Hey, good afternoon, everyone. Thanks for joining the OpCo Conference. I'm here with ORIC. We're going to do a fireside. Got Jacob and Dom with us. Hey, guys, welcome. Hey, Matt. Thanks for having us. I'll okay, I'll start off with a softball. So just tell me kind of about the ORIC philosophy and your DNA, because it seems, you know, when I look at the cancer targets that you're going after, you know, new ones kind of seems like a little bit ahead of the curve, maybe trying to push the science a little bit. You know, what is it, what are your core capabilities that allow you to do that? Yeah, it's a great question, Matt. I think it's a couple different things. One is, we—we generally like to stick to our knitting. And what I mean by that is, with very rare exception, you'll see us focus our pipeline on solid tumors, small molecules. Even within the solid tumor space, it tends to be prostate, lung, and breast, because those are the three main areas of expertise that we've got internal at the company. We spend a lot of time talking to KOLs in those three areas. So we have a very, I think, heightened sense of what the unmet needs are in terms of either current validated targets and drugs that are going after those targets, or even kind of the newest unvalidated targets in terms of novel science. And then I think it also helps that we've got a full slate of internal discovery capabilities. When we're in an area that is really trying to push the science with a novel, unvalidated target, we can build that expertise at ORIC itself. I think it helps us, hopefully, like you said, to use your words, stay one step ahead of the curve. Mm-hmm. I guess we can start with 944, which is, you know, prostate cancer program, I guess, from a catalyst perspective, probably the most timely coming up here. You had phase I, early phase I data that you shared with us around JP Morgan. Pfizer is supposed to have a pretty important phase II randomized readout that I think, you know, we'll talk about in terms of read-through to you guys. But I guess, first of all, what gave you the idea of targeting the EED domain for prostate cancer? Yeah, look, I would say here we were actually agnostic as to whether we were going to target EED or EZH2. What was really interesting to us was PRC2 as a complex. And the reason I say that is PRC2, obviously is a validated target in epithelioid sarcoma, and follicular lymphoma based on where tazemetostat has gotten its approval. But because the biological rationale is so strong for PRC2 dysregulation within prostate cancer, basically everybody with a PRC2 inhibitor has also looked at prostate cancer. Unfortunately, nobody has shown, prior to Pfizer good results in prostate cancer, but it was pretty clear to us that the reason for that was poor drug properties. So we have a strong network within the industry. About almost five years ago now, we got to talking to the Mirati senior management team, and they had a PRC2 inhibitor that was early, preclinical stages at that point. What they were pitching us on was that they saw the same issue with PRC2 inhibitors, which was the poor drug properties. They decided they were going to be agnostic as to whether they were going to focus on EZH2 or EED. They made a whole bunch of compounds that were EED inhibitors, a whole bunch of compounds that were EZH2 inhibitors, and then they put them all through the same paces to see which would hit the high bar TCP. It was this one that cleared that high bar TCP in terms of the drug properties and the other preclinical and in vivo properties. So what I like about it is it was an empirical experiment that they ran. It was the EED inhibitor that won. We can get into some of the theoretical rationale around why EED ought to be better than EZH2, in two different compounds that have like-for-like drug properties. But really, in terms of Mirati solving the drug property question here, it happened to be an EED inhibitor that won the day. And so, I love that it was just an empirical preclinical experiment that they ran. Yeah, let's go into that. Maybe some of the differences between ORIC-944 and Pfizer's PF-06821497, which I think is an EZH2 or EZH1 inhibitor. EZH2. Yep. Yep. They all play, they all play on the same bigger complex of PRC2, as you mentioned. But what, you know, what do you think, is different about yours versus Pfizer's? Yeah, so if you even stepping back from just Pfizer, if you kind of look at the whole—that whole space and see what's held the drugs back, in terms of when I say poor drug properties, really it comes down to two primary things, which is short half-life and/or CYP autoinduction. And so, in the case of tazemetostat, it's got both issues. It's got a short half-life, and it also has CYP autoinduction. You get this phenomenon of dose-dependent decreases in exposure, which obviously is the opposite of what you're trying to accomplish in terms of a good PK profile. Now, the Pfizer drug seems to not have CYP autoinduction, but it does have a short half-life, at least based on the data that they've presented thus far. So I think that still has room for improvement. Now, what we presented earlier this year was the first, single-agent clinical data for ORIC-944, which showed that we don't have CYP autoinduction, and we actually have a very good half-life and one that's compatible with QD dosing. And so I think that that ought to give us a better PK profile. It got ought to give us less interpatient variability. You can already see that in the PK and the PD data that we