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All right. Good afternoon, everyone. Thanks for joining us. So we'll get started here with the next fireside. With us, we have Oreck Pharmaceuticals. From the company, we have Jacob Chakko, as well as CFO Dominic Piskelli. Gentlemen, thank you so much for joining us and looking forward to the conversation. Thanks for having us. Excellent. So, you know, maybe just at a high level, Jacob, if you want to give us kind of like, you know, the pitch on Oreck and what you guys are working on, and you've got two programs and got some very interesting data from a competitor that's going to read through to you guys later this year. So maybe just kind of tee it up for us before we kind of dig into the questions. Sure thing. Happy to, Derek. So at Orick Pharmaceuticals, Orick stands for Overcoming Resistance in Cancer. In a nutshell, that's the mission of the company. We have two late-stage programs, one for prostate cancer, one für lung cancer. Both are differentiated in their own ways versus the competitors that are out there. Both are either, say in the case of her enzimetastat, our prostate program, It's already in its first phase three study, a study called Himalayas 1 in castration-resistant prostate cancer. I'm sure we'll get into some of the details of that. And then anazertinib, our lung cancer program, is, we think, headed towards its first phase three studies, which would start next year. So both programs are going well in terms of development. We're well-funded with a healthy balance sheet, long cash runway. And let's dive into any specifics you'd like to discuss. Excellent. Well, why don't we start? So, you know, pretty consequential readout for you guys in terms of the upcoming readout for Pfizer's Mepro1 with Mevrimetastat. So I guess, you Know, we've discussed your expectations around that trial and particularly like their announcement in terms Of the data is coming for Q. So now we know that. So how does that read through to RINCY? How does it read through To Himalayas 1? Yeah, I chuckle a little bit, Derek, because we probably get as many questions about Mevrametastats at this point as we do about our own program, RINCI Metastat, and at this point, I feel like we can speak in a pretty educated fashion about Pfizer's program. So I think what folks caught was in Pfizer's Q2 quarterly call, they mentioned some further specificity around mevrometastat timelines. And so they narrowed the guidance to Q4 this year for the first readout of their first phase three study, mevpro1. That obviously has, I think, positive implications if you do the trial modeling and event modeling, event accrual modeling that the street is doing and obviously that we've done. So under a whole variety of assumptions you can make around control arm performance, control arm distribution, meaning distribution of patients to various aspects of the control arm and how each of those components of the control arm might perform, you know, really in any sort of reasonable scenarios you can construct, including assumptions you make around enrollment curve and exactly when Pfizer was fully enrolled and whatnot, them narrowing that guidance to Q4 seems to have positive implications in terms of how that study is likely to read out. I think more broadly, as you folks just take a big step back and look at the mechanism of action, look at that data that Pfizer has produced now in not just one population, but actually two different populations within castration-resistant prostate cancer from two different phase one data sets. And then subsequent to that, a randomized data set in the post-Aboradarone CRPC population, which is the one that we're all talking about. You look at our own data with rinzimetastat, obviously in uncontrolled setting, but phase one data across those two different populations. You now have about half a dozen different data points, all of which point to the synergy of adding a PRC2 inhibitor, which is what these drugs are, in combination with an AR inhibitor. And so all of that should play out quite favorably in addition to now the stats and trial modeling folks are doing around MEVPRO1. Excellent. So I guess when you think about the trial, what would constitute, I guess, clinically relevant data? I mean, I think we had done some work around stats, and I felt pretty good about it hitting statistical significance. But is that enough, or are we looking for a specific hazard ratio that, again, would be more clinically relevant? Yeah, look, I Think in terms of actual trial expectations is probably a question that's better suited to Pfizer as opposed to us. I think from our own perspective as drug hunters, drug developers, you obviously want to see as clinically beneficial a profile as possible on behalf of patients. You have a pretty good sense of what the control arm would do in this patient population. Maybe if you take a step back, Derek, from just the stats of the phase three trial alone and just think about the actual patient experience and what physicians in this space are looking for, really what you're looking for is you have three big androgen