Good morning, everyone. Thanks for joining us at the Goldman Sachs Annual Healthcare Conference. Thrilled to be joined today by the team from ORIC. Maybe you guys could start with a brief introduction and then give us an overview of the company and pipeline with a focus on near-term value drivers.
Sure. My name is Dominic Piscitelli. I'm the Chief Financial Officer, and I'm joined with Matt Panuwat, our Chief Business Officer. For those of you that are not familiar with ORIC, we're a clinical stage oncology company. Our focus is small molecule solid tumors. Given the team that we've assembled here at ORIC, the three areas of focus for us are prostate cancer, lung cancer, and breast cancer. We have two clinical programs that we'll talk about throughout the presentation today. The first one is ORIC-944. This is an L-asteric PRC2 inhibitor that we actually licensed from Mirati back in 2020. We're studying this in combination with AR inhibitors in prostate cancer. The second program is ORIC-114.
This is a brain penetrant EGFR HER2 exon 20 program that we're studying in three distinct non-small cell lung cancer mutations, which include EGFR exon 20, HER2 exon 20, and EGFR atypical. Looking forward over the next 12 months or so, we've got a number of readouts across both programs. We'll probably touch upon those throughout the presentation. The goal is to start two phase three studies in 2026, one for ORIC-944 in the first half of the year, and then a second phase three study, which will be our first phase three study for 114 as well in 2026. A lot to cover in a busy next 12 to 15 months for us.
Perfect. Since we spoke last year, 944 has become kind of front and center to the pipeline. Maybe let's start with a high level. Why are you so excited about the target and this asset?
Yeah, so PRC2 inhibitors have been studied in prostate cancer for many years, dating back to GSK, Constellation, Epizyme. The issue that's really plagued the first-generation PRC2 inhibitors has really been poor drug properties. What I mean by that is poor potency, poor in vitro potency, poor in vivo activity, short half-life, CYP autoinduction. All these things have really kind of resulted in lackluster results when combining with AR inhibitors. What kind of changed that was Pfizer. Pfizer, back in the first half of 2023, presented some really compelling data with their PRC2 inhibitor called Mevrometastat in combination with their AR inhibitor, enzalutamide. Basically, what they showed in two different patient populations, both metastatic CRPC, they basically showed a three- four fold increase in radiographic PFS in what you'd expect to see there with enzalutamide alone.
That really kind of reinvigorated the interest on the programs. The two caveats there were it was relatively small ends and it was single-arm data. I guess it was early this year, in February of this year, at ASCO GU, they presented their first randomized data set. These are patients that were required to see abiraterone, and they could have seen up to one round of chemo. What they showed here was a radiographic PFS of 14.3 months in the treatment arm versus a control arm of 6 months, which was Enza alone, hazard ratio of 0.5 so really, really compelling data. In addition to that, they showed good PSA response. They had a PSA 50 of 34% in the treatment arm and about 15% in the control arm as well. PSA 90 was 12% for the treatment arm and about 8%.
Just really good overall data set. If you compare that to some of the recently approved agents, it's actually the 14.3 months comparison is pretty favorable against that as well.
Okay. You mentioned this has been kind of a challenging target because of poor drug properties. Can you talk about some of the specifics on 944? How have you guys overcome those challenges?
Do you mind taking that one?
Sure. Yeah, that was kind of the fundamental philosophy and sort of what we wanted in a molecule like that. There's been a number of early-generation PRC2 inhibitors that went into the clinic with some success, not so much in prostate cancer. None of the early-generation molecules were optimized for prostate cancer. It's much more difficult to treat cancer preclinically. Many of those were optimized for hematological malignancies and had some success there. When they went into prostate cancer, have not had much activity, which is supported by their preclinical data. Again, not much in vitro potency, really limited in vivo potency. A lot of them are associated with CYP autoinduction, where you get lower exposures over time. Too, a lot of them have drug-drug interactions with a lot of drugs and things like that.
Really just not optimized for something that you want in prostate cancer. Knowing that, we licensed this program several years ago. The molecule that we're working with now, 944, seems to have solved all of those problems preclinically. What we saw preclinically is essentially all of the pharmaceutical properties that you want in a molecule are essentially orders of magnitude better than kind of what came before. Better solubility, better half-life, better metabolic profile, much higher potency. We were really excited by the preclinical data. The program went into the clinic. Now we have a single-agent experience that we have seen with our profile. It looks great from a pharmacokinetics, from a pharmacodynamic aspect. What we've shown, our molecule has about a 20-hour half-life. Easily once daily, all of the early-generation molecules are about two hours half-life.
