All right, I think we're just at about time, so I think we're gonna get started. Want me to welcome everybody once again to the 44th Annual TD Cowen Healthcare Conference. Thanks so much for joining us. I'm joined here today by CEO of Arrowhead Pharmaceuticals, Chris Anzalone. Thanks for joining us. It's great. Thank you for having us. All right, so lots going on at Arrowhead these days, from everything from pulmonary to cardiometabolic, upcoming PDUFA dates, new data coming out. And on recent earnings call, you kind of, kind of really discussed the thinking from a strategic perspective in terms of these two new pillars, right? So maybe give us a sense of what went into the prioritization into cardiometabolic and pulmonary, and really why that's the right move right now for Arrowhead, based on where you guys are. Sure. Again, thanks for having us. It's a real pleasure to be here. So let's see. So broadly speaking, it was time for us to pick verticals, right? You know, and the history of this company has been one of rapid innovation and rapid transition from idea into the clinic, and we're able to do that en masse, you know, in these early programs. As programs become later stage, two things happen, two things change. You know, one, programs become more expensive, of course, and second, they start to require deeper domain experience. And so it made sense, you know, for us, as we progress, to start prioritizing certain areas. Cardiometabolic was a no-brainer, right? Between APOC3, plozasiran and ANG3 zodasiran. We are covering a number of important indications, I think. And it's, and it's not just long term, it's near term. You know, we have, we have a phase III study that we'll read out this year. We expect an NDA by the end of the year. We'll be in market, you know, sometime next year, in FCS. So, so what we see in cardiometabolic is, is over the next several years, a really, a really important train of value creation. You know, between these two drugs alone, you know, we can treat, FCS, roughly in this order: FCS, HoFH, HeFH, and then ultimately, with, with one, of those, presumably, ASCVD, with a, with a, you know, resulting from a, a broader cardiovascular outcome trial. So there's a number of areas to build value, I think, over time, with those two drugs alone. You overlay on top of that, additional cardiometabolic candidates will be coming down the pipe. We've talked about Inhibin E, this is an obesity target, as well as other, you know, metabolic concerns, right? That'll be in the clinic this year. We also have the ability to target adipose tissue. We haven't disclosed what targets we are focused on in the near or midterm there yet, but we will. I expect at least one of those will be in the clinic this year. And so between Inhibin E and potentially additional hepatic targets, as well as all these adipose targets, you know, this makes for a very large train of value creation in the cardiometabolic field. So that that's a bet we're gonna make. You know, and my job here is two things. You know, one is to mitigate risk, and the other is to expand our upside potential. We can do both of those things with cardiometabolic. You know, with all of these indications, all of these targets, we are not a binary play here, right? You know, we've got a number of shots on goal. And of course, the flip side of that is we have a number of areas we can create value. So cardiometabolic is easy. Pulmonary, you know, is a very attractive space. It's. We've talked about this in the past. There are 16,000 pulmonologists in the U.S. We like the idea of building a commercial force to address that relatively, you know, small market with a number of targets. And we think pulmonary is a target-rich environment. We don't expect, you know, 2 or 3 or 4 drugs coming out of that platform, but we expect 8 or 9 or 10. And so that makes sense for us to make a bet there, too. Which is not to say that we're not gonna partner within pulmonary. I think there's plenty of space there to do both. You know, to have wholly owned assets, to have partnered assets. So that made great sense. Now, these are our two sort of early pillars, if you will. We expect additional ones going forward. You know, we've got the possibility of skeletal muscle at some point. We've got two drugs in the clinic right now. I don't wanna get ahead of ourselves. And CNS will be coming down the pike this year and beyond, and so that's another potential pillar, you know, as we see data and as we see how that may fit into our broader strategy. Okay. All right, so there's a lot there to kind of unpack. And maybe to your point, just before we drill into pulmonary, I mean, you mentioned in the context of this restructuring that you kinda wanna decentralize the CMO role. So I guess when you look at cardiometabolic, when you look at pulmonary, what does that look like to us? And then what kind of changes are you actually looking to implement as you really consolidate there? Yeah, yeah, so they're not massive. You know, what-- You know, we will... I can foresee having a head of these verticals, right? You know, a head of cardiometabolic, who has, you know, deep experience doing, you know, filing NDAs and doing phase III studies in various aspects of cardiometabolic. That person will lead that vertical. Same thing for pulmonary, and then same thing for, you know, any additional verticals that we develop. Okay. All right, so let's get into pulmonary. Right, there's a, there's a lot here. We