receptor inhibitors that get used widely today. So that's enzalutamide, apalutemide, and darolutemide. And in combination with those three drugs, you also have a fourth drug called abiraterone. Those four are the ARPIs, and the ARPs are the mainstay of therapy today for prostate cancer patients. The issue is, as good as those ARPAs do for patients, and with abiratorone in particular, which is the drug that we're talking about following at this point, what happens is once patients in the CRPC setting progress on abiraterone, there really are no other good options to give them. Now, you can do an AR switch. You tend to get anywhere from four to six months of additional PFS when you do that AR switch. It's a tried and true treatment methodology for physicians. And what I mean by that is it's another oral agent. They're generally well tolerated. Physicians are very used to giving those AR inhibitors. Obviously, the downside to that, though, is four to sixth months of PFS. And so really, the holy grail in that space has been, what do you give a patient that's progressed on abiraterone if you're trying to get more than that four to six months of PFS? And so while in the trial design, you obviously include chemotherapy as one of the options, nobody wants to give their patients chemotherapy in that setting. And so in terms of what would be clinically meaningful, if they can get anywhere from two to three months of additional PFS above and beyond what you can get with your other standard of care, in particular an AR switch, any of that would be clinically meaningful. Obviously, they're going to have to show a bit more than that in the phase three trial because they're also going to have to show that they can also do better than chemotherapy. But really, if they get any control arm performance in the six to seven-month range, which is what folks seem to be quoting, their own trial is powered for 6.75 months of PFS in the control arm, anything approaching a double-digit PFS would be game-changing for those patients. Got it. I guess, what do you expect from a safety perspective from that trial? I guess, you know, how does that read through to you in terms of, like, what you offer with RIN-Z? Yeah, I think one of the key aspects of the differentiation here for RINZ-Metastat is thus far has been and is very likely to continue to be is the safety differentiation. And where that comes down to is this is good old-fashioned drug development 101 as you think about the pharmacokinetic properties of these drugs. In the case of Mevrimetastate, which is Pfizer's drug, it looks to have about a four- to five-hour half-life. in the case of rinzimetastat, a Oryx drug, we have a 20-hour clinical half-life. And what that extremely long clinical half life gives us the benefit of, in addition to the fact that we're combining with darolutamide, one of the three big AR inhibitors, whereas they're combining their drug obviously with their AR inhibitor enzalutamide. Enzaludamide is a SIP inducer. And so what that means is that it's a well-known, well-documented SIP inducer. It pushes down the exposure of drugs that are metabolized by CYP, which is most other drugs. And so, because of that DDI that they have with enzalutamide and their relatively short half-life of mevrimetastat, they're having to give very large doses of the drug. And, so, you know, in their randomized data that they presented and in the phase three study, in either case, they are giving grams of drug in order to overcome those two shortcomings, the short half life as well as the DDI with enzelutamid. In the case of rinzimetastat, our go-forward phase three dose is 400 milligrams once daily in combination with darolutamide. So the reason we can go with such a low dose is because, one, we have that 20-hour clinical half-life, but also, secondly, darolutamine is not a SIP inducer, so we don't have a DDI to overcome. Where that really shakes out is in the PK of the two drugs. And you can imagine the PK curve for the combination of mevro and enzalutamide shows you with two very large peaks during the course of a 24-hour period, and that's where you get C-max-driven toxicity. Pfizer themselves have said that they believe it's C-Max-driven toxicity that they see. And so you see on-target tox that you would expect to see. It's just at relatively high levels. So you see both GI tox and heme tox. In the case of the rinzimetastat combination, we also see that on-target tox. Of course, you should see on target tox, but we see less of it and less severity of it. and that's because of that much better behaved PK profile of the drug. That safety differentiation is key, and this is a space that has been well conditioned to that. So as you look at the three big AR inhibitors, Pfizer's drug enzalutamide was the first that they acquired from Medivation. That was the 1st AR inhibitor to market. Six years later came apalutomide from J&J, and its main differentiation was a slightly safer, better tolerated profile, not a better efficacy profile, the same efficacy profile but better safety, darolutamide, Bayer's drug, which is now a $3 to $3.5 billion a year drug