Eric Joseph, Senior Biotech Analyst with J.P. Morgan. Our next presenting company this afternoon is Relay Therapeutics, and speaking on behalf of the company is Chief Executive Officer Sanjiv Patel. There's a Q&A session after the presentation. Just raise your hand, we'll get a mic over to you if you have a question, and if you're tuning in via webcast, feel free to submit questions via the portal. So with that, thanks, Sanjiv, for joining us. Thank you.
Thank you, Eric, and thank you to J.P. Morgan for the invitation. This afternoon, I'll be making a series of forward-looking statements which are subject to the normal risks and uncertainties. Actual events may differ materially from the actual projections, intentions and expectations laid out. So with all that said, we'll begin. Relay Therapeutics was founded in 2016 as one of the first of a new breed of biotech that sits at the intersection of leading-edge computational and experimental techniques. Our approach has been to focus our Dynamo platform on making small molecule inhibitors against validated targets. Our platform to date, we believe, has been very productive. We have four clinical programs already created entirely in-house by our approach and one further program that's being held at IND. We're even more excited about what lies ahead.
We have more than seven preclinical programs, and we've expanded from oncology into genetic disease. We've moved from being a small molecule inhibitor company to now working on chaperones and degraders, and we have an extensive platform. All underpinning this is a wonderful team and an extensive balance sheet. So let's start with what's driving all the excitement is the platform. Our Dynamo platform was created eight years ago, and over time, we've added a constellation of tools both on the experimental side, like cryo-EM, room temperature X-ray crystallography, as well as tools on the computational side, such as generative AI, machine learning, and long timescale molecular dynamics simulation. Over the eight years, we've added and subtracted tools, depending on what's been working. Our experience has allowed us to combine different tools to solve different problems, and the more times that we solve problems, the better we get.
But most importantly, we've been able to integrate the tools more tightly, and so we have computational tools such as generative AI, working very closely with robotics and the creation of medicines that are actually in the lab. So over time, our platform has become more and more powerful, and it's all knitted together through our team. But a platform is only as good as the output, and so if you go back in time to the start of our company, we focused our platform on creating a SHP2 inhibitor, which is a fast follower program. So we tried to create as many chemotypes as we could in a short time period as we could, and we eventually created RLY-1971, which we believed had the potential to be a clinically differentiated program, and it was acquired by Roche Genentech in 2020.
Then we started to focus on solving a problem that conventional techniques couldn't solve, creating an isoform-selective inhibitor for FGFR2. We were pleased to create RLY-4008, which went into the clinic in 2020, and we've been able to generate validating clinical data that our platform has indeed created an exquisitely selective FGFR2 inhibitor. Then we moved our platform into trying to solve one of the precision medicine's holy grails and create a mutant-selective PI3K alpha inhibitor, and RLY-2608 went into the clinic in late 2021, and again, last year, we were able to show validating data that the platform has indeed done what it said it could do. And so all of this shows a very productive platform, and it's all manifested now in an extensive precision medicine pipeline that's spread across precision oncology and genetic disease.
If we look forward to our focus in 2024, for RLY-4008, which is our selective FGFR2 inhibitor, we will round out the pivotal cohort for our ICC fusion, pivotal population, and we'll continue to gather data on RLY-4008's activity in other alteration types outside of fusions and other tumor types outside of cholangiocarcinoma. All of this will come together in the second half of the year, and we'll engage with regulators and determine our go-forward development strategy. For our platform, we've already talked about, it's been extremely productive, and we will unveil another what we believe to be innovative target that we will show later in the year. The main focus of 2024 for us will be on our breast cancer portfolio.
