Hi, everyone. My name is Maury Raycroft, and I'm one of the biotech analysts at Jefferies. It's with great pleasure that I'd like to welcome the ORIC management team with me here today. I've got Jacob Chacko and Dominic Piscitelli. Thanks so much for joining us today. Thanks for having us, Maury. We're going to do fireside chat format. Maybe to start off, for those who could be new to the story, maybe give a brief intro to your company and the two key programs 944 and 114. Sure. Happy to do that. Thanks for having us, Maury. I'll keep it very brief so we can get into your questions. ORIC stands for Overcoming Resistance in Cancer. In a nutshell, that's the mission of the company. Our area of focus within oncology is specifically small molecule drug development within solid tumors. Just given the expertise of the team that we've assembled at ORIC, we tend to focus primarily on Lung cancer, prostate cancer, and breast cancer as the three areas of focus. The two programs that you referenced, ORIC-944 for prostate cancer, that's being developed in combination with, it's a PRC2 inhibitor being developed in combination with two different AR inhibitors. We just had data on that last week. I'm sure we'll talk about that. ORIC-114, which is a brain-penetrant inhibitor of three different populations within lung cancer targeted therapy populations. EGFR exon 20, EGFR atypicals, and HER2 exon 20. Both of those programs right now are in varying stages of either dose exploration or dose optimization. Big picture, both are headed to phase three study starts next year in 2026. Obviously a lot on our plate. Got it. Yeah, it's a good intro and overview. You mentioned the data you reported last week, which was an early cut of 944 plus apalutamide or daralutamide in prostate cancer. Maybe recap what you reported for PSA responses along with the safety profile and talk about how this compares to Pfizer's Mevrometastat as benchmark data. Sure thing. There has been a history of PRC2 inhibitors that have been developed in prostate cancer in combination with one of the major androgen receptor inhibitors. Pfizer has clearly shown the most compelling, at least randomized data in that setting. That is what you referenced with their compound, Mevrometastat, in combination with their AR inhibitor, enzalutamide. In that randomized study that they presented earlier this year, they had a PFS of 14 plus months in the treatment arm. In the control arm, which was enzalutamide, they had a PFS of roughly six months, which is exactly what you would expect. A pretty profound treatment effect. There are various safety profile signals that we can talk through in more detail later. The important piece of that update, though, that they provided, because they're obviously quite a bit further ahead of us in terms of timelines, they've got randomized data, they've got PFS data, but importantly, they also included PSA activity, so PSA waterfalls, which, as folks know, on the hierarchy of prostate cancer endpoints, you often look at things like PSA50 and PSA90 as early indicators of what ought to translate to long-term durability. What Pfizer showed was a 34% rate of confirmed PSA50s in the treatment arm as opposed to 15% in the control arm. They had a 12% rate of confirmed PSA90s in the treatment arm as opposed to 8% in the control arm. That, for us at an earlier stage of development, was something that we can start to try to compare to right away. As part of the data update last week, which was a data update from our dose exploration work of ORIC-944 in combination with two different androgen receptor inhibitors. One is apalutamide, which is where we partnered with Janssen & in terms of free drug supply for that part of the study. The other is daralutamide, where we are partnering with Bayer for free drug supply for that part of the study. We are looking at 944 in combo with both of those AR inhibitors. What we saw was a confirmed PSA50 rate of 47% as opposed to what Pfizer showed with 34%. In our case, that does not include one additional response that is pending confirmation. Then a confirmed PSA90 rate of 24%. Obviously quite good out of the gates in terms of just early PSA activity, both in terms of the breadth and the depth of the PSA activity. Importantly, on the safety side, there are two major classes of toxicity that you should see with the PRC2 inhibitors. Folks know tazemetostat is the approved PRC2 inhibitor that people are familiar with. You should see heme tox and you should see GI tox. Those are the two big classes of toxicities. What Pfizer showed in their ASCO-GU update was an 80% rate of diarrhea, a 60% rate of dysgeusia, which is a change in taste sensation, a 40% rate of alopecia, and multiple other AEs that were above the 30% level. What we saw was dramatically lower rates of GI tox, lower rates of anemia, certainly no alopecia. Just overall, already have a profile that on both in terms of early efficacy as measured by PSA activity, but also most importantly, safety looks to be quite differentiated. Got it. Yeah, a lot of details there. The PSA information, want to dig into that. Your PSA waterfall plot looked impressive. The responses there are a leading indicator for durability measured by our PFS since the relationship is validated across prostate cancer studies. With Pfizer's data, that's even more relevant to this point because the mechanism is similar to what you guys are doing. Maybe talk about the Pfizer PSA data, how that translated