You can see kind of the dramatic difference in kind of PK properties. We have been very excited by that. Now we are in a combination study with AR inhibitors.
Okay. You kind of touched on this, but maybe we can be more specific. The mechanism is expected to be more of a combination approach. In terms of single-agent activity, what have you shown?
In terms of single-agent activity, PRC2 inhibitors do not have a lot of single-agent activity in the clinic. What we have seen, and I think others have shown, is stable disease in prostate cancer. That is supported by the preclinical data. Where you see the dramatic benefit preclinically is obviously in combination with the AR inhibitors. You see pretty dramatic synergy. Many companies, including Pfizer, essentially just went straight into a combination study. They did a very quick dose escalation across all solid tumors, had a handful of prostate cancer patients, again, showed some stable disease in prostate cancer. That is essentially what we have shared as well.
You reported data from a phase 1b study about a week ago now, I think. Can you just walk through the highlights of those results?
Yeah. This was the initial data on the combination. Just a reminder, this is a combination we're combining both with apalutamide from Janssen and with darolutamide from Bayer. We do have clinical supply agreements that Matt was able to secure for us for both those programs. This is dose exploration. We started at 600, 800. What we showed last month is really 400, 600, and 800. What we did see here, again, being the caveat, this is only dose escalation data, we showed a PSA 50 of 47%. That excludes one patient that is still pending confirmation. We showed a PSA 90 of 24%. That does compare to Pfizer's 34% PSA 50 and their 12% PSA 90. Overall, it looks pretty good. Again, early data. Obviously, we need to show more durability at a later date.
We were absolutely pleased with this. What you'd expect to see with PRC2 inhibitors from a safety standpoint, on-target tox really consists of both GI and heme tox. If you look at the Pfizer data they presented at ASCO GU, they had like an 80% rate of diarrhea, 60% rate of dyschezia, and about a 40% rate of alopecia. We've seen much better safety standpoint. We've seen much lower diarrhea. I think our diarrhea rate, which was our most common treatment-related adverse event, is about 50% or so, 53%. We only had one grade- 3. From a safety standpoint, we seem to look a little bit cleaner. Obviously, this is an N of 17 percent randomized study. Overall, both from a safety standpoint and efficacy standpoint, we're starting to see good activity.
What Pfizer really did show us, which is really important here, they showed us that with a PSA 50 response of 34% compared to 15% in the control arm, they started doubling the PSA response. They also showed that that translated into a nice PFS benefit. Obviously, that's the next step for us. Given that they've shown that, that obviously bodes well for us as well.
Okay. You've kind of described a wide therapeutic index for the program. I guess talk to us about the doses that you're moving forward with if you've made those decisions and what else you need to the extent there's still additional data that's necessary.
Yeah. So we're still doing some more dose exploration with both programs. I think what we said on the call is that we're most likely to move forward with the 400 and the 600 for the combination with d arolutamide. And then with apalutamide, even though the 600 and 800 looks good, we do want to kind of push the envelope a little bit and see what we can see what the 1200 makes. So we have started that cohort as well. One thing to keep in mind here is that both apalutamide and enzalutamide are inducers of certain CYPs. And drugs like 944 and Mevrometastat as well are metabolized via CYPs as well. So you have this kind of drug interaction with these two compounds. So basically, you have to increase the dose. So again, these are just hypothetical.
As we move forward in the two combinations to the dose optimization, we'll most likely have a higher dose for the 944 with apalutamide than we would with the 944 with darolutamide.
Okay.
Because darolutamide does not have the CYP interaction.
I see. That makes sense. In terms of patient baseline characteristics between your study and the Pfizer study, can you tell us anything that we should be aware of as we look to compare these two trials?
Yeah. Both the Pfizer randomized data and the data that we presented last month, these are patients that had failed abiraterone and were allowed up to one round of chemo. From that perspective, the patient population is the same. What is different is we actually allowed other therapies. If you look at our patient characteristics, you saw that we had immunotherapy, PARP inhibitors, and other agents as well. If you look at the prior therapies, we had a median of three lines. If you look at Pfizer's disclosure, they did not give the specifics, but it is probably closer to one prior line. Based on that, it looks like our patients are more pretreated than the Pfizer patient populations.
