Thanks so much for joining us. I have to read some disclosures, and I don't have them printed, so I'm going to grab them from my phone. Sorry. Thanks so much for joining us here to discuss IDEAYA. We've got Yujiro Hata and Andres Briseno. I'll let you guys introduce yourself in a second, but before I get started, I do need to read some disclosures. We are required to make certain disclosures and public appearances about Goldman Sachs' relationships with companies that we discuss. The disclosures relate to investment banking relationships, compensation received, or 1% or more ownership. We are prepared to read aloud disclosures for any issuer upon request. However, these disclosures are available, and our most recent reports available to you as Client Center or firm portals. Okay, with that out of the way, welcome. Thanks so much.
Maybe we can just start kind of high level. I'd love to get a bit of an overview of IDEAYA, what you do, and focus kind of on the key value drivers over the next couple of months.
Sure. Well, thank you, Corinne, for the invitation. We very much look forward to participating again this year. So IDEAYA Biosciences, we were founded about nine years ago. We're a leading precision medicine oncology company with a significant focus in an emerging area called synthetic lethality. Within that, we now have four first-in-class programs in the clinic, darovasertib, which is a PKC inhibitor in a registrational trial for frontline metastatic uveal melanoma. We also recently just presented in an oral presentation at ASCO in the neoadjuvant uveal melanoma setting. Beyond that, we have IDE397, a phase II MAT2A inhibitor targeting MTAP deletion. Our third program is a PARP inhibitor also targeting HRD solid tumors, as well as Pol Theta, our fourth program in the clinic, also targeting HRD solid tumors.
We have a fifth program that we're targeting to get into the clinic with Werner helicase before the end of the year. We have two more candidates. Hopefully, we'll have time at the end that we're targeting to deliver by the end of the year. So, you know, we do anticipate hopefully 7+ , possible, first-in-class programs in the clinic in the next couple of quarters.
Great. Maybe let's start with the most recent update, because you did have data last week in an ASCO in the neoadjuvant uveal melanoma space. I mean, maybe let's just start with a brief refresher on what exactly you presented.
So the data that was presented was from our Australian investigator. It was 15 patients worth of data, and within that, you know, at least our feeling is that the data well exceeded our expectations. So in quick summary, I would say, you know, we saw a significant tumor shrinkage, and, you know, I think that was great to see as monotherapy. Corinne, as you know, we're testing it as a combination in the metastatic setting, but it's pretty clear to us in the neoadjuvant setting, monotherapy is sufficient. And then, lastly, was really around the eye preservation rate. So all of the patients that were enrolled into this study were basically on track to get their eye removed because their ocular tumor was of a certain size or location.
And remarkably, within that group, three-quarters or 75%, we were able to get them off of the enucleation track. In addition, we did present an early snapshot of our data. We've enrolled now, I believe it's 43 patients. So enrollment is taking off. Within that, we shared 8 patients worth of data that have been on for more than 4 months, and we see very consistent results.
Great. Maybe you could contextualize for us how, like, the 75% preservation of the eye, how is that clinically meaningful, or how does that compare?
So I think it's really important to first start with the unmet need. So there are no approved therapies, systemic therapies, for both neoadjuvant and adjuvant care. You know, when we started this journey about a year, a year and a half ago, at least in the clinic, I mean, our expectations when we got the feedback from the KOLs is that even a 10% eye preservation rate would be a game changer in this indication, because the alternative is we're going to remove your eye for those patients. So, that was our expectation going in, and obviously, you know, based on the early data thus far, we're just well north of that type of target. So hopefully that will bode well, as we now are preparing for this Type C meeting with the FDA.
Great. And we do expect another data set from the company-sponsored study that you referenced. Remind us the differences between those two studies and what we, how we should think about what that trial will show?
Yeah, so that's correct. We're guiding in the second half of this year, two key updates, including from our phase II company-sponsored study. It is going to be a larger data set. We anticipate it'll be 30 patients or more. We do want to have ideally 4-6 months of follow-up, for each of the patients to really see what we hope is, really the full potential of the molecule. Probably the main difference between, our company-sponsored study versus what we saw at ASCO is that not only will we have enucleation patients, but we'll have these smaller to medium-sized tumors as well. We are considering for our next update in the second half, do we combine that with the regulatory feedback, or do we separate them? So that's still under discussion.