As you could see from the San Antonio Breast Cancer Symposium just before the holidays, PI3K is indeed a very important therapeutic target in breast cancer, and the emerging profile of RLY-2608 is very encouraging and allows us to double down now and go as aggressively as we can to execute a broad clinical program for RLY-2608, both in doublet and in triplet combinations, and we'll deprioritize our second PI3K alpha mutant selective inhibitor, RLY-5836, so that we can put all our effort against RLY-2608. Let's talk a little bit more detail now about our breast cancer portfolio. As we've said, the foundation of it is our PI3K alpha mutant selective franchise, but we also have a pan-mutant approach as well as a H1047R specific approach, and we have a CDK2 inhibitor and an ER alpha degrader.
Both of those two programs have been paused but stand ready to be restarted at any time. Why are we so focused on breast cancer? It's because it's such a huge opportunity. The market for hormone receptor-positive, HER2-negative breast cancer for adjuvant, neoadjuvant, and first-line metastatic treatment is over $27 billion. The emerging standard of care in this field over the last few years is created by now, standard of care being CDK4/6 inhibitors combined with endocrine therapy backbone. So for us at Relay, we see two, emerging trends. The first one is that there are now novel therapies in development that could supplant these existing standard of care.... And the second one is there's room for additional therapies to be stacked on top of the standard of care. But to do this, you need to have two things.
First of all, you need to be able to demonstrate efficacy on top of the standard of care, and secondly, you have to have a profile such that the tolerability of this third agent is gonna be able to be stacked on the first two. We believe 2608 has exactly that profile, because firstly, PI3K alpha is a therapeutically important target. 14% of all solid tumors have a PI3K alpha mutation, and it's concentrated such that 35% of hormone receptor HER2-negative breast cancer patients have this mutation. That's over 150,000 patients in the U.S. alone. So this is a significant opportunity.
Unfortunately, the current non-selective PI3K alpha inhibitors have a tolerability profile that is challenging, and you can see here the three most common adverse effects that lead to dose discontinuation and dose reduction are high grades of and high rates of hyperglycemia, diarrhea, and rash. Capivasertib, which is also approved in this population, also unfortunately has a very challenging tolerability profile. So all of this leads to dose discontinuation and reduced dose intensity, and unfortunately, that caps efficacy. And what you can see here is the response rates, the CBR, and the median PFS is capped. The CBR is in the kind of mid-40% range, and the PFS is around seven months.
We believe that if you could create a tolerable profile through creating a mutant-selective PI3K alpha inhibitor, that you could get greater dose intensity, you could keep these patients on medicine longer, and it would eventually result in greater efficacy. The second thing that I wanted to share with you is the great data that we saw at San Antonio, that showed that you could take a non-selective PI3K inhibitor and combine it in earlier and earlier lines of therapy. Roche Genentech reported out a study with inavolisib, palbociclib, and fulvestrant, where they showed a doubling of PFS, and that's a wonderful result. Unfortunately, it was only in a very small segment of the first-line patient population. It was in endocrine-resistant-only patients, and it was in metabolically selected patients that were essentially metabolically very fit.
They had to be, because they were trying to minimize the tolerability or maximize the tolerability profile of the triplet. So we believe that if you could create a much more tolerable safety profile with a pan mutant alpha, PI3K alpha selective molecule, you could address a much greater patient population than the inavolisib triplet could. So we think there are various ways for a PI3K alpha inhibitor to be successful in the clinic. First one, obviously, is to create a selective molecule. Secondly, that should then result in a more tolerable safety profile. And thirdly, that could result in greater efficacy. And fourthly, that could address a much greater patient population. The unfortunate issue, though, is creating one has been challenging, and the industry has used all the tools that it has and has been unsuccessful.
So we set out in 2016 to do exactly this with our Dynamo platform, and we created the first full-length structures using cryo-EM of both the wild type and the mutant PI3K alpha. We then built what was, at that time, the largest molecular dynamic simulation and identified a novel allosteric pocket, and that eventually led to the discovery of RLY-2608, which entered the clinic in the back half of 2021. We went through dose escalation in monotherapy and then started the dose escalation trial in combination with fulvestrant in April of 2022. And what you can see here is a very flat PK profile with doses above 400 milligrams BID exceeding 80% inhibition of the target, which is the target that we had set ourselves.
