Thank you for standing by. Welcome to the Revolution Medicines Q2 2025 Earnings Conference Call. At this time, all participants are in a listen-only mode. After the speaker's presentation, there will be a question and answer session. To ask a question during the session, you will need to press star one one on your telephone. You will then hear an automated message advising your hand is raised. To withdraw your question, please press star one one again. Please be advised that today's conference is being recorded. I would now like to hand the conference over to your first speaker today, Ryan Asay, SVP of Corporate Affairs. Please go ahead. Thank you, and welcome everyone to the second quarter 2025 earnings call. Joining me on today's call are Dr. Mark Goldsmith, Revolution Medicines' Chairman and Chief Executive Officer, and Jack Anders, our Chief Financial Officer. Dr. Steve Kelsey, our President of R&D, Anthony Mancini, our Chief Global Commercialization Officer, and Peg Horn, our Chief Operating Officer, will join us for the Q&A portion of today's call. I would like to inform you that certain statements we make during this call will be forward-looking because such statements deal with future events and are subject to many risks and uncertainties. Actual results may differ materially from those in the forward-looking statements. For a full discussion of these risks and uncertainties, please review our annual report on Form 10-K and our quarterly reports on Form 10-Q that are filed with the U.S. Securities and Exchange Commission. This afternoon, we released financial results for the quarter ended June 30, 2025, and recent corporate updates. The press release is available on the investors section of our website at revmed.com. With that, I'll turn the call over to Dr. Mark Goldsmith, our Chairman and Chief Executive Officer. Mark. Thanks, Ryan. It's good to be with you this afternoon. Today, I'll highlight the progress we've made this quarter with a look ahead to the strategic priorities and milestones on the horizon for Rev Med. I'll then pass the call over to Jack, who will provide a financial summary before I share closing remarks and open the call for questions and answers. At Rev Med, we remain steadfast in our commitment to revolutionizing treatment for patients with RAS-addicted cancers through the discovery, development, and global delivery of innovative targeted medicines. We have a compelling pipeline of three distinguished clinical stage RAS(ON) inhibitors: daraxonrasib, a groundbreaking RAS(ON) multi-selective inhibitor; elironrasib, a differentiated G12C-selective covalent inhibitor; and zoldonrasib, a groundbreaking G12D-selective covalent inhibitor, for which a full report was published recently in Science describing the innovative chemistry, mechanism of action, and biological impact of this unique RAS(ON) inhibitor in preclinical cancer models. We are executing well and making meaningful progress in advancing all of these programs, which we believe have the potential to transform treatment for patients living with RAS-driven cancers. Starting with our efforts in pancreatic cancer, daraxonrasib is our most advanced clinical program. We were pleased to announce recently that daraxonrasib received breakthrough therapy designation from the U.S. Food and Drug Administration in previously treated metastatic pancreatic cancer with KRAS G12 mutations. This designation underscores the large unmet medical needs for patients living with pancreatic cancer and the urgency of advancing development of daraxonrasib on behalf of patients. Toward this objective, we continue to make progress across our active and planned daraxonrasib registrational studies in pancreatic cancer. First, RASolute 302, our ongoing global phase III trial in patients with second-line metastatic pancreatic ductal adenocarcinoma, or PDAC, has been enrolling well, and we expect to complete enrollment this year to enable an expected data readout in 2026. Notably, with robust contributions by U.S. investigational sites to date, we are winding down enrollment in the U.S. while continuing to enroll patients outside the U.S. to ensure we have a reasonable geographic mix to support global registration. Second, we continue progressing toward initiating our first-line metastatic pancreatic cancer registrational trial, which we plan to conduct as a three-arm trial comparing daraxonrasib or daraxonrasib plus chemotherapy to chemotherapy. Later this year, we expect to share the trial design and clinical combination data that inform this plan and to initiate the trial. Third, we also continue progressing toward a registrational trial with daraxonrasib as adjuvant treatment for patients with resectable PDAC. Later this year, we expect to share the trial design and initiate this trial as well. For patients with pancreatic cancer specifically bearing a KRAS G12D mutation, the clinical activity and tolerability profile we've reported for zoldonrasib is quite encouraging and suggest it as a remarkable inhibitor of this common cancer driver. We continue to follow patients in the ongoing monotherapy trial and are currently studying several combination treatments, including as part of a RAS(ON) inhibitor doublet with daraxonrasib in combination with standard of care regimens and with other novel targeted agents. For example, for patients with pancreatic cancers carrying both a RAS mutation and deletion of MTAP, Tango Therapeutics announced that a first patient was dosed in a collaborative phase I trial evaluating their PRMT5 inhibitor TNG462 with either daraxonrasib or zoldonrasib. Such novel combinations have the potential to provide differentiated options for patients with these cancer genotypes. Moving to non-small cell lung cancer, RASolute 301, our phase III trial of daraxonrasib in previously treated patients with RAS-mutant non-small cell lung cancer, continues enrolling patients in the U.S., and we are now activating