Good afternoon, everyone. I'm Judah Frommer, one of the SMID Cap Biotech analysts here at Morgan Stanley. Welcome to the 22nd annual global healthcare conference. We're very pleased to have Yujiro Hata, the CEO of IDEAYA, with us today. I'm just gonna read a quick disclosure before we jump into questions. Please see the Morgan Stanley Research Disclosure website at www.morganstanley.com/researchdisclosures. If you have any questions, please reach out to your Morgan Stanley representative so with that, Yujiro, maybe we could start with a quick overview of the company for those that are less familiar with IDEAYA.
Great. First, Judah, thanks so much for the kind introduction, and, great to be part of the Morgan Stanley conference, event this year. IDEAYA Biosciences, we were founded just about nine years ago. We have a core focus in emerging area of precision medicine oncology, called synthetic lethality. Today, we've advanced four, what we believe are potential first-in-class programs in the clinic. Our most advanced asset is darovasertib. This is in a registrational trial for potential frontline approval in metastatic uveal melanoma. We also have a key update we're guiding for in the second half of this year, including a type C meeting with the FDA that's scheduled for the third quarter , to hopefully get, endorsement and support around a registrational trial in the Neoadjuvant Uveal Melanoma setting.
In addition, we've guided towards the second half, phase II clinical efficacy update as well, in this indication. Next is we have a phase II program called IDE397. This is a what we believe is a potential first-in-class MAT2A inhibitor targeting a very large patient selection biomarker called MTAP deletion. We also have our third program in the clinic, in PARP, IDE161, in phase I dose escalation. We also have a fourth program in the clinic in Pol Theta with our partner, GSK. We're targeting to have our fifth program in the clinic with Werner helicase by the end of the year, and we're also guiding towards our sixth, seventh, and eighth development candidate by the end of the year.
That's a great overview. We're gonna try to unpack as much as possible in the time allotted. And I should mention, if there are questions from the audience, please do raise your hand, and we'll try to work those questions in. So starting with darovasertib, you had an impressive data update at ASCO in Neoadjuvant Uveal Melanoma from your IST and separately with the company-sponsored phase two study. Can you provide a recap of the data and what's deemed clinically relevant in this setting?
Yeah, no, great way to start. So yeah, Judah, as you mentioned, we had an oral presentation at ASCO a few months ago. This was 15 patients that were enucleation patients, and really, the high-level summary is in the predominance of these patients. We saw a very robust ocular tumor shrinkage of greater than 30%. In addition, we saw the vast majority of these patients that were going to get enucleated where we were able to deliver a result where we were able to preserve their eye. So we think, you know, both of these are really important, clinically meaningful outputs these patients on the IST.
And obviously, that's gonna be a big part of our discussion with the FDA in terms of what are the relevant endpoints, both in terms of potential primary endpoints as well as secondary endpoints. Lastly, I should have mentioned at that ASCO update, we believe we've continued to demonstrate a reasonable, manageable AE profile, that we believe further provide support around the risk-benefit profile, specifically in the neoadjuvant setting, which, as you know
... becomes even more critical in the pre-metastatic setting.
Okay, great. So we are expecting a second-half update from the company's sponsored neoadjuvant study. How many more patients, and how much more follow-up can investors expect versus the June update?
Yeah, so we're anticipating a fairly robust data set for our second-half clinical data readout. Here in aggregate, we anticipate it'll be over 50 patients, will be a combination of our phase II company-sponsored study, as well as our IST data that we shared at ASCO. I would say primarily, we're gonna combine that data set because that's the data that we did provide to the FDA. And what we you know, promised the public is that we'll share a data set that's largely similar to what the FDA reviewed to provide that feedback as part of the Type C meeting. Here, what people should anticipate is a very full data set as it relates to adverse event profile, and in terms of clinical efficacy.
People will see a waterfall, very clear visibility around what kind of ocular tumor shrinkage we're seeing-
... what is the eye preservation rate we're seeing? We also anticipate being able to share a spider plot type data set as well. So I think hopefully it should, you know, very much round out in terms of what we're seeing overall for this program, in the neoadjuvant setting, and obviously now we're in that range of over 50 patients. We would hope it's a fairly definitive data set as it relates to preliminary phase II data.
Okay, great. And you recently noted as part of your earnings that you have scheduled a Type C meeting with FDA for . Can you remind us of what you hope to gain alignment with FDA on as part of the meeting? And how will you provide the update on the feedback? Could this update come with the phase II company sponsor data update?