presented. And then hopefully that all leads to ultimately a better safety and a better efficacy profile, although we'll we'll, you know, that time will tell as we put that into the clinic in combo with AR modulators, whether, you know, all of that stacks up to Pfizer. There's some speculation that in prostate, it might go through a non-canonical pathway. Do you think the biomarker data that you've presented dispels kind of that idea? Yeah, that's a great question because we do get that question from time to time. There's, I think, one paper out there talking about the non-canonical pathway, and I think there's actually a series of papers that then came out after that debunking that one paper. Obviously we're a trust but verify bunch, so we did our own experiments internally, both preclinically as well as looking at the clinical data, the PD markers that you mentioned. We don't see any difference, in terms of like—if you've got two like-for-like drugs, we don't see any difference in terms of ability to downregulate the target here. There should be no difference in terms of long-term tox, long-term efficacy. Now the one area that EED ought to have a benefit over EZH2 that seems pretty clear at this point is long-term resistance. What I mean by that is EZH2 inhibitors are susceptible to bypass resistance from EZH1 and also to acquired mutations in EZH2, and that's not an issue for EED inhibitors. And so, that ought to benefit us in the long term in terms of long-term resistance. But otherwise, you know, in anything that we've looked at, and we'll present some of this data hopefully later this year, at least the preclinical data that gives us even further confidence about the, you know, supremacy of the canonical pathway here, we don't see any differences between the two. Gotcha. So then I guess, you know, assuming Pfizer does read out mid-year, I think there's some speculation, maybe ASCO. Pfizer's also having an R&D day later this month, so maybe that's something to keep an eye out on. But assuming it does look good, you know, that—that should be good for 944. Yeah, I think that's an absolutely fair characterization observation, Matt. And I think that, I think, you know, that look, this is my own interpretation is that I think the data are kind of hiding in plain sight, I like to say, from Pfizer in the sense that, you know, it's an open-label randomized study that they're going to read out later this year. And it's a study that they've been touting now for, you know, almost a year in terms of various public statements from the most senior folks at Pfizer. So, I think as people try to read the tea leaves and try to figure out whether those data are going to be positive or not, I think Pfizer is telling you that the data are going to be positive. You know, to the extent that even as recently as the end of last year, my understanding is that, again, in a public forum, they said that they're starting phase III studies for this program this year. So, you know, I've got to believe that the data readout is going to be positive. It's really more, from our perspective, a question of the actual nuances of the data. What does the actual radiographic PFS look like? What does that imply in terms of, you know, powering for Pfizer's, you know, phase III studies and just thinking about some of the more operational details in terms of study timelines and duration that you're expecting and how many patients you'd want to have as part of a pivotal trial? I think it's more those kind of data that, you know, at this point, I think would be informative to us. But otherwise, I think we are fairly certain it'll be positive and that it'll have a strong read-through to 944 for all the reasons we just covered. Yep. Do you have any early thoughts about a partner for 944? Darolutamide, apalutamide, neither of them are partnered up yet. Is one better than the other? You know, look, I think you—like I mentioned in my introductory comments, Matt, we spend a lot of time talking to KOLs, and I—and we know the prostate KOLs very, very well. I think if you talk to prostate KOLs, they would tell you that enzalutamide, apalutamide, and darolutamide are all fantastic drugs have done a phenomenal job for those patients, for men with prostate cancer. And—and if you try to sort of bifurcate between them, there's not a huge difference, not a lot of daylight in terms of the efficacy or safety profiles of any of the three drugs. So I think that's to our benefit, actually, that—that we have, you know, a—a number of parties we could think about potentially partnering with here. I think for us, it'll, at the end of the day, come down to, you know, who's—who presents the strongest case for becoming a partner with them. Because I think we've got a novel mechanism here with PRC2 and—and what we think is a best-in-class profile with 944. And so I think any of the above partners would be fantastic. I think, as you alluded to, it's quite helpful that Janssen and Bayer with apalutamide and darolutamide don't have a label in this specific area, of prostate cancer. So they—they ought to be quite hungry to get into that area. I can tell you that they're obviously well familiar with the Pfizer data. And, and so, you know, we look forward to further discussions on that front. Is the kind of standard of care second- and third-line prostate changing now that Pluvicto's on the market? Some of the other radioligand therapies are making headway. We've seen some M&A and ADCs. Ambrx got acquired. Cabazitaxel still kind of