wanna talk about ARO-RAGE, we wanna talk about MUC5AC and MMP7. But when you look at kind of the landscape of, of the indications that you can address here, you have asthma, you have COPD, potentially IPF, and some others down the pipe, right? How are you prioritizing which target to go into which space? And maybe let's focus on ARO-RAGE first. What are the updates this year gonna look like? Sure. So, RAGE, to us, feels like a severe asthma, and maybe in the future, less severe, but in the nearer term, severe asthma drug candidate. What's attractive to us about RAGE is that it's essentially undruggable, but has been a well-validated target for some time. You know, it tickles a number of different pathways, and so it's sort of a pipeline within a drug. You know, it's not just something that could potentially decrease IL-13, for instance, but different, a whole variety of pathways. And so, it's a broad player potentially. Now, within asthma, you know, we think there's probably 1 million or so potential patients with severe asthma in the United States. You know, people often think about this as those, you know, with type 2 inflammation and those, you know, not showing type 2 inflammation. We think, given where RAGE is on this inflammatory pathway, we should be able to address both those populations. So, you know, we'll know that going forward, you know, as we get into a phase 2 study, but at least theoretically, we think that we can address that entire market. Okay, so when we look at kind of the cadence of data before you enter a phase 2 study now, so when we're – when, when can we expect full dose ranging from phase 1 in asthma, and then what are we looking at when it comes to the high FeNO patients? Yeah. Maybe also, why do they make sense for RAGE right now? Yep, yep, sure. So, so here's what we've seen so far, and then I'll, I'll get to, you know, to future data. We've seen a good safety profile. I think we've been in, you know, among our, our, our, our three pulmonary programs, I think we've been in, in 150 or, or so, human subjects, and we've seen, you know, we've seen a good safety profile so far. Second, we've seen good knockdown with ARO-RAGE. We've seen that in healthy volunteers all the way up through the highest dose, which is 184 milligrams. And it appears that we're just crushing RAGE. You know, we've been talking about circulating sRAGE, you know, where we see knockdown in the 90%-95% range. That's impressive, and we feel great about that. But keep in mind that that's in circulation, and we know there are extra-pulmonary sources of sRAGE. So we would expect that knockdown in the lung is even higher than that. In fact, we've seen that. You know, we've seen within the BAL sRAGE reduction that is even greater than what we've seen in circulation. So it feels to us like we are, you know, we really do have our boot on the neck of that pathway in healthy volunteers. We will have patient knockdown data shortly. I'm not sure when we'll be able to talk about that. You know, probably at our next earnings call, we could probably talk about it. It's still ongoing, but so far, we've said this publicly on several occasions, it's mapping, you know, quite close to what we've seen in healthy volunteers, and so we expect good knockdown, continued good knockdown in patients. So then the next step is, okay, so what does this all mean? And we are enrolling high FeNO cohorts as we speak. We'll be looking at three different dose levels, 92 milligrams, 120, and 184. The reason for those three is that, you know, we see very good knockdown. We see essentially complete knockdown at 184, and something like 80%-85% knockdown in the 92 milligram cohort. And so we're curious to see, to know how steep that dose response curve is, and so we'll do 120 in the high FeNO cohort. That will help us to, you know, to design the phase 2 studies. In any event, you know, we'll have these high FeNO patients in over the next couple quarters. And so my expectation is that we'll have data from those sometime in the third quarter. Okay, so when we're talking about RAGE knockdown, right? I mean, we've seen, like you said, 90%+. I mean, do you have a sense of what that actually correlates to when it comes to actual lung function, right? And when are we gonna actually see some of these, like, potentially FEV1 data or something like that- Yeah, yeah From asthma patients? Yeah. So I don't have a good answer for you. We don't know how much knockdown you need, and if we were seeing 60% or so knockdown, I think that would be a more valid question because, you know, because who knows? But given that I think that we are crushing it, I think that we are, you know, getting, you know, near complete knockdown, you know, in the lungs, it really shifts to the veracity of the target, right? You know, theoretically, this target, knocking down RAGE, you know, should give us a number of, of good, you know, downstream effects. If that theory holds, the type of knockdown we're seeing, we would expect, you know, would translate into clinical benefit. Having said that, you don't know until you know. And so we won't really know that until a phase 2 study. You know, we are measuring FEV1, of course, in the phase 1, but that's really more of a safety measure. You know, we're only dosing, you know, single doses or as many as 2 doses, and so it's not really enough time to see changes in FEV1. And of course, FEV1 also can be a bit noisy, and these are small studies, and so we