Good morning. Thanks for joining us for another session at the 44th J.P. Morgan Healthcare Conference. I'm Brian Cheng. I'm one of the senior biotech analysts here at the firm. This is a highly anticipated presentation, and we have the CEO from RevMed, Mark Goldsmith. I will now pass the mic to Mark for a short presentation, followed by a live audience Q&A. Mark, the stage is yours.
Thanks for the introduction, Brian, and good morning, everyone. It's really great to be here at the J.P. Morgan Healthcare Conference and to share an overview of Revolution Medicines. We've made meaningful progress and have a transformative year ahead of us. As today's presentation will include forward-looking statements, please refer to our legal disclaimer shown here on slide two. At Revolution Medicines, our mission is bold: to revolutionize treatment globally for patients living with RAS-addicted cancers through the discovery, development, and delivery of innovative targeted medicines directed against common mutational drivers of human cancers. We have been pioneers in the RAS-targeting field, introducing a number of scientific drug discovery and clinical breakthroughs through creating breakthroughs that create compelling opportunities for patients.
RevMed is a late-stage clinical oncology company pushing the boundaries in three common RAS-addicted cancers: pancreatic, non-small cell lung, and colorectal cancer, with four RAS(ON) inhibitors in the clinic and a deep pipeline behind them. We have eight ongoing or announced registrational phase 3 trials, an extensive aggregate clinical experience to date with more than 2,500 patients having received one or more of our RAS(ON) inhibitors. Today, our clinical stage pipeline consists of four investigational drugs that target the major oncogenic drivers. RMC-6236, our most advanced program, is a groundbreaking and promising RAS(ON) multi-selective inhibitor; RMC-6291, a highly differentiated, highly active, and well-tolerated RAS(ON) G12C selective inhibitor; RMC-9805, an innovative, highly active, and well-tolerated RAS(ON) G12D selective inhibitor; and our newest clinical compound, RMC-5127, a RAS(ON) G12V selective inhibitor.
As I'll briefly describe later, these clinical programs are backed by a rich pipeline of preclinical and discovery programs, including an innovative and exciting new class of inhibitors that has provided a fifth RAS(ON) inhibitor drug candidate on its way to the clinic. As a company singularly dedicated to RAS-addicted cancers, we are well-positioned to bring forward new treatments aimed at changing the global standards of care for patients with common cancers. In pancreatic ductal adenocarcinoma, for which cytotoxic chemotherapy remains the standard of care for most patients, more than 90% of tumors harbor an oncogenic RAS mutation. There's a profound need for RAS-targeted therapies for this devastating disease. Likewise, approximately 30% of non-small cell lung cancers carry an oncogenic RAS mutation, including 18% with non-G12C mutations. New, effective, targeted treatments remain a significant unmet need.
In colorectal cancer as well, more than 50% of tumors carry an oncogenic RAS mutation, and there remain high needs there. The depth and breadth of our RAS(ON) inhibitor portfolio designed to target oncogenic RAS mutations broadly allows us to aim for clinical impact across RAS-driven settings, including early and late-stage lines of treatment and directed against tumors carrying diverse RAS driver mutations. Our integrated scientific workflow focused on RAS-addicted cancers is engineered as a virtuous cycle of innovation that leverages the research bench, the clinical bedside, and commercial insights that inform how we discover new ways of targeting RAS through our highly productive tri-complex inhibitor platform, develop new investigational drugs through robust and parallel clinical development plans, and systematically expand our commercial and operational capabilities to deliver potential new therapies to patients globally.
I'll review highlights of each of these three areas of our mission, beginning with development activities. Pancreatic cancer is our most advanced area of clinical development, with multiple registrational trials already underway or planned for initiation this year. RMC-6236 has an unprecedented clinical profile across lines of therapy, across RAS mutations, and across treatment regimens. The clinical durability observed so far in second-line appears promising relative to PFS and OS rates reported for cytotoxic chemotherapy in the second- or first-line treatment settings. This investigational drug was recently recognized by the U.S. FDA through the awarding of a Commissioner's National Priority Review Voucher, which noted RMC-6236's potential to change the way pancreatic cancer is treated. In first-line metastatic disease, we have also seen a compelling emerging profile, both as monotherapy and in combination with chemotherapy.
