Great. Thanks for joining us everybody. I'm Terence Flynn, the pharma analyst at Morgan Stanley. I'm very pleased to have Arvinas with me today. Before we get started, for important disclosures, please see the Morgan Stanley research disclosure website at www.morganstanley.com/researchdisclosures. If you have any questions, please reach out to your Morgan Stanley sales representative. Thanks so much for joining us today. We have Randy Teel, who's Senior Vice President of Corporate and Business Development, and Ian Taylor, Chief Scientific Officer. Thanks so much both for being here today. Maybe Randy, to start, I just thought given Arvinas is a pretty recent public company, you could provide kind of an overview of the company and the strategy. Then Ian, we'll go over to you for some more detailed questions on the pipeline. Thanks again for being here. Absolutely. Thanks very much for having us too. It's great to be back in person again. Yeah. Arvinas, we were founded back in 2013. The original protein degradation company. Our founder was Craig Crews from Yale. He's been working on PROTAC degraders since the very early 2000s, 2001 I think the first paper was. Again, we were founded in 2013. Got all that IP from Yale, and have been focused very much on oncology and neuroscience. Branching out a bit from there, but that's primarily where the focus is. By the end of the year, we'll be a you know, fully late-stage development company. We've got two pivotal phase III trials starting with our partners at Pfizer for the breast cancer program, which is ARV-471. We'll talk about a lot about that today, I'm sure. We also have a program, two programs in prostate cancer, the first of which is Bavdegalutamide, and will be in a pivotal phase III study in the second half of next year. Really moving on from being a research stage company. We've shown that the platform works. So exciting to be in that place where we're really focused on execution, getting those trials up and running. And obviously great to have a big partner in Pfizer to help us do that on the ARV-471 side. In addition to that, you know, Ian and team were gonna bring through four more INDs through the end of next year, including our first neuroscience IND, so a lot coming from that perspective. We continue to be able to invest quite heavily in the platform and in the preclinical programs. Ian will talk a bit more about the platform, but we're in a great position, you know, financially, and we feel fortunate to be there, that we can still be investing and making sure that we're bringing through the next tranche of programs too. Mostly oncology, like I said, about 75-25 with neuroscience, so that's a huge area of opportunity for us as well. Great. Congrats on all the progress. The other question we get a lot is just as we think about the protein degradation space, obviously, you know, as you mentioned, Randy, you guys were first, have a lot of, you know, Craig Crews know-how. There are other companies working in this space, some public, some private. Maybe Ian, you could just give an overview of kind of your platform, how it differentiates versus some of those other approaches and what you see as the competitive advantages. Yeah, we get that question a lot. I mean, as Randy Teel said, we're the first company in, we're the pioneers, had IP starting back with Craig Crews. Honestly, you know, it's hard for us to now differentiate because all these other companies have looked and seen what we've done and largely copied us. But we're very proud of the platform we've built. We have a very broad platform, so we really start by looking for ligands for both the targets of interest that we're going after, so like the androgen receptors, the estrogen receptors. We've built our own screening capabilities both internally and externally. Internally, our own DNA-encoded library screen, where we have basically 1 billion compounds now, where we're looking for ligands. We're also looking for new E3 ligases to hijack and ligands for them. The bulk of the platform that we've built is really to optimize PROTACs, to optimize their ability to form the trimer complex. That includes the linker. We have computational chemistry, we have structural biology built in-house. We have artificial intelligence approaches that we've actually built in-house, but we've also brought in externally with Randy's help. From a competitive standpoint, I don't think there's any company in the space, and there's a lot of them out now, that have the breadth of the platform that we do, all to optimize the compounds to degrade the best in these difficult areas. Undruggables is a big space that we believe where PROTACs are going to differentiate themselves in the long run versus any other modality. I mean, we all know there's a long list of targets that have been historically undruggable. We wanna go after those. That's how we feel we differentiate really in the competitive advances, is the breadth of it. Every individual piece, probably other companies are doing as well, but I don't think anyone's put it all together like we have. We've, you know, we've been doing it the longest, and we have the most experience. Okay, great. Maybe we'll dig into some of these, some of the drugs now. Obviously, as you said, you have, you know, two later stage programs. You've guided first to