASCO will only be from cohort A1. So I'm curious where things stand with the other cohorts, especially cohort A2, which is, I think, the Zim plus FOLFOX arm. And obviously, that one will be important to helping understand the contribution of Dom if that cohort varies from the 7-8-month number you're talking about. So I'm just curious where things stand there. Sure. So that cohort actually enrolled sequentially to the first one. So the final patient actually just was enrolled a few weeks ago. Keep in mind, not only was it sequential, but since it's essentially a single-arm study, the fact that you don't have an experimental arm is another thing that probably slowed its enrollment. So it's probably trending a year behind the initial cohort. I'll also mention that, as you've probably seen on ClinicalTrials.gov, we have two additional arms that are probably more designed to take on that contribution of components that will be run in a randomized fashion and with a larger end. The other thing that may be important about that cohort that you just referenced, that we recognize it's another opportunity, albeit a single-arm, non-randomized data set, that'll give people another look at how zimberelimab chemo compares to historical numbers for other anti-PD-1s such as Keytruda or nivolumab chemo. So we think it'll be an interesting data set as well. But it's at least a year behind this cohort. Got it. Thanks very much. Thank you. Our next question comes from Jonathan Miller with Evercore ISI. Your line is open. Thanks, guys. A couple on HIF2 from me. Obviously, we're very excited to see the 100-milligram cohort release and get a better sense for HIF2 efficacy here versus the competitor. But I'm wondering why, well, specifically, the 50-milligram cohort isn't going to be part of that same release. That was enrolled before 100 milligrams, no? So I understand 150 just got finished. But why not include 50 in your end-of-year release? Secondly, this quarter, as well as last quarter, you highlighted that you're already hitting. Sure. Sure. Happy. I was going to answer that because I'll forget what you said. Your brain is younger and faster than mine. So I'll forget the first question. So let me just answer the first one, and I'll take your second question. So the 50-milligram cohort was actually enrolled after the 100-milligram cohort. And it was basically we added both the 50, and then we wanted to go with the higher in the context of Optimis. So the 50-milligram cohort, just very recently, was fully enrolled. And in fact, it won't be part of the medical conference presentation because clearly, it won't be mature. But whatever we know about it, you'll be able to get that out of me without much inducing. So we'll share whatever we know about it. In fact, when we first saw the very earliest data, even when only 15 patients or so had been scanned, the data were looking interesting. To your point, it's actually, even though it's 50 milligrams, that's 2.5 the PD equivalent of the Merck belzutifan clinical dose. The 150-milligram cohort is just starting, as you noted. 50 came after 100. Okay. Makes sense. Last quarter, in this quarter, both, you highlighted that ORR at the 100 mg dose, I assume, is already similar to belzutifan, the implication there being that given belzutifan's time to response, that ORR could, in fact, deepen as you get more scans under your belt. So in the intervening three months, have you seen ORR increase? I mean, I noticed that in both this quarter and last quarter, using similar language, saying that you're hitting similar ORR levels to belzutifan. But now that we've gotten presumably more scans on these patients, do you see those late responses, or I suppose I should say later responses, more akin to belzutifan's time to response? Yeah. So if we were using the same language, it was because we were reiterating what we said at the end of the when we gave the last update, as opposed to it's a fresh description. So all we would comment is the data continue to look good along the trajectory of what we were seeing then. And we have no plans to give updates until the medical conference. And then you'll see the full picture. All right. Fair enough. Sorry. The way to do that is you're right that this is a mechanism where the response kinetics were on the slower side, and the average time to response was about four months in the LIGHTSPARK study. So similarly, some of our responses may take more time. Okay. Makes sense. And then lastly, just as we think about the two different TKIs that you're exploring as combinations here, can you give us a little bit of color about what you're looking for to pick between them? You've highlighted the importance of safety versus Lenvima as a driver here. So are there clear no-go signals that would push you one way versus the other? Or is it something else that you're really looking at? Yeah. So I would say it's more strategic in timing. And we're thinking about different settings. And I think what you're going to see - and this is primarily for competitive reasons, not playing any games - as this year goes along, we'll be very transparent about our development strategy. Some of this, it's not even that we're in the