There's been a lot of change, you know, I think, in the company, you know, the last couple of months. Just kind of walk us through that, and then we can kind of start digging into some of the questions. Yeah, for sure. Got through the hardest part because you pronounced everybody's name. Yeah, nailed it. Good job. I should just quit right now. That's right. Hey, maybe just to go back a little bit, so I took the role in May, and at the time, we announced that we would be, you know, we were looking forward to HS data. In the third quarter, we had just announced a positive PsA trial, and that, you know, we were going to look at the data and that we were really gonna take a look at the business, and make some decisions around the portfolio of the business going forward on the back of that data. And so, you know, that's what we did in August. We read out a positive HS trial. We're very pleased with the outcome there. But notwithstanding that, we did make the decision as a business to deprioritize internal development of HS and PsA, right? And to really focus our resources and our energy around lonigutamab, which is our program in thyroid eye disease, right? You know, we did that for multiple reasons, right? Notwithstanding the fact that the data were positive, and we think that that program or those programs are absolutely approvable and commercializable, that you know, they might benefit from an organization with existing footprint, you know, in infrastructure, in those kinds of areas. And that TED, the early data that we read out earlier this year, we were very excited by, right? And that we were gonna focus our resources around taking that program all the way. And so part of the announcement in August was that we had also restructured the company in line with the prioritization and the change in strategy and the focus and strategy. And all of that combined enabled us to extend our cash runway into mid-2027, which fully funds the pivotal program in TED. So that's kind of where we are now. Got it. Perfect. So I think everyone would expect me to start with Lonni, but I'm gonna actually start with uveitis. Sure. Obviously, as you mentioned, you're not moving forward in HS, not in PsA, but you have an ongoing uveitis trial. Thank you. So maybe just walk us through the rationale for IL-17 there. And I guess, you know, what are the kind of variables that you're gonna have to think about, depending on the data, about either feature? Like, would you develop that specific indication, or would you look to partner? Like, what do you do with the program, depending on the data? Yeah. So let me start, and then I'll turn it over to, to Shep, maybe. So, you know, so Uveitis is the third program that we were running with izokibep, right? That trial, we finished enrollment earlier this year, right? So that program is effectively fully funded. And I think in the same way that we have with HS and with PsA, right, we're gonna look at that data and then make some decisions about what do we do with that indication going forward. And, you know, Shep maybe can talk a little bit about, you know, what are Why, why did we do that trial? Yeah. You know, what is Uveitis? You know, how do we think about that? Yeah. I think the rationale is pretty strong, having worked on Cosentyx secukinumab on similar trials in uveitis, and looking at izokibep, which is a tenth smaller than a monoclonal. Also, being a small protein therapeutic, we have done preclinical studies, which have shown very nicely that 10 mg per kg IV of secukinumab equates nicely to 160 milligram QW, which is the dose we currently have in uveitis. The 10 mg per kg IV for secukinumab showed a very nice response compared to placebo. And when I was still there, when we moved to subQ, we didn't see the signal we were expecting, and we know exposure is critical. Mm-hmm. The other element that we have in our preclinical studies is that we did show that a subQ in primates, when we measured in aqueous humor at that dose, is really penetrating the eye. Okay. We have great confidence that we are exposing patients in uveitis at the right, you know, sort of exposure with a small protein therapeutic on a validated target. Hopefully, the outcome we see might change the paradigm for addressing the unmet need in uveitis. So what's the trial design there in terms of like, you know, how many arms, and are you just looking at the one dose? And like, what's the efficacy measure? Like, again, this is a new indication to me, so anything- Yeah. So, so far, there's only Uveitis There's only Humira, which has done- Yeah the VISUAL-1 study. Our study is akin to the same. Okay sort of patient demographics, characteristics, and the same mandated protocol decrement of a blast of steroids, starting at 60 milligrams, going to 0 milligrams by week 15, and then looking at treatment failure on a Kaplan-Meier curve and hoping to see a delta that's commensurate or better than what is currently shown by Humira. Okay, so there's a steroid taper as part of this? Correct. Okay, gotcha. Yeah. Interesting. So you have two