presenting some data for ARV-471, the breast cancer drug from the VERITAC phase I trial later this year. My guess is probably San Antonio Breast in December, giving us a pretty prominent venue. Maybe just remind us the patient population in this trial versus the phase I-B trial. Any similarities or differences that we should consider as we think about, you know, the data that's gonna be coming out later this year? Yeah. The big difference with VERITAC versus the phase I is that the patient population is earlier. In the phase I, we basically opened it up, okay, I have up to two prior lines of endocrine therapy, three chemotherapies. In the VERITAC study, it's limited to only one at most chemotherapy and one endocrine therapy as well. Really kind of tightened it from before it was probably fourth, fifth, sixth line, and now we're more in the second, third line. That's probably the biggest difference between the two. People ask about ESR1 mutations. We didn't put any restrictions or any targeting enrichment there, VERITAC relative to the phase I. In the phase I we've talked about, we've had about 50% of our patients were ESR1 mutants. I suspect that that'll be about the same population, just 'cause that seems to be where it's running these days. 50% of the patients in the late stage post CDK4/6 are about 50% ESR1 mutant. That is the big similarity between the two. It's still all 100% post CDK4/6 inhibitor-treated patients. That's important because as we know from publications, there's a lot of ER independent disease that emerges. You always have to be mindful of that, you know, if the patient's tumors are driven by something other than ER, you can degrade ER all you want, you're not really gonna get a response. The fact that we've seen the CBR around 40% that we've seen in that context, where 60%- 70% of the patients are no longer solely driven by ER, we've found that to be quite a remarkable result so far. Okay, great. Is that the CBR 40%, is that the range, you know, again, plus or minus recognizing like one patient can swing it either way. Is that kind of the expectation you've been setting for investors? Yeah, exactly. Right, exactly. We still have more patients obviously, than we had, showed before. Still a smallish number, but yes, we expect our data that as far as to basically consolidate around that number, we would find that to be a very successful result of the VERITAC trial. Yeah, at the doses, and that would be the big thing that people will see. We have two different doses, 200 and 500, and so when we have the data, people will see why we selected the dose. Yeah. Going forward from the phase III study that we did, so. Yeah. What about biopsy data? Again, I just don't remember the requirements. I know in some of the prior studies, again, it was kind of ad hoc, like if- Yeah. The patient elected to get a biopsy to have biopsy data. Is that something that's built into this trial or is it more- Still optional. Okay. Still optional. It's hard to make it mandatory if you want the study to enroll. Right. Of course, that's the goal, is to keep it enrolling, to be able to select the phase three dose. We'll have more biopsy data, but it'll still be from the minority of the patients. It's just the way it goes. That's why we have a neoadjuvant study that we've talked about. The study is solely focused on getting tissue pre and post. Yeah. That's where I think more of the definitive degradation data will come from. We will have more, and we will show what we have. Yeah. later this year. Okay. Again, the other study is this combination study with Ibrance. Yeah. You know, touched on this. I think now the data is coming first half of 2023. Maybe just remind us. I think initially, the data was coming in tandem, so my expectation was maybe both in the San Antonio Breast. Now it sounds like this is first half of 2023, so maybe any color on that decision. The second question is just as we think about what that trial is designed to show, like, what are you hoping to see there to drive kinda next steps? Right. Maybe I'll start there with the second question. Yeah. It really was a study design just for PK and for safety. PK obviously being important, you don't want a drug-drug interaction between ARV-471 and IBRANCE that would affect the exposure of IBRANCE. Our preclinical data suggests that won't be the case, but that's why we run the study to see. Then we also don't expect to see any overlapping toxicity based on the individual profiles of the molecules. Again, that's why you run the study. That was the main driver for the study, remains the main driver. Now, we recognize that people always wanna have efficacy. Obviously, we're gonna be following our patients for efficacy, and that was one of the reasons to delay the study to first half of next year rather than the end of this year, because we wanted the data to mature. From a company perspective, we don't want it. We feel like we've kinda gotten past the point where we have to show interim updates all the time. We wanna have when we give our updates, we want them to be more fulsome, to use that word. That's one of the reasons to delay. We also recognize that because most of those patients in that study will be post CDK4/6, you know, people are gonna say, "What's your bar for efficacy?" Well, we say it's a safety and PK study, but there