Q2 2025 Revolution Medicines Inc Earnings Call
Good day, and thank you for standing by. Welcome to the revolution medicine's, 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
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I would now like to hand the conference over to your first Speaker today. Ryan AC 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, medicine's 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'd 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 10K and our quarterly reports on form 10q that are filed with the US Securities and Exchange Commission.
This afternoon, we released Financial results for the quarter ended, June 30th 2025 and recent corporate updates. The press release is available on the investor section of our website at redmed cam 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 revmed. 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 revmed, we remain steadfast in our commitment to revolutionizing treatment for patients with grass addicted. Cancers through the discovery development and Global delivery of innovative targeted medicines
we have a compelling pipeline of 3, distinguished clinical stage grass on inhibitors.
DX on raseed a groundbreaking grass on Multi selective inhibitor.
Are on raseed, a differentiated g12c, selective, covalent inhibitor.
And zeldon raseed 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 wrasse on inhibitor and 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 directs on rapid is our most advanced clinical program.
We were pleased to announce recently that your axon raised received Breakthrough Therapy Designation from the U.S. Food and Drug Administration in previously treated metastatic pancreatic cancer with COS G12 mutations.
This designation, underscores the large unmet medical needs for patients, living with pancreatic cancer, and the urgency of advancing development of of duraxe, on raseed, on behalf of patients.
Toward this objective. We continue to make progress across our active and planned. Drax on raseed. Registrational studies in pancreatic cancer.
Online, metastatic pancreatic ductal adenocarcinoma 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 our investigational sites. Today, 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 3 armed. Trial comparing drafts on raseed, or directs on raseed plus chemotherapy to chemotherapy.
Later, this year, we expect to share the trial design and clinical combination data that informed, this plan and to initiate the trial.
Third. We also continue progressing toward a registrational trial with Dax on rasib as adjuvant treatment for patients with respectable pedak. In later this year, we expect to share the trial design and initiate this trial as well.
For patients with pancreatic cancers, specifically bearing a rash g12d mutation, the clinical activity and tolerability profile. We've reported for its old on raseed, is quite encouraging and suggests. It is 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 RASson inhibitor, doubling it with Durex on Raseed. This is 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 and a collaborative. Phase 1 trial evaluating their prmt5 inhibitor TNG 462 with either DirectX on Ras of Brazil on raseed.
Such novel combinations have the potential to provide differentiated options for patients with these cancer genotypes.
Moving to non small cell lung cancer Resolute 301. Our phase 3 trial of DirectX on Route Sub in previously, treated patients with Ras mutant non small, cell lung, cancer continues enrolling patients in the US and we are now activating trial sites in Europe and Japan as planned.
Evaluating directs on Ras have been earlier lines of therapy for patients with non small cell. Lung cancer is also an area of strategic priority for rebed.
We recently showed clinical evidence that directs on raseed can be combined productively and tolerably with pendulum with or without Platinum double chemotherapy with these results in hand. You're working toward initiating a registrational trial. And 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 mutant-selective inhibitors, earlier on Razem and Zold on RAS-ed in patients with RAS G12C or G12D non-small cell lung cancer, respectively.
First, we recently reported an updated clinical data set from patients with previously, treated krash g12c, non small cell lung cancer, treated with the Lyon massive as monotherapy that showed a highly competitive profile, including differentiated safety and tolerability that it along with a compelling objective, response, rate and progression-free survival.
we recently announced that A Lyon Raza was granted breakthrough therapy designation by the FDA for locally Advanced or metastatic cos g12c, non small cell lung cancer following prior, systemic therapy, including anti-pd1 and chemotherapy
This designation is a recognition of the significant unmet medical need and a lan riffs 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 a lure on raft of with other inhibitors.
In particular, the RAS-on inhibitor dlet of a l on raseed and Dax on raseed was shown to exhibit significant anti-tumor activity in advanced, non-small cell lung cancer patients who had progressed on treatment with a K, rash G12C of inhibitor.
This observation mirrored similar findings that we had previously reported in patients with krash g12c. Colorectal cancer
Your patience with an acceptable, safety and tolerability profile.
These findings suggest that Aeron Rasib and various treatment configurations warrant evaluation in patients with RAS G12C, non-small cell lung cancer.
And we continued work to prioritize among the multiple options for advancing development of this differentiated grass on g12c, inhibitor.