Then from a data cut from last summer, what you can see here is 17 patients at 600 milligrams BID, and it shows very early but encouraging signs of efficacy. In the five measurable patients, you can see that we have one partial response, and in the patients on the swimmer plot, you can see six out of seven of the clinical benefit rate-eligible patients reached the benchmark. And so remember, that's in context of response rates in the non-selective inhibitors of 20%, in terms of the response rate on the tumor dimensions and in the mid-40s on the CBR. We were very small N, but showing signs of target engagement, and what we were much more encouraged about at this stage is the tolerability profile.
What you can see here is the glucose, and what you can see is that we're seeing no grade 3 hyperglycemia at doses that we can believe from the previous slide are clinically efficacious. That grade 3 is something that we wanted to avoid and we believe is a clear sign that our molecule is selective and the Dynamo platform has done exactly what we'd hoped it can do. Now, if you look at this safety profile in context, you can see for RLY-2608, low rates of hyperglycemia, diarrhea, and rash. And if you put that in context with some of the non-selective inhibitors in the trials, you can see that various trials have been run with different metabolic entry criteria.
If you look at the generalized patient population, which is on one side of the slide, you can see a very challenging tolerability profile for the non-selective inhibitors. Whereas if you look at the other side of the slide, you see a very selective patient population with much more metabolically fit patients, and that leads to a better tolerability profile. You can see, although it's early, RLY-2608 has a great safety profile and we believe has the potential to have a safety profile that is much more generalizable in its use than the non-selective PI3K inhibitors are. So all of this gives us the confidence now to accelerate RLY-2608 as rapidly as we can towards clinical development. And so we will now accelerate our doublet.
So we've been through dose escalation, now it's complete, and we have 17 patients at 600 milligrams BID that were in the dose escalation cohort. If you remember back to July of last year, we commenced the 600 milligram BID expansion cohort. I can say that that is now fully enrolled. So we have now 37 patients that have been fully enrolled, 600 milligrams BID, and we're about to open another expansion cohort at 600 milligrams for a further 20 patients. And then for Project Optimist reasons, we'll open a 400 milligram BID 20-patient cohort. So as you move into the back half of 2024, we'll have an extensive data set on safety and tolerability for the doublet, and we'll have an emerging data set on durability.
As we come to the back half of the year, we will share this data with you, which should be very informative as we design our pivotal trial. As we've talked about, there is a much more extensive patient population that is in need in early and early lines of therapy. To address this, we've initiated a triplet trial with RLY-2608, fulvestrant, and ribociclib. We'll do this in dose escalation with the two labeled doses of ribociclib, and we'll also use the two expansion cohort doses of RLY-2608. Again, in the back half of this year, we'll share safety data, which will be early for the triplet. But all of this data should provide us with a huge amount of information as we think about design of the pivotal cohorts as we move into 2025.
So to summarize, we've initiated the 600 mg BID expansion cohorts. We've already enrolled the first 20 patients in that cohort. We'll share data as we come to the end of the year on the doublet cohorts from 400 and 600 mg, and we've initiated the triplet, and we'll share data in the second half of the year on that. So all of that is an extensive development program for RLY-2608, and obviously explains the deprioritization of RLY-5836, our second pan-mutant PI3K alpha inhibitor. So I'll move on to our FGFR2 inhibitor, RLY-4008. Unfortunately, these patients that have FGFR2 alterations have been underserved because they've only been able to be treated with pan FGFR inhibitors, which are plagued, unfortunately, with toxicities of hyperphosphatemia and diarrhea.