trial sites in Europe and Japan as planned. Evaluating daraxonrasib in earlier lines of therapy for patients with non-small cell lung cancer is also an area of strategic priority for Revolution Medicines. We recently showed clinical evidence that daraxonrasib can be combined productively and tolerably with pembrolizumab with or without platinum doublet chemotherapy. With these results in hand, we're working toward initiating a registrational trial in first-line non-small cell lung cancer in 2026 and expect to share the trial design in connection with the initiation. Clinical development efforts also continue across our RAS(ON) mutant selective inhibitors elironrasib and zoldonrasib in patients with KRAS G12C or G12D non-small cell lung cancer, respectively. First, we recently reported an updated clinical data set from patients with previously treated KRAS G12C non-small cell lung cancer treated with elironrasib as monotherapy that showed a highly competitive profile, including differentiated safety and tolerability, along with a compelling objective response rate and progression-free survival. We recently announced that elironrasib was granted breakthrough therapy designation by the FDA for locally advanced or metastatic KRAS G12C non-small cell lung cancer following prior systemic therapy, including anti-PD-1 and chemotherapy. This designation is a recognition of the significant unmet medical need and elironrasib's potential to serve these patients. Currently, there are no RAS-targeted inhibitors with full FDA approval for treating patients with KRAS G12C non-small cell lung cancer. Second, we also recently expanded the clinical evidence supporting the potential benefit of combining elironrasib with other inhibitors. In particular, the RAS(ON) inhibitor doublet of elironrasib and daraxonrasib was shown to exhibit significant anti-tumor activity in advanced non-small cell lung cancer patients who had progressed on treatment with a KRAS G12C off inhibitor. This observation mirrored similar findings that we had previously reported in patients with KRAS G12C colorectal cancer. Third, we showed clinical evidence that elironrasib can be combined productively with pembrolizumab in first-line non-small cell lung cancer patients with an acceptable safety and tolerability profile. These findings suggest that elironrasib in various treatment configurations warrants evaluation in patients with RAS G12C non-small cell lung cancer, and we continue work to prioritize among the multiple options for advancing development of this differentiated RAS(ON) G12C inhibitor. Fourth, we continue to advance zoldonrasib for patients with RAS G12D non-small cell lung cancer. We recently shared promising data for patients with previously treated RAS G12D non-small cell lung cancer. We are following these patients and enrolling an expansion cohort to generate a robust data set. We are also evaluating its potential in combination settings to inform potential registrational opportunities. Fifth, we were pleased to announce recently a new clinical collaboration with Summit Therapeutics to evaluate combinations of Summit's ivonescimab, an advanced PD-1/VEGF bispecific antibody, with each of daraxonrasib, elironrasib, and zoldonrasib. This collaboration builds on promising initial clinical evidence we have reported indicating that daraxonrasib and elironrasib can deliver additive anti-tumor activity with an acceptable safety and tolerability profile when combined with a PD-1 antibody. The new cohorts will assess whether combinations with a next-generation PD-1/VEGF bispecific antibody can unlock further therapeutic impact. Beyond our first three clinical stage RAS(ON) inhibitors that are progressing nicely, the next asset we are preparing to enter clinical development is RMC-5127, a RAS(ON) G12V selective inhibitor. We expect this program to be clinic-ready later this year to support the planned initiation of a phase I trial in 2026. We continue investing to produce next-generation assets to build on our momentum and support our commitment to creating the leading global RAS-targeted franchise. Among these investments are collaborations that will enhance our discovery efforts. This includes our work with Aethon, announced last year, to discover novel bispecific antibodies that can complement RAS(ON) inhibitors. We also recently announced a significant drug discovery collaboration with Iambic to use their cutting-edge AI capabilities and generate customized models through training with our proprietary data. This work may be particularly impactful by enhancing our lead discovery and optimization processes directed against both current and new drug targets. This exciting collaboration brings together AI and our well-validated drug discovery capability to help ensure that we continue building a highly impactful and sustainable pipeline. The progress I've outlined today is enabled by a strong operational foundation and the capabilities, talent, and financial wherewithal needed to scale the efforts to meet the ever-growing opportunities afforded by our pipeline. Our position of financial strength has been meaningfully bolstered by our recently announced partnership with Royalty Pharma. This partnership supplements our strong balance sheet by providing us with an additional $2 billion in committed capital through a highly flexible mix of synthetic royalty and debt instruments, which are available to us upon achievement of agreed-upon milestones. This capital access gives us the firepower, autonomy, and strategic agility we need to advance our ambitious clinical development and commercialization plans. Importantly, it also provides the financial muscle behind the commitment we announced through Rev Med to direct and execute independently on a global development and commercialization strategy for our promising RAS-targeted portfolio. This financial strength, combined with our maturing pipeline and organizational