arms, patients who take steroid only Yep and patients who take izokibep and steroids and follow them up to the event rate or a primary efficacy endpoint determined by treatment failure, which looks at multiple parameters of inflammation in the eye and also best-corrected visual acuity. Gotcha. And so what did Humira do in their trial? So what, is there like an efficacy bogey that you're looking for? They had a delta of around 28%- Okay at week twenty-five. Gotcha. And then the Cosentyx data that you talked about, like, or the experience there, like, what, what does it look like? And ultimately, you kind of made the case for why izo is probably better there, but, like, what level of activity can you even just see from Cosentyx? Yeah. So the response around the ten mg per kg was around 60%, and in the thirty mg per kg was a difference of 8%. So really respectable, and placebo was much lower. So a huge delta in those response parameters. Okay, so very good activity, at least. Absolutely. Yeah. Got you. Okay, great. So and then, yeah, obviously, you know, it's a big market opportunity. So, you know, kind of looking forward, you'll have to just make a decision depending on the data, you know, what the next steps are in terms of either commercializing or partnering or- Yeah. However. Absolutely. We'll sort of make the decision- Yeah in the same way we did around HS and PsA. Got you. I mean, it might be worth, you know, I guess, talking about sort of that, the opportunity, right? And what is that, especially, in light of the fact that we are not moving forward with HS and PsA- Yeah Internally, right? You know, it does open up the potential, for example, for, like, orphan pricing. Okay. And so that's, you know, that will be, you know, part of the consideration for us. Got you. Yeah. Anything to add there, Shep? No, I wouldn't add anything else other than, you know, I think the it's a very underserved market. Right. There is only steroids and Humira available right now, and when you look at the size of the market in the United States, it's pretty significant. You have seventy thousand patients, and you wouldn't need too many treated on a biologic within the orphan pricing regime to have a pretty interesting market opportunity. We'll take a look at the data when we get it. Okay. Mina said, make some decisions then. Any more, you know, detailed timing on when Is it, like, very end of the year? Are we talking Christmas time? Like, what is it gonna be, you know, under the tree or what? I'm not sure that we've got any more- Okay to say on that, but, you know, we do expect it this year. It's worth a shot. Yeah. All right, so now we can move to lonigutamab. Sure. So I guess, you know, obviously, we've seen some data, but let's take a step back and just understand. Yeah. So how does Lonnie differ from, you know, kind of the competitive molecules? Obviously Tepezza is out there, as well as, you know, VRDN-003. So just kind of looking at, you know, some of the, you know, other options in the IGF-1 space and, you know, why you think, you know, this might be better or at least, you know, more competitive. Yeah, and again, maybe I'll start and then turn it over to Shab. I mean, just to say, Tepezza has been obviously really important for patients, but we do think that there is, you know, real opportunity. We do expect the market to go subQ, right? This molecule is really intended to be a subQ, and we have shown the first in-patient subQ data, right? And we think that that's really important, and that has been sort of a foundational principle for us, I guess, as we think about the development program, and especially the phase 2, right? I think there is that kind of market opportunity, and, you know, I think there are differences scientifically around the molecule that Shab can talk to, but there's also an approach to development that we think is also differentiated, and we can talk about that a little bit, too, but do you want to start on the science? Yeah, sure. Fantastic. I think, we are very excited, as Mina said, that we are the first to really have a subcutaneous therapy that we are exploring, in thyroid eye disease. There are really, I think, three critical key attributes, on this validated pathway that separates our molecule in a place where we believe will potentially give us an upside for patients around the therapeutic potential and holistically on the benefit-risk profile. And I think the first one is the potency we have, on this target. If you look at the Viridian and Tepezza, you know, KD associations, we have a difference of around 70%, in terms of potency with tepro and maybe around 20% with Viridian. So what does that tell us? It shows on the data that we presented in our proof of concept with forty milligrams, that we are already reaching robust clinical activity after one dose at the first time of assessment at three weeks with a very low exposure. And therefore, if you look at Tepezza at twenty mg per kg patient, that's sixteen hundred milligrams versus forty and ten mg per kg with Viridian, that's eight hundred