The industry has always looked to try and find a solution for creating an exquisitely selective FGFR2 inhibitor, which the theory would be to dial out some of these off-target toxicities and allow greater efficacy. Again, I'm pleased to say that we employed our Dynamo platform back in 2017 to create what we thought and what is now the first exquisitely selective FGFR2 inhibitor, and it went into the clinic in September of 2020. Here we are, just over three years later, and we've now treated 450 patients across a range of alterations and tumor types, and it speaks to our clinical execution capability. We've been able to share data that is validating across cholangiocarcinoma fusions, and we believe has the potential to be differentiated from the non-selective FGFR inhibitors.
Also, at the triple meeting last year in the fall, we were able to share data for the first time to show our RLY-4008 has a broad activity across alteration types, outside of fusions, and also outside of tumor types that are not cholangiocarcinoma. So our plan for this is to enroll the pivotal cohort for cholangiocarcinoma, which is now fully enrolled, allow the data to mature, which hopefully should mature across the course of 2024, continue to collect data in tumor types outside of cholangiocarcinoma and alteration types outside of fusions, and to look at the totality of the data in the second half of this year and determine a go-forward regulatory pathway, and we'll update you in the second half of this year. Moving on to our final clinical program, RLY-1971, which is a SHP2 inhibitor.
This was the first of our programs that went into the clinic, and as we've said, this was licensed to Roche Genentech in 2020, and we were excited about doing that transaction because we wanted to try and combine RLY-1971 with as broad a precision oncology portfolio as we could, and obviously, Roche Genentech was the ideal partner. We've been very pleased with the collaboration to date. RLY-1971 is in three different combination trials, firstly, with the KRAS G12C inhibitor, secondly, with their PD-L1, and thirdly, with their EGFR inhibitor. The data disclosure strategy here lies fully with Roche Genentech. All we can say is we are very encouraged by the way the collaboration is going, and we continue to retain meaningful economics in that. So to summarize, here we are, eight years later. The Dynamo platform has produced a very extensive precision oncology pipeline.
We have a rich range of catalysts as we look out towards the year ahead of us. We have an execution culture as a company. The last four years, we've shown the same slide around the objectives that we've set out to achieve. Each year, we've achieved every single one of the objectives that we've set out to achieve. This year, we hope will be no different, and we look forward to being back here in a year and going through all of the milestones that we've been able to achieve. And to summarize, those milestones are for RLY-2608, sharing the additional clinical data, both on safety and efficacy, in the back half of this year. For our triplet combination, which we've just initiated, we look forward to sharing early safety data in the back half of this year.
For RLY-4008, our FGFR2 inhibitor, we look forward to sharing data, both on the data that we are collecting, as well as of the regulatory strategy in the back half of this year. We will also reveal an additional target that the Dynamo platform has created. Obviously, the data disclosures for RLY-1971 lie with Roche Genentech. We have a tenured team that is stable and has an execution culture. We have $811 million on the balance sheet as of Q3 of last year, and that should take us into the back half of 2026. So we look forward to executing across the broad range of catalysts that we have. With that, I thank J.P. Morgan again and invite your questions. Thank you. So I'm joined by Don Bergstrom, President of Research and Development, and Peter Rahmer, Chief Corporate Development Officer.
Okay, well, great. And just a reminder, if folks have questions, just, we'll bring a mic over to you, if you have, just raise your hand. Maybe it'd be a good place to start by picking up on some of the updates in breast cancer with 2608. I guess having sort of nominated 600 milligrams BID as one of the expansion dose cohorts, and you'll also be looking to fill out the 400 milligram dose cohort. I'm curious to know sort of what informed, you know, 600 milligrams is the upper end. Perhaps you could kind of speak to a little bit of the experience at higher dose levels, 800 and above.
Maybe, Don, maybe you can take that one.
Yes. So, we had announced in August of last year that we would open the first expansion cohort at 600 milligrams twice a day, and that was really based on the totality of the data that we were seeing. We've yet to identify a maximum tolerated dose, so 600 is not an MTD, but it's a dose that we feel represents a potential optimal dose based on PK, PD, safety and tolerability, and early antitumor efficacy signals, as outlined by, by Sanjiv in his remarks. You know, I think we continued dosing through higher doses, 800 milligrams, 1,000 milligrams. We're still collecting data on those doses on the patients that were enrolled in those doses.