One thing that they did say is they had about 40% of their patients had seen chemo, where about 30% of the patients in our study had seen chemo. We had a smaller percentage of patients. We did say that the responses that we saw were consistent, both patients that had seen prior chemo and those that did not. That was not different for us. Pfizer did not provide any color on that in their disclosure.
Okay. As you think about the development program maybe broadly, Mevrometastat has set a precedent here. I guess what have you learned from that data and their execution that's informing the way you think about these trials?
Are you going to take that one, Matt?
Sure. I think the first Pfizer phase three study that they started last year is very similar to the randomized study, similar to the data that we've shown. This is in a post-abiraterone setting. Patients have failed abiraterone. They're allowing chemotherapy. It is very consistent with the data they've already reported. I think that is a very good place to start. From there, they're essentially moving in earlier lines of therapy. Their second study will be in patients with metastatic CRPC that have not seen an androgen receptor pathway inhibitor. That is their next study. I think what they have said so far is that they will be starting their third phase three this year, which will be in the castration-sensitive setting.
They're essentially taking kind of a middle, early line metastatic CRPC setting and then going earlier from there. I think that makes sense both mechanistically. It makes sense from a commercial standpoint. It makes sense from an unmet need. Just where you would go in prostate cancer if you have an oral therapy kind of in combination with standard of care.
As you look at Mevrometastat, are there any limitations for that drug that you think you can overcome? Are you thinking about this as an attempt to be like a best-in-class profile? What will drive the competitive landscape here?
Yeah. I think a couple of things. I think the bar is to really be as close to a profile as they are. I think that would be a very significant commercial success. I think we say that because prostate cancer is such a significant opportunity. We have seen that with the androgen pathway inhibitors, where you have abiraterone, enzalutamide, darolutamide, and apalutamide, all relatively indistinguishable. They all have very similar clinical efficacy. The safety profiles are slightly different, but all of them are significant blockbuster programs. Even apalutamide and darolutamide that were approved seven years after enzalutamide, they're all easily blockbuster status. I think if we're in the range of Mevrometastat, that is a very good opportunity for us. We are striving for potential best-in-class. I think the data we've seen before, again, it's still very early. Our PSA responses are trending higher than Pfizer's.
The confirmation of our PSA responses are higher than Pfizer's. The safety profile looks a little bit better than Pfizer's. I think we have confidence that there are ways to differentiate. We definitely have a once-daily therapy, which we think obviously makes a big difference. Their drug in their randomized study was dosed twice daily at 1,250 BID, so 2.5 grams a day. They are plagued with a very short half-life. They are plagued with drug-drug interaction with enzalutamide. To get exposures that they need, they have to dose very significantly, much higher than we do. I think our molecule seems to be differentiated from the data we can see so far.
Yeah. Maybe just to add to that, this is prostate cancer. This is huge. There are 40,000-50,000 patients in metastatic CRPC on an annual basis.
The perfect analogy is the AR inhibitors, right? The big three AR inhibitors are enzalutamide, apalutamide, and darolutamide. If you look at the sales of those programs, enzalutamide, and Matt and I were both at Medivation. enzalutamide was approved in 2012, and it is doing $6 billion in sales worldwide. apalutamide came six years later, and it is still doing close. It is running right at probably $3 billion. Darolutamide came after that, and it is doing $2 billion. The point being, this is prostate cancer. There are a lot of patients, and there is a lot of durability here. Even being as good as Pfizer, being second to market, potentially two years behind, that puts us in a great position. To Matt's point, I think there is potential for us to differentiate whether it is on safety or on efficacy.
Obviously, we need to run the studies, but that potential is definitely there.
When should we anticipate an update on the phase three programs from Pfizer? Could that further de-risk the trials that you guys are running?
I'll take that one. Yeah. I think just based on obviously what Pfizer has said is that their primary completion date for their first phase three is the end of this year. I think they're guiding to a data readout next year, 2026, and launch next year. That is their timeline for their first phase three study. Obviously, the second one will be after that, they said, and the third one hasn't started yet.
Are there any other programs in development that you think about when you consider the competitive landscape?