growing 60-plus percent a year, that phenomenal growth is not because of differentiated efficacy. It has the same efficacy as the other two AR inhibitors, but it has even better safety and better tolerability. And so my point being, this is a space that is very accustomed to accruing more and more share to new kids on the block that just have a better safety profile. Gotcha. I mean, we want to talk about some of the differences and kind of the learnings from MedPro. So you guys are targeting EED rather than EZH2. I guess what do you believe could eventually be some ofthe advantages down the road taking that approach? Yeah, so first of all, just from a terminology perspective, because we sometimes kind of catch ourselves halfway through a conversation with an investor and just have to level set on the different targets we're talking about. So the complex is called PRC2, and the PRC1 complex has three different subunits that can be drugged. Essentially two are the ones that folks have focused on, which is either EZH2 or EED. So in the case of mevrimetastat, it's an EZh2 selective inhibitor. In the caseof rinzimetastat outward drug, it is an EED inhibitor What that means is that Pfizer is going about its inhibition of PRC 2 through the enzymatic complex, so EZ H2. And in the case of rinzimetastat, we're going at it from allosteric inhibition through the ED subunit. Now, it really doesn't matter which subunits you drug in terms of initial ability to inhibit the PRC2 complex. And so in the caso of mevrimetastat and the case rinizimetastate, they have similar potency. What really is the difference is obviously a very different half-life, as I talked about earlier. Now, where it comes to play, though, is in termsof long-term resistance. And this is probably what you're alluding to, which is that there have been numerous, at least preclinical studies that have been done to elucidate the biology and would suggest that selective EZH2 inhibitors are susceptible to acquired resistance or bypass resistance from EZ H1, so compensatory resistance from easy H1 or acquired resistant mutations in easy H2. And those are two things that an EED inhibitor would not be susceptible to, obviously, or for that matter, a dual ECH1, ECH2 inhibitor. So right now, that's theoretical. It's preclinical. We will actually have a poster at ESMO where we dive into a bit more of that preclINICAL biology to kind of peel that back and show those resistance mutations popping up in response to ECH3 inhibitors. The reason why thus far, clinically, we just don't know is there just hasn't been a long enough experience for either us or Pfizer to elucidate that, but that advantage ought to go to an EED inhibitor. Gotcha. So, basically, we will have to wait for pretty long-term data to really see if there's any potential differentiation on efficacy and resistance mechanisms. At least in terms of clinically, yes. Yeah. Safety, though, we can get that fairly soon, or we already know. Safety, you've already got it. We already got that. You got it, yeah. Excellent. Well, maybe on that vine of safety, so, you know, PRC2's been in the news with TAS kind of being pulled, and also Fulcrum's drug, but maybe just talk about kind of the perception of the class in terms of safety, particularly given, you know, what's going on there, but, you know,, even in light of, you knows, maybe your and kind of Pfizer's moves with, you know, even starting trials and basically engaging with the FDA, you know, within the class. Yeah, there was a little bit of a brouhaha in the first half of the year, which was really around this risk of secondary malignancy that folks had observed with tesmetastat, and, you know, I think what we thought of as old news, because the Tasmetastat label has been around for, was around for years, and folks should have been very well aware that in the Tasmentastat label was a low risk, but a risk nonetheless of secondary malignancy. It was at the rate of 1.7% rate of secondary Malignancies was what was quoted in their label. And you have to keep in mind that that was the preclinical or the nonclinicle toxicology studies that you do in these spaces are intentionally designed to be very sensitive to pick up these kind of signals. And in Tazmetastat's preclinical work, there had been a very strong signal of secondary malignancy risk that was on the order of about half the rodents passing away from secondary malignancies or showing evidence of secondary malignacies. And so despite that extremely strong signal preclinkally, what it translated to was a 1.7 percent rate in the actual clinic and what made its way into the label. Now, in the oncology space, you know, for folks that have been in the uncology space for a while, you don't tend to get scared away by a low risk of secondary malignancy, and the reason is because there's lots of oncology therapeutics that have a low-risk of secondary Malignancy. In fact, when you look at the prostate space specifically, the drugs that really today make up a lot of the therapeutic interventions in prostate. So that would include chemotherapy, radiation, Pluvicto, enzalutamide, for that