But as we continued seeing experience with the 600 milligram dose, we anticipated, based on looking at that PK curve, that a clear question that regulators, especially FDA, would have around dose selection is always: Can you go to a lower dose and see similar benefit for patients? So based on that, we opened the 400 milligram cohort to have that data to facilitate interactions with FDA. So I think where we are right now, we feel the 600 milligrams likely represents an optimal dose, but again, we're still collecting data on other doses. Doesn't rule out that we couldn't open another cohort at a higher dose to explore it, but I think we're really encouraged by the data we're seeing at 600 milligrams today.
Sanjiv, you I think did a pretty great job of sort of kind of speaking to the unmet need that's sort of left on the table in less metabolically fit patients with the competitor triplet update, excuse me, with inavolisib. Can you just maybe speak a little bit more to I guess the size of that opportunity? And I guess, is there sort of an upper bound in terms of metabolically unfitness, for the lack of a better term, that you think you may not be able to address with RLY-2608?
Look, I think that, and as we talked about, the opportunity is broad. If you just look at the absolute numbers of 150,000 patients in breast cancer a year with a PI3K alpha mutation, you just see the scale of it, and obviously, you start to look at the subsegments inside of that. We believe that there are opportunities in the later line, as we've talked about, in combination with fulvestrant, and there, the tolerability profile that 2608 could achieve could obviously allow us to get greater efficacy. But I think that the inavolisib data from San Antonio in the triplet showed an absolutely wonderful result of the doubling of PFS.
And so one of the questions that I think some people have had, obviously not us, is: Is there gonna be additional benefit from a PI3K inhibitor in combination with a, on a stack of a CDK4/6? The trial clearly showed there was. And so the INAVO120 study, we believe, only addressed about 20% of the addressable frontline patient population because of the fact it was in endocrine-resistant patients and because they put these metabolic criteria around hemoglobin A1C and fasting blood glucose. And so if you lift that, and the whole addressable patient population that remains is 80%.
I think the question for us is, as we generate data, and the safety profile that we've already created shows that in hyperglycemia, we're not seeing those high rates of Grade 3, which is, I think, what physicians are really worried about because that leads to potential hospitalization and having IV insulin. I think the question, as the data plays out across the years, how much of that 80% can we address? Our belief is that we can address a large chunk of that. And so I don't know, Don, if you have any, any additional comments.
Yeah, the only other thing I'd say, Sanjiv-
Yeah.
Can you flip back to the slide?
Yeah.
-that's got the comparison across the five groups by metabolic fitness? Yeah, I think it's really interesting when you look at the experience with the inavolisib and its Phase Ib trials, because I think Genentech was actually quite clever in terms of teasing out the impact on baseline metabolic status on the risk for hyperglycemia. And you can see in that arm F over in the far right, that reflects patients who are largely excluded from the INAVO-120 trial. So these are patients who either have, in that case, either BMI over 30 or an A1C over 5.7%.
As you can see, those patients, despite all getting prophylactic metformin, still had a 70% rate of any grade hyperglycemia and a 44% rate of grade three hyperglycemia with blunted efficacy of the triplet. So I think what that speaks to is that there is this significant population of less metabolically fit patients that are very challenging to be able to address with a non-selective inhibitor, given the hyperglycemia liability, even with prophylactic metformin being used. In contrast, our population for RLY-2608 includes a number of these patients who either have BMI over 30 or hemoglobin A1C over 5.7%. As shown here in the slide, we've yet to see grade three hyperglycemia.
Just consistent with what Sanjiv's saying, we think with loosened metabolic inclusion criteria, there is a potentially much larger population that we'd be able to address with a selective inhibitor.
Making you work for it.