But, you know, I think either way, we're really excited to give that update in the second half.
Yeah. And how do these data and kind of the robustness of results inform your strategy as you think about neoadjuvant and adjuvant uveal melanoma on the forward? And what do you plan to request as you go into this Type C meeting with the FDA?
Yeah. So first, our interest and intention is to evaluate this molecule both in the neoadjuvant and adjuvant setting. From a regulatory perspective, in this upcoming meeting in the second half, our primary focus will be to get endorsement for what we hope should be an accelerated approval study, specifically in the neoadjuvant setting. And as it relates to that, our plan is to bring forward both an accelerated approval study design, as well as for full approval. So that's our objective for this upcoming Type C meeting. We would then, at least our current plan, is to then go back to discuss the adjuvant trial after that.
Okay. This approach obviously would be a pretty, like, paradigm-changing-
Mm.
A treatment paradigm, treatment regimen in uveal melanoma. So I guess, what do you think you need to show to change behavior as you think about going to the physicians and convincing them to use this in neoadjuvant and adjuvant uveal melanoma?
Yeah, so I think typically in these kind of situations, it's really driven by three things primarily. First is the unmet need, and the great news here is, you know, at least personally, at least we think there's no greater unmet need than the neoadjuvant setting in uveal melanoma and oncology today, as we just walked through. Second is, what's the risk-benefit profile? And here, Corinne, as you know, we've evaluated darovasertib as a monotherapy agent for years. You know, we've been in, you know, now over 100 patients as monotherapy, and at least our perspective is that the AE profile is highly manageable. And we also know from the metastatic setting, we've been able to keep patients on the treatment for multiple years. So that's the second.
And then finally, third is, what is the effect size we're seeing? And at least right now, based on parameters of tumor shrinkage, we'd like to use response criteria as potentially the primary endpoint for accelerated approval. And then second, as we talked about, at least in the enucleation patients, the preservation rate we're seeing is so well north of what we were hoping for when we started this process.
Yeah. Maybe before we talk about the metastatic setting for a bit, how are you thinking about the market opportunity here in neoadjuvant uveal melanoma and adjuvant as well?
Yeah, so I, I think a good place to start is, you know, there is a competitive molecule that was approved in the frontline setting of HLA-A2 positive metastatic uveal melanoma, and that patient population, we believe, is, you know, roughly about 1,000 patients. So if you start from there, we think the primary setting uveal melanoma is at least 10 times that size. And so I think the good news there, at least on this other example, we already have real sales numbers, and I think, as you know, when you're trying to project into a new market, that becomes one of the key aspects. But here, we have real numbers to rely on. And then how we get to that 10X number, one is purely annual incidence.
We know in the pre-metastatic setting, the annual incidence jumps to about 8-10 thousand patients, you know, which is almost double. The next is around duration treatment. So, you know, our CMO recently mentioned at ASCO that we are in the process of amending a protocol where we would treat up to 12 months in neoadjuvant, up to 12 months in adjuvant in our existing phase II study. So that's another multiple, would just be duration. And then lastly is around total prevalence. So when you look at the metastatic setting, there's not a significant jump between annual incidence and prevalence because OS is so short. That's not the case in the pre-metastatic setting. So we know that there are a lot of patients that are sadly not doing anything.
They're doing wait and see, because there's no good therapies available for them, and so we should capture a portion of that, and that's why we think this is a, a very much of a significant opportunity. And duration, you know, frankly, we, we could really be at the start of this journey, and so there could be a subset of patients that want to stay on it as long as they can.
Okay. Maybe we'll take that as a segue to the metastatic setting. So maybe first, just you're enrolling patients in a registrational trial. When are the next expected updates?
Yeah, so the primary focus right now, in terms of updates, on the metastatic frontline trial that we have started last year, is where are we in enrollment relative to the target? So, most of our analysts are projecting a late 2026 launch, so we've been pegging our enrollment targets to, hopefully enable that timeframe. So what we can say right now is that not only are we on schedule, we're slightly ahead of schedule. So that's great, and we're still in the process of activating sites, in particular, in Europe. As opposed to the readout here, the primary endpoint is progression-free survival, which is, would be the primary endpoint for accelerated approval. There, all that really matters is the hazard ratio, so this will be a blinded study.