to our PFS benefit, and how does that information inform your strategy? Yeah, so if you look at what Pfizer presented, everything hung together quite nicely in the sense that the treatment arm got 14 plus months of radiographic PFS. The control arm did six months, so they more than doubled the performance of the control arm, which was enzalutamide alone. You go and look at the other correlative measures, as you mentioned, look at PSA50 rates. Their PSA50 rate of 34% in the treatment arm more than doubled the PSA50 rate that they saw in the control arm, which was 15%. In their case, because again, they're further along, and they were able to, at that stage of the game, even start to look at recessed response rates. Because as folks know, a lot of these patients in this particular setting of prostate cancer have bone-only disease. You really need a pretty large sample size just to get down to enough that have measurable disease that you can start to talk about RECIST response rates. There as well, they doubled roughly the RECIST response rate in terms of ORR for the treatment arm versus the control arm. All the correlative measures held together. Obviously, what we've got at this earlier stage of the game is, like I mentioned earlier, the PSA50s and the PSA90s. As you mentioned, those things ought to translate long-term into those durability measures. Folks ask about other correlative measures that might be looked at, especially in this population where there's bone-only disease. Certainly, one of those measures, ctDNA, is something that we're looking at as well. We haven't shown those data yet, but happy to discuss. Got it. Part of your update, and with Pfizer's update as well, was just discussing the baseline characteristics. Maybe talk about the differences there between your study and Pfizer's study and how could that affect results and maybe focus on prior treatments used, including prior chemo. You do not want to overinterpret because we've got a small data set here, but do you have any anecdotal insights into baseline characteristics? Yeah, I'll take that one, Maury. Based on the information that was disclosed by Pfizer, if anything, the patient population that we had enrolled was actually more pretreated. Remember, both these studies required prior abiraterone and up to one round of chemo. One thing, though, is we allowed other therapies as well. We saw immunotherapies, we saw PARP inhibitors and other agents as well. If you look at our median prior therapies, it was three. If you go back and look at the Pfizer, if you did the math based on what they disclosed, it's closer to one. Based on that, it appears we have a more pretreated patient population based on this disclosure. If you look at their, they also disclosed that they had about a 40% or so pretreated with chemo, and we had about a 30%. We did go on to disclose that the fact that the PSA responses were consistent both for the patients that had seen chemo and those that did not see chemo as well. They did not provide that level of detail. Got it. Maybe talk about just the dosing strategy too. You're evaluating 944 in combo with apalutamide and daralutamide. You've talked about some provisional phase two doses. Maybe talk about how you got to those doses and what you still need to learn around picking the optimal dose. Yeah, so people who've been following the story for a while know that we started with single-agent dosing with ORIC-944 in the clinic, and that enabled us to get a really good handle around the drug profile, the drug properties of ORIC-944, and understand what it looks like as a single agent. Importantly, as a single agent, we dosed anywhere from 100 mg daily up to 900 mg daily. One thing that we've sort of glossed over as part of this discussion here is just differences between our drug and Pfizer's drug in terms of the drug properties themselves. Pfizer's drug appears to have about a four or five-hour clinical half-life and is being dosed b.i.d. In the randomized results we just saw from them was 1,250 mg b.i.d., so two and a half grams of drug per day. In the phase three, they're taking forward a dose of 875 b.i.d. in a fed state, which apparently gives them same exposure as the prior formulation I just mentioned, but apparently better safety. That's still 1.8 grams of drug per day. Obviously, with ORIC-944, with a 20-hour clinical half-life, that's compatible with QD dosing. That's all we've ever explored with 944. It leads to really well-behaved PK properties and exposure properties. Along those lines with 944, we are then combining with apalutamide and with daralutamide, which are the two big AR inhibitors. I think people are probably familiar that because we already knew the single-agent experience, knew where the DLTs were as a single agent, we got to start out of the gates with efficacious doses of 944 in the combinations. The real big difference between apalutamide, daralutamide, and enzalutamide, as you look at those three drugs, is that apalutamide and enzalutamide are both CYP inducers. Daralutamide is not a CYP inducer. The relevance here is just that when you combine drugs with either apalutamide or enzalutamide, you essentially have to dose up your drug to get back to the same exposure, to sort of back solve for the same exposure. What I'm saying is that the combination doses that we take forward in combo with daralutamide for 944, those doses will be lower than the doses that we would take forward with