Forth. We continue to advance zolon rasib for patients with Ras g12d non small cell lung cancer. We recently shared promising data for patients with previously treated rash 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 registration opportunities.
Fifth, we were pleased to announce recently a new clinical collaboration with Summit. Therapeutics to evaluate combinations of summits, Ivan smab and advanced pd1 vegf by specific, antibody. With each of directs, on raseed, Aeron, raseed and sold on raseed.
This collaboration Builds on promising initial clinical evidence. We have reported indicating that directs on raseed. Ander on raseed can deliver additive anti-tumor activity with an acceptable safety and tolerability profile when combined with a pd1 antibody.
The new cohorts will assess whether combinations with a Next Generation pd1. Vegf by specific inhibitor can unlock further therapeutic impact.
Beyond our first 3 clinical stage Ras on Inhibitors that are progressing nicely. The next asset we are preparing to enter. Clinical development is RMC 5127 a wrasse on g12v selective inhibitor.
We expect this program to be Clinic. Ready later this year to support the plan initiation of a Phase 1 trial in 2026.
And 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 aeon and out last year, to discover novel by specific antibodies that can complement Ras on inhibitors.
We also recently announced a significant drug Discovery collaboration with imic 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, directly 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 progresses 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 meaning including bolstered by our recently announced partnership with royalty Pharma.
This partnership supplements, our strong balance sheet by providing us with an additional 2 billion dollars 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 for revmed to direct and execute independently on a global development and commercialization strategy for our promising grass, targeted portfolio.
This financial strength, combined with our maturing pipeline and organizational capabilities, empowers us. Our intention is to become a fully integrated global oncology company that discovers, develops, and delivers innovative targeted therapies on behalf of patients worldwide who are living with Ras-addicted cancers.
I'd now like to turn the call over to Jack to provide more specifics on our royalty farmer, partnership, and summarize our second quarter results. Jack, thanks Mark.
Before turning to the second quarter of financial results, I would like to review a few key highlights from our Royalty Pharma transaction.
Dead.
We have structured, the funding arrangement to be flexible.
With 1.25 billion or almost 2/3, reserved as optional for revmed and to be drawn at our election.
Subject 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 evolved.
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.
Turn into expenses R&D expenses for the second quarter of 2025 or $2.24 million.
To increase in R&D expenses was primarily due to increases in our clinical trial related expenses.
And Manufacturing expenses for our 3 clinical stage programs.
With the rocks on raseed being the largest driver of the increase, given the program is in 2 phase 3 trials.
Personnel-related expenses and stock-based compensation expense also increased in 2025 due to additional headcount.
GNA expenses for the second quarter of 2025 or 40.6 million compared to 21.7 million for the second quarter of 2024.
The increase in GNA 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 drawn to be received in June, was accounted for as a liability. On our second quarter, balance sheet.
This liability will accrete or increase through interest expense on our income statement and future royalty payments. We pay on net sales of directs. On receipts, it will be applied against and reduce the liability balance on our balance sheet.
In the second quarter of 2025, we recognized approximately $900,000 in non-cash interest expense related to the transaction, and we 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 increased 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 of medicine's organization is determined to build the leading Global targeted medicine 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 a 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 recognise the continuing extraordinary efforts of revmed 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 1, 1 on your telephone and wait for your name to be announced.
To withdraw your question. Please press star. 1 1 again, please limit to 1 question and 1. 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 Securities. Your line is now open.
Hey good, good afternoon, thanks for taking my question and yeah, nice to hear that the um brass salute 302 studies winding down us sites. Um, Mark could you comment on how you're tracking towards completing enrollment xus and perhaps? Um, you know, any comments on the rough? Geographic, distribution of patients uh, would be interesting, I think. Um, and then a question on the plan, first line pedex, study where you sort of reaffirmed, uh, plans to run uh 3 armed study here and um obviously a lot of interest in the the chemotherapy combination uh where you're doing work still and um obviously with with the go to optimize portability and I believe maintaining those intensity here. Um how important is potentially clinical efficacy assessments for these chemotherapy combinations to support advancing 1 or perhaps more of these uh plan combinations into first line. So, thanks so much.
Thank you, Michael. Those were meaty meaty questions. Uh, so the first question is about 302, um,
Uh, it it is making very good progress. I don't think we can, we can share with you a breakdown of of actual distribution. That, of course, continues to evolve.