wouldn't expect to, you know, anything to be powered for changes until the phase 2 comes out. Okay, so but in the studies where you're measuring FEV1, admittedly, that it is a safety, are we, are you planning to release some of that when you actually put out the sRAGE knockdown data? You know, at some point, we'll talk about those. I don't expect in the near term there's other than as a safety marker, you know, the good news is, you know, we're not seeing changes there, and so, you know, the safety profile continues to look good. Okay, so in terms of cadence, well, you know, you said we're gonna get full healthy volunteer and asthma patient dosing data, let's say Q2-ish, and then high FeNO data Q3. Would you assume that you could potentially start a phase 2 this year based on what this data looks like, or are you gonna need that kind of time in Q4 to get ready for a phase 2 and maybe start early next year? No, my expectation is that we can start a phase 2 by the end of this year, or at least, you know, at least file to begin. Will we be dosing patients this year? Probably not, but I would consider us starting that study or those studies by the end of this year. Okay. So, excuse me, maybe help us contextualize just a little bit. When you, when you talk about RAGE knockdown, you talk about it in the context of, you know, it's been historically difficult to drug. You know, when you look at some of the available asthma drugs that are on the market, you know, you say that there's solid evidence, validated target. I mean, what, what kind of clinical efficacy are we talking about? Just even extrapolating, right? Obviously, you have to validate this when it comes to the clinic, but, like, why does this target make sense based on how validated it is? And like, you know, relative to the drugs that are out there, what kind of FEV responses might be in the realm of reasonable? Yeah, well, so we clearly have to be competitive with the biologics that are around. You know, we think that we have the chance to provide pulmonologists with, you know, with another tool here. You know, we would expect, if the theory holds, you know, and if knocking down RAGE really does do what we expect it to do, we certainly would expect to be competitive with current biologics and maybe superior to some of them. Okay. But you would focus on the severe asthma patients primarily. Yes. For the time being. Okay. Yes. All right. So then for MUC5AC, give us a sense of timing. When are we gonna get the first data? 'Cause this is a different target, right? This has to be expressed in patients, right? 'Cause it's really not upregulated in healthy volunteers. That's right. So we would actually need patient data to get a sense of how strong the actual knockdown is. So when are we talking about for that first data? Yeah. Yeah. So that's exactly right. My expectation is to have data also in the third, you know, late third quarter sometime. You know, we're still enrolling patients, and so it's hard to give more granular guidance than that. But again, as you say, we have gone all the way up through the highest dose in healthy volunteers, and now we are dosing patients, and so we'll see what that looks like. We're really excited about that target. I mean, it's... You know, this is the root cause of, you know, of mucus plugging, for instance. And so if we can get a handle on this thing, that's really important. Now, you know, the follow-up question, you know, would be, how much knockdown do you need? The answer is, of course, we don't know, but at least, you know, in our animal models, almost any knockdown was, you know, was helpful. You know, and you know, imagine in these severe asthma patients, in these COPD patients, you know, with a massive overproduction of MUC5AC, any reduction, you know, could be helpful. And so I think more is better, but generally, sort of my, you know, our collective gut says, you know, anything over 50% is gonna be helpful. Okay. So and then MUC5AC, you're focusing on COPD first or asthma first or simultaneously? What's kind of the thinking? Probably COPD first. You know, we, you know, we'll see what the data look like, and of course, we have not started designing phase II studies yet, but my expectation would be that that would be the primary focus of COPD. You, you go into, first go into some of these more refractory patients. Would you try to recruit treatment-naïve? I think, what, what are you kind of thinking in terms of where it could fit into the treatment landscape? It's too early to tell. You know, we'll stay tuned on that. You know, as we get data, you know, we can start to talk about what the designs look like. Okay. So MUC5AC data, first looking around Q3 as well. Okay, so in terms of then shifting to MMP7, I mean, there's a lot of conversation. We've had the IPF panel, IPF-PH panel the other day here. You know, there's a ton of different targets in IPF, historically very difficult to actually show some kind of clinically meaningful improvement there. Why does MMP7 make sense? And I guess give us a sense of where it's kind of situated in this, like, milieu of different pathways that are contributing to IPF. Right. So MMP7 is a well-validated target. You know, the way we came across that is the same way we came across RAGE and MUC5AC and others, in that, you know, we would convene these KOL panels, and, you know, we show data, you know, we show data with tool triggers. You know, this is the kind of knockdown we can get. These