Good afternoon, ladies and gentlemen. My name is Leah, and I will be your operator on this call. After the presentation, we will conduct a question-and-answer session. Instructions will be provided at that time. If at any time during the conference you need to reach an operator, please press the star key followed by zero. Please note that this call is being recorded today, Wednesday, June 23, 2021, at 2:00 P.M. Pacific Time, and will be available on the investor section of Arcus website at www.arcusbio.com. I would now like to turn the meeting over to Katie Bock, Vice President of Investor Relations and Corporate Strategy from Arcus. Please go ahead, ma'am. Thank you. Hi, everyone. Thank you, Leah, and thank you all for participating in today's call on such short notice. Today, we will be discussing this afternoon's announcement regarding the interim analysis from the ARC-7 study. Joining me from Arcus are Terry Rosen, Chief Executive Officer; Juan Jaen, President; Jennifer Jarrett, Chief Operating Officer; Bill Grossman, Chief Medical Officer; and Kartik Krishnan, Senior Vice President of Clinical Development. I'd like to remind you that on this call, management will make forward-looking statements within the meaning of the Securities Laws safe harbor provisions. For example, statements about our clinical development programs, timelines, and the potential of the Arcus-Gilead partnership. All statements other than historical facts involve risks and uncertainties that may cause our actual results to differ. 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 those filings. This conference call contains time-sensitive information and is accurate only as of the live broadcast today, June 23rd, 2021. With that, I'll turn the call over to Terry. Thank you very much, Katie, and thank you all for joining our call today and for your interest in Arcus. We really appreciate your engagement. As Katie mentioned, the point of today's call is to discuss our announcement this afternoon regarding the interim analysis from our ongoing ARC-7 randomized phase II study. We really recognize the intense focus around this disclosure, and I have to say, we're all genuinely excited to finally have the opportunity to see the data, share our assessment of this data set, and convey the potential opportunities that they afford us. First, I'll spend a few minutes reminding you why we have a TIGIT program, which now includes two TIGIT antibodies in the clinic, and then we can do a deeper dive into the ARC-7 study and results from the interim analysis. I'll round out the call with a number of the other exciting things that we're doing here at Arcus as we continue on our journey towards becoming what we genuinely believe will be a fully integrated commercial biopharmaceutical company. Since our founding only six years ago, we've built a robust drug discovery capability to create highly differentiated small molecules. Our small molecule portfolio and focus today include both immuno-oncology targets and mechanisms such as the ATP-adenosine pathway, as well as cell intrinsic targets such as HIF-2 α and AXL. We also recognized from day one the essential need to own important backbone antibodies against PD-1 and TIGIT, which we could combine with our small molecules to create and develop rationally designed combination therapies. We invested early and heavily to secure access to high-quality PD-1 and TIGIT antibodies. Through these efforts, I'm pleased to say that we now have five clinical-stage molecules, of which the majority have moved into randomized or registrational trials. We also have another molecule, our HIF-2α inhibitor, AB521, expected to enter the clinic in the second half of 2021. This will bring our total clinical-stage molecules to six. We have also built what we believe is one of the best oncology development capabilities in the industry, particularly when you think about a company of our size. Our goal has been to advance our molecules into randomized clinical studies as quickly and efficiently as possible. That brings me to TIGIT and ARC-7. First, let me touch on the rationale for TIGIT as a target. TIGIT is an immune checkpoint receptor expressed on immune cells, including T cells and natural killer cells, and it's typically co-expressed with PD-1. Activation of TIGIT by its ligand, CD155, results in suppression of these immune cells, leading to impairment of antitumor immunity. Clinical studies have shown that the combined inhibition of TIGIT and PD-1 results in synergistic antitumor activity. Most notable in this context were the CITYSCAPE phase II data, which showed a significantly higher response rate and progression-free survival for an anti-TIGIT plus anti-PD-L1 doublet versus the anti-PD-L1 antibody alone. Early on, we recognized the importance of TIGIT as the next backbone immunotherapy and in- licensed our first TIGIT antibody. At that time, we made the decision to silence the Fc function. We believed then and continue to believe now that depletion of intra-tumoral Tregs was not a requirement for the clinical activity of TIGIT antibody, and in fact, that long-term depletion of Tregs in the periphery could result in unwanted toxicity, and that the potential depletion of intra-tumoral cytotoxic