Draxanrasib is currently under investigation and evaluation in three randomized registrational studies in pancreatic cancer. RASolute 302, our second-line metastatic phase 3 trial, recently completed global enrollment and will read out in the first half of this year. And RASolute 303 in first-line metastatic disease and RASolute 304 in resectable disease have both been initiated. Zoldanrasib , our covalent G12D selective inhibitor with a highly differentiated safety and tolerability profile, has also shown encouraging anti-tumor activity in pancreatic cancer. We are advancing this compound towards two first-line combination registrational trials in pancreatic cancer in 2026. RASolute 305 will evaluate zoldanrasib for pancreatic cancer in combination with chemotherapy, and RASolute 309 will evaluate the RAS(ON) inhibitor doublet of zoldanrasib plus draxanrasib as a chemotherapy-free approach for patients.
I'd like to briefly summarize the clinical rationale for this collection of trials starting with RMC-6236. RASolute 302 addresses an urgent unmet need for patients, provides the fastest entry point into pancreatic cancer, and is an important opportunity to potentially establish an overall survival benefit. RASolute 303 in the first-line metastatic disease setting is evaluating RMC-6236 monotherapy and in combination with gemcitabine and nab-paclitaxel, or GNP. This study tests two important and independent hypotheses: a chemotherapy-free RAS-targeted monotherapy treatment paradigm and a combination regimen containing a RAS-targeted drug plus chemotherapy. This parallel approach is intended to create treatment optionality for patients and their physicians, with the potential for an improved survival benefit supporting new standards of care in first-line treatment.
RASolute 304 in the adjuvant setting evaluates RMC-6236 monotherapy following surgery and perioperative chemotherapy in patients with resectable pancreatic cancer and has the potential to show improved long-term disease-free survival for these patients. If successful, these trials together could establish new standards of care for the majority of pancreatic cancer patients across lines of therapy. Finally, the highly attractive safety and tolerability profile seen so far with RMC-9805 also allows us to test two distinct hypotheses for patients in first-line metastatic pancreatic cancer carrying a RAS G12D mutation, including both a first-of-its-kind registrational study of a chemotherapy-free RAS(ON) inhibitor doublet and a combination treatment regimen with chemotherapy. Building on encouraging monotherapy results in previously treated pancreatic cancer patients, we have been evaluating RMC-9805 in combination with cytotoxic chemotherapies that are current standards of care treatments.
Today, I'm pleased to share initial clinical data from the combination of RMC-9805 with FOLFIRINOX. As of a December 1st, 2025, data cutoff date, the initial safety and tolerability profile for the combination of full-dose RMC-9805, that is 1,200 milligrams q.d., and full-dose in the modified FOLFIRINOX regimen was largely consistent with the well-known profile of FOLFIRINOX alone, and a favorable dose intensity for RMC-9805 was also maintained. 63% of patients achieved an objective response, including both confirmed and pending confirmation partial responses. The disease control rate was 95%, and the vast majority of patients remained on treatment as of the data cutoff date. We believe that RMC-9805 in combination with chemotherapy could be an important option for patients with pancreatic cancer harboring a G12D mutation.
This year, we also plan to share supporting results from the RMC-9805 plus GNP combination and from the RAS(ON) inhibitor doublet of RMC-9805 plus RMC-6236 at a medical meeting or meetings coming up. These findings support our intention to move swiftly into registrational trials with these regimens for first-line treatment. A second area of focus where we saw considerable advancement in 2025 was non-small cell lung cancer. We've shared encouraging initial safety, tolerability, and anti-tumor activity data that strengthen our belief that our first three assets may have a role in the non-small cell lung cancer treatment armamentarium as monotherapy or in combinations. First, RMC-6236 has shown a compelling profile as monotherapy in previously treated patients.
RASolute 301, a global randomized registrational study currently underway evaluating RMC-6236 monotherapy in previously treated metastatic non-small cell lung cancer patients, continues to enroll well inside the U.S. and internationally. Early combination data from first-line patients treated with RMC-6236 plus pembrolizumab were encouraging, and we are planning a first-line registrational trial. Second, let's consider our mutant selective inhibitors, RMC-9805 and RMC-6291, in patients with non-small cell lung cancers harboring RAS G12D or G12C mutations, respectively. We have reported highly encouraging initial safety, tolerability, and anti-tumor activity for RMC-9805 monotherapy in non-small cell lung cancer, and we continue enrolling an expansion cohort of second-line and beyond patients. Just last week, we announced that this investigational drug has received Breakthrough Therapy Designation from the FDA, our third BTD award for a RAS(ON) inhibitor.