viewed as like a salvage chemo. Like, where do you see kind of this market going, and how can you stay on top of that as you think about designing your own trial? It's a great question, Matt. I think one of the things that helps here is for folks to keep in mind that it's such a massive market we're talking about here. So in contrast to some of the targeted therapies, you know, for lung, where you're obviously talking about more circumscribed populations, in this case, it's, you know, really an all-comers prostate population you're looking at. And so, notwithstanding the great results from Pluvicto or, you know, from any of the other novel mechanisms that are being brought forward in prostate cancer in these lines now, we are very, very confident that there will be plenty of patients to enroll in these studies. I again, if you do your KOL calls, I think what you're going to hear is that quite a few of these patients in the community setting are actually treated by a urologist. You know, enzalutamide, apalutamide, darolutamide as these second-gen AR modulators have done such a phenomenal job for patients. People are really just looking for longer ways to keep patients on those drugs. So if you've got an oral, you know, safe, easy-to-take pill that you can just add on to one of those second-gen AR modulators, I think it's a very easy sell to the KOLs, both from a clinical trial perspective as well as even more importantly from a long-term sort of just real-world perspective in terms of commercial prospects for a drug like this. So I think there's room for lots of different mechanisms here is what I'm telling you. MorphoSys has had an EZH2, EZH1 tulmimetostat that they've tested in prostate but discontinued. Was that a, you know, another one of these PK issues you alluded to before? Hey, Dom, you want to cover that one? Yeah, sure. So yeah, so Novartis acquired MorphoSys. I think definitely the driver there was a BET inhibitor for myelofibrosis. You're right, when you looked at CPI-0209, the drug probably seemed to be better than CPI-1205. But if you look at the data they presented so far, you know, they did have significant grade three treatment-related adverse events. It was almost 50%. They had a high frequency of dose modifications and discontinuations. The half-life was about six hours, as well. So they did have a program in prostate cancer that they were moving forward with. They did present some data at ASCO in 2023, and they discontinued that program as well. So, you know, obviously we haven't seen what we don't know what Novartis is going to do with them, but we don't kind of view them as a competitor at this point. Okay. But your safety so far in the phase I you've presented has been much better. Yes. That's right. Yeah. What are we kind of thinking in terms of updated monotherapy data for 944 later this year? Yeah. So what we've said here from a guidance perspective on the program for 944 is that we expect to initiate the combination studies in the first half of this year with one or more AR inhibitor. And then with regards to the mid-year update, we have kept that very broad. So what we're saying is that could be one of many things. It could be just a preclinical update where we show some additional in vivo data comparing our molecule with some competitor data, both as a monotherapy or in combination. It could be a, you know, some additional clinical data from the monotherapy study that we presented earlier this year, or it could just be a general business update on where we are at the program and kind of how we're thinking about next steps. So, it's kind of TBD on what we're going to show there. Okay. Fair. Should we switch to ORIC-114, which is, Exon 20? Sounds good. That's good, Matt. Yeah. You know, nice, compelling data at ESMO. Obviously, I think the pitch is that it's brain penetrant. I'm probably answering my next question, which is effectively kind of what is your value prop here? Because Exon 20, unlike prostate, is a much more niche market. As you know, there are several competitors there. ArriVent just had a pretty successful IPO claiming to do kind of the same things you are. So kind of how do you view 114 versus the others? Yeah. So this again is one of those areas where our deep KOL relationships, I think, put this target on our radar many, many years ago. And the main reason was when you talked to the KOLs, they told you that at the time, there were no drugs approved for it. Obviously, amivantamab from Janssen now is approved for EGFR Exon 20 and lung. But even the late-stage programs in late-stage development had one of two issues or two of two issues, the two issues being lack of CNS activity and then the second one being toxicity, either EGFR wild-type related toxicity or off-target toxicity, which nobody really talks about in this space. And if you look at the kinome trees, you'll see there's very, very dirty kinome trees across multiple of the compounds in the space. And so you end up seeing either EGFR wild-type toxicity in the form of diarrhea or GI tox and rash, skin tox, or you see, you know, a whole host of off-target things like QTc prolongation, anemia, liver enzyme elevations. I mean, it's a whole host of badness in terms of the tox. And then on the efficacy side, like I mentioned, lack of CNS activity. And you've seen this play out time and time again across the various targets in targeted, you know, TKI land and non-small cell lung cancer. And Matt, you've covered lots of these companies, so you know better than others. You