capabilities, empower our intention to become a fully integrated global oncology company that discovers, develops, and delivers innovative targeted therapies on behalf of patients worldwide living with RAS-addicted cancers. I would like to turn the call over to Jack to provide more specifics on our Royalty Pharma partnership and summarize our second quarter results. Jack? Thanks, Mark. Before turning to the second quarter financial results, I would like to review a few key highlights from our Royalty Pharma transaction. This funding arrangement provides for $2 billion in committed funding comprised of up to $1.25 billion in synthetic royalty on future sales of daraxonrasib and up to $750 million in corporate debt. We have structured the funding arrangement to be flexible, with $1.25 billion, or almost two-thirds, reserved as optional for Rev Med and to be drawn at our election subject to achievement of specific milestones. This innovative funding provides us with flexible access to $2 billion in committed capital at a competitive cost and without equity dilution to our shareholders or compromising control of our clinical assets. We expect to use this financial flexibility as we progress our programs, as our cash flow and capital needs evolve, and as we continue optimizing our capital formation strategy as the company and portfolio mature. Additional details on our Royalty Pharma partnership can be found in our filings with the SEC. Moving to our financials, we ended the second quarter of 2025 with $2.1 billion in cash and investments. This balance includes the receipt of the first royalty monetization tranche of $250 million from our partnership with Royalty Pharma. Turning to expenses, R&D expenses for the second quarter of 2025 were $224.1 million compared to $134.9 million for the second quarter of 2024. The increase in R&D expenses was primarily due to increases in our clinical trial-related expenses and manufacturing expenses for our three clinical stage programs, with daraxonrasib being the largest driver of the increase given the program is in two phase III trials. Personnel-related expenses and stock-based compensation expense also increased in 2025 due to additional headcount. G&A expenses for the second quarter of 2025 were $40.6 million compared to $21.7 million for the second quarter of 2024. The increase in G&A expenses was primarily due to increases in personnel-related expenses and stock-based compensation expense associated with additional headcount and commercial preparation activities. Net loss for the second quarter of 2025 was $247.8 million compared to $133.2 million for the first quarter of 2024. The increase in net loss was primarily driven by higher operating expenses. With regard to the accounting for the Royalty Pharma transaction, the first $250 million royalty monetization tranche we received in June was accounted for as a liability on our second quarter balance sheet. This liability will increase through interest expense on our income statement, and future royalty payments we pay on net sales of daraxonrasib will be applied against and reduce the liability balance on our balance sheet. In the second quarter of 2025, we recognize approximately $900,000 in non-cash interest expense related to the transaction and expect this to grow for the remainder of the year. We are updating our 2025 financial guidance and expect projected full-year 2025 GAAP net loss to be between $1.03 billion and $1.09 billion, which includes estimated non-cash stock-based compensation expense of between $115 million and $130 million. The increase in expected GAAP net loss is primarily the result of our decision to pursue global development and commercialization independently and increase expenses that result from our growing confidence related to our robust research, development, and commercialization plans. That concludes the financial update. I'll now turn the call back over to Mark. Thank you, Jack. The Revolution Medicines organization is determined to build the leading global targeted medicines franchise for patients living with RAS-addicted cancers. We believe our strong financial condition and access to a large quantum of additional capital to fuel our expansive development and commercialization plans for our compelling portfolio of investigational drugs will empower us to establish new global standards of care for patients living with RAS-addicted pancreatic, lung, and colorectal cancers. Our momentum is made possible by the support of our patients and caregivers, clinical investigators, scientific and business collaborators, advisors, and shareholders. I'd also like to recognize the continuing extraordinary efforts of Rev Med employees whose tireless commitment to patients drives this progress. This concludes our prepared remarks, and I'll now turn the call over to the operator for the Q&A session. Thank you. At this time, we will conduct the question and answer session. As a reminder, to ask a question, you will need to press star one one on your telephone and wait for your name to be announced. To withdraw your question, please press star one one again. Please limit to one question and one follow-up question. Please stand by while we compile the Q&A roster. Our first question comes from the line of Michael Schmidt with Guggenheim. Your line is now open. Hey, good afternoon. Thanks for taking my questions. Nice to hear that the RASolute 302 study is winding down U.S. sites. Mark, could you comment on how you're tracking towards completing enrollment ex-U.S. and perhaps any comments on the rough geographic distribution of patients would be interesting, I think. A question on the planned first-line PDAC study where you sort of reaffirmed plans to run a three-arm study here. Obviously, a lot of interest in the chemotherapy combination where you're doing work still. With the goal to optimize tolerability and, I believe, maintaining dose intensity here, how important