Indeed. So you have two expansion cohorts at 600 milligrams. I guess one is fully enrolled, 20 patients, and another one that opened in the fourth quarter. I guess, is there sort of a meaningful difference between the patient populations comprising those two cohorts?
You want to take that one?
Yeah. Sure, yeah. The only real difference in the second 20 that we've just recently initiated, one of the things that we're seeing, given that we are the only mutant selective inhibitor open for all mutations right now in clinical development, we do see a little bit of an overweighting of kind of the non-hotspot mutations. And so we will try to get a bit more balance back to the study by making sure in this next 20, there are only helical or kinase domain mutations. And we'll also restrict that to patients with measurable disease only. And the goal there, again, is as we get, you know, that this should grow the 600 milligram population to about 60 patients and have pretty good distribution to what we would see in the general patient population.
Okay. In another meeting we were all part of, somebody asked a question about recruitment rates in the INAVO120 study. Kinda using that perhaps as an analog for what enrollment might look like in a pivotal study with RLY-2608. That being said, you ostensibly would have a wider field to pursue in terms of addressable patients. So I guess, maybe you can just kinda talk a little bit about sort of that timeframe and how you might be able to sort of improve on that if you're pursuing a pivotal study.
I mean, the first thing is this is not a small patient population. So as we talked about, the, you know, the numbers here are large, so hopefully, this is not a rare disease. The second thing is the INAVO data obviously removes the doubt around, is there gonna be therapeutic benefit from adding a PI3K alpha inhibitor? And so I think we-- it's have a wind in our sails already, and maybe, Pete, you can just talk about the, the length of time.
Yeah. I mean, if you look at that, their study, they enrolled that. They did, they ran that over the course of about 3.5 years or so. It was 325 patients enrolled across 225 or so sites globally. Certainly, they have a very robust clinical trial infrastructure to execute that against. Part of the reason why we were so excited to partner our SHP2 inhibitor with them. As we think forward to us running our own global randomized phase III study, I think as Sanjiv alluded to, there's a number of tailwinds.
Not to mention our own data, which we would intend to share in greater detail we get to the back half of this year before we would anticipate, you know, the quickest kickoff that we could get to of a randomized phase 3 study. Which, you know, for us, we have yet to have a regulatory interaction, so I don't wanna put the cart too far before the horse. But we think that we might be able to have the data in hand to start those discussions this year.
Hello. Rune Vestermark, Copenhagen, Denmark. So as a diagnostic developer or biomarker company, I love when someone say they have a precision medicine pipeline. Can you speak a little bit to how your strategy is towards biomarkers, and is it something you do yourself, or are you partnering with other companies?
You wanna take it, Bill?
Yes. So, you know, I think there's... It's really two parts to how we're approaching this. So one is in the context of our clinical trials, especially in our non-pivotal trials, how are we recruiting patients? And I think in these early trials, we are using local testing to recruit patients. Many of the centers we're using are running their own panel-based diagnostics and are routinely identifying patients who either have PI3K mutations or FGFR2 alterations for enrollment.... We then are pursuing confirmatory testing on a centralized platform using both plasma-based diagnostics for circulating tumor DNA and tissue-based diagnostics. We have presented at an earlier scientific conference the concordance between plasma and tissue for FGFR2 fusions, where we've shown high concordance. And it's been shown by others for PI3K that there's high concordance between plasma and tissue.
Then obviously, there's the question as we move into pivotal trials and start developing companion diagnostics, we are working with partners with experience in the companion diagnostic space and anticipate that, you know, we will work with partners to bring a companion diagnostic forward. Again, for both FGFR2 and PI3K, there are existing panel-based companion diagnostics today. Foundation Medicine has both FGFR2 fusions for cholangiocarcinoma and PI3K mutations for breast cancer on their platform. But we anticipate, you know, as we go forward, would find the optimal partnering solution for bringing a companion diagnostic to market.