T cells, which are the very same cells that we're trying to reinvigorate, could diminish the potential synergy between TIGIT and PD-1 antibodies. Consistent with how we pursue all of our programs, shortly after we selected our first anti-TIGIT antibody, domvanalimab, which we call dom, we initiated work on a second differentiated molecule directed against the same target. We recognized that an Fc functional antibody with the potential to deplete TIGIT-positive cells could be beneficial for certain tumor types. More specifically, in solid tumors, TIGIT is found only on immune cells and not on cancer cells. In certain hematological malignancies, the cancer cells actually express TIGIT. In this case, depletion of the TIGIT-bearing cells would be beneficial. We recognized the optionality that this provided and specifically designed our second molecule, AB308, to be Fc-enabled. Certainly, investment is now paying off. Domvanalimab has the potential to be the second or third TIGIT antibody to the market and potentially the first in certain settings. We have another anti-TIGIT molecule right behind it in phase I combination studies with zimberelimab, and we expect to initiate our first expansion cohorts with this regimen later this fall. We believe we're the only company with two anti-TIGIT antibodies in clinical development. Before I get to the results of the interim analysis, I really want to step back, take a moment to thank our patients and investigators for participating in the ongoing ARC-7 study. As a reminder, we designed this study to target patients with first-line metastatic non-small cell lung cancer with 50% or greater PD-L1 before the release of the CITYSCAPE data. The CITYSCAPE study utilized a PD-L1 antibody, the results that we will discuss today represent the first public discussion of randomized readouts for a TIGIT antibody combined with a PD-1 antibody in this setting. The ARC-7 study includes three arms: zimberelimab, which is our PD-1 antibody; zimberelimab plus domvanalimab, to which I'll refer as the doublet; and zimberelimab plus domvanalimab plus etrumadenant, which is our adenosine A2a/A2b receptor antagonist, and which was previously known as AB928. I'll refer to this third arm as the triplet. This randomized study has a target total enrollment of 50 patients per arm, or 150 total patients. As a reminder, the CITYSCAPE results in the PD-L1 high patient population were based on 29 patients per arm. ARC-7 was designed to provide us with a lot of valuable information, notably not just how the doublet performs relative to zimberelimab alone, but also whether etrumadenant might add efficacy to that doublet. If positive, this triplet combination would allow us to develop a completely novel and differentiated therapy for this patient population. This arm is really the type of combination that Arcus is all about: unique and rational differentiation, which creates a potential home run for patients. Let me just give you a reminder that our partner, Gilead, and we have been blinded to the ARC-7 data. We blinded ourselves to maximize the integrity of the study and to preserve our ability to use this study for regulatory purposes. This first interim analysis, therefore, was designed to provide us with an early look at these data to inform our future development decisions for both the doublet and the triplet. To the results from this interim analysis. As you know, we've been very clear that we would not share quantitative data from this interim analysis at this time. This is an ongoing study that is still enrolling, and as a result, it is critical that we not disclose data that could potentially bias investigators or impact our ability to complete enrollment in the study. The intent of top-line releases is to preserve the ability to present the results at a medical conference, which we obviously want to be able to do. Today, I'll share as much qualitative information as I can. The initial decision we made based upon the results of the interim analysis is that we and Gilead agreed that both ARC-7 and ARC-10, which is our registrational study for domvanalimab plus zimberelimab in the same population, should continue as planned. In addition, Gilead and we agreed that the results of this interim analysis support the continuation of our ongoing joint efforts to prepare for additional phase II studies for domvanalimab. Before diving into further details, I would first like to remind folks, given that this is an early look, clearly the total number of disease evaluable patients in this interim analysis was relatively small, and the data still need time to mature in the ongoing study. Also, as with any ongoing clinical study, and because this is an early look, the data could change over time. I'll now spend a few minutes on each of the arms. The first thing that we wanted to confirm with this study is that zimberelimab showed activity similar to that of other marketed anti-PD-1 antibodies in this setting. In fact, the results to date continue to demonstrate that zimberelimab has activity similar to that of the marketed anti-PD-1 antibodies. Having our own anti-PD-1 antibody provides us with a huge amount of optionality. The performance of this first arm is an important observation