That will come, you know, once enrollment is complete and sufficient follow-up has occurred.
Remind us what the prior study showed and what this study is powered to demonstrate with respect to PFS?
Yeah, so we haven't gone into the specifics of the powering assumptions, but really the quick summary is historical PFS, and this indication that's across half a dozen trials has been in that two to three-month range. In the frontline setting, data that we presented in an oral presentation at ESMO last year, we had a PFS that was higher than seven months, and the subgroup of patients with hepatic-only disease, we saw a PFS that was approaching a year. So by every standard, we're just, you know, we're significantly above what we've seen before, and that's what gives us the confidence, and so I think the powering assumptions we've placed is that we're gonna hit that type of objective.
Okay. And as you mentioned, there is a competitive agent in this space, so talk to us about how you think about the market opportunity in metastatic uveal melanoma?
Yeah, so in terms of metastatic uveal melanoma, you know, here I would start with annual incidence. You know, and this is predominantly in the U.S. and Europe. We believe it's about 4-5 thousand patients annual incidence. Total prevalence is probably in that 10-12 thousand patient range. Right now, there's only an agent approved in HLA-A2 positive. We believe that represents about a third of that population, and the remainder is HLA-A2 negative, where there's nothing approved, and that's the significance that we're running a frontline trial in that setting. But I would say important to highlight that our drug works irrespective of HLA-A2 status, so we are not giving up on the A2 positive.
So there, assuming approval in HLA-A2 negative, we would continue to publish data in a peer-reviewed setting in positive, and target to get on compendia for pricing and reimbursement.
Okay, great. Are there any other indications where you see a role for darovasertib or the combination? Maybe you can just expand on what those look like.
Yeah, so I would say our primary focus is to have this agent penetrate the patient journey in uveal melanoma because we think the opportunity is so significant in neoadjuvant and adjuvant, beyond the metastatic that, that we just walked through. I would say beyond that, our probably next biggest focus is in, cutaneous melanoma. So we know that GNAQ/11 is present in about 4% of skin melanoma. We've already shared some data publicly, and, and really, the quick summary is the data looks very similar to what we see in uveal. We're seeing, responses there, and we're seeing quite significant durability, which is encouraging. So there, the primary focus is, really around finding these patients and enrolling them.
Okay, great. Maybe we'll switch gears here and go to IDE397. Maybe first, it's a MAT2A inhibitor being developed in patients with MTAP deletion. Maybe if you could just briefly remind us of the mechanistic rationale for this molecule and how it differs from the PRMT5 inhibitors that are also in development here.
Yeah, so here, the patient selection biomarker in question is called MTAP deletion. Corinne, as you know, is a very large biomarker, represents about 15% of all solid tumors. There are probably two primary targets that have been pursued today in this pathway. One is PRMT5, as you mentioned. There are these second-generation molecules, which are called MTA-cooperative PRMT5, and the second is MAT2A. So the similarity is that both of these molecules, the patient selection biomarkers, MTAP, the way they do it is different. So I'll focus on MAT2A primarily because that's our asset in phase II, which we're, you know, clearly first in class or have the opportunity to be first in class there. And here, this is all around depleting SAM levels.
So, MAT2A is involved in the conversion of methionine to SAM, and if you inhibit MAT2A, you deplete SAM levels. And we know the role and importance of SAM has several key important factors, including being the key substrate for protein methylation of PRMT5. And that's where if you look at all the various CRISPR screens, MAT2A comes out as one of the top hits for synthetic lethality with MTAP. The second, which I won't get into too many specifics, but is around the combination rationale with PRMT5. And here we know, for those second-generation PRMT5 inhibitors to work, a critical aspect is to be MTA, to be bound to the binding pocket of PRMT5. MTA and SAM compete at that same binding pocket and have a similar KD.
So it's not just about having elevated MTA, it's also about what are your levels of SAM.
Mm-hmm.
So if you can deplete SAM levels, you really influence the stoichiometry of these two key cofactors. So, beyond that, we have a lot of data that we've been generating independently. We've now looked at over 20 models. We've been doing great work with Amgen. We just actually ran into Jay Bradner in the hallway.
Mm-hmm.