apalutamide, basically to get to like-for-like exposures. What we mentioned on the call last week is that we had started out of the gates testing 600 milligrams of 944 and 800 milligrams of 944 in QD doses, daily dosing in combo with each of apalutamide and daralutamide. From there, because of the difference, as I mentioned in the DDI properties, the CYP induction of APA versus daro not having it, the next direction was essentially to go down a dose of 400 milligrams of 944 with daralutamide, which is now completed, was part of the data set last week. We are currently actually going up a dose to 1,200 milligrams of 944 in combo with apalutamide. Got it. Just based on that 1,200 mg dose, do you think that could lead to better efficacy? Do you think there's any safety risk there with going to that higher dose? No, because again, you have to keep in mind, we talk about a 1,200 mg dose of 944 in combo with apalutamide, but keep in mind, because APA is a CYP inducer, it's not like the exposure is the equivalent of 1,200 mg of 944 single agent. The exposure is south of that. That's why you're taking it up to the 1,200 mg dose of 944 in combo with apalutamide, just to back solve for the right exposure. I wouldn't count on it being an appreciably different either efficacy or safety profile for that matter. We mentioned on the call last week that with daro, we did start to see in the daralutamide combination, we did start to see tox at the 800 mg cohort level of 800 mg 944 with daralutamide. We do not yet see where that line is with apalutamide, but again, to be very clear, that is because APA is a CYP inducer and pushes down the exposure of 944. That is why we are testing 1,200 mg of 944 with APA, to try to find where that tox line is. Obviously, one of the points of dose exploration is not only to establish early efficacy and safety profile of a compound, but importantly, to figure out where the tox threshold line is so that you know what you take forward for Project Optimus dose optimizing. Got it. Makes sense. Looking forward, your protocol allows assessment of both metastatic CRPC cohorts post-abiraterone and also post-ARPIs, including ab, enza, APA, and daro. Can you talk about the types of patients that you aim to enroll in the dose expansion phase? Do you anticipate you'll enroll in almost equal split for both patient cohorts or will you enrich one more over the other? Yeah, so the data update last week was exclusively focused on the post-abiraterone population. Within metastatic CRPC, the patients who, as Dominic mentioned, have all had post-abiraterone, they all had abiraterone progressed. They could have had up to one prior line of chemotherapy. They also could have had a whole smattering of other investigational approved agents, as we outlined last week. We also mentioned on the call that we have just recently started to enroll that post-AR inhibitor population, meaning that a patient has progressed on either enzalutamide, apalutamide, or daralutamide, the three big AR inhibitors. We're starting to look whether in that population, we can also see the same resensitization with a PRC2 inhibitor in combo with an AR inhibitor. I do not know how the enrollment's going to trend between the two populations, where I know that the post-ABI population obviously had a huge head start. We have more of those patients now, and we'll just kind of keep monitoring how those enrollment trends look as we go forward. Those are obviously, again, as we outlined on the call last week, two populations of high interest to us as we think about potential future phase three studies. We have said that the first phase three study for us is slated to start first half of next year, first half of 2026. Those two populations you just highlighted, the post-abiraterone population within metastatic CRPC, as well as the post-AR inhibitor population within CRPC, are both of high, high interest to us as potential first phase three studies. Got it. Makes sense. You have also guided to having two additional data updates later this year. Dose escalation data second half of the year, and then finally the combo dose optimization data in fourth quarter of this year or first quarter of 2026. What will you report in these data updates, and will you be able to provide any perspective into durability? Yeah, I'll take that one, Maury. With the second half update, what we've said is we expect 20-25 patients' worth of data. As we said on the call last week, enrollment is going much better than anticipated. This is really post-ASCO, GU, post-APHYSER data. We'll probably exceed that number, being north of 25 patients. This being still the dose exploration portion of the study, the focus is still on PSA responses, looking at safety and tolerability. We may show some additional information, maybe around how we selected the provisional RP2Ds for the dose optimization portion of the study, but that's really the focus there. The other update, the latter part of this year, Q4 of this year or Q1 of next year, that'll be from the dose optimization portion of the study. That is where I think we'll get a good look at some early durability data. What we mean by that is really looking at a kind of a four-month or a six-month durability analysis, landmark analysis, and just looking to see that patients are on the drug and staying on the drug for a period of time. It will definitely be not fully mature data. Obviously, that'll take some time before we get there. Got it. That durability