There's somewhat of an ongoing debate about whether selective inhibition or mutant selective inhibition of alpha is the key to extending clinical benefit in breast cancer, or whether you might need some contribution from wild type or other PI3 kinase isoforms. Can you sort of speak to, you know, your present thoughts on that paradigm and the extent to which the INAVO120 incrementally informed that hypothesis?
Don, do you want to take that one? It's our favorite question, this.
Yeah, so, I mean, I'll start with what our experience has been. And we've had the opportunity now across all of our PI3K programs. We've made a number of different inhibitors with various ranges of mutant selectivity, and that's allowed us to go and actually start to ask whether we can isolate the contribution of potential wild-type suppression to the activity that we see.
I think what I'd say is that when we go into models that are truly PI3K driven, you could take a model like inavolisib that shows you almost no mutant selectivity, or, you know, molecules that are really, say, H1047R specific, that show you a wide window in mutant selectivity, and there's no decrement in activity or efficacy for the highly mutant selective molecules, which would suggest that there's little contribution of inhibition of the wild type to the mutant. Now, it's hard to tell from the INAVO120 experience, because presumably they are getting robust mutant inhibition, which, you know, is associated with some of the glucose signal that you're seeing there.
So, it's hard to really tell whether that is informing the question, but I think on everything we've seen so far, both preclinically and now with our early data in the clinic with 2608, would suggest that the contribution of wild-type inhibition is negligible.
Yeah, I don't think we would characterize it an overly scientific, robust debate, but certainly a little bit of a debate nonetheless.
Sure. I guess adjacent to the PI3 kinase debate is one node, you know, down in the pathway, AKT. And you do have capivasertib now approved here. I guess, can you talk a little bit about sort of the what that represents as a sort of a competitive benchmark as your program evolves, or what it might represent operationally, perhaps, as a headwind to conducting your, you know, future trials?
You want to take it, Pete?
Sure. Yeah, I think we would actually welcome the experiment of going head-to-head against capivasertib. It is a, you know, by all traditional measurements, probably more of a multi-kinase inhibitor than what I would characterize as the current generation of targeted agents. It brings with it a host of side effects that are not contributing, or we would contest, don't really contribute to the activity of the agent and are just hindering dose intensity. And that's, you know, precisely what we are solving with 2608. Mutant selectivity allows you to hit the target actually driving the cancer harder, maintain dose intensity, and aggregate some of those off-target side effects to drive to greater benefit for patients.
We do think, and I think, you know, we're hopeful that our data will continue to demonstrate that throughout the course of the year, that in a head-to-head study against capivasertib, we could bring much greater benefit to patients.
Okay. All right. Maybe just a question on lirafugratinib, RLY-4008. I guess if we're thinking about, practically speaking, in terms of the pivotal development path forward for that agent, I mean, there's the CCA population and one part of the barbell, the other. And perhaps a non-CCA tumor-agnostic bucket that you could pursue. Maybe you can just kind of set the stage in terms of what additional, either data or regulatory interaction kind of needs to transpire in order to you know, be able to have a solid view on whether a tumor-agnostic pivotal path is on the table for that agent.
Yeah. Fir st of all, good for you on trying to pronounce the name. We keep saying 4008.
Yeah, we can't do it.
Yeah, I think, you know, the main thing we have to do is we have to generate more data. This is the simplest answer. We have the CCA pivotal cohort fully enrolled. That's maturing. As we said at the triple meeting this past October, we're pausing regulatory and commercial activities against cholangiocarcinoma to let the tumor-agnostic data catch up. I think what we'll do is let the tumor-agnostic data mature a bit further, add some more patients, get some more durability, probably have an FDA interaction.
With both more mature data in hand and some feedback from the agency, we can come back and probably have a bit of a robust discussion as to what is the path forward for 4008, and is the data generated as such to really justify additional resources for us to put towards it?
Okay, great. Okay, good. If there are no questions from the floor, I think we'll leave it there for time. Thanks very much to the Relay team, and thanks, everybody, for joining the session.
Thank you.