for both Arcus and Gilead, which shares the rights of this molecule with Arcus. Second, we wanted to demonstrate that the doublet and triplet provide superior anti-tumor activity relative to zimberelimab alone. Both arms with domvanalimab-based combinations showed encouraging clinical activity that Arcus and Gilead believe is sufficient to continue enrolling our existing studies as planned and to continue with our preparations for additional phase II studies. We're doing that together. In particular, we were intrigued and actually quite excited about the activity seen in the triplet arm, which is the first data set reported for an anti-TIGIT and an adenosine receptor antagonist combination. Allowing the data to mature will enable us to better assess the relative contributions of each of domvanalimab and etrumadenant. Given the exciting data from the triplet, we look forward to evaluating this regimen in other studies. In summary, we are encouraged by the data we have seen to date in all three arms, and particularly the two domvanalimab-containing arms. As with all clinical studies, we understood there would be a trade-off between an early look and data maturity. We're excited about the data and thrilled that they support the continuation of our ongoing TIGIT development plan and strategy. The opportunities in this space are enormous, and our approach has been thoughtful but expeditious. Generating randomized early data on study arms to support our future investment in both the doublet and the triplet is an example of just that mindset. A key observation from this initial data set is that the time to response across all arms is rather long, with an average time to response of over three months, and therefore, the study and the data will benefit from greater maturity and more disease assessments. In fact, more than 25% of our responders did not achieve a partial response until after their second tumor scan. We find this extremely encouraging, a hallmark of the profile of benefits associated with immunotherapy-based therapies. Data from ARC-7 will be submitted later this year for presentation at a medical meeting. What does this mean for the Gilead option? The mechanics of the option are such that Gilead gets to first determine whether a triggering event for an Arcus program has been met. If they make this determination upon delivery of a data package, Gilead would have a certain period of time, typically a few months, to make a decision. As a reminder, Gilead gets what we say, one bite at the apple for domvanalimab after a triggering event has been met. Also, once Gilead opts into a program, they become responsible for 50% of the joint development costs. Since this was a blinded study, when we unveiled this data to the Gilead team, they shared their excitement to continue moving forward, particularly the domvanalimab combinations, including the triplet, given the potential differentiation of this combination. I'm sure they will also communicate this with all of you. However, Gilead has determined that it will not start the opt-in review period at this time. They expect to make a decision on the opt-in by year-end, following maturation of the ARC-7 data to confirm the results that were observed in this interim analysis and to better understand the relative contribution of domvanalimab and etrumadenant. Both parties recognize the importance of moving quickly here. This is also why we will continue with our phase III plans, and the timing for the opt-in should not slow down the first patient in for these studies. Since Gilead's option also includes AB308, I wanted to spend a minute on the status of our second TIGIT antibody, which is actually advancing very quickly. As a reminder, this molecule is in a phase I/I-B study in combination with zimberelimab. This also has the potential to advance as a pivotal program for hematologic malignancies, even as we advance domvanalimab in solid tumors. We started this study with two important advantages resulting from our extensive clinical experience with TIGIT. One, we started dose escalation of AB308 directly in combination with zimberelimab, and two, we started at a dose level of AB308 that we predicted, based on our prior studies, would be relatively close to the dose level we would want to take forward. In fact, AB308 achieved full receptor occupancy in our first dosing cohort. We've already completed enrollment of the second dosing cohort, and we expect that the second or third dosing cohort will likely be our going-forward fixed dose for AB308 and zimberelimab, putting us in a position to start our expansion cohorts later this year. Before we move to Q&A, I want to update you on the other events happening over the next several months. First up will be an update on our ARC-8 study for AB680, which is our small-molecule CD73 inhibitor in first-line metastatic pancreatic cancer, expected to be presented in the fall. The data set will include updated data from the ASCO GI presentation in January from the dose escalation portion of the study and data from the dose expansion. We continue to be very excited about the potential of this molecule in what we all know is a truly devastating disease. Second, we will be initiating the first clinical