is potentially clinical efficacy assessment for these chemotherapy combinations to support advancing one or perhaps more of these planned combinations into first-line? Thanks so much. Thank you, Michael. Those were meaty questions. The first question is about 302. It is making very good progress. I don't think we can share with you a breakdown of actual distribution. That, of course, continues to evolve. As indicated, we're winding down the U.S. enrollment. There continues to be enrollment outside the United States, and the final numbers will ultimately be determined by that. It's hard to give you much more information than that. We're sort of like landing a Navy jet on a moving aircraft carrier. There are a lot of parts that all have to synchronize to get to the finish line. It's looking very solid. We're in very good shape, and I think we'll be in a good position to share data in 2026. With regard to the three-arm study and the chemo combination component, I think you asked sort of two subparts. One is, are we still studying it? The second was, what role does efficacy play as a parameter in that? Steve, do you want to comment on each of those questions? Are we still studying the chemo combinations, and what role does efficacy play? We are still studying the chemo combinations, but we're very, you know, we did promise that we would share the study design and the rationale behind that study design in 2025. We're getting closer to the end of 2025. You can infer that we're pretty close to the end of the assessments that we need in order to inform the study design specifically. With regards to the efficacy assessments explicitly, of course, they will be important in informing the study design up to a point. The primary basis for the ongoing assessments that we have is obviously safety and tolerability. We are relying very heavily on the second-line data that we have for daraxonrasib, which, as we have previously reported, seems to exceed the outcomes for chemotherapy in first-line pancreatic cancer. That's already a fairly strong driver of our decision to move forward with that study. There will be some supplementary efficacy information for the analyses that we've done specifically in first-line patients, and we will share that information when we share the study design as part of the rationale. I hope that we'll have a pretty comprehensive package and a persuasive one for you at that time. Very helpful. Thank you so much. Thank you. Our next question comes from the line of Marc Frahm with TD Cowen. Your line is now open. Thanks for taking my questions and also following on Michael's questions. Hopefully, it's meaty. Could you maybe characterize the chemotherapies you're zeroing in on and how closely you'd expect that to, you know, the chemo in the combination to resemble kind of a standard of care first-line regimen versus maybe how much you've had to dose adjust to make things tolerable? On the guidance for data potentially being in 2026 for the second-line trial, is that referring to the final analysis, or is that inclusive of all of where you're projecting all of the interims to occur as well? Oh, okay. Thanks, Marc. I appreciate the questions. The first question, remind me again, had to do with chemotherapy. Sure. The regimens we're looking at. The regimens, yeah. As we've indicated, I know we've talked about this with you before, that all of the dosing that we're looking at is well within standard practice. We're not pushing outside of that at all, nor do we think we're going to need to do that. I think we're using very active doses. You know, within chemo, as we've discussed before, doses that are higher at the beginning of a treatment regimen often become lower. In fact, very typically become lower throughout the course of multiple cycles simply because they started at MTD. By definition, they're barely tolerable, and they get less and less tolerable over time. I think we're well within that range, and that's by intention. The second question had to do with when we say a readout of data in 2026, what do we mean? All we can really reference right now is the first analysis. We can't really predict what would happen at that time. It all depends. That first analysis might be the final analysis. It might be an interim analysis. There are potential additional analyses after that, but they're all event-driven, and we don't really control the timing. It would be very hard to tell you all possible scenarios here. It is the first interim that's likely in 2026, given kind of current event rates and enrollment rates. We can't skip the first interim. The first analysis is always going to be the first out analysis. We do think there will be a report in 2026, and we're optimistic that we'll be able to deliver on that. The enrollment has been very robust, as we're indicating here. We're having to sort of slow some things down to allow other things to fill some slots. I don't think that enrollment is going to be an issue at all. We just then have to let the events and a reminder that this is an OS event-driven readout. Even though it will read all the endpoints, it's OS-driven. We can't really predict that, even though we have models that attempt to predict it, but we don't know for sure. I think we're comfortable with 2026. Okay. Thank you. Thank you. Our next question comes from the line of Jonathan Chang with Leerink Partners. Your line is now open. Hi, guys. Thanks for taking my question. On the daraxonrasib combination data informing the front-line PDAC registrational study design, can you provide any additional color on what kind of data and how much data we can expect later this year? Thank you. Thanks, Jonathan. I think the best way to answer that, and Steve may want to add to this, is we are building a data set that allows us to make these decisions. That's usually our standard. If it's sufficient information to guide our decision-making, to give us confidence in moving