matter. They all show low risks of secondary malignancy. And so that's why a low risk of secondary malignant is not, in and of itself, something that would dissuade development of a drug in the space. Now, in the case of fulcrum, they obviously couldn't come to agreement with the FDA on what a phase three study would look like, but what folks have to remind themselves is that that was in a completely different division of FDA, completely different indication, not an oncology indication. They were developing their drug for sickle cell disease, where you're anticipating dosing younger patients, adolescents, for decades on a therapy. It's just a very different risk-benefit profile than what you see in the oncology space, certainly in the prostate space. And so I believe through the public comments that Pfizer made, through our own public comments, it became clear that there was, you know, we had not, certainly I can speak for OREC, we have not seen evidence of secondary malignancy in our preclinical studies. So remember I told you those models are extremely sensitive, and yet we saw no evidence of secondary maligancy or malignancy, I should say, in those preclINICAL studies. We have not see that evidence in the clinic of secondary malignacy, and I believe Pfizer has made some statements along those lines as well. And then, as you alluded to, I think folks should also take comfort with the fact that Obviously, we and Pfizer have had extensive dialogue with the FDA as we've been prepping for phase three studies that are now theirs is underway and ours is underway, and both companies are continuing with their studies. And they've also started a trial, right, an earlier line where the control arm could be like 24 months or something like that, right? Even longer than that, yeah. So, yeah, exactly. You're right to bring up. So, MEVPRO, well, MEvPRO2 is maybe the study you were alluding to where the controller arm would do a couple of years, but MEVPro3, even more importantly, which is in the CSPC setting, the castration-sensitive setting, is one where you'd expect the control arm to do four-plus years. And again, that study is still ongoing, and Pfizer has not made any indication that they've been asked to change the design of that study or to stop. Gotcha. So I guess, you know, focusing on RINCY, so what should we be kind of expecting? Sorry, Derek, just to interject, by the way, because, you Know, sometimes we do get the question from people saying, well, is it a risk that you may one day see a secondary malignancy with the program. And this is where I ask folks to maybe take a step back and see the forest for the trees, which is that in no way can we guarantee that we are never going to see a secondary malignancy with rinzimetastat, nor can Pfizer make that guarantee for mevrametastat. But the point, I just rattled off all the widely prescribed drugs in the prostate space that see rates up to the high single-digit percentages of secondary maligancy, and they're widely used in the prostate cancer space. And so the point is not that you need to come through this with no evidence whatsoever of ever seeing a secondary malignancy. At low rates, it is still a very positive risk-benefit profile in terms of what you're offering to these patients to treat what is guaranteed to be a fatal cancer. And, and so that's where I think that folks need to kind of focus on. Got it. No, very helpful. So yeah, maybe in terms of your updates for RINCY, maybe talk to us, you know, when should we get the next updates? And And also just for the Himalaya trial, you know, kind of timing that you guys have communicated to the street and if you guys will give, you know sort of any updates along the way on enrollment. Yeah, so as you know we give our guidance in January at our conference and we gave the guidance and we intentionally called it a program update. And the reason for that is we didn't specifically say it was a data update. So what this second half program update could include for Renzi Metastat could be an update on the Himalayas. One study which as you guys know we just started could be our thoughts on a potential second phase three study in prostate cancer, or it could be some additional data in either of the two patient populations. So that's a little bit of TBD, so we'll see on that. With regards to the timing on the Himalayas-1, as you guys know, we said we'd start that study. We've started that study, that's ongoing. We're assuming about a 16 month enrollment period for that study and we'd expect top line data for that in the first half of 2028. The primary endpoint for that is PFS, so similar to the MEPRO-1 study as well. Got it. Perfect. And I guess you kind of brought up, you know, a little bit there, but, you know, how should we be thinking about, you know, Renzi's expansion to other, you know, places in prostate? And, you know, I guess right now you're in the post-Abrams Abbey setting. Where else could you go, and is it going to be following the Pfizer playbook, or would it be something else? If you can elaborate on that. All excellent questions, all under active discussion internally at OREC. So