are the kind of cell types that we get knockdown in. You know, if you could do anything, what would you do? And we just kept hearing MMP7 over and over again. It has been undruggable. And we know that it is highly correlated in IPF patients. You know that the higher the MMP7 expression, the more severe the disease is. We know in mouse knockouts, MMP7 knockouts are protective against injury-induced IPF in those models. That's helpful. In fact, we've seen in our hands, reduction of around 50% gives us a benefit in these animal models. And so all that looked very attractive to us, and it's expressed in a cell type we can address. You know, it's involved in both inflammatory and fibrotic pathways. So it felt like a really good first IPF target for us. Okay. So then where are you at, at this point in terms of enrolling that? Would you... First, first data we'll get with MMP7, are we talking about healthy volunteers and IPF patients together? Yeah. So as with MUC5AC, we have gone all the way through the highest dose in healthy volunteers, and we are now recruiting patients. You really, you know, again, as with MUC5AC, you can't really see MMP7 knockdown in healthy volunteers because it's just not really produced. My expectation is that we will have patient data around the same time as MUC5AC, sometime in the late third quarter. Okay. So in terms of kind of the cadence of these, is this like a, you know, you present all of these at a medical meeting or something, or would you kind of put them out as the data is available individually? Yeah, we'll see. Decided. You know, I like to do both those things. You know, once we have complete data sets here, it'd be nice to top line some of them, but then provide, you know, the broader, deeper data set at medical conferences. Excuse me. I think, I wanna say it was at ERS last year, I think you mentioned the possibility of a TSLP-targeting- Mm-hmm. Compound. I mean, what's the latest on that? When can we maybe expect that to enter the clinic? And kind of how are you thinking about RNAi targeting TSLP versus some of the biologics that are out there? Yeah, yeah. So, we do have a TSLP candidate. We are kind of sitting on that right now as we see what RAGE looks like. You know, RAGE is sort of. It feels to us, at least theoretically, you know, RAGE, within RAGE, there is a TSLP knockdown as well, right? You know, because it includes that pathway. And so that is, it's an interesting target, but we're not gonna bring that into the clinic yet until we see what RAGE looks like. And also, you know, we view that as a component of a good, of a dimer, potentially. You know, we've got the ability to do dimers. We have not done much dimer work in the lungs yet, and so that's sort of our next-generation push. We've done a lot of dimer work in hepatocytes and other cell types. But TSLP could be a really nice component of a dimer. Okay, so when you say that, it's kind of implicated in this RAGE knockdown, I guess, do you have a sense of, you know, when you knock down RAGE, to what degree are you able to inhibit TSLP, really relative to the kind of knockdown we're seeing with some of the biologics out there? And I guess I'm trying to get at, you know, how competitive would you expect RAGE to be versus some of the TSLP-targeting drugs that are available? Yeah. So the FeNO data may give us some, may help us with that question, but it's hard. There's, you know, it's hard to measure some of these downstream effects. You know, you know, we talk about FeNO just because we can, not because it's the end all. You know, it is, it's... You know, it is, it is a way that we can measure, you know, IL-13 reduction. But there's a number of different pathways that we should be addressing with RAGE that are just much harder to assess. Okay, so you- Uh- It sounds like you'll probably wait until at least the high FeNO data with ARO-RAGE before you decide to move with TSLP. Or would you wait until you have, like, phase II data with RAGE until you advance that one? I don't know the answer to that. All right. Fair enough. All right. I think it's a lot on pulmonary. Obviously, you guys got a lot of other things going on. I do wanna touch a little bit on some of the timing to, filing and the upcoming data, right, with, plozasiran. Maybe first let me ask you, just because I know that's, it's a, it's an important point of consideration for you all: What's the latest on the CVOT? Which drug are you thinking? Which way are you leaning now? And maybe what's kind of the, the, the process that you're going through to decide which... whether it's plozasiran, this is the, APOC3 or the ANG3? Yeah. It's not easy. So the good news is, there's probably not a bad answer, you know? I think both those drugs will do well, CVOT. I really do, and our KOLs believe that as well. And so we're just... You know, we are, we're still in that process. We have not made a decision. My expectation is that we'll make that shortly, you know, over the next month or so, and then put together a protocol and then start talking to the FDA about what that protocol looks like. But we have not made that final decision yet. So fair to say that we would get a decision by Q1? Uh- Q1 column. Yeah, I think that's probably fair. I think it's probably fair. Okay. And, I mean, it seems like some of the lipid biomarkers that you've I mean, you had a whole deep dive analyst day looking at both drugs' profile. It seems like, you know, the kind of remnant cholesterol that