forward, to spend significant capital, and to commit patients to experimental arms in a trial, we feel that that's sufficient to share with you. That's all we can do to quantitate it at this point. Got it. Maybe just one follow-up on that then. Can you provide your latest thoughts on what you think the key considerations are as we think about which chemo regimen or regimens could be part of that front-line daraxonrasib registrational study? Thank you. I think Steve may want to comment on it and reiterate, but you know it's primarily a safety and dose intensity question. We can give you a little bit more color to that, but that's always been the question that we needed to resolve as we discussed starting back at the first conference of the year. Chemotherapy, I'll just say one more thing, and then Steve can clarify it here. Chemotherapy is dosed at maximum tolerated dose. Anything you add to that may end up compromising not only the dosing of the chemotherapy, but also the dosing of the active target agent as well. Since we believe generally continuous dosing is a very good idea for suppressing RAS pathway signaling and thereby suppressing inhibiting tumor growth, we need to optimize that. That really is the main consideration, but maybe Steve can give you. That was the primary consideration, minimizing dose interruptions and maximizing the dose intensity of the RAS inhibitor. We fundamentally believe that pancreatic cancer is a RAS-driven disease and that the best treatment you can deploy would be a RAS inhibitor. It's really important for us that the patients randomized to get the RAS inhibitor get the best chance on that RAS inhibitor, which means that the dose intensity has to be as high as possible and the interruptions need to be as infrequent and as short as possible. Chemotherapy, unfortunately, does a very good job of disrupting both of those things. Chemotherapy will cause toxicities that require dose interruptions of the RAS inhibitor, and chemotherapy may result in other things that may ultimately reduce the dose intensity of the RAS inhibitor. There are some critical constraints. We're not testing regimens that are unusual. We're not testing cytotoxic drugs that are not used in standard practice on a global basis. We're not testing the schedules or doses of those drugs that are not used in standard practice on a global basis. Ultimately, we have a few constraints. This is going to be a global trial. We have consulted very widely across the major geographic areas that will be participating in this study. I think that we will come up with a solution that is acceptable for everyone involved. Once we've dotted the I's and crossed the T's, we'll be very happy to share that information with you. We're just not quite ready right now to do that. For disclosure, we are very optimistic about this, and we've repeated this plan multiple times now. Understood. Thank you. Thank you. Our next question comes from the line of Ellie Merle with UBS. Your line is now open. Hey, guys. Thanks so much for taking the question and congrats on all the progress. Curious your perspective on RAS upregulation as a resistance mechanism and thoughts on RAS degradation versus inhibition, particularly in the G12D space. Thanks. Yeah. RAS amplification is a real issue. Firstly, let's start with I don't think it matters whether it's on the back G12D or not, frankly, because I think what I'm going to say is going to likely be true for all of the major RAS mutations in probably all of the major tumors in which RAS is a cancer driver. RAS amplification, that is, amplification of the mutant allele, the actual KRAS G12D, if you like, for G12D tumors, is a major cause of escape from RAS inhibitors because the tumors really, really love RAS, and they try everything they possibly can to continue to signal through RAS. If you give a mutant selective inhibitor, there are multiple other ways the tumor can escape by reactivating RAS. If you give a RAS multi-inhibitor, a lot of those additional pathways are shut down, and the tumor ultimately has to default to RAS amplification. The problem for the tumor is that mutant RAS amplification is unfavorable for the tumor. It takes a lot of energy for the tumor to do it. It takes quite a long time for the upregulation to become apparent and for the translation of the protein to actually overcome the RAS inhibitor. There are also therapeutic ways where you can get on top of RAS amplification. If you double down on inhibition of the mutant RAS allele with, for instance, a RAS(ON) doublet, which we're clinically testing right now, you can actually get over the mutant RAS allele amplification. Yes, we acknowledge that it's a problem. It seems to be more of a problem for RAS multi-inhibition than it is for mutant selective inhibitors. There are therapeutic ways of getting on top of it. Some of them we have in our discovery toolbox, and we just haven't shared them publicly yet. With regards to degraders versus inhibitors, I don't think there's any evidence anywhere in the global literature for any oncology target that a degrader is better than an inhibitor. I think that the jury will remain out until the degrader companies generate clinical data that exceeds the efficacy and safety of the inhibitors that we have currently in clinical development. I can't comment more than that. I just don't see any precedent right now for the degrader technology being superior to inhibitors. Ellie, thanks for that question. Just to highlight a point that Steve made, the tumor is a microcosm of natural selection. It is actually gratifying to see that these RAS-addicted tumors go to such great lengths to overcome daraxonrasib. It is because it is such an effective inhibitor of RAS, and they're so dependent upon RAS. I think it makes complete sense biologically. We believe it makes complete sense biologically and is a marker of how effective daraxonrasib really is on suppressing broadly the