Yeah. There's been a number of PRC2 inhibitors. I think now with the Pfizer randomized data, people are kind of re-looking at those. We are aware of several that are being studied in prostate cancer. Novartis has one that they acquired with their acquisition of MorphoSys. That is in a study. Broad solid tumors, prostate cancer is one of them. There are several out of China that are looking at prostate cancer. There are a number of them. Most of those molecules, at least what we've seen from their profile, they're more similar to the first-generation molecules than they are Mevrometastat or our molecule. They seem to have, again, kind of the short half-life, the poor pharmaceutical properties. It does not seem like they were optimized for prostate cancer. There are a number that are starting to go into development.
You've been developing this in combination both with apalutamide and darolutamide thus far. Can you talk about how you'd pursue pivotal development with either or both, or how do you make those choices on the forward? Can you talk about the partnerships that you or the kind of agreements you currently have with J&J and Bayer?
Sure. We do have a clinical supply agreement with each company, darolutamide from Bayer and apalutamide from Janssen. They're essentially just structured as they're giving us free drug. We meet with them. We get advice and feedback and things like that. For the most part, for us, we are running the study. We're paying for the study. We kind of control the data and everything like that. We are getting free drug for the current studies. Those are the molecules that we're focused on right now. Our protocol is written very broadly. We could also study ORIC-944 with enzalutamide or abiraterone. That also makes mechanistic sense, but we haven't done that yet. Our expectation is that we will select one of those to actually go into phase three. It doesn't really make sense for us to do more than one in a phase three.
We will want to see the data kind of play out for both of the molecules just to make sure to see if we can figure out which one is better from a clinical standpoint. Pre-clinically, there is no difference. They are the same mechanistically. I think strategically which one might be more interesting. So far, the data we have shown, we seem to have equal efficacy with both molecules. Both are extremely great drugs. For Janssen, I think Dominic said is doing $3 billion. They are both growing significantly. Darolutamide is the last one that came to market, but it is growing the fastest. That seems to have some safety benefits. apalutamide is once daily, so you can kind of split hairs. Both of them have their advantages. I think it will depend. I think both are great drugs. I think either would combine well with 944.
I think more data and more discussions with our partners might make it more clear which one we should select.
How much does the dosing matter? You mentioned that you have to dose higher. I think with darolutamide, you start to get to a lot of drug. How much does that matter in the calculus between the two programs?
Yeah. I don't know if that's going to weigh too much in, but obviously, we need to figure out what that dose would be. But to Matt's point, when you look at all three of the AR inhibitors from an efficacy standpoint, they're pretty much indistinguishable, even enzalutamide, apalutamide, darolutamide. So we don't expect to see any difference there. Obviously, everyone has a slight benefit. To your point, darolutamide, the fact that it doesn't have the CYP interaction is a slight benefit for it. But darolutamide is twice a day, where apalutamide is once a day. So each one has their own slight pros and cons. But we think they're both great drugs. We think both J&J and Bayer are great potential partners as we think about developing things longer term.
As Matt said, I think at the end of the day, we'll look at the data set that we have later part of this year. There's somewhat of a strategic discussion. Obviously, we'd love to get hopefully some free drug from one of the partners as well around that as well. We're ready to run that first phase three metastatic CRPC study ourselves.
Okay. What should we look for in terms of the next updates? How many patients, what kind of follow-up, and what are the benchmarks there?
Yeah. For what we've said for the next update, we've got two more updates on ORIC-944. One is in the second half of this year. What we said there originally was 20-25 patients' worth of data. Now we have exceeded our prior guidance for the first half. Enrollment has picked up post-ASCO GU, post-APHISU data. We'll probably be north of that 25 patient number. This is still from the dose escalation portion of the study. The focus here again will be on PSA response, safety, tolerability. Similar to the first half update, just more patients. In addition to that, we'll probably provide some color. We do expect to start the dose optimization portion of the study in mid-2025, so pretty soon.
Maybe we'll provide a little more color on the selection of the doses for the dose optimization portion of the study. We did say on the call two weeks ago that we have started enrolling post-AR inhibitor patients. Again, not promising anything. That's something we could potentially share as well, depending on how many patients we have and that data as well. The next update, which is going to be in Q4 of this year or Q1 of next year, will be from the dose optimization portion of the study. That will be at the provisional RP2Ds for both the combination with darolutamide and the combination with apalutamide. That's what I think is the more relevant data set. Obviously, we'll look at PSA responses. We want to continue to see good safety and tolerability.