wasn't a lot of data about patient responses post CDK4/6 with a CDK4/6 combo. Now there is more data. There's the MAINTAIN study that's come out, so we recognize people are gonna be looking at that data and comparing to ours, even though it is a safety and PK study. I'll say it again. We want that data to mature so that if you are gonna make that comparison, you at least have a better data set to compare. Waiting till the first half, and also to do it at a medical meeting. If we're gonna let it mature, we'd prefer to have it at some medical meeting as well. Okay. By maturing, do you mean basically having PFS, some kind of PFS data or? Well, you know, I mean, there'll be duration data probably. We're not really guiding on the specifics of the data, but, you know, there's. It's allowing more events to happen, more duration to emerge, so. Okay. I guess as we think about the phase three program, you and Pfizer have talked about starting that later this year. Maybe just remind us, kind of, I think you said two trials, a little more detail on those trials. Then will you have all the information you need from, again, VERITAC and again, this phase I-B to start those trials? Or are there any other pieces given, you know, it sounds like you want mature data from the phase I-B, that's an input into the phase three program. Sorry, a lot here. Yeah, yeah, no. I can keep going if you want. Well, I was gonna insert related point. Yeah. Which is we've gotten asked just because some of the SERDs have had some DDI questions with the CDK4/6 inhibitors. We've gotten asked if that was the reason to delay the phase I-B. Answer is no. Okay. We're still very much planning to start both the two phase three trials by the end of the year. Okay. That's not it. Obviously, just 'cause we are not sharing the data yet doesn't mean we can't use data from that to help us make our decisions, so. Okay. Yeah. There's really nothing on the ongoing studies that's gating for the registration studies. Okay. Got it. That will happen. Like I said before, when we roll out the VERITAC data, people will see why we selected the dose that we selected between 200 and 500. Okay. Obviously, we're exploring doses like that in the combination, but waiting for that data is not gonna delay the start of the registrational combo study. Okay. Any details you can share? I think one is a monotherapy study, one is a combo study, but just maybe, you know, design, patient population, anything on that side you can share at this point? I mean, we haven't really been that specific in the past, but certainly the monotherapy will be in the second line plus setting, and the combination will be in the first line. Yeah. Okay. Okay, great. How to think about the adjuvant opportunity. I mean, that's the other you know, bigger part of the market. I mean, is that a trial that would start down the road? Or there, how are you and Pfizer thinking about that? Yeah. We're definitely talking about that, planning for that. As I mentioned, we have a neoadjuvant study. We will have started that. We'll have some data from that. That That also will not be gating for the adjuvant. We're not gonna wait for that study to complete before we do the adjuvant. I think you've seen other companies do that as well. They've got a neoadjuvant overlapping with the adjuvant. We're thinking very much the same. Yeah. We recognize adjuvant is a huge opportunity. We wanna get there as quickly as possible. Part of that is selecting the dose, and the neoadjuvant will help us just judge that very briefly, as you can think of it almost like a run-in- Yeah for the adjuvant, but that's a big focus, obviously. Okay. Understood. Again, you know, you touched on the DDI questions with some of the SERDs, but the other is just the lack of activity of Sanofi pulling back from there now. I know you guys have talked in the past about differential activity of your PROTAC versus the SERDs, but maybe, Ian, you could just kinda remind us of some of the key points why you and Pfizer are still confident moving into that large phase three program, given some of those competitor data points over the last couple of months. Yeah, no, we've been very, very consistent over the years, and it has been years that, you know, PROTAC is different than a SERD. All right? PROTAC actively brings the E3 ligase to the estrogen receptor to ubiquitinate and degrade it. It's a very direct mechanism. It's a very efficient degradation mechanism. As opposed to a SERD, much more indirect. A SERD will bind to the receptor, kink it, make it look denatured, more hydrophobic. The cell now has to recognize that and ubiquitinate it. Or if you believe the Genentech data, it kind of, the SERD will block the estrogen receptor on the chromatin, won't let it move. The cell recognizes, "Oh, something's wrong," ubiquitinates it, and then degrades it. That's a very much indirect mechanism, much less efficient, and that's been very consistent with our data pre-clinically, where we look at degradation, we always see 471 is a much better degrader than these other SERDs, because it is that active direct mechanism. We've always felt that the best degrader will win. We've done a lot of profiling against fulvestrant, for example. Pre-clinically, people have seen that data, and we think that degrading is better than antagonizing. These other