decision-making process. We know. But we want to let time play out a little as we get closer to those studies coming online. And you'll see there's different lines of therapies. There's other combinations we're thinking about. In addition, you can imagine even that we might go in both directions in different settings. So we'll describe that as the year goes along. All right. Thanks very much, guys. Thanks, Jonathan. Our next question comes from Jason Zemansky with Bank of America. Please go ahead. Thank you. Good afternoon. Congratulations on the progress. Really appreciate you taking our question. Maybe just to take a step back on the adenosine pathway, just starting development efforts, it looked like the pathway was upregulated across a number of tumor types. While there are certainly very encouraging signals in colorectal and pancreatic cancer, there have been some admitted setbacks as well, both in cold tumors like prostate and, seemingly at this point, NSCLC as well. I'm curious, have you cracked the code at this point in terms of which tumors are likely to respond, especially as your data sets emerge and mature? Are there additional signals that give you confidence in the mechanism at this point, especially as you start to look longer-term at maybe some additional indications? Yeah. Thanks, Jason. So I think what we're probably looking at right now when we think about sweet spot, from what we've learned, and this was a big part of what we thought going in, is less the organ and more the biology and therefore the treatment. And what I mean by that is if you looked at the three studies that we're pointing to right now, Morpheus, PDAC, our own pancreatic study, and the colorectal study, they're both situations that were going right on top of immunogenic chemotherapy. And going into this, that was sort of down the middle of the fairway for us, where you have a setting where you're killing cells. It's in this immunogenic way with chemotherapy. And what's extraordinarily well understood about those settings is that if that ATP spills out from those initial cells dying, you produce a ton of adenosine. And so if you're able to mount any sort of immune response, those T cells are hit by adenosine. And that's physics. That adenosine, there's a million papers that are going to tell you if a T cell sees adenosine, it's going to sleep. And so the phenotype of the response that we're seeing in each of these studies is very similar. So the places that we are thinking about beyond the current settings would be just those, something where the standard of care is an immunogenic chemotherapy, but there's headway above that to actually get the benefit of when you think about that immune response that might be induced by chemo, that you can enhance that by mitigating the effects of the adenosine that forms. So that's the way we're thinking. What's the most we've learned to date? And there may be more you learn with time. But that's the primary learning to date. Go ahead, Juan. Yeah. Sorry. I think a third element would be tumors that tend to be very high in CD73 expression. So that pretty much takes you to GI tract and lung adenocarcinomas as the places where you have the convergence between a high level of CD73 immunogenic chemotherapy. Got it. Perfect. Thanks for the color. Thanks for the question. Our next question comes from Daina Graybosch of Leerink Partners. Your line is open. This is Jeff Liu for Dana. Thanks for taking our questions. So we have one on the Cas and one on the Truma. So I guess starting with Cas, we noticed Novartis has an oral ASCO for their HIF-2 inhibitor. How does Cas differentiate from that molecule? And in that context, what are your expectations for that ASCO presentation? And do you think Novartis's decision to discontinue its further development has any read-through to Cas and your program? I want you to comment what we know about the Novartis molecule. I'll start off zero read-through, but I'll let Juan comment on the Novartis molecule or whatever's known as it. Yeah. So our in vitro evaluation of the compound suggests that it's a reasonably potent HIF-2 inhibitor. In our hands, it's maybe an order of magnitude weaker than Cas is. As you know, there's much more that goes into making a high-quality drug, what it does in terms of pharmacokinetics, drug-drug interaction, PKPD. We'll have to see. But definitely going in, it was sort of not a great contender purely from a potency standpoint. Okay. Great. And then on the etrumadenant, how has the recent Roche PDAC data and the upcoming Arc9 data changed your view at all on etrumadenant's potential therapeutic opportunity relative to quemliclustat? And put another way, do you see any clinical settings where you'd expect the etrumadenant to outperform quemliclustat? And do you anticipate initiating any additional randomized phase 2 or phase 3 trials for etrumadenant this year? Thank you. So on the first question, while some people speculated otherwise, we look at both molecules, as we sit here today, as great molecules and great potential. And to be honest, if things continue along the way we've said this from the beginning, once we start to get good data, and the more good data that come, the