insight will give investors a lot to compare with Pfizer, and that should be an important perspective. Yeah, it'll give investors, strategics, and ourselves a lot of insight as well. Makes sense. You are collecting, Jacob, you mentioned the ctDNA data, and you said this is trending with efficacy on your conference call update last week. Maybe talk about the correlation there between ctDNA and durability and how much emphasis FDA has put on this as a correlative biomarker. Yeah, I mean, in prostate, I mentioned earlier, we've all been trained to start looking at PSA activity, so PSA50s and PSA90s on the hierarchy of endpoints as one of the first things you look at to see whether a drug is active within the prostate space. The thought is that that long-term will correlate to durability measures, which are the ultimate regulatory endpoints, things like radiographic PFS and OS. Interestingly, I think more recently people have started to look at ctDNA as well within prostate cancer. The reason being that there's literature out there that suggests that even higher correlations than PSA to long-term durability, you can see with ctDNA to long-term durability, things like radiographic PFS and OS. ctDNA may be an even better marker than PSA activity for those long-term durability that you ought to end up seeing. Because that is a bit of a newer measure, I'm not aware of any studies in prostate cancer that have used ctDNA as a primary endpoint. I think there's some now that are using it as a secondary endpoint. It's certainly something that we've been looking at. Main reason being, aside from any regulatory discussions, I referenced earlier that within these particular lines of prostate cancer, it is almost always the case that most patients don't have measurable disease. In other words, they'll have bone-only disease, which really doesn't qualify for using things like RECIST measurements in terms of looking at ORR. People have gone down the lines of using ctDNA because in the absence of measurable disease in a vast majority of your patients, you can measure ctDNA in all your patients. One thing that we mentioned qualitatively on the call last week during, I believe, the Q&A was that in response to a question about whether we've been measuring ctDNA, we said we in fact have been measuring ctDNA. As you said, Maury, we do see that high correlation between that and then the PSA activity that we're seeing. At least qualitatively, what we commented on is that in the vast majority of our patients, we see substantial reductions in ctDNA, including many that have complete molecular clearance. That should all bode well. That, as Dominic mentioned, could be part of an update in the second half this year that we'd include as a first look at the actual data from the ctDNA that we're measuring. Got it. Really helpful. You talked about starting the phase three study first half of next year, and you're trying to determine which setting that could be in. Are you leaning more toward the post-ABI setting in line with Pfizer's MEVPRO-1 because you've got a de-risking data set there already? Or would it be later line post the ARPI where there's no competition with almost an equal number of patients? Can I say yes? We're looking at both, and we have not planted a firm flag as to which of those would be of interest to us. They're both of high interest to us. Yeah, to your point, Maury, these are both very large commercial opportunities individually. Obviously, in the post-ABI setting, obviously, Pfizer is a little bit ahead of us, but they're not pursuing the post-AR inhibitor. There's some attraction that's there that we'd be the first PRC2 inhibitor in that space as well. Got it. What do you want to see in order to make this decision before you start the phase three in the first half of next year? Will you need to have a BDDL in place prior to starting your first phase three study? What we want to see is obviously we'll continue to look at the maturation of the data from our dose exploration. We'll obviously want to look very closely at the dose optimization data that we're going to be generating in the second half of this year. That's obviously we'll be generating that in combination with each of our combo partners, apalutamide and daralutamide, at two provisional RP2Ds to satisfy project optimist requirements. We'll clearly be looking in that data set for these early indicators of efficacy that we mentioned, PSA activity, ctDNA activity, recessed responses to the extent that we have a big enough data set to look for patients with measurable disease. We'll obviously be looking at the safety profile. Probably most importantly, we'll be looking at the durability within those populations. Now, of course, we won't have a mature radiographic PFS to look at, but we can certainly at some point start to do landmark analyses of looking at what% of patients are still on for four months or six months or whatever the right landmark analysis would be at that time. Aside from that, Maury, then it's obviously the standard regulatory conversations before a phase three study. Your question on what from a BD perspective would we need ahead of a BDDL perspective ahead of the start of that first phase three study, the answer is nothing. That was the reason for the raise last week was that we did a concurrent raise along with the data. The reason to raise in markets as atrocious as the one that we're in right now is because it's obviously a much stronger message