molecules are degraders, but they're suboptimal degraders. There's no two ways about it. They do not degrade as deeply as 471 does. In the end, we believe that degrading is the best way to go. I think what we're seeing is the suboptimal degraders having suboptimal results, where we think an optimal degrader will have optimal results. Pfizer shares that vision. They've seen obviously our data, that's why we've. The overall strategy is to make ARV-471 the endocrine therapy of choice. Yeah. Whether it be as a monotherapy or in combination with a CDK4/6 or a PI3K or any other mechanism that you could. Right. Can you just remind us on those degradation levels? I mean, you mentioned ARV-471 versus fulvestrant. Did you do the study versus any of the oral SERDs from Sanofi? Yeah, we've done. We've profiled every molecule that we can, that we know the structure of, and preclinically and seen that 471 has the deepest degradation, which is obviously right. We've degraded. We've shown our data as 90, 95% plus degradation with 471, and the other molecules don't approach that, so. Okay. Understood. Okay, maybe moving on to the other program. Again, I always call it ARV-110, but again, 'cause I can't pronounce the name. Bavdegalutamide. Again, here, I know now you're moving forward into phase three. I think there was maybe some, you know, hope for an upside scenario of maybe like a phase two that could lead to an approval. I know that was a more recent update, post the, you know, 2Q press release. So maybe you could just elaborate a little bit more on kind of the decision to go forward with the phase three instead of trying the accelerated approval path, which again, some, you know, a company like Clovis was successful for in the PARP space. Again, I know more of a question, maybe an upside scenario. Yeah. Yeah, that was our original strategy was to go for a single-arm accelerated approval path. We went to the FDA with that, but also with our study, the confirmatory phase three design. The feedback that we got, in terms of some of the inclusion criteria, exclusion criteria, as well as the fact that while they set our dose, our selected dose of 400 mg was okay to go forward with in the context of Project Optimus, they said, "But you have to really prove that a little bit more with the lower dose as well." We have some lower dose data, but not enough, and they said, "You need more patients on a lower dose really to prove that 400 is the optimal dose." Given that, we looked at the timelines. We looked at the fact that, okay, if you do a global randomized study, you're gonna have to do the confirmatory study. Timeline didn't shift that much in the end. We said, "Okay, the best way to do it, conserving patients, resources, et cetera, let's do the randomized study global." That means you have to go back to the FDA with that design. You have to go to the EMA with that design as well to make sure it's all harmonized 'cause you're gonna be doing both. That's why the study now pushes to the second half of next year. In the end, it doesn't cost us much time, and it's actually one less trial because we don't have to do the confirmatory study. While there was precedent for the accelerated approval, based on Project Optimus, some of the feedback that turned out not to be probably the best way to go. Yeah. Okay. In terms of some of that lower dose data, maybe just remind us when we are. I'm assuming sometime next year, but first half, second half? Yeah. That's a good question. I will say that none of the getting the second dose data because the study's already ongoing, we already have some data, is really not gating to the study. It's not like that's, we have to get that and then do all that planning. We can do everything basically in parallel. That's an important point. When we'll get that data, maybe Randy remembers. I don't know if we've guided to that. Yeah, definitely we haven't. I mean, it'll really inform the dose, you know, really confirm the dose for the phase three. Still, you know, planning to start that in the second half of next year. Okay during that timeframe. Okay. Got it. Are you enriching? I'm assuming you're enriching for mutations in that lower dose cohort, or is it still an all-comers? No, it's still an all-comers. PK, PD. Yeah, exactly. It's just, it's really. Okay A differentiation on PK, right? From our the dose that we proposed. Obviously more safety data. We'll obviously get efficacy data as well, but it's really just to show that it's a safe dose and it's the 400's differentiated, so. Okay. Is it just one lower dose? We're already, you know, had a trial ongoing anyway, so enrolling more patients at that lower dose doesn't slow us down much. Okay. Is it just one lower dose? Have we talked about? Yeah, I think it's just one more. Okay. The other question I guess is just the phase three trial. I know you talked high level. Maybe just remind us what the design is of that study, you know, in terms of patient population, endpoints, and again, anything else as we consider thinking about kind of enrollment timelines that could be relevant. Sure. It's gonna be in the AR mutant population that we talked about. Yeah. that we see the really nice signal. Again, late line population, post enza and abiraterone, essentially, where we believe that the AR mutations that they're responding well