milligrams. So we have a low exposure to begin with, which you can think in the future, you have low volume that will enable you to have an auto-injector, maybe by the time we launch, home use, with a single device, maybe, that fills in that single auto-injector. And so that's one characteristic of the potency that I think will help us also focus on safety, because safety in terms of exposure has been related to a Cmax, and then having potency and efficacy at a low exposure is very critical. The second thing is the efficient internalization that happens on this pathway with our molecule, which I think showcases in the rapidity of improvement across the endpoints that we measured in the proof of concept and in the dataset we showed in our cohort two at week six. And I think that is really critical because you need that rapid reduction in inflammation that is then seen in how the patient is responding, and that can also enable a deeper, earlier response that can then provide durability that's required in this therapeutic area. The third one, I think that's really unique, is we bind a different epitope, so a different binding site. Viridian and teprotumumab bind IGF-I receptor, where IGF-I also sits. And I think you have seen, a PD marker being used by, Viridian to say: We have the same engagement on IV as we are doing with subQ. Mm-hmm. Because there's that competitive inhibition that results in a high level, systemically, of IGF-1 in the 200%-400% above homeostatic levels. With lonigutamab, we bind peripheral. So if IGF-1 is sitting on the receptor, we internalize and degrade it. Mm. And so our increase in IGF-1 are in the order of 50%, 100%. We believe that hypothetically, there is an importance of looking at those levels because the insulin receptor has some homology with the IGF-1 molecule, and therefore, maybe there might be a perturbation of glucose handling- Yeah. -that results in hyperglycemia. Interesting. And so we believe that might be an important differentiation. And then in the dose ranging we are doing, we are really calibrating, which is something new that has not been done, a minimal effective dose, really focus on understanding what our Cmean, that enables the responses we want to see across the endpoint, and then just focus on a dose level and a dose regimen that optimizes steady state, which is Ctrough, and therefore not having an overexposure in Cmax. So we think these characteristics will help us really address the current paradigm, and being low exposure could also enable what we are focusing on, which is long-term chronic treatment. We see that patients in fixed dosing, some of them have fixed dosing, while they still have grumbling inflammation that recurs. When you look at some of the data, diplopia is not 100% in every patient. There is an opportunity with low exposure to continuously give patients that need that extra time to arrive at disease modification. I think this will really change the paradigm for treatment across Thyroid Eye Disease. Got it. So can you just, like, give us some, you know, insight on how you landed on the seventy mg dose, right? So obviously, you haven't actually tested it in patients yet, but you've done some modeling work. So, you know, what gets you confident, you know, you may see maybe better efficacy, but also not at the, the risk of seeing, you know, some adverse events, like on target adverse events? Yeah. And maybe I'll start- Go ahead, yeah. Okay, so maybe just to step back around the phase two, right? Sort of program design. So what we had announced previously when we announced the early POC data was that we were going to, we're going to have three cohorts, right? And then we would plan to have a phase two B trial that would start later this year. What we announced recently is that we're actually adding a cohort in order to complete our dose ranging work in patients inside the phase two. And what that enables is, you know, our ability to go and talk to the FDA later this year and to start that phase three program, right, in the first quarter of next year, and to potentially run the phase three programs concurrently, right? As opposed to that two B, and then sort of a sequential second registrational trial. And so that's kind of the overall design. And, you know, on your question about dose, I think more important than, you know, the seventy or the, you know, the individual doses is the totality of the data across both the doses and the regimens that we're trying, right? And when we put that against our modeling, right, to dial in that optimal dose that Shep is talking about, right? So I think it's important to step back and look at the totality of that phase two program and all of the dosing that we're doing, as opposed to, you know, is it, is it the seventy, right? Because there is a combination of both dose and regimen, right, that we're kind of dialing in. Yep. Okay. Yeah, I think exactly on point that we are driving, threading the needle in an optimal range where we are not overexposing patients, but making sure that whatever dose level and regimen