RAS pathway. Thank you. Our next question comes from the line of Kelly Shi with Jefferies. Your line is now open. Congrats on the progress, and thank you for taking my questions. For the front-line pancreatic cancer trial, as you guided, you will share the pivotal trial design later this year. Curious, at this moment, if the trial design has been signed off by the regulatory agencies, could we assume no interim data from second-line pivotal trials needed in the data package or sign-off based on the comments made from the opening remarks? Thank you. Thank you, Kelly. We don't typically give sort of blow-by-blow updates on our interactions with the regulatory agencies. It ends up being much less helpful than one might hope for. I can't really answer that specific question. I think what's lost here a little bit is, although it's not yet transparent to our investors, to our analysts, we're actually making very good progress. The fact that we keep reiterating that we're going to be on timeline for initiating is an indicator of where we stand. Beyond that, we just can't give you any higher resolution insight into it. It's coming soon enough. Days go by quickly. Okay, thanks. Thank you. Our next question comes from the line of Andrea Newkirk with Goldman Sachs. Your line is now open. Good afternoon. Thanks for taking the question. Maybe just given the reiterated timelines here for expected enrollment completion for Resolute, the top-line data next year, launch to follow in 2027. Just curious if you'd be willing to speak more on the extent to which you're already engaging in pre-commercial activities and what learnings you're taking from Lumakras or Krazati launches that you see to be applicable to the upcoming daraxonrasib launch in PDAC. Thanks so much. Thanks, Andrea. Just to clarify, I don't think we've guided to commercial dates. We have guided to data in 2026. I'm not agreeing or disagreeing with that particular date, but just clarifying that we've not guided to anything about the commercial timeline. With that said, Anthony Mancini can give us his view of our commercialization program status. Thanks for the question, Andrea, and thanks, Mark. I think what I'll say is that launch readiness plans are progressing very well. We've got a team of experienced and talented executives leading our commercialization team across Med Affairs, Market Access, Marketing, and Sales, and they're deeply engaged in market-shaping activities and planning, in KOL and advocacy organization engagement, and in really building our operational capabilities and launch readiness activities. An example of some of the market-shaping work that's going on is our Expect RAS campaign that's focused on educating the community of community oncologists primarily that RAS is a driver mutation in PDAC and that over 90% of pancreatic cancers have RAS mutations. We're continuing to add to that experienced and talented team, and starting to build our U.S. field teams more broadly now. We're learning from some of the other launches, not just the G12 off inhibitors, and putting the right resources in the right place, building the best strategies and tactics and operational capabilities so that we bring daraxonrasib with urgency to patients when we get that opportunity. We're confident in our ability to continue to hire the right talent with the right commercialization experience, both in the U.S. and internationally. Yeah. Thanks, Anthony. Maybe I could just add a comment sort of observing it as Anthony builds that organization. I think we're going to give this a really strong effort, and hopefully, we'll have a terrific approval that will go with it. Thank you. Our next question comes from the line of Jay Olson with Oppenheimer. Your line is now open. Oh, hey, congrats on all the progress, and thanks for providing this update. We have a question about your Summit partnership. Since you're planning to combine ivonescimab with all three of your RAS(ON) inhibitors, can you just talk about how you're going to prioritize those three combinations, especially with regards to which tumor types you would prioritize? I have a follow-up. Thank you. Thanks, Jay. I can't really give you much information about that. That's sort of an operational question more than anything. We continue with our commitment to pembrolizumab. As you know, we've talked about things that we'll continue to do with pembrolizumab, which is the really singular standard in first-line lung cancer in particular and also in many other indications. In parallel, we'll begin exploring how the bispecific antibody will behave jointly with these different agents. I'm sure they'll be studied across a variety of solid tumors. Initially, with dose escalations, we typically start with a wide net because we're trying to establish safety initially. Over time, once we get past any safety questions, we start focusing on very specific indications. It's too hard today in this context and at this stage to outline any of those more specific paths beyond the dose escalation. We're excited to be in the collaboration. We think it takes essentially the most advanced PD-1/VEGF bispecific antibody in the field with the richest pipeline of RAS(ON) inhibitors and puts them together. We think that's a very, very promising opportunity. Okay. Thank you for that. As you look into the future, do you think the combination of ivonescimab plus daraxonrasib has the potential to be an ideal combination in first-line non-small cell lung cancer? Ideal? You know, ideal is a fairly big word. I don't know. There will always be things that we'll continue to try to improve upon whatever is the then standard. I mean, it stands a chance of becoming a new standard of having differentiated impact. In the meantime, while we're doing that work, ivonescimab in other contexts will be—we'll see in more mature data as Summit and their partner elaborate that information. We'll get a better sense of how it performs