We believe the mechanistic rationale of this combination is significant. Corinne, I know you've been hearing us over and over on this one. Out of all the various combinations, one can pursue an MTAP deletion. We continue to believe this is the high conviction. This really is-
Mm-hmm
... the critical experiment being run clinically. At least from our vantage point, the primary reason why is there's a lot of various bypass and resistant mechanisms that we've identified specifically related to PRMT5-
Mm
including around this change of MTA levels. And so a lot of that data we now have.
Mm-hmm.
We are planning to publish that work to really hopefully educate the public on why this is the combination people should focus on.
Okay, that's helpful. We did see a number of the monotherapy updates-
Mm
around the PRMT5 inhibitors last fall. I guess, how do you think about the differentiation potential of a combination approach?
Yeah, so I would say, first and foremost, I would say two observations there. One is when you look at precision oncology in general, and I'm gonna generalize here, but obviously, it's not just about seeing responses. Ultimately, you need to drive durability-
Mm-hmm
... and, you know, we saw that very much front and center in the KRAS space.
Yeah.
Now the question is: What is the combination that makes significant mechanistic rationale that might have the opportunity to drive that durability? In particular, if you want to get into the earlier line settings of tumor types that we're interested in, including lung cancer and bladder cancer.
Mm-hmm.
Right out of the gates, the assumption, at least I think, should be, you're gonna need to go in combination if you want to really penetrate that frontline setting-
Right
... and hopefully address durability. So I think if I were to put at the top of that list, Corinne, what we're trying to really achieve through this combination is to deliver that durability, which - if you look at the swim lane plots that have already been published by the second-generation PARP inhibitors, as you know, one was presented at the Triple Meeting. At least personally, I just don't believe that durability is there yet, is there right now. So I think that's gonna need -
Mm-hmm.
to be delivered through this type of combination.
Yeah. You did also report some that you'd hit RP2D for the monotherapy a couple of weeks ago. At a high level, obviously, you didn't share the data, but what are you seeing in those monotherapy cohorts, and how does that kind of inform your expectations for the combinations?
Yeah, I would say here, Corinne, I think, you know, you're probably seeing some of our messaging communication of all this on this one. I would say we're becoming growingly excited about what we're seeing. You know, I appreciate that, you know, it's taken a bit of time to really you know, for us to identify what the right tumor types are, including squamous lung in particular, and then second, to really identify the right dose. So as you know, we had started the expansion phase probably about a year and a half ago, and through that, we were looking at roughly about four or five different doses. And within that, we narrowed it down to this one, 'cause this is where we are seeing, A, the most responses, including confirmed responses-
Mm-hmm
... by RECIST, and also, where we feel like we can treat these patients longest from an AE perspective.
Mm-hmm.
It was really finding that, that sweet spot. You know, we are becoming more and more confident on what we're seeing on the monotherapy side. But with all of that said, our continued central strategy in this pathway will continue to be rational combinations. And hopefully, what you'll see, by the time we end the year, is that IDEAYA will be viewed as one of the leaders in MTAP deletion, with one key category, which is the breadth of our portfolio in MTAP. We have- we're not just investing in MAT2A, we've invested very broadly across this pathway, and you're gonna start hearing more of that as our candidates start getting delivered.
Okay. I think I've got a question on that later-
Yeah
... but for now, I'm gonna stick-
Absolutely
-with the Amgen combination.
Sure, sure.
Just remind us the specifics of the collaboration and kind of where you are in that clinical study, when we could get next results, like, next data?
Yeah. So I think first, you know, we just start with our collaboration with Amgen. Look, I think, you know, we give them a lot of credit. You know, they jumped into a novel, novel combination with us around the strong mechanistic rationale, and I do think Amgen deserves a lot of credit for that. And I know the teams have generated a lot of exciting and important data, in particular, also on the preclinical side. You know, we've already published together at AACR. The construct is that it's a 50/50 cost share. Amgen is the holder and the sponsor of the IND and running the trials globally.
Mm-hmm.
The focus on the expansion phase will be in lung cancer, and the dose escalation, there is no tumor type focus, although all the patients are MTAP deletion.
Okay, and maybe we'll go to it now.
Yeah.
You've talked a little bit this year about some preclinical work around the MTAP space. I guess, what are you optimizing for relative to your existing, like, asset in the space as you think about bringing new candidates forward?