study for our HIF-2α inhibitor, AB521, also in the fall. We also expect to submit ARC-7 data for presentation at a medical conference by year-end. Last, we are currently evaluating etrumadenant in three different randomized studies. In TKI-refractory EGFR mutant lung cancer, in second-line plus colorectal cancer, and second and third-line metastatic castrate-resistant prostate cancer. We look forward to being able to share the data from these studies, which we hope will further validate the potential of etrumadenant in multiple patient populations. I wanted to wrap up with an update on our financial position. We feel we are fundamentally well-aligned with Gilead in how we are looking at these programs. We think it is unlikely we would advance our programs into registrational studies without the support of our partner. To date, Gilead has made a greater than $650 million total investment into Arcus through their upfront payment and equity investments, including having a 19.5% ownership to date, the most recent raise in February, and we believe their commitment to Arcus is as strong as ever. As a result, we have over $885 million of cash and cash equivalents as of the end of March and plenty of capital to prosecute our programs over the near term. We'll now open up the line to questions. As a reminder, to ask a question, you will need to press star one on your telephone keypad. To withdraw your question, press the pound key. Please be advised that you are only allowed to ask one question and one follow-up. Please stand by while we compile the Q&A roster. Your first question comes from the line of Alethia Young from Cantor Fitzgerald. Please go ahead. Hey, guys. Thanks for taking my question, and congrats on moving forward with all three arms. Just, I guess the question on everyone's mind is that, thinking of obviously the CITYSCAPE data and your internal bar being around the 50% or so, I'm just curious about how to think about views of competitive views around the doublet and the triplet. Does it need to be, kind of, in that range of 60% to be competitive? I know you don't want to give numbers, but is there anything qualitative you can do to help us understand how to stack this up, and how you view positioning this asset competitively? Thanks. Thank you, Alethia, and thanks for the question. As you said, we aren't going to get into any quantitative numbers. First of all, let me remind you of a couple of key things. Zimberelimab performed just like the market ed anti-PD-1. Both of the combinations met our internal thresholds to continue going forward. Our dataset is relatively small. It's clearly difficult at this point to compare it to the CITYSCAPE data. Clearly, we don't have the maturity of their dataset yet. Based upon everything that we've seen, we think that our combination of our anti-PD-1 plus our anti-TIGIT is going to look like any of the other anti-PD-1 plus anti-TIGIT. We feel that the data that we generated to date, if it holds up with the triplets, could offer a clear competitive advantage. That's part of the reason why we are actually feeling very good about having looked early. It's helping to inform how we think about the proportion of registrational studies. Do we actually start to shift toward a greater proportion where we might be taking on the triplet? We feel like the next several months, given where we are in the study, will actually help to see how that doublet and triplet arm actually end up separating with a little bit more time. Just as a follow-up, for the triple, should we expect some sort of further update there by the end of this year? Or is it more like in 2022? Because you said it takes like three or four months, it sounded like. Thank you, Alethia. We will present the totality of the data together at the medical conference we were talking about. Full update, both the doublet, the triplet, as well as the monotherapy. Great. Thank you very much. Your next question comes from the line of Robyn Karnauskas from Truist Securities. Your line is open. Thanks for taking my question. Alethia prepped me well. Let me just ask this clear question. It sounds like what you're saying is that both combos met the internal bar for going forward. I think going in, I think I even have written from you all that 50% or above would be good. When people say that, you use the word 'encouraging', they're worried that that doesn't mean that 50% bar was met. Can you make people feel a little bit better about the word 'encouraging'? That's the first question. Then it sounds like this combo, making a statement for the combo, is a lot more optimistic than even what we were thinking. Maybe give us a little bit more color around. Is Gilead looking at that combo as well? You said that basically they're going to make a decision by the end of the year. Does that mean they're going to get data in a few months, or is it because they have two or three months? When will they get that data? Could they often go later than that if they have to wait for more data? I know there are two questions there. Basically, can you make people feel better about the word encouraging? Second, a little bit more granularity about what that opt-in qualifying mark is. Thanks. Thank you, Robyn. You know how my brain