we choose covers the heterogeneity of patients who might be longer disease duration, high disease activity baseline, smoking, and anything and any other variable that is associated with an outcome in this disease, so that that becomes a very important consideration for that therapeutic outcome. Got you. Have you guys looked at just the single dose to see, like, the durability at all? Like, or you've looked at it, like, in clinical models. Just because I know you were talking about, like, trying to understand maybe dosing interval and maybe I think you're looking at three-week and four-week, right? Yep. Like, you know, can you get some enhanced durability, you know, relative to maybe what we see with some of the other IGF-1's? Yeah, I mean, I think the regimen is super important, and we are, you know, trying a wide variety of options there, right? So that second cohort with a 50 mg loading, right, was weekly, right? So we're kind of looking at sort of weekly up through Q4. Got you. Yeah. Got it. And then so in terms of just the interaction with the FDA on, you know, kind of future trials, so like I said, you kind of said seventy mg might be the dose for is going to be the dose for registration. I guess, when they're going to have interaction with the FDA, and is it prior to, you know, seeing the data for the seventy mg, or are you going to kind of have some internal data and share it with them? So how is that going to work just so that you're kind of on track to, you know, launch pivotals maybe next year? Yeah. So we, phase two is open label, right? So we do have data, and obviously we'll share that with them. We have said that we're going to meet with the FDA later this year, right? And once we've had that interaction and we have sort of the data that we think we need, right, that we will be coming back to the market, right, to report the outcome of that interaction and what does that mean for the phase three program, as well as additional data from the phase two. But, you know, at this point, you know, we have guided to a Q1 start, and, you know, and we feel good about that. What are the big discussion points with the FDA on the program? Like, what do you need to kind of, like, clarify or propose, I mean, again, is it necessarily the dose, or is it other things about the trial design that you might be doing differently? Yeah. So I think it's the totality of an end of phase II, where we want a comprehensive interaction- Mm-hmm. Around we are going in a new paradigm of chronic dosing. Mm-hmm. What are the requirements that would enable us to get a label in that particular paradigm? And then to your point, do you agree with where we are setting our dose to move forward to have the benefit risk profile we think would be important for patients? Got it, and then just from the phase I to like, how do you I mean, these are small trials, right? Mm-hmm. Small cohorts, too. So like, you know, there's a lot of variability, you know, in some of this data. So I guess, you know, one, how much should we trust this data? I mean, obviously, we know IGF-1, IGF-1R works, but like, you know, there-- it could compress in a larger trial. But also, are you looking at things just beyond, you know, the traditional measures of apoptosis, if you're looking at imaging and other things to really like, again, root out that, you know, this does This is different, right? Like, you're getting- Yeah. You know, better efficacy, you're seeing, you know, better improvements. Yeah. For sure, we're dealing with sort of the, you know, well, not small numbers here. That said, the phase II, right, I mean, as designed, it's going to be sort of 30-ish kind of patients, which frankly, in a TED setting, is not insignificant, right? The phase III trials are, you know, fairly small here, right? And so, you know, we think that there is data and it's meaningful, you know. And we have, I think, as an industry, all gotten smarter about TED, right? You know, audiograms, you know- Right MRIs, all of those things are a lot more prevalent now, right? And so I think there is more data and plus the modeling, and so we're going to look for sort of consistency across all of those things. Okay. What do you think about, again, the screening for hearing impairment or hearing issues like in the trial? So obviously not in the original Tepezza trials, but now, like, is there a sense that, like, now that we're looking for it and we're testing for it, like, the rates are, like, to be the same or go up? Like, I don't know. Yeah. Because obviously, you're screening out those patients, but now, you know, a patient can just be like: "Maybe I do hear some ringing. Yeah, there's some confirmation- Yeah bias, for sure. Yeah. So, like, what do you think about that, just now that that's going to be included in, you know, these trials? I guess we'll find out pretty soon enough, right? They're going to report it out pretty soon, what that's going to look like. But what's your take on that? Yeah, I think it's an important observation, which is also critical for how we look after