Um, you know, as indicated we're winding down the US, enrollment, there continues to be enrollment, uh, outside the United States and so the final numbers, uh, will ultimately be determined by that, but 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, a lot of parts that all have to synchronize, uh, to get to the Finish Line. Uh, it's it's looking very solid, we're in very good shape and I think we'll be in a good position to, uh, share, uh, share data in in 2026.
um,
With regard to the 3 armed study and the chemo combination component. I think you asked sort of 2 sub parts 1 is, are we still studying it?
Uh, and then the second was, uh, what role does efficacy, uh, play as a parameter in that.
um,
Steve, do you want to do? You want to comment on?
Each of those questions. So we still
Studying the chemo combinations and what role does staff have to see play.
We all still studying with emo combinations. Uh,
but we're very, you know, we did promise that we would share the
study design and the rationale behind that study design.
In uh, 2025 we're getting closer to the end of 2025. So as so you can infer that we're pretty composed to the close to the end of um of the assessments that we need in order to inform the
Study design, specifically.
Um, with regards to the efficacy assessments explicitly.
Um, of course they will be important. Um, in in informing the study design up to a point, um, the, the primary basis for our, um, the on the ongoing assessments that we have is is obviously safety and tolerability.
Um, we are relying very heavily on the the second line.
Data that we have for Direct or Raseed, which as we have previously reported.
Scenes to exceed the outcomes for chemotherapy in first line pancreatic cancer. So that's already a fairly strong driver of our decision to move to move forwards with, with that study. But there will be some supplementary efficacy information for the analysis that we've done specifically in first line patients. And we, we will share that information when we share the
When we share the study designers as part of the rationale, I hope that we'll have a pretty comprehensive package and uh you know, and persuasive 1 for you at that time.
Very helpful. Thank you so much.
Thank you.
For next question comes from the line of Mark Ram with TD Cohen. Your line is now open.
Listen, falling on on Michael's questions. Hopefully, it's meaty. Um, could you maybe characterize the chemotherapies your zeroing in on? And, you know, how closely you'd expect that to, you know, the the chemo in the combination to resemble, kind of a standard of care, firstline regimen, um, versus maybe how much you've had to, to dose, adjust to, to make things, um, you know, tolerable. And then on the, the guidance for data, potentially being in 2026 for a second, line trial, it 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 Mark, appreciate the questions. Um uh, the first question um remind me again had to do with chemotherapy.
Uh, character we're looking at. Oh the regimens. Yeah. Um, as we've indicated, I know we've talked about this with you before. That all of the, all of the dosing that we're looking at is, well, within
Standard practice.
Uh, we're not, we're not pushing outside of that, uh, at all, uh, nor do we think we're going to need to do that. So I, I think it's we're using very active, uh, Doses and 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, they typically become lower throughout the course of multiple cycles, simply because they started at the maximum tolerated dose (MTD). So, 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.
um, the second question had to do with when we say a readout of data in 2026,
uh, what do we mean?
Well, I mean all we could really reference right now is the first analysis. We don't, you know we can't really predict what would happen at that time. It all depends that person analysis might be the final analysis. It might be an interim analysis.
um and uh, there are potential additional analyses after that, uh, but they're all event driven
And so we don't really control control control the timing. So it would be very hard to tell you.
All possible scenarios here.
Okay, but, but it is the first interim. That's likely in 2 268 and enrollment rates.
Well, we can't skip the first interim. The first, the first analysis is always going to be the first out analysis. And we do think there will be a report in 2026 and we're, we're optimistic that we'll be able to deliver on that, you know, the enrollment has been very robust as as we're indicating here and um, you know, we're having to sort of slow some things down to allow other things to, to, to fill fill some slots. Um, 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
Uh, readout, even though it will read all the the end points. Um, it's OS driven and we can't really predict that even though we have models that that attempt to predict it, but we don't know. Uh, 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 lank Partners. Your line is now open.
Hi guys, thanks for taking my question on the duracon Raza combination data and forming the Frontline Pac. Registrational study design to provide any additional color on what kind of data and how much data we can expect later this year. Thank you.
Uh thanks Jonathan. I I think the best way to answer that and and Steve may want to add to this is
We, we are building a data set that allows us to make these decisions.
And 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, um, experimental arms in a trial.
Then we feel that that's sufficient to share with with you. Um, and that's all we can do to quantitate it at this point.