is, and that was a lot of words, but I think I got the totality of your question. First of all, what does encouraging mean? One thing to get that we want to make very clear is going along. During 2020, as we evolved from an independent company working by ourselves to an independent company collaborating with Gilead, we had a number of things that we've been working on from a communication standpoint. What I would say is that at this point, we've gotten to a situation where we're being very highly aligned in how we communicate on the same topic. One of the things that we talked about is that we don't want to get quantitative about this at this point. With that said, what does encouraging mean? Encouraging reflects a number of things. First of all, that zimberelimab performed as the marketed anti-PD-1 antibody. Second, that both the doublet and the triplet met the hurdles that we've talked about wanting to see for us to go forward. Over the course of the year, we've used the metaphor thumbs up, thumbs down. Gilead has communicated these data to give us a thumbs up. We want to pursue as we've planned. We're continuing the planning with our trial. To your point about the triplet and how we should contextualize the triplet based upon what we already have said about the doublet. Our look, we believe, is similar to Gilead, and that's why we're looking to have this additional few months period. If those data continue to hold up, I believe that Gilead shares our enthusiasm that the triplet could represent a truly differentiated opportunity from the other doublets that the rest of the world is pursuing. Quick follow-up, if I can. For AB308, a lot of questions obviously going into this around Fc-enabled versus Fc -silent. Your decision to continue on with this trial and continue on with the pivotal trial has anything to do with the fact that the current drug is sufficient, or do you not need Fc-enabled? How do we view the Fc-enabled versus Fc -silent debate? Can we learn anything from this press release? I'm done. Sorry. Thanks. No, thank you, Robyn. The one thing I should really make a point of, because maybe this helps with both your and Alethia's questions. One of the other things we talked about is that we weren't simply looking at a single numerical number. We've really looked at the totality of data. For example, the spider plots. I mentioned the time to respond. Virtually all of the patients, by far the vast majority in both the doublet and the triplet, remain on study. All of that encourages us as to how things will play out with greater data maturity. Coming back to the AB308 question, you should keep in mind that's exactly the same way we've been positioning that for ages. We've been moving it along. We recognize the opportunity and the optionality that it provides us in certain other settings and hematological malignancies. We're going to be very aggressive about that. The data and the speed at which that's enrolling are awesome for us. We're excited to have both of those. In terms of Fc-enabled versus Fc-silent, I think we'll start to switch the narrative, or at least come out of our mouths on that question. As you know, it's something that probably is never going to be proven, unless someone literally runs an anti-TIGIT plus the same anti-PD-X side by side. Based upon the totality of the data that we've seen to date, we feel we have an anti-TIGIT antibody that looks like an anti-TIGIT antibody. We don't expect there to be any differences between the Fc -enabled or Fc-silent function. Thank you, guys. I appreciate you taking all the questions, and congrats on hitting this milestone. And your next question comes from the line of Umer Raffat from Evercore ISI. Your line is open. Hi, guys. Thanks so much for taking my questions. Maybe three quick questions, if I may. First, I know there's a lot of focus on the 50% threshold for the combo arm. Let me go to the other side of the spectrum on the PD-1 monotherapy. I feel like there's a fair amount of spread even for the commercially marketed PD-1s. For example, CheckMate 227 brought PFS in the high range of 30%, whereas KEYTRUDA in KEYNOTE-024 is in the mid range of 40%. As we think about those two numbers in the context of 50%, that makes one of them look like only a 5% spread versus the combo, and the other one looks like a double-digit spread versus the combo. I'm trying to interpret that in the context of Terry, how you described the doublet being sufficient to continue, and the triplet being something you were intrigued and excited about. I would really appreciate any thoughts there. If you could also remind us what the median duration of follow-up is. Thank you very much. Thanks so much, Umer. I'm actually going to let Bill Grossman take that question. Hi, Umer. Thanks for the question. As you kind of refer to, there are a number of different studies out there for monotherapy PD-1, PD-L1, and PD-L1 high population. If you look at the majority of those studies, primarily KEYNOTE-042, IMpower110, as well as CheckMate 227, the range really is much closer, I believe. I think it's really in the 35%-40% range. KEYNOTE-024 did have a higher response rate, around 45%, and we think we're right in the typical range of all the PD-X antibodies