We are in advanced planning for RASolute 308, our first registrational study of a zoldanrasib combination regimen in first-line metastatic non-small cell lung cancer. O leranrasib , our RAS G12C selective inhibitor, has shown a strong and differentiated clinical profile in G12C inhibitor naive and G12C inhibitor experienced patients as monotherapy in combination with pembrolizumab alone or as part of a RAS(ON) inhibitor doublet with draxanrasib . We are continuing to evaluate both monotherapy and combination approaches with oleranrasib to inform our registrational path forward. Colorectal cancer is another area of high interest for Revolution Medicines. Given the genetically heterogeneous profile of these cancers, we learned early on that combinatorial treatment approaches would likely be necessary to maximize clinical impact in this setting.
We have a range of combination studies ongoing that include evaluating RMC-6236 and RMC-9805 as part of a RAS(ON) inhibitor doublet and evaluating each asset in combination with current standards of care and other approaches. We also continue supporting our collaboration with Tango Therapeutics, studying the combination of a RAS(ON) inhibitor with vopimetastat, a PRMT5 inhibitor, in patients with tumors carrying both a RAS mutation and MTAP deletion. We are also now initiating a first-in-human study evaluating the combination of our RAS(ON) inhibitors with Summit Therapeutics ivonescimab, a PD-1 VEGF bispecific antibody across multiple solid tumor settings. Finally, we have initiated the first-in-human study of RMC-5127, a RAS(ON) G12V-selective inhibitor, as our fourth RAS-targeted compound to enter clinical development.
In addition to our parallel development program for clinical-stage RAS(ON) inhibitors, we also recognize the importance of continuing to invest in potential new approaches with the potential to provide significant additional impact for patients living with these cancers. We are committed to sustaining our leadership position through continuous innovation, leveraging the productive virtuous cycle I described earlier. Our singular ongoing focus on targeted therapeutics for patients with RAS-addicted cancers has produced large and diverse clinical data sets, yielding important translational insights, differentiated expertise, and know-how. We continue investing to strengthen and expand our proprietary discovery platform in order to identify new potentially groundbreaking options for treating patients with RAS-driven cancers. I would like to share with you an example of the exciting output from this continued investment in innovation.
To frame the context, we've reported compelling clinical durability from RMC-6236 treatment in patients with pancreatic cancer that is highly consistent with our earlier preclinical findings. The Kaplan-Meier plot on the left recapitulates the encouraging overall survival we've observed for patients with the second-line pancreatic cancer treated with RMC-6236, and the graph on the right shows the preclinical progression-free survival effect of RMC-6236 across a panel of models of RAS G12D pancreatic cancer. These data highlight the strong preclinical to clinical translation observed for RMC-6236 activity. They also illustrate the harsh reality that most RAS-driven cancers eventually will find ways to develop resistance and circumvent RAS inhibition, most commonly by increasing RAS signaling. We owe patients new solutions for this eventuality and have concentrated our efforts in this area.
Here, we're proud to briefly introduce an innovative new class of RAS(ON) inhibitors specifically designed to overcome RAS-driven acquired drug resistance and thereby extend the clinical benefit of RAS(ON) inhibitors. We intend to advance the first compound from this class into the clinic this year. Let me briefly illustrate with the preclinical data on this slide. The two graphs on the left show the anti-tumor activity of RMC-6236 in two standard preclinical xenograft models: a RAS G12D pancreatic cancer xenograft on the top and a RAS G12C non-small cell lung cancer xenograft on the bottom. In both models, RMC-6236, shown in green, drove deep and initially durable tumor regressions relative to the control arm, but upon longer follow-up, we saw emergence of on-treatment escape and tumor regrowth.
We used tumors that escaped from treatment with a RAS(ON) multi-inhibitor to derive resistant models for further study, as shown in the middle panels. The resistant pancreatic cancer variant exhibited increased RAS signaling as its apparent mechanism of drug resistance, and the resistant lung cancer variant carries an increase in RAS gene copy number. As expected, RMC-6236 showed significantly reduced anti-tumor activity in these models selected for resistance. In contrast, compound RMC-055 from our innovative new class of RAS(ON) inhibitors, shown in the orange tumor curves, defeated acquired RAS-dependent resistance in these settings and drove especially deep and sustained regressions. Treatment with RMC-055 across a wide range of active doses was well tolerated.