we're thinking actively about what Himalayas 2 and eventually Himalayans 3 will look like. There's obviously a lot to do within the prostate space itself. As part of our first half update, the data update, we provided not only a data update on the post-Aboradarone CRPC population, but also a second population within CRPC, which was post-AR inhibitor. So patients who had progressed on either enzalutamide, apalutemide, or darolutamide who we were then giving darolutemide as a re-challenge essentially. It's an AR inhibitor re-schallenge, which as you know is not a thing. AR inhibiter after AR inhibitor doesn't work, you should really be getting two months of PFS for everyone because at the very first scan, you're seeing progressions. And that was not the case for us. So when we saw at least as good early landmark PFS out of that population as we did in the post-Aboradarone population, and that was something that gave us a great deal of confidence in not only the mechanism, but also what a second study might look like. So Himalayas 2 could be in that CRPC setting post-AR inhibitor. But another population that's really captured our attention is obviously CSPC, castration-sensitive prostate cancer. And so, you know, any therapy that has been studied in the CRPC setting when it's then investigationally, you know, been successful in the SRPC setting, when you take it into the CSPC works just as well, if not better. And so that would obviously be of high interest to us as well. So that would be something more akin to like MEVPRO3, what Pfizer's third phase three study is. So those are both of high interested to us. And right now, we're just letting the data mature. We like what we're continuing to see out of our own phase one data. So keep in mind, we get to see the ongoing follow-up of our phase one data in CRPC in the two different populations. We like how those data are continuing to develop. And we'll continue to monitor that and make some decisions about one or more phase three studies to start next year. Got it. I mean, anything else on RINCY or kind of MedPro or just the CRPC space that you would flag in terms of what we should be watching for the second half a year and maybe early part of next year. Yeah, I mean, you know, so we'll have our own data that's developing in that space. You know, the other thing that we're working on internally is obviously we get asked by pharma parties that have their own favorite new mechanisms in prostate cancer, what this PRC2 mechanism does to expression of things like KLK2, for example, or PSMA or STEEP1 and all very interesting targets in the prostate cancer space, and all of which have their expression increased through PRC2 inhibition. And so we're continuing to do some more preclinical work in those areas, but certainly we're also thinking about other early clinical work that we might start in some of those areas to see where else beyond AR inhibitor combinations might we develop rinzimetastat within the prostate cancer space. We've also shown preclinkally quite a bit of evidence around combining PRC-2 inhibitors with other targets in other therapeutic areas beyond prostate, so including breast cancer, colorectal cancer, lung cancer. So some of those are combinations with KRAS inhibitors. And so we have a lot on our plate, Derek, in terms of running down some of these opportunities, prioritizing some of These opportunities, and just figuring out what is going to be the most efficient and yet comprehensive development plan that we can undertake for rinzimetastat to execute this opportunity as quickly as we can. Excellent. Maybe shifting gears to Eno, maybe just give a little background on that program and where you guys are kind of in development there. Yeah, so enazertinib is our brain penetrant compound for two different populations within what are broadly called the atypical EGFR mutation. So one of those populations is EGF-R exon 20, and then the other population is more specifically pack mutations or atypical mutations. The terminology gets used by different people in different ways, but those are the two broad populations within EGFR that we're looking at. Those are populations that folks know well because there's a lot of competitors that have tried and failed in those populations. There's a Lot of ongoing competitors in those Populations. The main issue has been, Derek, really some combination of either safety liabilities, either on-target safety liibilities or, in many cases, off-targent liabilities. and then the big, big, big issue has been a lack of CNS activity and the reason why that matters so much for these targeted therapy populations is, look, some of us came, some of the people on the ORC team, myself included, came over from a company called Ignita that all about a decade ago was working on targeted therapies in the lung cancer space and I used to remember back then there was an active debate about whether you wanted a therapy to be brain penetrant or not because on the one hand, brain penetrance was quite important because so many of these patients, It's about 35%, 40% of patients in the frontline setting present with