Yeah, so I would say the primary objective for the Type C meeting with the FDA will be largely around what are the clinical endpoints? Because you know, we are attempting a study here, obviously, hopefully with endorsement from the FDA, which is a trial that's not been attempted before, right? So I think we've been saying for quite a long time that several of these key what we think are clearly areas of clinical benefit, like eye preservation, you know, can we positively impact endpoints such as visual acuity, we think are relevant. However, you know, Judah, as you know, when you look at historical neoadjuvant regulatory approvals, you know, typically you've seen as primary endpoints in a randomized fashion endpoints such as event-free survival as well as relapse-free survival....
I think for us, some of the key points of clarification we would like to provide, is, you know, what is the FDA's perspective on some of these additional novel endpoints, such as eye preservation and visual acuity? So that's first. And in addition to that, you know, what would be their perspective of the use of some of those endpoints, either as a primary endpoint or a secondary endpoint? And this will, I think, be important as it relates to the next topic I'll bring up, which is around event-free survival, relapse-free survival, because when you look at historical neoadjuvant, trials, typically what you've seen is EFS and RFS used as the primary endpoints, and when they're utilized as the primary endpoints, oftentimes, needing to show superiority versus the control arm, right?
So now here, you know, will it be required as a primary, you know, or will it be required as a secondary? And in that context, could impact sort of the various gradients of what one might need to achieve as it relates to EFS or RFS. And I think to quickly to go through the kind of menu of possibilities there, right on the far, you know, right or most, you know, stringent or highest bar for us, would be, we would have to demonstrate superiority. The next one over would be, either equivalence or non-inferiority, and then I would say, you know, the least stringent for us would be around, no detriment, to EFS, RFS. And we think that will largely be based on what is the perspective of the FDA on some of these more novel endpoints.
Do they view those as clinically important? So hopefully, we can get clarity on several of these items. The last piece I should have mentioned would be around what is the population we evaluate? So we will look at, ideally, two cohorts. One will be enucleation, the other plaque therapy. If randomized, enucleation would be drug versus obviously getting enucleated. The plaque therapy cohort would be darovasertib followed by plaque versus plaque alone. And we also view that ideally, you know, could we focus on the high metastatic risk population? Because if we can, we should be able to get the readout, such as visual acuity, as well as EFS, RFS faster, right? But then, obviously, we wouldn't want to be limited in the label to just the high-risk group.
So what is-- obviously, we appreciate this will all be a review issue-
-but we can obviously get that feedback from the FDA as well. So I know I put out a lot there.
Yeah.
but obviously somewhat of a complex equation, but a lot of key pieces we hope to get, hopefully an endorsement and resolution on.
Okay. No, that's great color. So if we move on to the phase II-III registrational study you're running in frontline metastatic UM, can you elaborate on the study design and next updates for this study?
Yeah. So the high level, you know, which we felt was, you know, a really great outcome with the FDA, is this is an integrated phase II/III trial, where we, in the same trial, could get accelerated approval. Here, the primary endpoint is progression-free survival. There, our targeted objective is to enroll roughly 230 patients. As we've mentioned publicly recently, we've been already enrolled a triple digit enrollment, so we're almost halfway there, or largely halfway there. And then, for full approval is OS, and so we would add additional 120 for that. Here, it's randomized against standard of care, which we anticipate will be PD-1, PD-1 plus CTLA-4, as well as DTIC.
Here, in terms of historical PFS, obviously, these are time to event endpoints, but for whatever it's worth, historical PFS has been reported at roughly 2 to 3 months .
Based on some of those benchmarks, and historical PFS has been reported in that 10 to 12 month range.
Got it. And if we move on to the adjuvant uveal melanoma setting, that's another large market. Do you have plans for that setting?
Yeah, so great question. I would say we are seriously evaluating the adjuvant portion. I think some of it is going to depend on the outcome of the FDA on the neoadjuvant piece and what exactly, you know, study design will we need to implement. So, for example, you know, if it is a randomized study, where obviously, you know, we do have the ability to look at some of these clinical benefit endpoints, and obviously, if we're evaluating endpoints such as EFS and RFS, I think the bigger question for us is because in the neoadjuvant setting, you're getting in front of the adjuvant setting, you know, do we need. You know, is it worth it for us to run a full randomized adjuvant-
study and trial? Because obviously, that will be a larger trial. These endpoints will, you know, likely take longer to read out. So I think once we, you know, have that endorsement on the neoadjuvant piece, and we provide that update, we'll make that evaluation for the adjuvant portion.