In a related experiment shown on the far right, treatment with RMC-055 arrested tumor growth and drove deep and durable regressions in the parental tumor models, even after they'd begun progressing during initial treatment with RMC-6236. Hence, we believe that RMC-055 and other compounds in this promising new class of RAS(ON) inhibitors have the potential to offer additional benefit for patients with RAS-addicted cancers by countering common RAS-dependent mechanisms of resistance. They may enable exciting sequential and/or combination treatment strategies designed to extend even further the durability of therapeutic effect. This year, we plan to share more information about this class of compounds at a scientific meeting and to bring a first compound into the clinic as our fifth investigational drug targeting RAS.
This vignette is a direct output from our continued investment in elucidating the fundamentals of RAS cancer biology, uncovering the clinical and molecular effects of treatment with RAS(ON) inhibitors, and deploying our differentiated drug discovery engine. We are building a world-class end-to-end global oncology enterprise to deliver RAS(ON) targeted therapies to patients living with RAS-addicted cancers. As our late-stage programs progress, we are ensuring that our organization is ready for successful commercialization. We've established the operational foundation necessary to move with speed and agility, focused initially in the U.S. and extending into priority international markets. Leading this work are seasoned executives with track records of launching some of the most impactful oncology products of the last two decades, and we continue expanding our capabilities in order to deliver these important new therapies to patients.
Our aim at RevMed is to create the industry-leading global targeted medicines franchise for patients with RAS-addicted cancers. To date, our organization and collaborators have discovered major insights and created valuable know-how in advancing groundbreaking RAS(ON) inhibitors, developed pioneering RAS(ON) inhibitors, and advanced into multiple late-stage registrational trials across a range of indications and lines of therapy, and scaled the organization, positioning RevMed to deliver global launches. A strong financial position with $1.9 billion as of the end of the third quarter, with an additional $1.75 billion in committed capital available to us under our agreement with Royalty Pharma, enables broad execution to serve unmet needs across the important opportunities I've outlined today. 2026 will be a year of growing impact for RevMed, with key milestones to track across our clinical programs as well as in advancing new programs and growing our capabilities.
In pancreatic cancer, we expect to provide several important data disclosures on RMC-6236 in the first half of 2026, including an expected readout for the RASolute 302 trial and sharing updated monotherapy and combination data in the first-line metastatic setting with initial durability measures. We also plan to initiate two registrational trials with RMC-9805 in the first-line metastatic pancreatic cancer setting this year. As I mentioned, RASolute 305, studying the combination of RMC-9805 plus chemotherapy to initiate in the first half of this year, and RASolute 309, a chemotherapy-free RAS(ON) inhibitor doublet, evaluating RMC-6236 plus RMC-9805 to initiate in the second half of the year.
In non-small cell lung cancer, we aim to substantially complete enrollment this year for RASolute 301, our ongoing RMC-6236 monotherapy study, and two first-line metastatic registrational trials in non-small cell lung cancer are planned for 2026. RASolute 308 will evaluate the combination of RMC-9805 with standard of care, expected to begin in the first half of 2026, and a trial of RMC-6236 in combination with standard of care, expected to initiate in the second half of the year. We also expect to provide an update on our registrational strategy for RMC-6291. In colorectal cancer, we plan to share an update on combination strategies in 2026 as we look forward toward pivotal trial opportunities. In earlier programs, activities related to RMC-5127 are ongoing to enable us to identify a recommended phase two dose in the second half of 2026.
Finally, we plan to initiate, as I mentioned, a first-in-human phase one trial with a first investigational drug from the innovative and exciting new class of RAS(ON) inhibitors that I previewed earlier today. Our organization is driven by a tireless commitment to patients living with RAS-addicted cancers. We believe that each asset in our pipeline has the potential to transform the treatment landscape for difficult-to-treat RAS-addicted cancers. We strive to achieve such impact every day through every trial and for every patient enrolled in our studies. I'd once again like to thank the patients, caregivers, clinical investigators, and advocates who partner with us in this critical work, and to acknowledge the extraordinary team of revolutionaries who drive transformative science on behalf of patients. Thank you very much.
Thank you, Mark, for the wonderful presentation. Let's start the Q&A.
For those who are in the audience, feel free to raise your hands. For those joining us virtually, you can submit questions on the portal. Mark, maybe just to start off, big picture question. Do you see yourself building something bigger? How do you balance your goal in building a bigger machine than taking strategic transactions in front of you? And ultimately, where do you see RevMed in six months and five years?
I'm shocked.
Maybe not five years.