Yeah. So I would say, on the, on the combination specifically with Amgen, what are we optimizing for?
No, the, your next asset.
Okay. So here, you know, I would say our central focus on the next candidate, so one, they're not in the MAT2A target space. So first, I wanna just get that-
Yeah
... off the table. I would say our primary focus is really to identify the right molecules that are either competitive in the arena, but in particular, combine well with IDE397.
Mm.
We think IDE397 is a great molecule, and the advantage we have is we can evaluate our compounds preclinically to ensure that they combine well, whether that's DDI-related efficacy, so on and so forth.
Mm-hmm.
So I would say, Corinne, that's our primary focus. That doesn't mean we may not independently advance them as monotherapy, but our primary focus is to enable combinations with IDE397.
Okay. Maybe we'll switch gears get again and go to IDE161, which is the PARP inhibitor. I guess for that program, maybe you can just refresh us on what you've shown in terms of clinical data to date.
Yeah, so we've shown early clinical data, and the particular early clinical efficacy data, where we have reported early responses in the dose escalation. Here. You know, there, we did show a patient in CRC as well as endometrial cancer. In terms of the tumor type focus, we are also looking at both prostate cancer as well as breast cancer. Personally, I think from a monotherapy vantage point, probably the most opportunity for an agent like this is to focus on tumor types where PARP inhibitors are not approved, including in endometrial and CRC. And then the remainder of the PARP focus will likely be around some of these key rational combinations that we've been working on for about two years.
As you know, we recently announced a partnership with Merck to do the combination with Keytruda and endometrial cancer, and that's irrespective of HRD status. So that's looking at high MSI as well as microsatellite stable. We have about another half a dozen conversations going that we think could enable a whole class of cancer therapies, and that's what you'll see that strategy unveil from now to the end of the year.
Okay. And in terms of... I guess you've talked about this, you talked about this a little bit, but in some of your programs, you're really focused on the combination approaches. How do you think about this one as a monotherapy versus a combination, and, and in which indications like, which of those two strategies makes the most sense?
So I would say for IDE161, in endometrial and CRC, I think they're, you know, more monotherapy activity we can demonstrate, I think obviously, the better. And because PARP inhibitors are not specifically approved there, I think there is an opportunity. I think it's just too early. We need more data to demonstrate that. But I would say similar to a lot of our other programs, in particular in the metastatic setting, I would say our significant focus is around these key combinations that we're putting in place. So the Merck Keytruda one, we're excited about, and then I would say this next wave of combinations you're gonna start seeing from that program-
Mm-hmm
... we think are highly compelling.
... Okay. In the past, you've put out some press releases in terms of the early results you're seeing, et cetera, but as we think about the next clinical updates that you wanna share, how many patients should we be expecting?
Mm-hmm.
What kind of duration? How many doses? Just talk to us about those parameters.
Yeah, so we have not given specific guidance on when the next data update will be for IDE161. We've guided towards program updates. We actually gave some updated guidance recently in our last earnings, that we're gonna target to pick an expansion dose for phase II in the second half of this year. So I think here, what I could highlight is that we've cleared multiple doses. We're continuing to do the dose escalation on that front, so hopefully we'll be able to achieve that objective. And then I would say second is around enabling these additional combinations. So that would be the primary focus for us-
Okay
as we close out 2024.
Okay. There are some other assets that have sort of come into the space behind y'all. I guess, how are you thinking about the competitive landscape as it's evolving with respect to PARP inhibitors?
Yeah, no, I think. Look, I think we've been on the forefront of PARP, and, you know, with our academic collaborators at CRUK. And I think this target is a target that just makes a lot of sense in the DNA damage repair area. I think it's always great when you have people that are trying to follow you into the clinic. And I think that's great for the whole field. You know, more data we generate quickly, the better. So but we think IDE161 is gonna be a very tough molecule to beat.
Okay. You're also working through some pre-IND work for a Werner helicase program. This has obviously been a pretty tough target to crack. So what enabled you to generate the breakthrough in terms of getting a Werner helicase program?
Yeah, so yeah, you're—I mean, you're right, Corinne. It's been a very long journey with Werner helicase, so you know, maybe you know, taking one step back on this target. This was one of the earliest targets that we started on at the founding of IDEAYA. It's been, you know, over a seven-year journey of drug discovery, and one thing is very clear to us with Werner and the synthetic lethal with high microsatellite instability.