know, when you have a non-brain penetrant compound, you end up getting worse durability. And the reason is that you can't handle, you know, 35% of patients who at initial presentation present with brain mets. And then of those 65% of patients that don't have brain mets, overt brain mets at initial presentation, you know, you talk to the docs and they'll tell you actually quite a few of them actually do have brain mets. They're micro mets that you don't yet see on imaging. And even if they don't have brain mets at that initial presentation, they will eventually develop brain mets at eventual presentation. And so amivantamab is a great example of this. If you look at the PAPILLON study that obviously was quite positive that everyone was, you know, quite enthusiastic about, ourselves included, when we saw those data because it's great for patients. At the same time, they put out a New England Journal of Medicine paper that shows you that when you bifurcate the patients as to those with versus without brain mets, they have a very different hazard ratio. That's even after they had preselected those patients because they didn't allow patients onto the study who had active brain mets at initial presentation. They had to have been treated with surgery or radiation before coming onto the study, and they still got these disparate outcomes between the two populations. So those are the two things it comes down to: the safety and the CNS activity. We think in our ESMO update, while early, we've already shown that we're very much checking those two boxes in terms of the differentiation for this program. We feel passionately, I hope you can hear, in terms of the differentiation of this compound. Even though it's a crowded space, we think it's a crowded space with some drugs that have, you know, really subpar profiles for patients. Yeah. Are you the only game in town that you're aware of that is allowing patients with active untreated brain mets in your trial? Yeah. So I mean, if you look at this—I'd, you know, urge everyone to do this—is go look at the phase I, phase II criteria for the enrollment criteria and inclusion/exclusion criteria. What you'll notice is that really, other than Blueprint with BLU-451, it was only us that was taking these patients who had either a prior Exon 20 inhibitor already and weren't kind of excluding those patients from the studies and/or, you know, patients who had active brain mets so that hadn't already been treated with surgery or radiation. And that's why if you look at the Blueprint update that was provided last year by them, you'll see that quite a few of those patients had prior Exon 20 inhibitors and had active brain mets. It was the same thing for us in terms of the patients that we enrolled, where it's a dramatically different patient population that was enrolled into our study versus what has come before on both of those two metrics. Now, the Blueprint announced that they've deprioritized really their whole EGFR portfolio. You know, again, to use your words, we're the only game in town now that is taking these patients, at least in the early-stage studies. I think that speaks volumes in terms of, you know, our confidence in the profile of this drug. I can tell you, after ESMO and the presentation we made, we got a very strong reception from the KOL community as well with investigators who are really enthusiastic about putting patients onto the study now that haven't had prior Exon 20 inhibitors and other things because they now believe in the profile of the compound. Yeah, I think like the immediate reaction at ESMO, a lot of people focused on ORR, which probably is never fair for any phase I trial. But on top of that, if you really were getting a much sicker patient population than others, then it makes it doubly unfair. Maybe walk me through some of the highlights of that, specifically the one patient that had a complete remission, including intracranial CNS response. Yeah, yeah, happy to do that. I mean, so if you, there was a slide in the ESMO presentation that we presented where we tried to lay out as clearly as possible just the different populations that people were looking at when they quote, you know, the ORRs. Because I think what comes top of mind for most people is in the second-line setting, so post-chemo and then prior to an Exon 20 inhibitor, you'll see that kind of the best profile in this space, which a couple of different drugs have all kind of coalesced around 40% ORRs. Obviously, a decent amount of tox, but, you know, somewhat manageable or at least more manageable than, say, mobocertinib or poziotinib was able to do on the toxicity side. And then no real CNS activity. And that's in the context of, you know, about 35% of the patients having been enrolled into these studies that had brain mets at baseline. If you instead look at what we saw in our study, 86% of the patients had brain mets at initial presentation. It's like not even in the same neighborhood as what others have enrolled in terms of being almost 3x the number. And then also, like I said, all those patients had prior Exon 20 inhibitors as well for our study. Whereas for the other studies, you know, you can count on one hand the number of patients who had had a prior Exon 20 inhibitor across all those other compounds and studies in their early-stage phase I, phase II studies. So dramatically different patient population. The patient that you're alluding to, we did spend some time talking about that one patient vignette. The reason was because there was no