out there. Our performance is right in line with what we had hoped, and we were hoping that we wouldn't see necessarily an underperformance in a patient population, which was not the case so far. Your next question comes from the line of Geoffrey Porges from SVB Leerink. Your line is open. Yes, this is [Nasim] on for Geoff. Congratulations on the progress. Are the study responses confirmed responses, are they investigator-assessed, or independently verified? A follow-up is, what is the longest duration of response on the combination arm? Thanks. I'm going to let Bill Grossman handle those questions as well. Yes. Right now, we're just primarily looking at unconfirmed response rates. They're based on investigator assessments right now. We will be looking at, with longer follow-up, studies to confirm all those responses. As Terry mentioned, it's early days in the follow-up period. We will be looking at that as well. Your last question was around the response. Is that correct? The longest responder? Yeah, the longest duration of response. Yeah. In the combination arm. Correct. In the published numbers in the two different combination arms, the longest durable response we have is right around eight months at this time. Thank you. That's very helpful. Your next question comes from the line of Salveen Richter from Goldman Sachs. Your line is open. Good afternoon. Thanks for taking my question. Could you just help us understand what the gating factors are for Gilead to opt in here in this program? Yeah. Thanks, Salveen. Obviously, you won't have a chance to ask them, but I think that part of this is that they have the opportunity to let their data mature a little bit more. They're able to do it. If you ask me, it's actually smart. The data looked quite encouraging to us, but I think that they find it valuable. When you look at how these data are playing out, as we talked about the time to response, the spider plots, it gives them a few more months to just see if everything holds up the way things are looking today. Great. Thank you. Your next question comes from the line of Mara Goldstein from Mizuho. Your line is open. Great. Thanks so much for taking my question. I had a question just on, firstly, on the presentation of data and where you anticipate that may occur, as we're close to the second half of the year, and many of the bigger clinical conferences are really coming up very quickly. Secondly, I'm just curious, given that you're approaching that phase II dose in AB308, it appears. By the time you round out the year and have a data package for Gilead with domvanalimab, where will you be with the AB308 study? Actually, Bill can probably handle both of those. Why don't you go ahead? For the first question, the medical conference is still to be determined. Once we get more data maturity, the plan is to make an abstract by the end of the year. As you point out, there aren't that many conferences towards the end of the year, but we'll be looking at our opportunities for presentations at the end of the year once we see the next data cut. Then, as far as the AB308 package, as Terry mentioned, we're in our third cohort for dose expansion right now, and we do expect either the second or third cohort expansion to be our recommended dose for expansion to go forward. We are exploring additional flat dosing combinations in that study, as well as the expansion cohorts. We'll be looking at presenting that study, again, at a medical conference as soon as we can in the near future. Okay. If I could just also ask, just on the doublet versus the triplet combination, and I understand you're not necessarily giving specific data. Could you maybe help us understand what you are seeing in terms of inflection differential between those two different arms? All I would say at this point is that both look very interesting, but the triplet certainly looked like it was doing something more, and we think we simply will, with a few months more data maturity, also bring in not only more data, but more patients. That'll help us to ascertain whether and how meaningful that difference is. Okay. All right, thanks. I appreciate it. Thank you, Mara. Your next question comes from the line of Yigal Nochomovitz of Citigroup. Your line is open. Thank you very much. Just following on the last question, Terry, regarding the doublet versus the triplet. I know you're not giving numbers out, but can you please confirm that the doublet and the singlet were comparable in terms of the separation between the triplet and the doublet? Did you see a similar separation there between triplet and doublet, and doublet and monotherapy? We don't want to get into specific quantitative numbers, but certainly, there was a separation between the doublet and triplet, which were separated from the singlet. Okay. Another question, since you mentioned that the time to respond was over three months for all the arms and that the study would benefit from a greater duration, and then you said that 25% didn't respond till the second scan. I'm just wondering if the time to respond for the triplet was, in fact, a little faster than the doublet? I think it's way too early and way too few patients to start to make those types of comparisons. I would just say, if