I have very little to say about the latter part of your question since, obviously, we have a well-established company policy of not commenting on rumors or speculation, so I won't be able to address that particular question. But with regard to what are we building, it's not our goal to build something big. It's our goal to build something that's impactful.
We have tremendous momentum that I just summarized. We have an extraordinary organization that grew by something like 400 people in 2025, reaching into every corner of all disciplines that we need to be able to deliver these products on behalf of patients eventually around the world. So we're committed to that vision. There's a lot to do between where we are today and achieving that vision, and we'll need to continue adding to those resources in order to achieve it.
Historically, when you look at the data disclosure from RevMed, we have seen data at your own time. We have seen it at conferences. We have seen it at earnings. What's your take in disclosing data today, which I totally welcome? What's the rationale in disclosing today at the conference of the year?
Why did we disclose data at the conference, the most important conference of the year?
Is that what you asked?
Yes.
Look, our general feeling is, and I think most investors who talk with us understand that we share data when the data are mature enough to show something that indicates a direction that our program should go. And I think the two things I showed today are very much linked to what's going to happen later in the year. Sometimes conferences aren't convenient. Their abstract deadlines don't happen. They don't check with us when they set the dates for abstract deadlines. So we just choose to keep moving things forward with urgent needs that need to be met. And the only way for us to move clinical programs forward is to provide the data that supports it in order for investigators to understand why they should participate and for patients to make decisions about whether to participate.
So I think we'll continue to do that.
Maybe turning to the second-line trial that you're running, can we talk about the risk that you see in the study? There's certainly a lot of wiggle room for error when you look at what you have presented for the draxanrasib performance in the second-line PDAC setting. What keeps you up at night in relation to the second-line study's outcome?
Well, I mean, at this point, it's going very well. It enrolled extraordinarily rapidly. We've completed enrollment. We've covered the territories that we needed to cover, which took some management to get that accomplished. And we'll await the data. Of course, it's an experiment. And so while we think there are a lot of data that justify conducting the study, and we certainly have high hopes for it, it's an experiment. And we'll see the results when we see them.
You have narrowed your guidance for the second-line to now first half. Have you seen the data in a blinded setting, and do you have a sense of how close you are to the events? And I hear this question quite a lot where there's some question of whether you have seen the interim. What's your take on those questions?
Well, the thing that we do track is OS events, deaths, in the trial because it's an event-driven trial. So we have to track that. There's no way around that. It's, of course, blinded, so all we know is a total number. And we have a target number after which we will be able to unblind the data. So it's a very process-oriented thing. There's really not a lot of wiggle room in it. And we don't get to take a peek until we unblind it.
As we look into the top line in the first half, what can we expect there? And can you talk about what weight it carries towards the path to approval?
I'm sorry. Say that again.
Is it sufficient for you to file for an approval based on the top line in the first half?
Well, we don't know that because we don't know the results. So it may be an interim analysis. I mean, it starts as an interim analysis under the plan. And remember, it's overall survival-driven. So it's powered for overall survival, but that means it's overpowered, if you will, for progression-free survival. And when the data are unblinded, we'll have those numbers. And there's several different scenarios that could play out in it. And one of those could mean that the trial is completed and we move forward.
And one of those could mean we have some of the results that we need and not all of them. We just don't know. I mean, of course, we've designed it with some assumptions in mind and a great deal of statistical work behind it. But at the end of the day, we just have to see the results, and then we'll know which way it will go.
If I do my math, let's say mid-year top line, in the most blue-sky scenario where this top line is sufficient, submission potentially the fall, you have CNPV, so potentially one to two months of review. Do you think that it's possible that you could get approval this year?
Yeah, I wouldn't want to speculate on that. I mean, there are so many factors in there that we don't control.
Probably if you asked your question more broadly, what do I lose sleep over? It's things we don't control as opposed to things that we do control. And there are a lot of macro external events, very high-level macro events, but then there are practical things like the FDA and how it prosecutes things. And they've made a public commitment to be very efficient and to move very quickly, and that we're working very well with them on that. But we don't know what all that will actually translate into, and we have no control over it. So I think for us to speculate today would literally just be speculation.
I'll take one question from the audience. No question.
How should we interpret zoldanrasib's performance here that you presented here today relative to draxanrasib's performance in the past, mono or combo of chemo that we reported back in September?