relative to PD-1. The initial information is encouraging, but it's hard for us to see into the future. This work for us is being done on the presumption that it will play out. We're excited to see more options, more opportunities, more potential benefit for patients. Excellent. We'll look forward to that. Thanks for taking the questions. Thank you. Our next question comes from the line of Ami Fadia with Needham & Company. Your line is now open. Hi. This is Poorna on for Ami. Thank you for taking our question. Just wondering, for the data update that's expected in 2026 for RASolute 302, is there any scenario where with the data update you could seek some sort of accelerated approval, and what would that look like? The second question is a follow-up on the Summit Therapeutics one. Could you elaborate on how the combination of RAS(ON) inhibitor with PD-1/VEGF inhibitor can improve response or efficacy in the last two months? Thank you. Sure. Yeah. Thanks for your question. The first question is, do we envision the possibility of an accelerated approval? I think that might mix up a couple of different things. I mean, there's an accelerated approval pathway, which, as my friend Steve Kelsey often points out, is not often the most accelerated approval pathway. It's just called accelerated approval because you can do that in a different data set. We're going to have a complete data set. That's the whole point of the randomized control trial and the progress that's being made now. We expect to have a package of data in 2026. The question is, how fast can they move on it as opposed to will we pursue an accelerated approval path? I think just to differentiate those. We'll move as fast on it as we can, and we hope they'll move as fast on it as they can. Beyond that, I don't think we can speculate today about timing. We, of course, are preparing ourselves to move this absolutely as efficiently as possible. When When we do open the envelope and see what the data show us, there won't be any hesitation on our part to move those data forward. We'll be well prepared for it. It'll be a well-oiled machine. Hopefully, by then, we will have also set things up with the FDA to maximize their ability to move as well. I guess the other comment would be that the breakthrough therapy designation does create some efficiencies or some speed in the review process that we'll take advantage of. That's a benefit of having the breakthrough therapy designation in our hands. I think that's about all I can probably say on that. Yeah. Okay. The bispecific, what was the question on it? It was, oh, why was. Training and efficacy by the combo of the VEGF with the RAS inhibitor. Yeah. Dr. Wei Lin is with us, our Chief Medical Officer, and maybe he wants to comment on PD-1 with and without VEGF and why there's the possibility that it adds incremental value. Yeah, sure. Thanks for the question. Thanks, Mark. Historically, if you reference back to, say, EGFR, which RAS is a downstream node from EGFR, the combination of targeted therapy using EGFR, so prototype plus VEGF, there's actually crosstalk between these pathways, such that there's actually improvement in both response rate as well as progression-free survival. There have been a number of trials that actually demonstrated that. Now, that has to prove itself in RAS, but at least that's in theory. There could be interaction between those two pathways that can enhance anti-tumor activity and potentially even translate to improved progression-free survival. Yeah. To add to that, we've already demonstrated, albeit with a relatively early data set, that the RAS inhibitors, both daraxonrasib and elironrasib, in combination with an anti-PD-1, do deliver greater punch, at least as determined by response rates. We didn't present any durability data. We've seen that many times in preclinical models. Particularly, the RAS(ON) inhibitors are so effective at suppressing the RAS pathway that they reverse some of the local immunosuppressive effects that occur inside a RAS-driven tumor. That makes them more sensitive to the impact of an anti-PD-1 antibody when it unleashes the immune response. That additivity, we think, is already there. Whether the VEGF itself contributes, the VEGF antagonist contributes to RAS-driven signaling versus just tumor growth, I don't think we can dissect that out. It's a reasonable bet that if the bispecific antibody is superior to the monospecific PD-1 antibody, then when you combine it with RAS, it'll be superior to the monospecific PD-1 antibody combined with the RAS inhibitor. That just makes sense. It'll have to be experimental to show. Great. Thank you so much. Thank you. Our next question comes from the line of Alec Stranahan with Bank of America. Your line is now open. Hey, guys. Thanks for taking our questions and congrats from me on the updates as well. First, on zoldonrasib and elironrasib, are there any particular data points you're waiting on before pushing these into additional studies? When do you expect to have the information in hand to make that decision? Second, on the Iambic collaboration, how do you see your in-house data maybe synergizing with their platform? What kind of conclusions do you think you'll be able to draw leveraging their AI technology that, I guess, you wouldn't have been able to make on your own? Thank you. Thanks a lot, Alex. zoldonrasib and elironrasib, you're looking for sort of what data packet will impact our decision-making. We have those studies really already underway, and they've been well described. In some cases, we've shown relatively small early data sets that are quite encouraging. We believe those data sets, but of course, we continue to follow patients to make sure that there aren't latent tolerability or safety signals. That's one of the things we do. We often expand then to make sure we have enough data to permit the FDA or regulatory bodies and so on. There are quite a number of things, and