Okay, that makes sense. And you touched on pieces of this in your answers, but just to wrap up the Daro section, can you discuss the unmet need that remains in uveal melanoma and the market opportunity for Daro in general?
Yeah, look, you know, I've been working on oncology since the 1990s, and, you know, I think, frankly, I'd have to say, out of many tumor types that are out there, you know, uveal melanoma continues to be one of the highest unmet medical needs.
Sadly for patients, there are no systemic approved therapies for either neoadjuvant setting. There are no systemic approved therapies for the adjuvant setting, and we believe for the predominance of these patients with metastatic uveal melanoma, of which we believe the majority are HLA-A2 negative, there are no approved therapies, right?
So we're seeking frontline approval, in the metastatic setting for HLA-A2 negative. Obviously, by default, if you're the first approval in neoadjuvant, and if we pursue adjuvant, that would also be in the frontline setting.
Got it.
You know, sadly for these patients, for survival, right, I mean, these are. It's a really tough situation, right? I mean, historically, it has been viewed as a 10- 12 month survival.
That makes sense. Okay, so moving on to IDE397, your MAT2A inhibitor. You recently showed impressive monotherapy data in bladder and non-small cell lung cancer. How are you thinking about a monotherapy strategy, given you have combination studies with AMG 193 and Trodelvy?
... Yeah, so I think for us, that's going to be a question we're going to continue to you know generate data on, to really think about what our registrational path forward is, and you know we'll be publicly guided as our objective to do that next year in 2025 , so here we're continuing to generate monotherapy data in lung cancer as well as urothelial cancer. You know really for us the quick summary is we do believe we've demonstrated preliminary clinical proof of concept. We do believe we have an active agent as a single agent as well as an acceptable AE profile based on the expansion dose we've selected. In parallel as you mentioned we have two key combinations ongoing one with Amgen with PRMT5.
I know they have an upcoming presentation coming up here at ESMO. There we've publicly noted, as part of our last earnings release, that we've recently now financially budgeted to prepare for that expansion phase with Amgen. Here, the priority tumor type focus will be non-small cell lung cancer. The next now shifting to Trodelvy with Gilead. So that combination is focused specifically on MTAP deletion urothelial cancer. Here what we can say is the dose escalation is going well. We, I believe we just recently cleared the first cohort. We don't think this is going to be a very long dose escalation because we're our initial dose cohort is starting at the approved Trodelvy dose. So we'll it's likely that we won't need to dose escalate beyond the second cohort.
Hopefully, we'll be in a position to also expand in that combination, perhaps, maybe as even as soon as the end of the year, obviously, pending on the results and the cadence of enrollment. And then lastly, you know, Judah, I think, as you know, one of our broader objectives is hopefully to build one of the broadest industry portfolios in MTAP. So we have two additional internal programs in MTAP deletion, including a target goal to have a second development candidate in the MTAP arena by the end of the year. So we would hope that should be positioned for the clinic by middle of next year. And so that is a very important strategic imperative for us.
Okay, got it. So maybe just a couple more pointed questions on the combos. So if we start with PRMT5, can you just walk us through briefly the mechanistic rationale for pairing a MAT2A inhibitor with a PRMT5 inhibitor? And just again, remind us what the next updates are for that combo.
Yeah. So here, you know, we've generated a lot of data with Amgen on the mechanistic rationale, and I know, you know, our plan is to publish preclinical data with them in a peer-reviewed setting around the mechanistic rationale. And this will, you know, include, I would say, a substantial amount of preclinical data, and also further support around the mechanistic rationale, some of that we can cover right now.
Mm-hmm.
So first, I would just highlight that the objective around the combination with MAT2A and PRMT5 is not about hitting the PRMT5 pathway harder. These are two distinct targets that we believe have complementary mechanisms to fully suppress the MTAP deletion pathway. In particular, we believe that by inhibiting both MAT2A and PRMT5, we can also help address certain very key bypass and resistant mechanisms that we've identified with PRMT5. Essentially, every preclinical model that we've tested to date, we see greater efficacy in combination than either maximal efficacious dose as independent agents. So I think that gives us high conviction. The two pieces to be aware of in terms of the mechanism, one is around this interplay between two key cofactors.