Uh got it, maybe just 1 follow up on that then.
Can 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 Frontline, uh, directs and rest of registration of study. Thank you.
Comment on it. Reiterate that 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, you know, that we needed to resolve. As we discussed starting back at the first conference of the year.
Chemotherapy to say 1 more thing. And then if you can, can clarify it here
Chemotherapy is dosed at maximum tolerated dose.
so anything you add to that may end up compromising, not only the dosing,
Of the chemotherapy, but also the dosing.
of of
active targeted agent as well. And since we believe generally continuous dosing is a very good idea for suppressing, grass pathway signaling, and, and, and their thereby suppressing inhibiting tumor growth. Um, we need to optimize that so that really is the main consideration, but maybe maybe Steve can give you.
that was the primary the primary consideration was the minimizing dose interactions and maximizing the dose intensity of the rats Inhibitors and we fundamentally believe
The pancreatic cancers are Ras driven disease and that the best treatment you can deploy would be a Ras inhibitor.
And so, it's really important for us that the patients that are randomized to get the RAS, inhibitor, get the best chance on that rats 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 and chemotherapy, unfortunately he does a very good job.
Of disrupting, both of those things. So chemotherapy will cause toxicities that required? Those interruptions of the Rat inhibitor and chemotherapy may result in other things happen. That may ultimately, reduce the dose intensity of the, the rats inhibitor. Having said that, there are some very 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 and we're not testing reg. Uh,
The schedules or doses of those drugs that are not used in standard practice on on a global basis. So I think that um, ultimately we have a few constraints, we have, this is going to be a global trial, we have consulted very widely.
The major Geographic areas that will be uh participating in this study. And I think that we will come up with a solution that is, uh, acceptable for everyone involved. And, um,
We'll, you know, as I say once we've, once we've dotted the eyes and crossed the teas, we, we will be very happy to share that information with you. We're just not quite ready.
And it it will be the plan.
Understood, thank you.
Hey, thanks so much for taking the question and congrats. Um, on all the progress, um, curious your perspective on Wrath of Regulation as a resistance mechanism and stop on raft. Degradation versus inhibition um particularly in the g12d space. Thanks.
um,
Yeah, rats amplification is a real issue.
Um,
Rats ampl. So firstly, let's let's let's start with, uh, I don't think it matters, whether it's all about g12d or not. Frankly because I think the the what I'm going to say is going to likely to be true for all of the major Ras mutations uh in probably all of the major tumors in which rats as a cancer driver, but
Uh, Ras.
Rat. Amplification, that is amplification of the mutant allele the actual kras g12d if you like for G or D from tumors.
Is a major.
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 rats. Amplification is 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 rats inhibitor. And there are also therapeutic ways where you can get on top of, uh, Ras amplification, if you double down on in on inhibition of the mutant rats allele with, for instance, uh, a rat on dlet, which we have we're we're clinically testing right now. You can actually, uh, get a get over over over the, uh, the mutant ratio. Um, amplification so, 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 selected inhibitors.
And uh, and there are therapeutic ways of of getting on top of it. And some of them we have in our uh Discovery tool box 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 are degrader is better than an inhibitor.
And, uh, I think that the jury will remain out until the degraded companies generate clinical data that exceeds the efficacy and safety of the of the Inhibitors that we have currently in clinical development, so, um, can't comment more than that. Uh, I just don't see any precedent right now for the degraded technology being Superior to, uh, inhibitors
Yeah, thanks for that question. And and just to highlight a point that Steve made, the tumor is a microcosm of natural selection. And so it's actually gratifying to see that these rats addicted. Tumors go to Such Great Lengths, to overcome directs on raseed. It's because it's such an effective inhibitor of Ras and they're so dependent upon Ras. So, um, we're I think it makes complete sense biologically. We believe it makes complete sense biologically and, uh, is a marker of how effective directs on really is on suppressing, broadly, the rest that way.
Thank you.
Our next question comes from the line of Kelly Shei with Jefferies. Your line is now open.
Uh, congrats on the progress, and thank you for taking my questions, uh, for the, uh, Frontline, pancreatic cancer trial, uh, as you got it, I will, uh, you will share the pivotal trial design later this year, curious. Uh, at this moment, if the trial design has been signed off by the Regulatory Agencies, could we assume no in from data from second line to the trials needed in the data package from start of based on the comments made from the opening remarks. Thank you.