there are so many different options there that it would be very difficult for us to sort of lay out a complete delineation of every study and exactly which data will be coming when and would make the difference. Therefore, we've simply not described it except when we think we're close to something where we can have meaningful guidance about when something's going to happen. I think both zoldonrasib and elironrasib are doing very well, and they do create some fantastic opportunities for us. You can bet we're working on those. We'll just ask for patience until we're ready to give more complete stories about them. With regard to Iambic, I think basically it comes down to this for us. We have tens of thousands of tri-complex inhibitors that have been carefully crafted by our amazing chemistry group with feedback and input from our cancer biology organization. That creates a massive data set around, you could call it simply SAR, but it's a massive data set. Our chemists are very familiar with it because they made all of those compounds. It's a lot of information to keep in your head and to be able to access sort of on a moment's notice. AI has no problem with that. It accesses all of that information iteratively, very, very quickly. The notion here is that we ought to just get more firepower out of processing that information, that multidimensional information, which accounts to undoubtedly many millions of data points, if not even a larger scale than that. It's very large data sets across many different parameters. It can process those and give us, give the chemists a hand in helping to prioritize which things that are worth synthesizing and which things aren't. Iambic, in particular, has built their neural plexor technology to facilitate this. They've done it on a particular scale for a particular set of goals and actually created very quickly their own lead molecule and then developing candidates to take into the clinic. That's not related to RAS per se, but it sort of validated the effectiveness of their technology. They have their own uses for it. They and we agreed that feeding that AI model or updating the AI model by incorporating our proprietary data may deliver insights that the model can predict for us or produce for us that can make it more efficient. That could be applied to RAS targets. That could be applied to non-RAS targets. We have everything from modest ambition goals to very high ambition goals. We'll see as we prosecute this to what degree it delivers. In the meantime, we are for sure investing in our own internal AI capabilities. This is a very nice component of an overall strategy that's growing here with regard to the use of machine learning, essentially, largely, but also more broadly, AI to make us even better at something that our organization's already pretty good at. Thank you. Thank you. Our next question comes from the line of Peter Lawson with Barclays. Your line is now open. Great. Thank you. Thanks for the updates. Just a follow-up on the commercial build-out, kind of how large would the U.S. field team be, and kind of what milestones do you want to hit over the next 12 months as regards to the build-out? Yeah. Hi, Peter. Thanks for the question. I'm going to hand you over to Anthony, who may be somewhat disappointing for you on this particular point. That's sort of somewhat strategic and competitive information, but Anthony, give it a try. Thanks, Mark, and thank you, Peter, for the question. We have initiated the build-out of our U.S. field team. In fact, we already have parts of the field team in place. We have an MSL team, and we have a thought leader liaison team already in place. We've started to build the rest of our team, including our access and sales leadership. It's really been impressive to see the caliber of talent that continues to be really interested in making our mission come true. That's the goal. All I'll say to fulfill Mark's point earlier is that we're really pleased with the field build, and we're really pleased with our progress on launch readiness so far. Okay. Thank you so much. I realize it's difficult to talk through those. On the PRMT5 combo, what tumor types are you prioritizing? Is it lung versus pancreatic or broader kind of MTAP deletion? Firstly, the current study that's ongoing is being sponsored by Tango, not by Revolution Medicines. The overlap between MTAP deletion, which creates the susceptibility to PRMT5 inhibition, and RAS mutation is largely pancreatic cancer. The focus there is mainly on pancreatic cancer. There's about, as you know, I mean, almost pretty much all pancreatic cancer is RAS-driven. About 92% of it is, frankly, RAS mutated. Somewhere between, depending on geography, somewhere around 20%- 25%, I would say, would have some form of MTAP deletion or loss of function. It turns out that around between 20% and 25% of pancreatic cancer have both, and that would be the target population for the combination largely. The overlap, there are some RAS-mutant lung cancers that also have MTAP deletion, but the numbers are a little bit smaller there. Yeah. If I could add, I think that Tango, I think they might use the number of 30%, something like that. We're not disagreeing with that. It's hard to nail that down. They probably have the most information since they study that. I'm sure they would also be quick to point out there are other tumor types in which MTAP deletion occurs, but they're less commonly sites for which RAS mutations occur. We don't capture them in our thinking so much. I agree with Steve's points. Great. Thank you so much. Thank you. I'm showing no further questions at this time. I would now like to turn it back to Dr. Mark Goldsmith for closing remarks. Thank you, operator. Thank you to everyone for participating today and for your continued support of Revolution Medicines. Thank you for your participation in today's conference. This does conclude the program. You may now disconnect.