for us as a small biotech to be able to say that first phase three study is funded and does not require a BD partnership from pharma. Certainly, we'll look at some point here to extend the free drug supply agreements that we have in place currently with Janssen and with Bayer to cover a phase three study. In terms of economics or meaningful rights, none of that is going to be exchanged ahead of the first phase three CRPC study. Got it. You have the cash to run the study. Would you want to wait for Pfizer's phase three study to read out before starting yours? No. I mean, the name of the game here is close a timeline gap. We want to start first half next year. If we sit around and start to make things contingent on a bigger BD deal or make it contingent on seeing more data, it's just we're just going to push back the timelines. I think it's really important to us. Pfizer's articulated their timelines. They're quite aggressive. They say primary completion date for that first phase three study, end of this year, and that they're going to launch next year. It behooves us to move as fast as we can into that phase three study and get going. Got it. Maybe just talk about the choice of picking APA or DARO for the pivotal study and what the trade-offs are for advancing with either J&J or Bayer. Look, J&J and Bayer have been phenomenal partners to us. They've obviously, aside from the free drug supply, we talk to those prostate teams all the time. They've given us great feedback on the phase three protocols, great insights into these populations, even into as we think about prioritization of different phase three populations in which the first study may start. They've been phenomenal partners, really great to work with. We know all the folks up and down in those organizations. We see no differences between either one of them as a partner. The two drugs are phenomenal. I mean, folks are obviously enzalutamide, apalutamide, and daralutamide. We've sort of glossed over it, but those three drugs have transformed the prostate landscape. They collectively do $11 billion of sales. Even though apalutamide was the second one to market six years after enzalutamide, it is a $3 billion a year drug growing 25% a year. Daralutamide was third, and that is a run rating to $2 billion a year growing 75% a year. My point is that those are great drugs, and either one of them would be phenomenal partners or phenomenal combo agents for us in a future phase three. Got it. With J&J and Bayer, they both have their own AR inhibitors, but not sure how much you can comment on this, but do you get inbounds from other pharmas in the prostate cancer space that do not have an AR inhibitor? Yeah, I can't comment on that a whole lot other than to say that we know every major pharma that's got a prostate franchise or is building a prostate franchise super well at all levels from the Head of R&D to the Head of Prostate to the Head of BD. We know them all really, really well, and they have all taken note of the PRC2 mechanism. Got it. I wanted to dig into the mechanism a little bit more, wondering if there's benefits or trade-offs of targeting EED versus EZH2 subunits of PRC2, or does it not make much of a difference, is kind of like what we see in the preclinical data? Yeah, I mean, I could do a fireside chat on just that question, so I'll try to keep it to a very short answer at a high level, which is that if you have two drugs that are equally potent, equally good drug properties, one targets EZH2, the catalytic subunit of the PRC2 complex, the other targets EED, the subunit of the PRC2 complex, they will both be equally good at initial inhibition of the PRC2 complex. The reason I say initial inhibition is that there is biological theory out there that long-term, it would be better to target EED, which is what we do with 944, because that's not as susceptible to things like bypass resistance from EZH1 or acquired mutations in EZH2. We'll see whether that theory plays out in the clinic long run, but otherwise, there's no differences in targeting one versus the other. Got it. One of the questions we get is just whether we have to be better than Pfizer to be competitive because you're coming from behind by about two years potentially. What are your thoughts there? Do you have to be as good or better? Yeah, my thoughts there is you don't have to be heroes in an indication that's this large. What I mean by that is you just have to be as good as Pfizer and close the timeline gap in terms of the commercial launches. The reason I say that is there's obviously dozens of studies out there that look at the empirical data of commercial launches. If you have a completely undifferentiated profile for a compound that comes two years later after the first entrant, all the empirical studies tell you that that undifferentiated second entrant ought to have 30%-40% of the market, while the first player retains 60%-70% of the market. The reason those percentages are relevant here is that if that's all we can do is be no better than Pfizer and just be the second player to market with an undifferentiated profile, 30%-40% of the markets we are talking about, these markets are so large that that obviously still makes it a quite commercially attractive opportunity, even as a second undifferentiated entrant. The point being here, obviously, is even in the early data we presented last week, we actually think that there's many reasons why either on the safety side or the efficacy