One is elevated MTA, which is what's often people view drives the synthetic lethal with MTAP deletion, and then the other is the presence of another key enzyme called SAM. We know that MTA and SAM compete for the same binding pocket of PRMT5. What we're trying to do is to influence the stoichiometry between MTA and SAM levels. As we know, with MAT2A inhibition, you deplete SAM levels, and if SAM and MTA compete for that same binding pocket, it's not just about elevated MTA, it's about can you deplete the levels of SAM to sort of tip it in the favor of greater PRMT5 suppression. We also know in different tumor types, you do see variability of MTA, so this could become critical as you also expand the horizon of tumor types.
Lastly, as I mentioned earlier, is around certain compensatory resistant mechanisms. One of the observations we have also seen is around, in the presence of PRMT5 resistance, is around this overexpression of MAT2A, which would mean you're putting more SAM into the system. And so there are several, I would say, key factors involved in terms of the mechanistic rationale. So you know, we think this is going to be a critical combination, in particular, if you want to have a viable approach clinically to hopefully target the frontline setting, especially in a tumor type like lung cancer, which, Judah, as you know, is a very high bar, right? Here, you're going to be competing likely with KEYTRUDA , chemo doublet or triplet, which, you know, is going to require quite a result to be able to displace.
Okay, got it. And similar question for the combination with Trodelvy in urothelial cancer. If you could walk us through the mechanistic rationale and again, the updates for that combo we should expect.
Yeah. Here the rationale around the topoisomerase, or in this case, Trodelvy, is really revolved around the topoisomerase payload.
Mm-hmm.
So you may know or recall that one of the combinations we explored in the early days was around the pemetrexed combination with IDE397. And a lot of that rationale with pemetrexed is pretty much identical to why we're interested in this topoisomerase payload. We you may know that there has been retrospective studies done with Trodelvy that has identified that agent in particular has demonstrated a higher response rate in MTAP deletion versus other genetic alterations. And we believe this is all related to the impact of topoisomerase, specifically in the folate pathway. Lastly, really how MAT2 really links in, as we know, MAT2's impact to the purine and pyrimidine pathway, which has a critical role as it relates to nucleotide pools.
And we know nucleotide pools plays a critical role in the repair of DNA damage that's related to topoisomerase DNA damage. So basically, what we're trying to do is to prevent that repair that's delivered by topoisomerase, to basically magnify that effect, which is why we're bringing these two mechanisms together. I would also highlight that we don't believe PRMT5 and MAT2 are interchangeable here, because PRMT5 is further downstream and does not impact the purine and pyrimidine pathway in the same way that MAT2 does. So yeah, here, you know, as highlighted earlier, we're in the dose escalation. We've cleared that first cohort. We do anticipate activity early here based on the fact that we're starting at the approved dose of Trodelvy in the first cohort.
We have mentioned publicly before, IDE397 is being dosed at one half our expansion dose, which we do believe is an active dose.
Got it. Okay, and just to wrap up here, maybe a little bit more on the market opportunity for IDE397 in these priority tumor types you highlighted.
Yeah, look, you know, we think MTAP deletion today is one of the largest, if not the largest, markets in precision medicine oncology.
Yeah.
Right? Here, you know, it's been reported at roughly 15% of all solid tumors, and you know, just for example, in non-small cell lung cancer, MTAP deletion frequency has been reported at roughly 15%. In urothelial cancer, which is another key tumor type for us as well, has been reported as, you know, 25%- 30%. Pancreatic cancer has also been in that similar range. Gastric esophageal cancer as well, in that 20%- 30% range. So as you appreciate, these are enormous figures that we're talking about, and then lastly, there's no approved therapies for MTAP deletion patients, sadly. So from our perspective, you know, this market area is completely wide open, and we think is one of the most substantial commercial opportunities.
With all of that said, you know, what continues to be a core anchor focus for where we believe will unlock the greatest opportunity, both for patients and commercially, are going to be through rational combinations.
Okay, great. Moving on to PARG. So, if we think about IDE161, can you discuss the potential for this target and how it differs from PARP inhibition?