more this is something one would contemplate. You might even think about combining the two at some point because there are certain situations where you may be able to generate adenosine through a mechanism that's not CD73 mediated, in which case blocking its action could be advantageous. So what we're going to say is, as of today, we've just seen and you'll see the data for yourself so you can decide. We think we've got very compelling data with both molecules. Going to your question about Novartis, I'm just going to use this as an opportunity. We've lived under an umbrella of some early studies done that, frankly, were with very bad molecules. We always talk about it's the molecule quality, it's the combination, and it's the setting that makes the difference. So we think going forward, there's still a whole lot more to be learned with these, despite the fact that each of them could be on a trajectory. In fact, we're starting the pancreatic trial as late as early next year and as early as late this year. We do expect to do more with the TIGIT. The only reason we are sharing specific details of what the plan will be and obviously, after you see the details of our data, there'll probably be more questions about exactly what we're going to do in the future. But we're still working through those details together with Gilead. We're preparing for discussions that we'll be having with the FDA. We want to think about exactly what would be the ideal control. That control and standard of care has evolved. When we started, it was Regorafenib. Now, it's moved much more in the direction of Lonsurf plus Bev. So there's a number of things that we want to work through. But you can definitely expect and when you see the data, you will expect that we'd be crazy to not be doing something more with the molecule. So we're working through that. Yeah. Well, I mean, obviously, it means a lot. I think it says a lot that I got an oral presentation at ASCO. To get any presentation accepted at ASCO has gotten to be a high bar. So hopefully, the fact that we had an oral presentation accepted tells you that the clinical community is at least finding the results and the study meaningful. All right. Fair enough. Thanks for taking our questions. Thanks. Our next question comes from Li Watsek of Cantor Fitzgerald. Your line is open. Hi there. This is Rosemary also Li. Thank you so much for taking my question. Just a quick one on your NextGen programs. How are you thinking about prioritization as you have all these late-stage trials going on? And how does inflammation fit in with your oncology franchise? Thank you. Yeah. So I think the question was sort of the early-stage portfolio. Given that we have all these late-stage things, how do we think about it? So we were talking about the collaborators and the collaboration and what it enables us. And in fact, it's another unusual aspect of the dynamic that we created with this collaboration. When we set this up with Gilead day one, well, people don't always take these things at face value. It was really designed to be an R&D engine type of collaboration. So clearly, disproportionately, given the number of late-stage programs we have, dollars are being invested correspondingly. With that said, we've continued and this was when we discussed the most recent equity investment that Gilead made. One of the things that we discussed at that time and there's a $100 million fee that they'll be paying shortly that maintains the relationship. There was a big emphasis on continuing to enable the discovery part of it because clearly, if you look at what we're generating, we started as a blank piece of paper. We're generating what we believe are good, high-quality molecules for targets of interest. And the most notable one that's moving along nicely and we think is going to be a big deal is our AXL inhibitor, which recently has gone into patients. And it performed well in healthy volunteers and generating some initial PK data. And that will be the first AXL inhibitor that actually tests the hypothesis. It's going to have the PK and the selectivity that we'll be able to hit AXL hard and see how that works out. So the early-stage portfolio continues with the same emphasis and investment that it has previously. To your question on the more immunological component of that, we haven't shared the most recent targets that we're working on. And we'll probably hold off on that for some time. It may even be within a year that we'll start to talk about that. But along with Gilead, increased our emphasis there. As we built the company, we have a very strong immunology-biology group. And I think you'll slowly see the percentage of the portfolio that looks like it includes immunology inflammation increasing. But it's not like we've defined some particular percentage. We're still at a stage of our evolution where the biggest driver would be best players. So best target, we'll get the next emphasis in our drug discovery group, whether immuno-oncology, oncology, or I'll use the term de novo, I&I. Got it. Thank you so much. Thanks. We have no further questions in the queue. So this concludes today's call. Thank you very much for joining. Thanks, everybody. Appreciate it.