brain metastases. The brain is often the first site of progression. And it ends up being what pulls in the PFS of these compounds is because especially the huge portion of patients that have brain metástases initially just do much worse on drugs that are not brain penetrant. The flip side of the debate was people worrying about, well, are you going to get some kind of toxicity related to getting the drug in the brain? As it turns out, now it is dogma in that thoracic oncology space that you want a drug to be brain penetrant, because physicians realize what an issue these CNS metastases are. And what was a head-scratcher for us, no pun intended, was that in this space, as you looked at the other drugs in development, the other dogs were not CNS active, not CNR penetrant. And so it was a real shortcoming of the space in both of these populations. And that's really where anazertinib has tried to make its name for itself, is really with that profound CNS activity. Can you maybe just talk through the development strategy for Eno and where you guys have been focused? Yeah, so we're pursuing it in two different patient populations, EGFR Exxon 20 and the atypical. We had a pretty extensive update in the second half of last year at ESMO Asia. And then, as you probably know, we have a poster at ESMo this year focused on the atypicals. So when we look at that space in particular, we talk about what the benchmarks are there. If you look at the competitors out there, I think from a systemic response rate, it kind of focuses on the low to mid 60% systemic response. What's interesting though, when you look these competitors, the CNS response rate really drops off pretty considerably. And you see some of them in a kind of 30% and some of em are not reported as well. We think for a good active CNS active drug, there should not be that big of a gap between the systemic response as well as the CNX response. So hopefully when we have a data update later this year we can show hopefully we're better on one of those benchmarks and hopefully as good as on some of the others. The other thing we're seeing with some of these benchmarks, with some these other competitors is a lot of off-target toxicities. This could be in the form of QTC prolongation, anemia, excuse me, or elevated liver enzymes as well. So we'll have that. Exxon 20, we'll have, again, we're studying it in three different approaches there. That's EGFR, exxon20, it will do monotherapy, then we're doing it in combination with chemo, and we're in doing it in combination Emevathimab as well. Gotcha. So I guess when we get all this data, I guess what's the next steps that you wanna take? And obviously with RINDSY, you're moving into registrational trials. With ENO, is there an independent path to kind of bring to market, or do you want to partner this asset? Where do you think is the best way to, or what's the best path to creating value? Yeah, you know, it's interesting. When we talk about rinzimetastat and the path forward versus enozertinib and the path forward, I would say that there's a different lens that we look at the two of them through, Derek. And what I mean by that is in the case of rinzipetastat, because it's in development in massive indications in prostate cancer, any one of the indications we've just rattled off is a multibillion-dollar market in the U.S. alone. For that reason, you know, we've never tried to be heroes in the way that we've, you know, set our aspirations for Renzi. And what I mean by that is, while there's many reasons we think that our profile is going to end up being better than Pfizer's profile, and certainly on the safety side alone, we don't have to be better. We can be just as good as them. And in such large markets, you Know, even if you are, you Now, a second to market with a relatively undifferentiated profile versus the first mover, you can still accrue such a large portion of the market that it's still incredibly commercially attractive. It's a different litmus test we would use in the case of the lung cancer program. And what I mean by that is those are relatively smaller markets, and for that reason, you really need to be best. And it can't just be sort of tied. And so along the criteria that Dominic mentioned, what we're going to want to see out of our own data and what will wanna prove to others from the data is that he gave you three criteria. So he talked about the off-target toxicities of the other drugs, he talked about the systemic response rate of the other drugs and he talked about the lack of CNS activity of the other drugs. We will need to be better than the other drugs on at least one of those criteria and at least as good on the other criteria to satisfy ourselves and others that the drug is better than others, not just kinda tied for first place. And so assuming that we can prove that we will then elucidate what the phase 3 strategy is going to be. But like I said, we have aspirations for that first phase 3 study to start next year for endosarumin. Gotcha. And as you think about the overall, so again, smaller and different type of opportunity relative to RINCY, but what do you think that