Yeah, so maybe, you know, starting with the similarities and differences with PARP. So as you mentioned, the primary similarity between PARG and PARP is that they're both obviously involved in DNA damage repair in a very similar pathway, specifically around PAR chain synthesis biology. They've been described as counter-opposing mechanisms, where PARP is involved in that disruption of PAR chains, and obviously, through PARG inhibition, specifically, if you inhibit that process, it's really what you're doing is extending these PAR chains. Ultimately, both biomarker settings have been in HRD. I would say the primary difference here is, we believe mechanistically, is the unique role of PARG, specifically in replication stress, which is not observed with PARP inhibitors.
We believe that is really the key MOA delineation of why we believe there may be a relevant population where PARG inhibitors could be effective where PARP inhibitors are not active. I would say bigger picture for us here, Judah, I would say a very significant thrust of our focus is also to identify patient populations outside of HRD. That's why, for example, our first partnership with Merck on the KEYTRUDA combo is an endometrial cancer, specifically looking at high MSI, as well as microsatellite stable, that's agnostic of HRD status. You may know that recently we acquired a bispecific ADC topoisomerase. Here, we anticipate the PARG mechanism can amplify the efficacy of topoisomerase-based DNA damage.
And if that's the case, then we think that's a significant application, and there, the biomarker would be more driven by the antigen of the ADC asset. So look for us to double down on that aspect, not with our own asset, but as well as other pharma conversations that are ongoing today.
Okay, got it. And, and you started touching on this, but maybe just a little more expansion on your clinical strategy in, in both the, the mono and combo therapies, including, you- like you mentioned, with KEYTRUDA , and what would be the next updates that we should home in on here?
Yeah. So maybe first start, chart talk on the guidance. So really right now, our guidance for the program is targeting the monotherapy expansion phase in the second half of this year. We continue to feel good about that guidance. Second, we've also guidance about hitting our FPI with Merck on KEYTRUDA as well in the second half. We anticipate that's going to happen imminently, so we feel good about both of those pieces of guidance. We have not, at this time yet, given any clinical data update guidance.
Mm-hmm.
In terms of monotherapy, I would say our core focus there is in HRD.
Mm-hmm.
Here, I would say a significant focus on indications where PARP inhibitors are not approved, and I would say in order, I would sort of focus on endometrial cancer, and then second, on CRC. In terms of combination development, I think we covered some of this, but, as you probably saw, some, you know, fairly exciting data with Imfinzi-
Mm-hmm.
-and that whole arena in MSI and endometrial cancer in combination with DNA damage repair. So I think a very similar approach to that. I would say our probably bigger focus on that combination will be, can we amplify the effect, specifically in the microsatellite stable setting? We do have more mechanistic data on the interplay of PARP and impact as based, as it relates to immunotherapy. I think there we're considering sharing some of that data at, potentially at the R&D day at the end of the year. And then lastly, you know, as noted earlier, around the topo ADC combinations. So I think there, you know, we are considering can we enable a clinical combination there in the fairly near to medium term?
And then, of course, advancing our own topo ADC into the clinic to enable our own combination. So, we think that's quite exciting. We think the mechanistic rationale is strong. And I would say within all of those parameters, I would say probably our biggest priority, our kind of bigger interest is probably in that topoisomerase ADC combination.
Got it. Okay. So with the remaining time, I figured we could try to pepper you with some questions on your preclinical program.
Mm-hmm.
So maybe we start with the Werner program that's in collaboration with GSK. Can you expand on the history around this target and what makes you excited about it? What are next steps for the IND here?
Yeah, I would say there's a lot of exciting aspects to Werner helicase. So, you know, I'll make some general statements here. But if you look at a lot of the major CRISPR screens that have been done by, you know, several leading academic institutions, including the Broad Institute and the Sanger Institute, it's pretty clear that, one of the most significant synthetic lethal targets that drop out in terms of, you know, robustness of the synthetic lethal interaction is Werner helicase with high microsatellite instability, without a doubt. So it's one of the most robust and consistent interactions. I think the really... the big challenge here has been drugging, Werner because it is a helicase.
Mm-hmm.
Second here, as you know, it's a large patient selection biomarker, right? High microsatellite instability is prevalent in roughly 15% of gastrointestinal cancers, and as we all know, there's not a lot of great options refractory post-PD-1 for these patients. So we think the unmet need is there, it's significant, and then lastly, you know, we do think this is hopefully the next wave of agents in DNA damage repair, which is Werner helicase is a non-essential gene, right? Which would hopefully, as long as you have a selective molecule, should hopefully be able to drive a much wider therapeutic window.