Yeah, thank you Kelly. Um,
We don't typically give uh, sort of blow by blow updates on our interactions with the Regulatory Agencies. It's it ends up being much less helpful than uh, than than my hope for. So I can't, I can't really answer that specific question but um, I think what's lost here a little bit.
Is although it's not yet transparent, you know, to our investors to our analysts.
We're actually making very good progress. The fact that we can keep your integrating that we're going to be on timeline for, uh, for initiating is an indicator of where we stand, uh, but beyond that,
We just can't get give you any higher resolution um you know, 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. Um, maybe just given the reiterated, um, timelines here for expected. Um, enrollment completion for resolute, the top line data next year, launched the following 27,
Just curious if you'd be willing to speak more on the extent to which you're already engaging in pre-commercial activities. Um and what learning you're taking from uh Luma crack or Croatia launches um that you see to be applicable um to the upcoming Direct on rapid launch um in Pak. Thanks so much.
Uh, thanks Andrea. Uh, just to just to clarify. I don't think we've guided to commercial.
Commercial timeline with that said.
Uh, Anthony Mancini can give us uh, his view of our commercialization uh, program status.
Now, thanks for the question. Andrew, and thanks, Mark. I think, uh, what I'll say is that launch Readiness plans are progressing, very well. We've, uh, got a team of experienced and talented Executives leading, our commercialization team across Med Affairs, Market access, marketing, and sales, and their
Their deeply engaged in in Market shaping activities and planning and in kol and advocacy organization engagement, and it really building our operational capabilities and launch Readiness activities. Um, and an example of some of the market shaping work that's going on is our expect graph campaign that's focused on uh educating uh the community of uh Community. Oncologists primarily that Ras is a driver mutation in Pak and that over 90% of pancreatic cancers, um have RAs mutations. Um, we're continuing to add, uh, to that experienced and talented team, uh, you know, and and starting to build our us field teams uh, more broadly now, um,
We're, we're learning from, uh, some of the other launches, not just, not just the g12 off Inhibitors. Um, and putting the right resources in the right place, uh, building the best strategies and tactics and operational capabilities. So that we we bring directs on raseed with urgency, uh, to patients
When we get that opportunity and 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. And maybe I could just add a comment sort of observing it as Anthony builds that organization. I think we're going to give us a really a really strong effort. And, uh, hopefully we'll have a, a terrific approval that will go with it and and great label. When the time comes,
thank you.
Our next question comes from the line of J. Olsen with a nightmare. 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 and since you're planning to combine Ivon smab with all 3 of your Ras on Inhibitors, can you just talk about how you're going to prioritize those 3 combinations and especially with regards to uh which tumor types you would prioritize and then I have a follow-up. Thank you.
Uh thanks Jay. Um, can't really give you much information about that. That sort of an operational question more than anything. Um, you know we continue with our commitments to pemberley map. As as you know we've talked about things that we'll continue to do with embolism at which is the
The these really singular standard in in first line lung cancer in particular and also another some other indicate many other indications. Uh but in parallel, we'll begin exploring. How the 5 specific antibody uh will behave in in you know, jointly with uh these different agents and I'm sure that we studied across a variety of of solid tumors. Um, you know, initially with dose escalations we typically start with a wide a wide net because we're trying to establish safety initially. And then over time once we get past uh any safety questions, then we start focusing on very specific indications uh, too hard today and in this context uh, and at this stage to to outline in any of those more specific paths beyond the beyond the dose escalation, but we're excited to be in the collaboration, we think it takes essentially the the most advanced. Uh uh veg fp1 by specific antibody in the field with the richest part.
Line of grass on Inhibitors and puts them together. And we think that's a very, very promising opportunity.
Okay, thank you for that. And then, I guess, as you look into the future, do you think the combination of Ivan smap plus? The daxon raseed has the potential to be an ideal combination in the first line. Non small cell lung cancer.
Ah, ideal.
Summit in their partner. Um, you know, uh, elaborate that information. And so, we'll get a better sense of how it performs relative to pd1. The initial information is encouraging, but it's it's hard for us to see in the future. Uh, this work for us is being done on the presumption that it will play out. And, uh, we're excited to see more options, more opportunities, more, uh, potential benefit for patients.
Excellent. We'll look forward to that. Thanks for taking the questions.
Our next question comes from the line of Ami Fadia with Nidam and Company. Your line is now open.