opportunity is for ENO? Yeah, so I know it is relatively small, but it is definitely not small. If you look at the EGFR exon 20 in the U.S. alone, it's about 2% of non-small cell lung cancer, so call it 4,000 or so patients in the U.S. alone. EGFR-A typical is actually slightly bigger than that. It's about 2.5%, 3% of non-small cell lung cancers are called 6,000 patients. So the EGF-R exon 20 by itself, we think in the US, it's about a $1.5 billion total addressable market, and we think the EJFR-AT typical is probably $2.5 trillion addressable market in the USA alone. So we don't think these are small. If you look at targeted therapies and you have a drug that is truly best in class that is differentiated that should gather the majority of the share so we think this is a sizable opportunity I think people are under calling it hopefully with data from competitors and our own data in the second half of this year people start giving us a little bit of credit for it yeah and then I maybe just last question in terms of the cash runway so you guys can kind of talk about you know being well funded so you know I think you've funded most of these trials but maybe just walk us through again what's funded what would need additional funding and you know ultimately some of the levers that you pool to do that yeah so we ended the second quarter with 388 million in cash and that gives us cash runway into the second half of next year and 2028 excuse me and and that does include the Himalayas one study and does include a phase three study for you know certain of as well so there's a fully burdened number the important thing is that cash run it takes us into the second half in 2028 which is past the top line data readout from the first phase three study for RENZI metastat, which is the Himalayas One study. So we're in a good position from a cash perspective. Obviously, we're biotech at certain points. We'll have to raise more money, but we feel pretty good on the position we're In today. Excellent. So maybe to wrap, you know, in terms of layout, the next 12 to 18 months in terms Of catalysts that we should be watching for that really impact you guys. Yeah, I mean, we'r obviously going to have a lot of data, substantial amount of data from our own two programs now with RENZY metastate and an I think that one of the underappreciated aspects of the story, Derek, is just how efficiently you can do the CRPC study. So with a sole primary endpoint of radiographic PFS, and so you don't have a co-primary of overall survival. Obviously, you'll want to see or FDA will want to See a trend in overall survival, but that's not a co primary endpoint. What it means is you can get your answer pretty darn fast. And so for a study that we initiated just a month or two ago, when we're saying you're going to have a first half 2028 phase three readout, it's funny when we think about it was not that long ago that we were talking to investors about OREC having two different assets in phase one. But because of how fast things go in oncology, in particular, how efficient the development is in the CRPC space, by the second half of 2028, you're gonna have our first phase three redoubt. And that's for an indication post-Aboradarone CRPC that, as Dominic alluded to earlier, is a $3.5 billion a year indication in the U.S. alone. And so, you know, 600-patient trial, you can kind of just do the math on how much that costs. It's actually pretty efficient to do a trial, both in terms of speed and cost in the CRPC setting. And like I said, Himalais-2 could be a post-AR inhibitor CRPC study. Again, roughly the same size, same timeline, same kind of cash needs for a study like that as you do in the post-abiraterone CRPC setting. That itself is a very large indication, just as large as that post-aberaterone indication. And so you're going to get a lot of data from us over the next, you know, call it 18 to 24 months, including the first phase three for rinzimetastat. And then, like I set, a substantial amount of data on anazertinib that'll show whether that's also going to be a phase three program. And then while I hesitate to speak for others, I think you're obviously going to get a lot of data from our competitor, Pfizer, with Mevrometastat. So in Q4 this year, we're going to get their MevPro1 readout. They've said that Mevpro2, as of their August earnings call, they said Mevro2 phase three readout was coming in the next 12 months. And so there's a lot that's happening in both of these spaces. I guess maybe one more question. So with the Pfizer data, they might provide just very high level information. So I guess if they were to provide kind of the more detailed data at a medical meeting following that, should we be thinking about ASCO-GU or when do you think we would actually get to see all the goods of the MedPro1 trial? Yeah, I have no idea. That's a question that's much, much better suited to them. And we're more focused on our own timelines right now. There's obviously ASCO GU, there's ASCO next year, but who knows when they would present those detailed data. Got it. Well, we'll be on the lookout. Gentlemen, thank you so much.