better vignette to highlight just the properties of this drug and the importance of this drug. This was a 55-year-old female who we highlighted had been on chemotherapy and progressed. Then went on to amivantamab and actually did quite well on amivantamab for almost a year, was in response, eventually progressed in the brain with small lesions in the brain. And that's why she had to come off of amivantamab. She would not have been eligible for any of the other studies. So exactly to your other question, other than us and Blueprint, those are the only two studies she would have been eligible for at that point because she had had a prior Exon 20 inhibitor already that would have excluded her from the other studies. And then if that wasn't enough, secondly, those brain mets had never been treated with surgery or radiation at that point. So she couldn't have gone on to those other studies. She, of course, could go on to our study even with both of those. And she had a complete response in the lungs. She had a complete response in the brain. She had a tox profile that was easily manageable and well tolerated. And so it really, you know, really spoke volumes about what that drug can do. And despite the fact that we're, you know, years later to the game here than all these other compounds that we've just talked about in the space, that patient that we just highlighted is the very first patient with a complete response in the brain who had active brain mets at initial presentation. That should tell you something about just what this drug is able to do. Yeah. What was the reaction from the KOL community? Did you see it kind of an uptick in enrollment after you presented the data? Yeah, we never had an issue with enrollment here, Matt, because, you know, this is one and, you know, I know you've covered other companies in the space and people kind of talk about what the commercial prospects are for some of these targeted therapy drugs. And I'm a big believer that what you see in terms of enrollment activity or demand for enrollment in the clinical trials is actually a very good harbinger of what the commercial prospects will eventually be. We've never had an issue for enrollment here, even from the earliest days of the study. And because it's a dose escalation in this early in the phase I, you have to kind of wait till you clear certain dose levels. So So if anything, we've had to throttle back enrollment even prior to the presentation of the ESMO data. I'd say what changed after the presentation of the ESMO data is we literally had investigators who were authors of studies for other drugs in the space who were asking to then be part of our study. And we had patients and we had clinicians who had patients who had never had Exon 20 inhibitors or in some cases never had chemo even, so totally treatment naive, where those clinicians were asking, can we find a way to get those patients onto our study? So the point being, I think the clinicians very much are believers in the profile that we presented at the time of ESMO. And I think it's, you know, one of the main questions we get is, given the number of drugs in the space, given the fact that amivantamab already has an accelerated approval, can we actually enroll Exon 20 population going forward? Absolutely, hands down, we can. The ESMO data helped us make that case. Interesting. What do you think is maybe the regulatory path of least resistance? Would it just be focusing on active CNS lesions and that could be like a single-arm trial or something else? Yeah, look, our team, our clinical team came from Ignyta, having developed entrectinib already in the face of a drug that had a full approval in front of it. You know, I was on the board of Turning Point Therapeutics, which was doing the same thing around the same target, I think. So the regulatory path of least resistance here is going to be really an all-comers population. So in other words, not limited to just those with CNS mets at baseline. But a standard single-agent accelerated approval that enrolls patients with and without brain mets, both. It would be a, you know, a second-line setting. And so patients would have had chemo already, but be naive to Exon 20 inhibitor. And that would be for the first, you know, the first pass for the single-agent accelerated approval. Obviously, the later stage confirmatory trial would then look to move into the front line like others have done where you're getting into a totally treatment naive population. There's three different populations here of relevance, Matt. We talked a lot about obviously EGFR Exon 20 for all the reasons that folks are so familiar with it. There's also HER2 Exon 20 and then very importantly, atypical EGFR mutations. Those are three different shots on goal that we've got here with this drug, which is quite potent against all three of those populations. Yeah, I do want to ask you about that next, but first maybe just in terms of how you would get the Exon 20 population into the front line, is that probably looking like a combination with amivantamab? It's a great question. You know, it could be similar to what Amy did, which is a combo with chemo as your treatment arm. The really interesting idea would be to combine with Amy because now you've got actually, you know, two different ways you're targeting EGFR with a small molecule and with an antibody. And obviously, Amy's bispecific, so you get some added benefit there. And with Amy not being brain penetrant and with 114 being brain penetrant, that could be a