you look at the spider plot, they look like you would expect in an immunotherapeutic regimen. Too early to try to call out differentials. Okay, thanks. Thank you, Yigal. Your next question comes from the line of Peter Lawson from Barclays. Your line is open. Hey, thanks for taking the question. Just as we think about the data being presented, could that be presented ahead of Gilead's opt-in, or would the Gilead opt-in delay data presentation? We probably can't get that granular with any knowledge we even have about exactly how that's going to play out. I would just say that we don't have enough fidelity to make a call on that. Thank you. Could you remind us about the opt-in time and events for Gilead around the adenosine? Yeah. I'll let Jen answer on that one. Yeah. We have not disclosed what the triggers for the adenosine programs are, nor are we. I just want to come back to Salveen's question as well, but also related to the opt-in for triggers. It is patient number-based, so we've not disclosed what that is. It's been redacted in the agreement, but it's patient number-based, so it's not based on meeting some sort of efficacy frame or anything along those lines. Got you. Just a final question around the spider plots, do they look encouraging, pointing downwards, or is there any kind of worry around the spider plots? They look wonderful, Peter. The spider plots, and that's one of the things we talked about as we were talking last year, that got asked a sort of qualitative question on the data. That's why we're excited. The spider plots are the telling story, and the pattern is very, very consistent. That's why we mentioned so many patients remain on study. That gives you how those spider plots are looking today. Give it a few more months, and I think they're going to look pretty beautiful. Perfect. Thanks so much. Congrats. Thank you, Peter. Your next question comes from the line of Zhiqiang Shu from Berenberg. Your line is open. Thanks for taking my questions. Congrats on the progress. I have a few questions to ask. Can you comment on the PFS? I know it's probably immature, but have you seen similar data around five to six months as compared to CITYSCAPE? The second question is about safety. I think, Terry, in your prepared remarks, you mentioned that without depleting Tregs, you may have a better safety profile, I guess. Have you noticed any better safety profiles compared to other Fc-enabled TIGIT antibodies? The third question, I think, I want to get a bit more clarity on the opt-in option from Gilead. I wonder, the decisions for them to delay making a decision to opt in, would that be associated with the fact that they want to see more data from your AB308 data package, given these two molecules are on dose? Thank you. Well, thank you very much for those questions. I'm going to let Bill answer the PFS and the safety question, and then I'll comment on the opt-in. Thank you. From a PFS perspective, that's a time-to-event endpoint that we have as part of our co-primaries in the study. However, at the current maturity of data, we don't have PFS. We don't have enough PFS data. That'll be forthcoming as the study matures with further enrollments as well. No PFS at this time. As far as safety, again, reiterating what Terry had said before, there are no unexpected safety signals across any of the three arms. The current safety profile really appears consistent with all immune checkpoint inhibitors or combinations that have been presented to date for our TIGIT antibodies. We haven't seen anything that is unexpected across all three arms. Coming back to the opt-in question, actually, I'd like to frame that. Interestingly, this is not actually a delay in the opt-in. In fact, what this is would've been like an early opt-in; Gilead has the time to look. It's smart. It shouldn't be interpreted at all in the context of AB308. I think Gilead, and we are both motivated to go as fast as possible. I should point out that the way this is all staged and how the timing works out is that both the ongoing studies and our planning, it won't be affected by when, if they choose to opt in prior to the end of this year, it won't slow us down in anything that we're either doing or planning. Great. Thank you very much. Thank you. And once again, if you would like to ask a question press star and the number one key on your touch-tone telephone. Your next question comes from the line of Jonathan Miller from Evercore ISI. Your line is open. Hi, guys. Thanks so much for taking my question. You mentioned a couple of times that the data is not mature enough to get a real sense of some very important metrics and that we should wait for that data to mature. That makes sense. When we see this data at a medical meeting later this year, at that point, do you expect to have enough follow-up to be giving us not just detailed ORR estimates, but to have a meaningful sense of PFS curves and separation there as well? It's a little bit hard to say right now because of that data split with TBD, from a PFS perspective, probably not, because if you look at the CITYSCAPE data, they're beyond the six-month mark, which I think is where we need to be able to across all of our enrolled patients. We will be able to at least express