Hi. This is Pune on for Army. Thank you for taking our question. Um, just wondering because they update that's expected in 2026 for residue. 302 is there? Any scenario where with the data update? You could see seek some sort of a approval and what would that look like? Um, and the second question is a follow up on the summit. Therapeutics 1. Could you elaborate on how the combination of Vasan inhibitor with pd1 budget. Inhibitor can improve response or efficacy in the last few months. Thank you.
uh,
Sure. Um,
Yeah, so first, thanks for your question. The first question is, do we envision the possibility of an accelerated approval?
I think we're kind of that that might mix up a couple of different things. I mean, there's an accelerated approval pathway, which is my friend. Steve, Kelsey often points out is not often the most accelerated approval pathway. It's just called accelerated approval because you can submit a different data set.
Um,
We are, we're going to have a complete data set.
That's the sort of whole point of the randomized control.
That's being made now and we expect to have a package of data in 2026.
So then the question is, how fast can they move on it as opposed to will? They will we pursue an accelerated approval path. I think, just to differentiate those and we'll move as fast on it as we can. And we hope they'll move as fast as possible. And if they can, uh, but, uh, you know, beyond that, I don't think we can speculate today about timing. Uh, we, of course, are preparing ourselves to move as absolutely as sufficiently as possible. Uh, when we do, you know, open the envelope and see what the data show us. Um, there won't be any
Um, hesitation on our part to move those data forward. We'll be well prepared for it. It'll be well over a machine and, um, hopefully by then, we will have also set things up with the FDA to maximize their ability to move as well.
Um,
and I guess the other comment would be that. The BTD does does create some efficiencies or some speed in the review process that will take advantage of. And so that's a benefit of having the BTD, uh, in our hands
I think that's about like probably say on that. Yeah, okay and then the buy specific.
Hopes the question on it.
It was, oh, why the combo of the media?
Yeah.
Um, Dr. White Lynn is with us, our chief medical officer and maybe he wants to comment on.
Td1.
With and without that Jeff. And why? There's the possibility that it adds incremental value? Yeah, sure. Thanks for the question. Thanks Mark. Um, the um, historically, uh, if you reference back to say,
Egfr, um, the uh, which Ras is a downstream note, uh, from HFR, uh, the combination of Target therapy, using egfr code and high plus um, that you have, there's actually cross talk between these Pathways so that there's actually uh, Improvement uh, in both uh, response rate as well as progression, free survival. There's been a number of Trials, actually demonstrated that now that has to be proven
Help, uh, in Wrath but at least. Um, that's, uh, um, uh, in theory, there could be interaction between those 2 Pathways that can enhance anti-tumor activity and and and potentially even translate to improved progression free survival.
Yeah, and to add to that, I mean, we've already demonstrated, albeit with a relatively early data set, but we've already demonstrated,
That the rest inhibitors.
And that makes them more sensitive to the, uh, impact of an anti-PD1 antibody when it unleashes the immune response. So that additivity we think is already there.
Whether the vegf itself, contributes the vegf uh antagonist.
Contributes to.
Ras driven signaling versus just tumor growth. I don't think we can dissect that out, but it's a reasonable bet.
That if the buy specific antibodies superior to the mono specific pd1 antibody, then when you combine it with rats, it'll be superior to the monospecific pd1 antibody combined with the rest of the day. But that just that just makes sense.
But it'll have to be an experiment with the show.
Great, thank you so much.
Thank you.
For our next question, comes from the line of Alex janah with Bank of America. Your line is now open
Hey guys. Uh, thanks for taking our questions and uh, congrats um, from me on the updates as well. Um, first on rasp and a on raseed, uh, are there any particular data points you're waiting on before pushing these into additional studies? And when do you expect, um, to have the information in hand, to make that decision? Um, and second on the Ambac collaboration, uh, have you see your in-house data as maybe synergizing with their platform, and 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.
Uh, thanks a lot Alex um, sold on and a later on.
Uh, you're looking for sort of what data.