Got it. Got it. Moving on to the Pol Theta program with GSK. Can you give us an update on where you are with that program?
Yeah, so Pol Theta Helicase, you know, another very interesting program. I would say here, really, we think the core application will be around combination with PARP inhibitors-
Mm-hmm.
and specifically to help address what's been identified as probably the most significant resistant mechanisms to PARP inhibitors, which is specifically around BRCA reversions, which has been connected to microhomology-end joining. And as you do further you know research into microhomology-end joining, you'll uncover that Pol Theta is viewed to be one of the key Achilles heel of that backup DNA repair mechanism. So that's sort of first and foremost-
Mm-hmm
... is this combination with PARP to hopefully help address one of the most important resistant mechanisms to PARP inhibitors. That asset is in dose escalation. I know, you know, even with a recent update from GSK, our understanding that's going well. Multiple cohorts have been cleared, and that's everything there is going as planned. GSK does have a very good molecule with, you know, a very high therapeutic window, so I think that's a very promising agent.
Got it. Okay. And you recently announced an option and license agreement for a potential first-in-class B7-H3 PTK7 bispecific ADC program with Biocytogen. So can you walk us through that program, a little bit of the background and next steps there?
Yeah, we're very excited about this asset. I would say... probably the single biggest strategic driver for us to bring this asset in was around what we just covered with IDE161 and PARP, our clinical asset-
Mm-hmm
... and the ability to amplify the effect of topoisomerase-based ADCs. And we had enough conviction around that mechanistic data we generated, that we felt it was critical that we be able to wholly own this combination. And then obviously, as we thought about ADCs, you know, this was a process where we looked at opportunities for about a year and a half. We looked at over 50 asset opportunities, spanning from preclinical to phase II stage. And, you know, we didn't want to bring in an asset that was just a fast follower, so we also wanted an opportunity, an asset, also had its own monotherapy path forward. So I would say we quickly narrowed down if we wanted novelty to bispecifics.
As you know, you know, people are working on dual payloads, novel payloads, novel antigens, but we, I would say, quickly narrowed to bispecifics.
Mm-hmm.
Second within that, we wanted an "and" format bispecific versus "or." So this means it needs to have both antigens to bind versus either, either or. And then finally, third, if you said bispecific, in an "and" format, we wanted to pick an antigen where we're truly in the game. So, for example, HER2 or TROP-2. So if you looked at those next wave antigens, it's not a really long list, right? So it's a pretty short list, and we narrowed to B7-H3 quite quickly. And then, obviously, if you asked a question around bispecific, there's two really critical questions, you know, which two antigens there's reasonable co-expression? PTK7 really jumped out, especially because of the co-expression of lung cancer with B7-H3.
And then, based on the data we saw, you know, we were compelled, and so, you know, this was a very obviously focused in-license we did, and that's very strategically well into our portfolio.
Okay, that makes a lot of sense. So maybe we could wrap up with, you know, some guidance you provided, that you're targeting two additional development candidate nominations in MTAP and the KAT6 pathway this year. Is there anything you'd want to highlight on either of those at this time?
Yeah, I think on the MTAP one, which is probably, you know, is an important area of focus for a lot of our shareholders. You know, we feel we've done, you know, a very good job preclinically to cover our bases on what key combination assets are in the MTAP pathway. And this is a key strategic goal by the end of the year to, you know, meet our objective to wholly own key combinations on this pathway. The other I would just highlight is that this candidate was picked sort of to be a fit for purpose combination with IDE397. So I think that's also very attractive.
And, you know, we continue to believe, as we just mentioned, how critical combinations are going to be moving forward in the MTAP deletion arena.
Mm-hmm.
On the second, on this KAT6 pathway here, you know, what I could mention here, Judah, which is, this is not a fast follower to Pfizer's KAT6. This has truly a differentiated profile. And here, our objective is really to address two key objectives. One is, can we have, an asset in this pathway that would not require fulvestrant in combination? And then second, you know, can we have opportunities that expand this opportunity beyond, breast cancer? In particular, we have a focused area in lung cancer.
Got it. Got it. Okay, I don't see any questions in the audience, so I think we can wrap up with that, but thank you very much. That was a great overview.
Great. Thanks so much for the time, Judah. Appreciate the time today.
Thanks.