That'll be kind of our first look at what's called durability. Maybe it'll be a landmark analysis, a four-month or a six-month landmark analysis. Obviously, we want to see that patient just staying on the drug. To be clear, if you look at the Pfizer data, we're not going to wait for full mature PFS data. If we did wait for that data, excuse me, we wouldn't be able to start this phase three study until 2027. That landmark analysis, and then we'd look to start that first phase three study in the first half of 2026.
Okay. In terms of your, I think you said this, but you would look to do the pivotal on your own. Would there be any interest in exploring an expanded partnership with either one of these potential partners?
Matt's a beady guy like a mansard.
Yeah. I think we're committed to running the first phase three. We just completed the financing. And so that gets us through the first phase three. I think in prostate cancer, there's a number of lines of therapies we want to consider. Prostate cancer, if you have an active molecule, you really want to be running three-plus type phase three studies. The other studies get longer and kind of bigger. I think at some point, it would make sense to have a big pharmaceutical company on board. We don't need that for the first phase three study. As we think about Pfizer, for example, their study that they'll run this year is a castration-sensitive study. That is a study where the control arm is likely to be enzalutamide. That has about a 50-month PFS.
The combination RBU would want to beat that. That is definitely within kind of the big pharma territory. That is the real significant commercial opportunity. I think for something like that, at some point, it would make sense for 944, most likely with a big pharmaceutical partnership.
Okay. Maybe we can turn to one for a decision earlier, design for potency against exon 20 atypical mutations HER2. Let's maybe just start with how the agent is differentiated versus the slew of other EGFR TTIs.
Sure. Yeah. This is another program we licensed a few years ago when we looked at the landscape. Mostly, it was designed for EGFR exon 20. That is one area of differentiation. Most of the other molecules were repurposed for EGFR exon 20. They were designed for sensitizing EGFR mutations and things like that. I think that is one. The second key differentiator is it is highly brain penetrant. It was prospectively designed to have that feature preclinically. We felt that that was missing. That is definitely a distinguishing feature of almost all of the target therapies in lung cancer. As we think about osimertinib in the sensitizing mutations, if we think about alectinib in the ALK fusions and things like that, you really need a brain penetrant molecule in lung cancer because most patients progress with CNS metastases.
That was kind of the fundamental differentiating feature of what our molecule can do preclinically. Now that we've put it into the clinic, we have shared data that it actually does, in fact, do that. It is a very highly potent and selective molecule. I think we've looked at that preclinically. From the clinical data, there's no off-target toxicities that we've seen so far. It is all primarily rash and GI, which is kind of what you would expect at certain doses. Our clinical trial design is also different from everybody else. We essentially allow patients to enroll in our study having any prior therapy as one. They are actually able to come into our study with active metastases. Because again, those were the actual, that's kind of how we want to see proof of concept.
Essentially, every other study out there excludes those patients. They have very stringent inclusion-exclusion criteria, sort of what patients most patients cannot enroll in these studies. We have seen patients. Again, we've shown a really interesting case study that we saw early in our study. A patient had progressed on chemotherapy, had progressed on amivantamab, which is the approved therapy for EGFR exon 20, came into our study with untreated brain metastases. Essentially, after the first cycle, we saw 100% complete response in the lung. After the next cycle, we saw 100% shrinkage in target CNS lesions. Essentially, 100% complete response in the brain, 100% complete response systemically. That is something that nobody else has shown to date. We think that kind of bodes well for the long term. That is kind of the update. We'll see more patients.
We'll see longer follow-up. Really, when we put out that data, there's been a lot of interest from investigators. One of those interests was looking at our molecule in atypical mutations, which was not something that was designed with our molecule. We did go back and profile our molecule against a number of atypical mutations. Serendipitously, it's actually much more potent in atypical mutations than it is even in EGFR exon 20, which I believe we are the most potent molecule out there for exon 20. We're obviously excited by that potential path as well. We're kind of looking forward to seeing that data. Basically, everybody else's data as well will come out this year. I think we'll really know if we have a best-in-class molecule or not.
Okay. You talked about this. You'll have data in the second half. I guess, what should we expect in terms of number of patients, type of follow-up? I think there's a couple of different cohorts here. How should we be thinking about those results?