What data packet, um, will impact our decision making? Uh, well, we have those studies really already underway and they've been well described. And we in some cases shown relatively small, early data sets,
Uh, that are quite encouraging and we believe those data sets. But of course, we continue to follow patients to make sure that there aren't latent. Um,
Tolerability or, you know, safety signals. So, that's 1 of the things we do. Uh, we often expand. Then to make sure we have enough data to convince the FDA or regulatory bodies and so on. So there's a there are quite a number of things and there. There are so many different options there. That, um, it would be very difficult for us to sort of, lay out a complete delineation of every of every study and exactly which data will be coming in and would make the difference. So, therefore, we've simply not described it except when we think we're close to something where we can have a meaningful guidance about when something's going to happen. I think both sold on and later on are doing very well.
Um and um they do create some fantastic opportunities for us and you can bet we're working on those. Uh we'll just ask for patience until we're ready to um get more complete stories about them.
With regard to ambach.
Um,
Yeah, I think.
basically, it comes down to this for us, we have
Tens of thousands of try complex inhibitors.
That have been carefully crafted by uh you know our our amazing chemistry group with feedback and input from uh our our cancer biology organization.
Um, that creates a massive data set around, uh you could call it simply s r, uh but it's a massive data set. Now, our chemists are very familiar with it because they made all of those compounds, um, but 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, you know, very, very quickly. And so, um, the notion here is that we only just get more Firepower.
Out of, uh, out of processing that information, that multi-dimensional information, which accounts to.
You know undoubtedly many millions of data points. If not you know even a larger scale than that, it's very large data sets uh across many different parameters and 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 and, um, I am a particular has used has built their neurop plexer
Model.
Uh or updating the AI model by incorporating. Our proprietary data May deliver. Insights that the uh that the 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.
Um, to what degree it delivers. And in the meantime, we are for sure investing in our own internal AI capabilities. This is a, a very nice, uh, component of an overall strategy that's growing here, uh, with regard to the use of machine learning, essentially largely. But uh, also more broadly AI, uh, to make us even better at something that our organizations 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. Um, just a follow-up on the commercial buildout. Got a power Lodge with the US field team, B, and kind of what Milestones do you want to hit over the next 12 months as regards to the?
To build.
Out. Yeah. Hi Peter. Thanks for the question. Um, I'm going to hand you over to, uh, Anthony who may be somewhat disappointing for you on this particular, uh, point that sort of
Some strategic and competitive information, but and we give it a try now. Thanks, thanks, Mark. And thank you, Peter, for the question. Um, we we have initiated the build out of our us field team. Um, in fact, we we, we already have parts of the field team in place. We have a, an MSL team, and we have a, a thought leader liaison team, uh, already in place. And, and we've started to build the rest of our team, um, including our access and, and sales leadership, uh, and it's really been impressive to see the the caliber of talent that continues to be really interested in, you know, making, uh, you know, making our mission come true. And that's, that's the goal. So all I'll say to to fulfill Mark's Point earlier is that we're we're really feel. We're really pleased with the field build and we're really pleased with our progress on on launch Readiness so far.
Okay, thank you so much. Um, realized it's difficult to talk through those. Um and then on the prmt5 combo kind of what tumor types are you prioritize in, you know,
Learning versus pancreatic or, you know, broader kind of anti deletion.
Do you want to comment on that?
well, firstly, um
The current study that's ongoing is being sponsored by Tango, not by Revolution medicines. Um,
but the overlap between mtap deletion, which creates the susceptibility to guarantee by omission and
And Ras mutation is largely pancreatic cancer. So the focus there is mainly on pancreatic cancer. There's about, as you know I mean almost pretty much all pancreatic cancer is rash, driven about 92% of it is frankly, rats, mutated.
and uh, somewhere between
Depending on geography somewhere around 20 to 25%, I would say were would have some form of endap, deletion or loss of function. So it turns out that around between 20 and 25% of our credit cancer, have both and that would be the target population for the combination largely does the the overlap there. There are some ratios and lung cancers that also have um mtap deletion. But the numbers are a little bit smaller.
Yeah, if I could add, I think that uh, that Tango, I think they might use the number of 30 30%, something like that. And we got, we're not disagreeing with that. It's hard to to nail that down. They probably have the most information since they since they study that and there are, I'm sure they would also be quick to point out. There are other tumor types in which, uh, and tap solution occurs, but they're less commonly sites for which rats mutations occur. So we they we don't capture them in our in our thinking so much. Um, so I agree with the group 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 Mark, Goldsmith for closing remarks.
Thank you, operator. And thank you to everyone for participating today. Uh, and for your continued support of Revolution medicines
Participation. In today's conference, this does conclude the program, you may now disconnect