you're looking at is a primary factor and when you're trying to decide which one to carry forward. Yeah. Again, you know, the good news, bad news is that both these drugs, you know, alter a number of lipid parameters that we think are important. So yeah. You know, we continue to comb through patient-level data to try to figure out which one might be best. Okay. So I, I think from a timing perspective for the APOC3 drug, I think we'll get FCS data still in Q3. Is that fair to say? That was the- Yeah, I think it's fair to say. You know, the- Yeah. So the last patient in, last patient, last visit, I believe, is in May. And then, you know, you've got to lock database and analyze the data. But I think third quarter is reasonable. Look, I expect that we will present those data at a medical conference. And so we'll see where that would be. My hope is that we would topline it, and then present the deeper data at a medical conference. Okay. And obviously, the read-through there from the FCS would then be into the much larger SHTG population, right? So- Yeah. I think you have two or three phase III studies with SHTG about to get underway, or are they now recruiting? What's kind of the status on these? No, so we have those protocols set, and we have begun communicating with the FDA around those protocols. There are three of them. You know, two just in the broad SHTG population, and then one will be in those patients with a heightened risk of pancreatitis. Okay. So I mean, we've got some ASO data and some in FCS. Shortly, we'll have it in SHTG. So I guess in terms of how long you think it would take to enroll and run the SHTG studies. I mean, it seems pretty clear that RNA has very clear benefits in terms of dosing, right, when it comes to ASO frequency. But I mean, what are we talking about in terms of timeline to potentially pivotal SHTG data? Are we talking about next year, or is it maybe- No, no, no. Closer to 2026, 2027? No, it won't be next year. But, you know, because, you know, it will be. You know, these will be year-long studies. And it'll take us some time to enroll them. We're not ready to give guidance on that yet, in part because we, you know, we haven't gotten our protocols blessed yet. You know, let's make sure that we know exactly what these protocols look like, and then we can start to make some guesses about how long it'll take to enroll. But, you know, you mentioned ASOs, and the data so far have supported... Did my mic just go out? There it goes. The data so far have supported our assumption that we should see deeper knockdown, and more durable knockdown compared to ASOs, and potentially a better safety profile. So far, that has held up. Okay, so I think my next question, I think, applies to FCS SHTG transition, but also, you know, HoFH, potentially to HeFH, and then potentially into mixed dyslipidemia. When you're thinking about kind of pricing in these ultra-orphan markets with the, with a certain drug and then inevitably trying to move into the larger markets, I mean, what- how are you thinking about that transition over time? I mean, obviously, I think you're gonna be, I don't want to say constrained, but impacted by potential earlier launches doing the same trajectory. But, give us a sense of how we should think about that kind of market pricing as you move from one to the other. Right. So, so look, I think that we expect to have open and transparent conversations with payers that, you know, the initial label I expect, you know, will be for FCS, both genetic FCS, as well as sort of clinically defined FCS. So, you know, these are the patients with triglycerides above 880 and history of pancreatitis. I expect the label to say that, and that's a relatively small market. And so my expectation would be that those will be priced—they'll be priced as an ultra orphan. However, we do expect, you know, to expand the label as we complete these SHTG studies and potentially, eventually, you know, in a broader mixed dyslipidemia market. And so, and so we would expect step downs in pricing, you know, should we be lucky enough to, to see approval in these broad markets. And so that's, that's our expectation, and I think that we can have those open discussions with payers that, look, you know, it costs X now, but, but, you know, should these, should these, these other studies pan out, and, and the label will be broadened to in- to include these other populations, of course, the, the prices would drop commensurately. Okay. So then for zodasiran, this is the ANG3 targeting drug. When can we expect that you'd start HoFH study, the, the pivotal HoFH study? And then, have you made a decision on whether you're moving into the heterozygous population? Yeah. So it's a good question. We are developing that right now. You know, of course, we need to communicate with the regulators, but our hope is that we can do a HoFH and high-risk HeFH phase III study, rather than just, you know, only HoFH. And so we'll have those discussions with the FDA. Now, the broader HeFH population, we have not had discussions with the FDA around what the approval endpoints there would be. You know, would that be simply lowering LDL, or would we require a CVOT? We have not had those discussions. Okay. And kind of what percents of the broader HeFH population are we talking about when it comes to the high-risk patients? You know, it would be a small pop... It'd be a small percentage. But, you know, it would- I think the FCS analogy is a good one, right? You