Yeah. For our 114 program, second half update, four readouts there. In the second line or later setting, we'll have three different cohorts: the EGFR exon 20, HER2 exon 20, and the atypicals. Again, this is second line or later. One thing Matt pointed out, we do allow patients with and without brain mets, including active brain mets, where a lot of others have kind of excluded those patients. Across those three cohorts, what we've said is we expect 30-35 patients' worth of data for each one of those, a total, call it, of 90-plus patients. Obviously, those would be across the two provisional RP2Ds that we've selected. If you guys remember, back in 2024, we did decide to move forward with the 80 mg and 120 mg once-a-day dose. That'll be that readout as well.
Early this year, we did bring in, due to better than anticipated enrollment, we did bring in one of our readouts for the first line EGFR exon 20 setting as well. There, what we have said is we expect 20-25 patients' worth of data in that data set as well. This will be kind of the first look. This will be more focused on top line. ORR will not be durability data. Durability data will probably come more in 2026 standpoint. We have put some kind of benchmarks for each of these out there. In the second line or later setting for EGFR exon 20 and atypical, the bar there is probably 35% or better. HER2 is somewhere north of that, probably 50% or better.
For the first line, EGFR exon 20 as a monotherapy, the bar there is about 55% or better for us to kind of think about moving that forward. Jumping to 2026, we have two more readouts with that program as well. One is in the first line, EGFR atypicals, and that is monotherapy. We also have the combination with amivantamab and the EGFR exon 20 first line as well. A lot of data, a lot of cards to flip in the next 12 months. As Matt said, there are a lot of competitor data sets that are kind of reading out from now till then as well. We can compare and contrast our profile and hopefully continue to show that differentiation both on safety and the CNS angle.
Okay. Maybe you could talk a little bit about the combination with amivantamab. Are you anticipating those will be additive or synergistic? Where do you think that kind of combination fits best in the EGFR landscape?
Yeah, sure. This is another collaboration we have with Johnson & Johnson. We are combining ORIC-114 with amivantamab. Interestingly, this will be the sub-Q formulation of amivantamab. It is still pending approval, but that is kind of the next generation molecule from them. We do view that this potentially could be synergistic. The combination, I think, scientifically makes a lot of sense. Amivantamab, I think some people might know, is a bispecific antibody. Half of it is EGFR. The other half is CMET. The two on-target resistance mechanisms that you often see with EGFR inhibitors is CMET. That would be covered by amivantamab. That would not be covered with 114. Also, C797S, so mutation in the cysteine where ORIC-114 binds, that would be covered by amivantamab as well. We bring the brain penetrance. We are inhibiting EGFR on the target differently.
There are a lot of potential benefits on combining the two. What we've seen with Amivantamab in the EGFR sensitizing mutations, they are combining with lazertinib. They see dramatic benefits in combination. They've also reported some data in atypical mutations, significant PFS and OS benefit is what they can see with the combination. We are hoping that should play out with ORIC-114 in the exon 20 space. Lazertinib does not have activity in exon 20. This kind of essentially would be replacing lazertinib in this type of mutation. We're obviously very excited to see that combination data as well.
Okay. Would that synergy play out in terms of duration, or would it be visible even in response rate data?
Potentially both. I think duration is what you really want to see. Right now, amivantamab is approved in front line in combination with chemotherapy. It has pretty high response rates in general. The PFS, we haven't seen a very significant PFS benefit yet in the EGFR exon 20 space, both with amivantamab or the other therapies as well. If the combination of amivantamab or 114 can approach anything kind of close to the lazertinib data in the other EGFR mutations, that would be dramatically better. I think that's where you'll see the real benefit.
Okay, great. Maybe we can spend our last minute or so talking about cash runway and how you think about sources of capital. What kind of clinical activities are embedded in the cash runway while you're at it?
Yeah. Concurrent with the ORIC-944 update, we did do a concurrent financing to raise $125 million in a pipe. With that, our pro forma cash at the end of March is $349 million. With that, we've extended our cash runway into the second half of 2027. Your second question is a good one. What's included in that? We don't risk adjust our cash runway. That's a fully burdened number that does assume we're kind of maintaining control of both assets, no strategic partnerships of any sorts. That also assumes we're starting the two phase three studies I alluded to before, both in 944 in the first half of this year—I'm sorry, first half of 2026. It's also starting the phase three study for ORIC-114 in the second half of 2026. That's a fully burdened number.
It includes all the CMC and everything associated with it.
Okay, great. I think that brings us basically to time. Thanks so much for joining us today, guys. Thanks to everyone who joined us here and online.
Thanks.
All right. Thank you.
Thank you.