are a signature for those tumors still being AR dependent. Right. Very similar to what we're talking about with the estrogen receptor. The discussion will be obviously the size, because it will be a targeted population, it won't be a huge trial. The thing that we'll be talking about with the FDA and the EMA is what the comparator arm is. We've not guided on that, but those are the main things. It's still late line, in terms of the global idea, in that mutant population. Okay. I know you haven't guided on the comparator arm, but what are some of the, like, the range of possibilities if you think about what, you know, what could be relevant in that patient population? Yeah. Is it like chemo? Is it like Taxotere? That's where the. Sure. You could consider having the other abiraterone/enza comparator as well as chemo. You can imagine that in Europe that might be more important than in the U.S., and that's part of the harmonization we have to do in talking to both. You could imagine basically a investigational choice. Okay. As well. I see a lot of those type of studies. Right. Okay. Got it. Understood. In terms of like how I guess you, we still don't know the size of it, but in terms of enrollment, I mean, you know, a year, is that fair? Well, all I'm gonna say is we're gonna go as fast as possible. Yeah. Employ as many strategies as possible to make it fast. 'Cause obviously we're in competition with other Yeah. Not just modalities, but other agents. Orion's out there, basically in a similar population. We know there's other degraders. Okay. BMF has, et cetera, so. Okay. Got it. The primary, assuming this is PFS? Yeah. Yeah. Okay. Got Got it. Almost it. Yeah. Okay. Great. Well, maybe moving on to 766. Again, this is another, you know, AR degrader. Just remind us again structurally, like what was this one designed to do that 110 can't? Sure. Bavdegalutamide, we always knew that it couldn't degrade one of the mutations in the ligand binding domain of the androgen receptor, L702H. All these mutations make the androgen receptor more promiscuous. They can be activated by more than just testosterone. That's why they're as resistance mechanisms to these other agents. We knew why bavdegalutamide or ARV-110 couldn't degrade it, there's structural clash. It just can't bind to that particular mutation, therefore it can't degrade it. Knowing that from our structural studies, when we designed ARV-766, we could see that it would degrade L702H, and in fact, it does. When we started that program, really started as a backup. ARV-110 was the first PROTAC in humans ever. We said, "You know, it'd probably be prudent to have a backup to that," because we weren't really sure what would happen. But if we're gonna have a backup, we want it to degrade L702H. When we started, L702H was like 2%-3% of the population based on the literature. It wasn't that much, but we still said, "Well, good to pick it up." Over time, since then, L702H has actually become the most prevalent mutation in the 9%-10% percentage range. It's actually become more important over time to have a molecule that degrades L702H. That's the main difference. Obviously, they're different molecules. They do have different other properties like PK, and some ADME, nothing major, but they're still different. We'll see how that plays out in the clinic in the phase one study. We're trying to generate that data as much as possible and get to be able to select the recommended phase two doses, because we will have multiple doses. Then see how that plays, how that profile plays out, and then be able to position 766 well to the 110 based on clinical data. 'Cause preclinically, we know what they look like. Clinically, we'll see. Right. What have you guys said in terms of data timing for that phase I-B? End of this year, right? End of this year. ARV-766, yeah. Yeah. This year. End of this year. Okay. Got it. Is this an enriched population? Like, are you only enrolling the L702H, or are you enrolling just an all comers just 'cause it's more about PK? Yes, exactly. Okay. It's all about speed, PK. Yeah. Safety, exactly, so. Okay. Um. Your expectation would be it would be about 9%-10% of patients would have the. Yeah, based on what we saw from the Vertex study. Yeah. That's basically where it was running. Okay. Got it. Of course, it still picks up everything else as well. Yeah. Yeah. The phase two for ARV-766 is also planned to start by the end of the year as well. Okay. We'll roll straight into that. Yeah. That would be a more enriched population, I would assume, right? Where you would only enroll the L702H. We haven't talked about the design. Again, it has a broader profile, so, I think just enrolling only L702H is not likely. Okay. it could be broader. Obviously, ARDENT was set up quite uniquely with four different cohorts. Right. Yeah. We were learning a lot in that study. I don't think we have to learn quite as much with the ARV-766 study, but. Right. You'll see that by the end of the year. Okay. I guess, you know, obviously, you guys have the Pfizer partnership. Randy, this is probably a question for you. As you think about one ten, again, is that a program that you feel like you guys can carry through commercially solo, or is that something where you'd be open to a partnership, as well? Yeah. I'd say we are confident that we can, for sure. Especially