It is, if not the most robust, one of the most robust synthetic lethal interactions in the cancer genome, and that's been verified not just by our work, but other great work that's been published in important papers like Nature, including from the Broad Institute, as well as the Sanger, which you may recall there were a couple of, back-to-back papers that were published on that front.
Mm-hmm.
One of the real challenges from a drug discovery perspective with Werner, as part of that, was A, this is a helicase target class, and helicases are notoriously difficult to drug. And, you know, it took us probably about four years to even just solve the crystal structure for Werner, and then it took us another year, year and a half, to get a co-crystal structure to be able to do structure-based drug design. And we can say with fairly high confidence, without a structure, you really have no path forward against this. And we ran every single screen you could think of chemically against this target. And the last piece that I would mention is, you know, GSK deserves just a tremendous amount of credit. They've been phenomenal partners.
Mm.
worked with us side to side. We just had a never-quit attitude, and-
Yeah.
Yeah, we're excited. You know, the GLP tox data is now behind us. Not only do we anticipate filing IND this year, but, you know, we hope to have our first patient dosed by the end of the year.
Mm.
And at least based on where we see the competitive landscape today, we do anticipate that we should be the first biotech company, at least, to have the Werner helicase inhibitor in the clinic.
Mm.
and we do believe we have a potential best-in-class molecule. We're not saying the specific feature, that's something that GSK has asked us not to disclose, but there's a very specific feature of this molecule, relative to the two competitors right now in the clinic with Novartis and Roche-
Yeah
... that we think could have a significant importance once we're in the clinic.
Of course. I know there's some limitations around what you can share, but could you double-click a little bit-
Yeah
On the competitive landscape? There's a couple of different features of the molecules that are up for debate.
Mm-hmm.
I think most obviously, the covalent versus non-covalent. How do you think about the parameters that are important as you're solving for this Werner helicase structure? And, could you just give us, like, what you can in terms of that competitive landscape?
Yeah. So that's exactly correct, Corinne. So one is I'm really happy you're focused on this target. I think we'll hopefully look back in the next 5-10 years and realize that Werner was perhaps one of the most important targets discovered in precision oncology. So it's great that you're focusing on this. And that's correct. Chemically, so far, based on what's been published, the main distinction of what's out there is around covalent binding versus non-covalent. We can't comment about what our molecule is-
Mm
... because, we haven't stated what that structure is at this point yet. But we do think there could be significant importance of that, whether it's covalent or non-covalent. The second, which I can state because we have mentioned this publicly, for this target, you wanna see regressions. And so, you know, we've seen a couple of other preclinical data sets out there publicly, where you're basically only seeing stasis. We think that's a lot less interesting, and we would say that's probably an inhibitor that was several generations ago. Lastly, there has been some combination data published preclinically, I believe around with the irinotecan, specifically around chemo combos. At least personally, we think that's probably less interesting versus specifically PD-1 combinations-
Mm
... which obviously has an important position in the high MSI setting.
Sure. Okay, maybe, maybe talking about your other partnership with GSK, you do have the Pol Theta program. So if you could just give us a quick update on that one. I know it's not been quite as much of a focus-
Yep.
From the investor side. So where are we there?
Yeah, look, I think Pol Theta helicase in many ways represents a lot of what IDEAYA is about. Another first-in-class molecule, another helicase inhibitor, and at least that we're aware of, we believe we are the first pharma or biotech company that has delivered back-to-back helicase development candidates in oncology. This primary focus, as I mentioned, is around HRD solid tumors, but specifically in combination with PARP, and in particular, GSK's niraparib. So if we kinda cycle back on PARP and what's happened in the last couple of years, Corinne, as you know, one of the challenges of PARP inhibitors is that they have not hit their survival endpoints. In fact, you know, label changes has, have occurred. And so now the question is why? You know, why are they not hitting some of these survival endpoints?
Mm.
We think a lot of that is related to acquired resistance to PARP inhibitors. If to break out that feature of acquired resistance to PARP inhibitors, we believe BRCA reversions is really one of the key problems that PARP has to face. If you dig into BRCA reversion, pathways that's activated is a backup DNA repair mechanism.