Right. Zoldanrasib is performing very well. Draxanrasib has also performed very well. They're different in their characteristics. And I think only over time, once we've completed randomized phase 3 trials, will we really be able to compare them. And our feeling is that we have to have some humility about it. We can make guesses about how certain things are going to play out, but we just need to conduct those studies. I think they're both exciting compounds. They're even more exciting in combination, we believe, which is why one of the arms of our first-line or one of the studies will be a combination RAS(ON) inhibitor doublet.
We're also able to combine zoldanrasib because of its very favorable tolerability profile. We're able to combine it with FOLFIRINOX quite readily. And that gives us an opportunity that we did not choose to take with draxanrasib . So I think there's both complementarity and then some actual overlap. And I think that'
s good for patients. As we think about the setup with 305 and 309, I think just to play devil's advocate, why not just combine both 305, 309 in just one study in a sense that chemo combo in one arm, Drax combo in one arm, and then the chemo control? What is the benefit ultimately of doing two parallel studies for the front line for Drax in a front line PDAC setting?
Yeah, it turns out to be entirely an operational question.
So it's not actually. It seems like it's interesting, but it's not that interesting. The cost is about the same. So there's really not a cost savings to run that trial as a multi-arm trial. And so then it comes down to what's most practical. And a larger trial will take longer to run as opposed to running two smaller trials in parallel. So that's one consideration. And there are various other just logistical aspects of it. So we make those decisions on a case-by-case basis. As you know, for our RMC-6236 trial, we're running a monotherapy arm and a combination arm compared to the same control. But think about the fact that you have to have the same control as well. It's complicated.
Going back to the CNPV that's in place for draxanrasib, I know we talked a little bit back at ESMO.
At that point, I don't think you fully know whether the CNPV is applicable just for PDAC or it is for all the indication or whether there is some restriction around the line of setting. Do you have that clarity today, and since you've got the CNPV, has that impacted your planning for draxanrasib or even other combination partnerships?
Yeah, I think these vouchers, as far as we can tell, are for a single indication. They're generally not for a whole class or for a whole program, and of course, we just spent the last 25 minutes talking about draxanrasib in the 302 study, so it's clearly the thing that most urgently needs to get out there, so I think that you can sort of infer from that. We've had a great relationship with the FDA.
They've been very committed to working with us, including under the CNPV regime. They're kind of inventing it as they go because it's a pilot program, and so we're kind of inventing along with them, but we're very positive about the interaction.
As you think through zoldanrasib's positioning, we have seen a few G12 data out there. How do you see your differentiation? What's your edge there with zoldanrasib?
Well, I think there are a number of characteristics that give it an edge. It's probably been studied in substantially more patients than any of the others, so we have a much more mature view of how it behaves. Its tolerability profile is so attractive that investigators and their patients consider it to be analogous to placebo and therefore can be run in a placebo-controlled way, which I don't know of any other compound like that.
Its activity level seems to be as high or higher than anything that we've seen so far with anything close to the same tolerability profile. We think it's a class-leading compound. Those sorts of things play themselves out over time. We've had a pretty vast experience with it now. I think we're pretty confident that this will be an important part of drug treatment options for patients.
Then turning to G12C oleranrasib , where does that go in terms of your priority list? Is laying out a plan near-term? Does it make sense? Does it hinder the growth of RevMed in any way? Does oleranrasib hinder the growth of RevMed? Just from a strategic standpoint, does laying out a plan for G12C have any impact in terms of your thinking around where the portfolio could go?
I have to admit, I'm not quite understanding. Is your question whether telling people what we're going to do with it has an impact or whether actually doing something with it has an impact?
Whether the next step, laying out a plan for the next step, would have any impact in terms of how your potential discussions are going or your plan for draxanrasib and also zoldanrasib?
Yeah, whether we disclose what we're doing or not disclosing it, we have to make our own plans. We think oleranrasib is a really outstanding compound. It's a little bit the little brother, little sister of the others because they've just addressed such important gaps in treatment regimens. The G12C space is obviously much more crowded. So we're being much more thoughtful.
We need to be much more thoughtful and careful in deciding how to move it forward. And before we advance it into a registrational trial, we want to make sure what we're doing is going to serve an unmet need and is going to have a place in the marketplace. And there are several ways in which that could happen. And when we're ready to move that forward, we'll tell everybody about it and explain our rationale.
Great. Just to wrap up, can you remind us how we should think about the data cadence this year? Which data update are you most excited for?
Which data update are we most excited for? Why don't we take a poll in the room and find out what the answer to that is? We probably agree with that. Thanks very much.
Thank you. Thanks for your time.