I think with the narrower indication, we feel very well situated to do that. The capital situation is really positive for us. We have an ongoing relationship in place with Foundation Medicine to do the companion diagnostic for that. So it's pretty straightforward. However, you know, of course, it's always true that if someone can convince us that they can help us go broader, faster, earlier, you know, at an earlier stage, you know, pre NHA, certainly we'd be happy to listen. But we feel pretty confident where we are, with the resources we have to move forward and still, you know, bring everything else, you know, into the clinic as well. Good. What would be the trigger for those pre-NHA studies? Like, what would you guys want? Would you just complete the phase three first in the late line, and then you would go to those studies? Or is that something you could run in parallel, essentially? I would tell you, yeah, overlapping. Overlapping. Okay. I don't think we need to have the data from those to go earlier. I mean. Okay. The reason to go earlier is to get into lines of therapy where AR is still driving. Yeah. You know, depending on the mutations. Right. If that's the general philosophy, then you don't need to wait for that. You wanna Right. Can do it overlapping. Because it's not that we degrade the mutations better, right? You'd expect that earlier in the treatment paradigm- Right. You've got more AR-driven disease. There's no reason you couldn't be active there as well, so. Yeah. Okay. Maybe just in terms of last topic, I mean, you touched on this, Randy, the four new INDs through 2023. Maybe just any update on kind of progress towards that goal? Is this something that are gonna be staggered over that timeframe, or is it more like back-end 2023 loaded, just as we think about kind of the rollout of those other INDs? Well, I think the clinical team definitely prefers a staggered approach. Not much more we can share in terms of timing. You will see, you know, more data come out as we get closer to that. You know, it's been nine months now, but we had BCL-6 data last year at ASH in December. Yeah. That's certainly one of them that's on the pipeline. Yeah. That could be an option. Haven't been more specific on timing yet, but it'll definitely be a different-looking situation, you know, this time into next year with all those new programs coming into the clinic as well. Yeah. Looking forward to it. Okay. I know KRAS was also on the list. I mean, is that one that's still high priority? I know there's been some questions on kind of the role of these agents in the frontline setting in lung cancer, but is that still a target of interest for you guys? Oh, yeah. Absolutely. KRAS, we've talked about this pretty openly, is actually multiple programs in one. Yeah. We pivoted away from G12C, that's where a lot of our activity was, because we do not see differential biology of a PROTAC using an irreversible warhead versus the irreversible compounds from Mirati and Amgen. Which makes sense, because you lose the catalytic activity of the PROTAC. We pivoted to G12D and G12V and a pan-KRAS. We've been investing a lot in KRAS. It makes perfect sense for a PROTAC, so we're pretty excited about that. We have MYC as another undruggable on the pipeline. We have the neural programs. Our INDs will come from, I think Randy said, from our named programs, but also from our unnamed as well. Right. We actually have more unnamed than named programs quite honestly. Okay. Got it. We could get some surprises. You'll get some. Okay. Great. Remind us on the CNS side. I know that's another part of your platform that's differentiated, the ability to get through the blood-brain barrier. Maybe just remind us of kind of the targets that you guys were going after with some of the initial programs and anything, you know, we might see later this year, maybe some more data on the CNS side. Yeah. I know that's still pretty important for you guys. Oh, yeah. Absolutely. Our three named programs are tau, synuclein, and then huntingtin, mutant huntingtin. Those are progressing well. All of our programs will have PROTACs across the blood-brain barrier, that kind of goes without saying, but we've been very, very successful. I think you will see data later this year, but we've not guided yet, showing some of that data on our programs. That'll be a little teaser for you. Okay. Is that one of the named programs or could it be an unnamed program? I'm not gonna disclose. You can't go make me go farther than that. Okay. I guess in terms of, maybe just last question in terms of balance sheet. I mean, Randy, you mentioned this, you guys are, given the Pfizer collaboration and the upfront, pretty strong position there. They also help fund a large portion of that program. Maybe just remind us what you said about kind of future cash needs burn. Absolutely. Yeah. As of the last earnings, we had $1.35 billion in cash. We've said that's multiple years beyond 2024. Obviously it's great to have that amount. Obviously, the burn will go up as we move multiple programs into phase three trials, but we feel great about where we are. Great. Well, thank you so much for being here today. Really appreciate it, Randy. Ian, nice to see you. Yeah. Nice to see you. Thanks so much. Yeah. Thank you very much. Thanks for having us. Thanks. Appreciate it.