side or both, we actually might end up with a better profile long run. Got it. All makes sense. In the last couple of minutes, wanted to shift gears and talk about 114. A few months ago, you updated your strategy there to focus on frontline EGFR exon 20, the HER2 exon 20, and/or the atypical EGFR, depending on the data sets. Maybe talk about the rationale there and the net impact on NPV with the launch timelines. Yeah, I think the main thing there, Maury, was for us to focus our efforts on you can't do all things as a biotech, and especially in the current market macro, it's hard to find the dollars to put to every single opportunity just because it's NPV positive. I think implicit in your questions, we look at NPVs, obviously the frontline opportunity is more substantial than the second line opportunity, and that's why we chose to prioritize the frontline opportunity. These are obviously all competitive populations within lung with a number of different competitors in EGFR exon 20 and EGFR atypicals and HER2 exon 20. We just chose to prioritize for future, meaning continue doing the second line studies we're doing now and the frontline studies we're doing now, but for the phase three efforts or the registrational efforts, focus on the frontline opportunities. By the way, the side benefit of that is with a new FDA regime where we're not quite sure yet how accelerated approvals are going to be looked upon in the future. There's the side benefit that by pursuing a frontline strategy where it was always going to be a randomized control trial that we were pursuing, we know that that's going to be ironclad for any future development strategy, whereas the standard playbook of single-arm accelerated approvals in the second line in lung, we don't take any chances on it. We're not pursuing that. Got it. For the second half of this year, you've guided to having a comprehensive data update from all four cohorts. Maybe talk about what we should expect for that update and what it would be at a medical conference or company-sponsored event. Yeah, so for the second line or later patient populations, we've got three distinct patient populations. We've got EGFR exon 20, HER2 exon 20, and the EGFR atypicals. What we said there is about 30%-35% patients for each of those cohorts we'll have in the second half of this year, and that'll be across the two provisional RP2Ds of 80 mg and 120 mg per day. The goal there is obviously looking at topline ORR. It's a little too early to look at any mature durability data. What we've also did with the update we provided in February, we brought in the topline data readout for the ORIC-114 in the first line, EGFR exon 20 as a monotherapy. What we said there is about 20%-25% patients' worth of data for that readout. With regard to the venue, we're kind of keeping that open. If it works out that it correlates with a medical conference, we'll do there or also just do an investor call like we did for 944. Got it. What's the benchmark that you want to see on the data? Yeah, so I think for EGFR exon 20 and EGFR atypicals in the second line, I'd say it's about 35% or better from an ORR rate. For the HER2 exon 20 in the second line, we'd say it's about 50% or better. Then the first line EGFR exon 20, we're calling about 55% or better. Got it. For mid-2026, you're going to have an update there from your frontline EGFR exon 20 combo with Amivantamab. Maybe talk about how that combo strategy with J&J came about and what's the status of the combo cohorts and how should we think about the benchmark for success on that one? Yeah, I mean, I could joke, Maury, that the way it came about was a fireside chat with you years ago where you were probably the first one to ask about what an Amivantamab combo with 114 would look like. Honestly, it was on our minds. It was on the minds of the folks at J&J that we know quite well. Both companies actually kind of mutually proposed it at the same time in the same meeting about looking at what a combo of Amivantamab and 114 might look like. Obviously, the reason being J&J has explored Amivantamab in combo with Lazertinib, which is their drug for other populations. The thesis being that if you have a bispecific antibody that covers MET mutations, it is a potential resistance mechanism. With 114, you have the brain penetration of 114 that can handle CNS mets and prevent future CNS mets. Obviously, you get better coverage of the various EGFR exon 20 mutations with two different agents. That was the rationale to study it. We have started that combo dosing now of 114 in dose exploration with Amivantamab, again, supported by Janssen providing free subcutaneous Amivantamab, which is the formulation we're looking at. We'll have data next year that'll inform whether that's the treatment arm that we choose to go forward with into a future phase three study. Got it. I think we're pretty much out of time, but maybe to close out, if you want to highlight your cash position and just the runway assumptions into the pivotal studies. Yeah, I'll do that real quickly. With the raise last week, our pro forma cash as of end of March is $349 million. That gives us cash runway into the second half of 2027. That does assume full success for both 944 and 114. That's a fully burdened number that we're providing. Most importantly, that is past the topline data readout we'd expect from the first phase three study for ORIC-944, which is mid-2027. Great. Jacob, Dominic, thanks so much for joining us today.