Mm
... which Pol Theta is that first step. There's domain, one is the helicase domain. Since our earliest founding, and the helicase domain, and that's ultimately what we brought into the clinic with GSK. So this is gonna be exciting. I think it will hopefully make a big difference for patients. I think ultimately, hopefully, where this will end up, this may be many years later, but GSK, you know, we hope would do a frontline study, you know, likely head-to-head against PARP, and hopefully deliver a great result as it relates-
Mm
... to OS.
Okay. You know, we've kind of done a really quick run through-
Yeah
... a very large pipeline, but kind of underlying all of that is the drug discovery capabilities. So maybe you could just spend a minute talking about how you leverage AI and machine learning to further the drug development that you guys have all done, and where do these technologies kinda fit in your discovery process?
Yeah, so I would say our platform, which is a highly integrated platform for several key areas, from target discovery, biomarker discovery, and a lot of what we just walked through, is what we think are world-class leading capabilities around drug discovery. And within that, there's several components, including a proprietary chemical library that we've created related to synthetic lethal targets we've identified. The others are on computational chemistry and structural biology in particular. And there, I think it's pretty safe to say we have leading capabilities there, based on the fact we've delivered a MAT2A inhibitor in the clinic, PARP, first in class, Pol Theta, Werner. What's powered a lot of those capabilities is around AI machine learning. And I would say the primary piece that...
As you know, in the AI machine learning area, in life sciences, it is being applied quite broadly in a lot of different areas, including, you know, interpreting clinical development data, putting regulatory even documents together, obviously on the target biomarker discovery side, as well as drug discovery.
Mm-hmm.
Our singular focus right now with that specific technology is in the area of drug discovery. And we've now basically generated data where we know that AI ML has actually quite significant capabilities as we're optimizing certain features of the molecule. So we know that if you just apply it broadly across, it's not as effective, but if you know what features of the molecule where AI ML actually can be quite informative, it can really accelerate what you're doing. I would say what probably differentiates us the most from all... targets that people... work there that's been done, it's been on target... think is, is less interesting as a sector.
Mm.
And that's where we hopefully will continue to differentiate ourselves moving forward. So look for us to actually double down-
Yeah
in this arena. This is, actually quite a big topic for us internally.
Okay. Any other assets in the pipeline or in early stage development that we haven't talked about, or that you wanna make sure before we wrap up here in a second?
Yeah. So I think just the last part, we would mention, you know, as we talked about in the very beginning-
Mm
... we have several. One is in the MTAP arena, and there we have two programmatic efforts there. One is a bit more advanced than the other, probably about a few quarters apart. And as we mentioned, the importance of wholly owning what we think are several key combination opportunities with IDE397.
Mm.
The second, you know, we're actually gonna hopefully note it for the first time here at your event, because of the interest around KAT6 from ASCO.
Mm-hmm.
We do have an opportunity in the KAT6 pathway that we're triangulating around in terms of a candidate. And this would be what we think is a first in class profile, potential best in class profile. So, but it's-
Mm
... it's in the specific pathway.
Really burying the lead here.
So,
You're burying the lead here. It took till the end of the thing to tell us what you got.
Yeah, exactly. Yeah. But I think one of the primary parts I would mention around this program and the KAT6 pathway is, you know, we've been working on it for several years, and we had optimization.
Mm-hmm.
The team's made phenomenal progress this year. And one of our key focus areas to differentiate is that we think there could be an opportunity not to have to combine with fulvestrant in particular.
Oh.
And so we think that could have a different profile, could potentially also expand the patient population beyond the current focus area right now.
Okay
... of the specific model in the clinic. So hopefully, you know, it gives you a sense, Corinne, that our portfolio is growing.
Yeah.
We're continuing to try to push the envelope, and we're excited to hopefully finish out the year strong in 2024.
Perfect. I love breaking news. Okay, maybe last question, 'cause it's biotech: cash runway. I know you have plenty, but just, an update.
Andres?
Well, yeah, we have $978 million of cash and marketable securities, and our public guidance is cash into 2028.
Perfect. Thank you. All right, with that, I think we'll wrap up. Thanks so much to the team from IDEAYA for joining us here to kick off the week at the Goldman Sachs Global Healthcare Conference. All right, thanks, guys.
Yep, thanks so much, Corinne.
Perfect.
Thanks for the time.