and show information on some of the durability of the responders. That type of data we'll be able to definitely include in a presentation around our response rates. Great. At that point, just of course, obviously, this depends on enrollment and follow-up, but about how many patients would you hope to have by that medical meeting later this year? I mean, certainly we're not actually disclosing anything quantitative about enrollment, but I'll tell you that the study is enrolling quite well. We've got over 60 sites up. It's doing well. Okay, thank you so much. Once again, if you would like to ask a question, press star one on your touch-tone telephone. You have a follow-up question from Robyn Karnauskas from Truist Securities. Your line is open. Hi. Sorry, I have another one. Two questions. Just thinking about the competitive landscape, there are a lot of people going after TIGIT. How much of your press release and lots of color is given around the thought to other people reading the data? Second, you've got a lot of catalysts for adenosine in the back half of the year. Could you set the bar for people who don't seem to give much credit to adenosine? What would be the bar for the next readout you have for adenosine, and why should people care about that data set? Thanks. Sure. Certainly, there are elements of keeping things a little tighter now due to the competitive nature of things. We feel we need to give qualitatively, let the world understand what we're seeing. I think we recognize this is quite a competitive field, and particularly as you start to think about these differentiators like a triplet that start to move you away from just how fast you can execute on a doublet in a given setting. I'll remind you that's what we've been saying all along, which is the unique aspect of Arcus. We want to give the color as to what we're seeing, but we will be a little tighter on that information. I also think maybe Jen can comment a little bit on how the rest of the year is going to play out insofar as the adenosine programs, which, by the way, we're extraordinarily excited about those and the fact that we've been saying for ages, the triplet is a key aspect of what we were interested in. I think it's a very logical juxtaposition of questions. Thank you, Robyn. Appreciate your questions. Yes. The most likely next data sets will be the ARC-8 update. That's for AB680, our small molecule CD73 inhibitor in first-line pancreatic cancer. We submitted an abstract for presentation at a conference. We hope that it will be in the fall. That's something we're very excited about. I think we mentioned in the past that we've also started a second-line cohort in that study to continue the sentiment of what we started with ARC-8. That'll be one extra data set from both the dose escalation data that was provided earlier, as well as the initial data from the expansion cohort. That'll be 20+ patients in that expansion cohort. We also hope to have, as we talked about at the beginning of the year, the presentation of the ARC-7 data at a medical conference. That will include data on the triplet arm, which I think we've tried to convey today, we're very excited about. This will be presented after the remainder of the year, and then in the first half of next year, we should have randomized data from all of the studies that Terry just pointed out. Specifically, ARC-6, which is the study evaluating etrumadenant in metastatic prostate cancer, we're very excited about the randomized data. Again, randomized data for etrumadenant plus zimberelimab in PD-L1-positive lung cancer. Great. Thanks. Your last question comes from the line of Mara Goldstein. A follow-up question from Mizuho. Your line is open. Thanks. I'll keep that quickly. One of the things that you guys have said is that the ability to do this interim allows you to make any adjustments to ARC-10, and I'm just curious as to, at this early juncture, whether or not you've learned anything that has prompted you to revisit any of your assumptions? Thanks, Mara. That's an easy answer. ARC-10 is proceeding just as planned. The one thing that I would like to highlight, though, because I think it's an important aspect of this, took on a very public and external flavor as we went through the year. As we always talked about, this was intended as an internal decision-making enhancing tool. In fact, probably the biggest thing that came out of it for us, taking that early look, is helping us think about what we might do differently insofar as the doublet versus triplet. You can imagine we're in full planning mode on a number of doublets. We're still continuing that, but we're building into planning the possibility that we may shift just how we think about doublets versus potential triplets and when we might start to execute on those, pending the data holding up as they get more mature. Okay, thanks. I appreciate it. Hey, thanks so much, Mara. These are all the questions we have. Please continue. Let me just thank everybody on this call again for joining. We really appreciate your continued interest and all of the awesome questions. We look forward to maintaining dialogue. Thank you. This concludes today's conference call. Thank you for participating. You may now disconnect.