know, it's sort of the population of genetic FCS is very small, but then, you know, it can become in the thousands when you include these clinical FCS. I think the same thing for HoFH to the high-risk HeFH, I think it goes from hundreds to, you know, to low thousands. Okay, great. So the last couple minutes here, I want to talk a little bit about financing strategy. I think you touched on this on the last earnings call. I mean, you had a nice equity offering recently. You, you kind of alluded to the potential of, for a debt component moving forward. You have a bunch of partnerships and potentially some more coming down the pike. So I guess maybe give us a sense of cadence of what you're thinking, why a debt component would, would make sense now, if you think it does still, and then when we might get an update on any potential partners. Sure. Yeah, so our financing strategy has always been a multipronged approach. You know, we're doing a lot of things here, and to rely solely on equity financing wouldn't make sense. To rely solely on partnering wouldn't make sense. To rely on debt, of course, wouldn't make sense. But a combination of those things do make sense, I think. As you mentioned, we had a good equity offering, I guess, what, late December, early January. And we expect to follow that up, you know, with a more structured finance transaction, you know, relatively soon, I think. We've been talking to a number of firms about, about, you know, about a structured transaction that would, that would include a royalty piece, you know, that would be for, for, you know, one of our products, and then could have a debt-like component to it. I think that we will get something like that done, you know, in the relatively near term. I think that that's- that gives us... I think that, I think that will, you know, that could be a source of a lot of capital for our balance sheet, but also give us, you know, more time, you know, to do a number of business development deals. You know, you can't control the timing of those deals, and so, and so we just need to make sure that we are properly capitalized so we can, we can do the right mix of business development deals rather than the first one that comes to us. So, I mean, when you're thinking about how to prioritize some of these different BD partnerships, I mean, obviously, like ex-US commercialization partners for some of these larger cardiometabolic indications seem to make sense, but, you know, you have a pretty wide pipeline at this point, too. You have skeletal muscle, I mean, you have even the adipose tissue or CNS. I mean, how are you prioritizing each of these, and like, are you expecting additional partners and beyond commercialization partners this year? Yes. So, let's see. You know, we would like to do ex-US commercialization partnerships for, you know, for the big cardiometabolic drugs. That doesn't have to happen this year because we really don't need those partnerships until we're in much larger markets, and so we've got a bit of time to let those brew. So, yes, it'd be fine to have them this year, but it'll also be fine to have them next year or the year after. Beyond that, we've got an awful lot of ammunition here, I think, to do business development. You know, we are making a commitment to pulmonary, but that's not to say that we will not do deals in pulmonary. You know, as I mentioned, that's a target-rich environment. And so we are. I think we can do platform partnerships in pulmonary for new targets that maybe we're not developing right now. We have three, we have three good programs right now that we like a lot. Doesn't mean that we will always, you know, leave those unpartnered. I think that we could do some partnering within pulmonary, but still have that as a core vertical for us. You look at complement space, you know, we've got C3 and Factor B. These are dynamite targets, and they're gonna work, I think. You know, RNAi is a very reliable technology, and we know how to deliver to hepatocytes. We know we have good expectation about what those knockdown profiles should be. The data for C3 have been very good so far. We're dosing patients as we speak. And so I think that could be a place for partnering. You know, we'll see about skeletal muscle. You know, could that be a vertical that we wanna hold on to or partner? We haven't made that decision yet. But that is possibly, you know, a space that we could partner, or hold on to. Look at NASH. You know, we've got a dynamite program in PNPLA3 that we developed for J&J. They decided to get out of NASH, and so we have that candidate back to us. That's a good defined, you know, genetically defined population. That's something that we could consider partnering or holding on to. All right. I guess last question, just because you mentioned it. I mean, are we gonna get, any data updates with the C3 or the Factor B asset this year? Let's see. So C3, I do expect you'll see patient data this year. Factor B, let's see. You know, it's possible that we could have knockdown data by the end of the year. We've just started that, as you know, and so we'll see how fast we can enroll that. But it's certainly possible we could have some data, you know, towards the end of this year. Okay, so C3, probably Q3, Q4, we're talking. I think that, I think that makes sense, sure. All right. Great, now we're a couple minutes over, so I appreciate everybody sticking around. It's good to see you. Always a pleasure. Yep. Thanks for joining.