really interesting treatment arm. You know, I think we're kind of thinking through all various permutations of that right now. Okay. So I think last time I spoke to you, you were kind of on the fence about whether to provide an update on that program this year. But when should we expect kind of an update from both the trial and the regulatory approach that you guys are going to go for? Dominic, you want to take that? Yeah. So what we've said here, Matt, is for this program, we're going to start the initiation of the expansion cohorts. As Jacob said, he kind of outlined it, three cohorts of patients that we're going to enroll there, right? EGFR Exon 20, HER2 Exon 20, and the atypical EGFR. That'll be in the first half of this year. The guidance series will provide an update in the first half of 2025. Now, obviously, with regards to Project Optimist, the goal here is we're going to probably move forward to potential RP2Ds in the expansion cohort. So we'll kind of provide an update in 2025 around all that. And the goal here could be to potentially start the registrational studies as early as the second half of 2025. Okay. So you're thinking initially maybe looking at two different recommended phase II doses for the expansion cohorts. Do you think that you're at a place now where you're near the recommended phase II dose or at least one of those recommended phase II doses? Because if you want to start in the second half, that's only another four months or the first half. Yeah, we feel good about where we are. We typically don't give the date, you know, play-by-play on where we are on each of the programs. But we feel good about where we are. So we feel comfortable with initiating all three of those cohorts in the first half of this year and move forward and again, have that data in the first half of 2025. Gotcha. All right. Let's talk about atypical EGFR because 114 was kind of a built-for-purpose, at least as I understand it, like a built-for-purpose Exon 20. But it sounds like there are some similarities in the binding pockets between Exon 20, EGFR Exon 20, HER2 Exon 20, and these "atypical" mutations. I feel like the EGFR field has come a long way in the last five years in terms of kind of segregating. I mean, obviously, first was T790, and then it kind of moved. Now there's the CS mutation, you know, post-osimertinib. It seems like we're better able to kind of differentiate a lot of these different biologies of the enzyme itself. So explain to us what going after atypical mutations means. Yeah, I think the short answer is because Jacob started the kind of introduction. The beauty of having this internal research discovery expertise in-house is you can do a lot of internal experiments around this. So even though it was purposely built for EGFR and HER2, we ran a number of internal experiments and we presented some of this at ESMO last year. And we showed some really interesting data, both comparing ourselves to other competitors in vitro, and we showed more potency as well. And then we showed, you know, really complete tumor regression in vivo as well. So that's what's really gotten us excited about this. Ironically, we're actually a little more potent against the atypical EGFR than EGFR Exon 20. So that obviously gives us some more reassuring given the clinical data that we've seen with EGFR X20. Again, as Jacob said, the patient population for EGFR atypical is actually 1.5 times the size of the EGFR Exon 20. When you combine these opportunities, we think it's pretty significant. This is definitely something that's gotten us excited. We're obviously moving forward to the expansion cohorts. Could you just kind of walk us through how maybe investigators are starting to group these different mutations together? Like in the future, what would be treated with osimertinib versus what would be treated with 114 versus another agent? Yeah. Yeah, Matt. I think what people think of as the classical EGFR mutations are the ones that would be treated with osimertinib. For these atypical mutations, which would include EGFR Exon 20 as well as these other non-EGFR Exon 20 atypical EGFR mutations, because of the homologies you mentioned in the binding side, it actually seems like I think clinicians would tend to group those two together as well. And obviously, we're not the only one. There's other drugs out there as well that are potent against EGFR Exon 20 that are also enrolling the atypical EGFR mutation. So that kind of further shows you that I think that's kind of one clustering as well. And then there's obviously kind of a, I think of it as like a, maybe it's an offshoot of the first bucket, which is the folks that progress on osimertinib, you know, and then eventually need some other drug to take care of them. I think at this point, there's lots of compounds that are trying to go after that population. All right. Great. It sounds like it's going to be an exciting year, both in prostate and, you know, maybe later in the year, we'll learn a little bit more about the Exon 20 program and kind of next steps for the atypical mutation profile as well. Yeah, there's a lot going on in the pipeline. I think, you know, as Dominic mentioned to you, you know, earlier in the call, we're looking at having these two programs in pivotal studies by second half of next year. There's obviously a heavy lift going on internally at the company. We're heads down focused on execution mode right now. All right. Looking forward to it. Thanks, guys, as always. It was a lot of fun. Thank you. Thank you.