patients. So in our studies, even in the phase II, we already did audiograms in patients at baseline and sequentially over time. And in any patient who had any subjective complaint of, let's say, tinnitus, we also checked the audiograms at that particular time point, and then, as was you know outlined in the protocol. It's really important. Number one, patients with thyroid eye disease, like any other autoimmune disease, there's a baseline risk of hearing issues, right? Because of the inflammation that could also go into the auditory nature of that proximity. And therefore, we want to assess at baseline and over time and really understand what is happening in both arms, placebo and drug- Mm-hmm to really enable us to see whether there is any significant worsening that happens in patients on drug. Yeah. That would then characterize what type of patients, based on hypotheses around, exposure, Cmax, whether this could be something that could be meaningful. Yeah. So far to date, in our course, we've not seen- Yeah any association with any of our exposure. Got it. I know we've talked about this in the past in terms of just like, you know, the hearing impairment seen in Tepezza, like, and what's going on there, even in the real world, relative to what we've seen, you know, with your agent. You know, again, can you just kind of tell us or share with us, like, how those are, are different and how the FDA might look at those differently? Because we've got some mixed feedback on that from KOLs in terms of, like, is what we're seeing with, you know, is this, like, kind of mild tinnitus, like, really a hearing impairment? It may be it's not termed that way, but some docs will term it that way. So, you know, clear it up for us, Shep. Yeah, no, I think, number one, we have to take a step back and really categorize tinnitus as a subjective symptom and not an objective hearing impairment or loss. The other observation has been, in real world, using Tepezza, is at baseline, patients who have been followed on audiograms, there's a certain percentage who have subjective symptoms who have developed sensorineural hearing loss, but there are patients without any symptoms- Right who have had audiogram changes of sensorineural hearing loss. So moving forward, the field should continuously monitor patients on instituting such a therapy and also follow, and understand what's happening. But I think it will also be dependent on the results we get out of our two phase III studies- Mm-hmm on what is the threshold and guidance we will be discussing with the regulators on how much monitoring is needed based on that, outcome. Got it. So maybe we shift gears to kind of the commercial, you know, aspect of TED. I mean, you know, since Amgen bought Horizon, you know, people have gotten a little bit less enthusiastic- Mm-hmm you know, with the market. So what do you think is going on? And obviously, like, why do you think, you know, TED remains as attractive, you know, commercial opportunity? Kelly, you want to take that? Yeah, sure. Absolutely. So I think from a market perspective, you see a lot of different mechanisms in the field now, but we think the IGF-1R is going to maintain. It's the most central mechanism to thyroid eye disease, and that's going to remain so, just as a threshold matter. And then kind of going from the IV solution to a subQ solution, you know, we see that being a big shift in the market, I think, for a couple of reasons. First, you know, the convenience is going to allow, you know, more patients to have exposure, and then this question of moving from the active population to the chronic population. It, having a solution that can be administered at home, lower exposure, you know, potential safety benefits, is going to allow the market to continue to expand. So we see a transition to subQ, IGF-1R remain in the forefront, and then potential market expansion as more solutions come in for TED patients. So what do you think that incremental, like, number or percentage of patients is? Like, that would, you know, maybe not take IV Tepezza today or IV VRDN-001 tomorrow, and then would want to, you know, move to a subQ. Like, basically, what market, you know- Yeah - component is not accessible right now? Yeah. Without giving the exact kind of point estimate on it, it's going to be a sub- we think it's going to be a substantial majority of the market is going to move to the subQ solution away from IV when it's available. And it will also open up the prescriber base. You see, the prescriber base now is, you know, majority oculoplastic surgeons with some endos. I think the sub- the prescriber base could start to change with the availability of a subQ, so really market expanding and for something convenient, you know, with the same type of efficacy and also, you know, with lonigutamab, lower exposure, you know, lower Cmax with the potential safety advantage. We're also, again, as Mina and Shep mentioned earlier, we're going to be looking at the potential for chronic dosing and what that might mean for depth and durability for patients. What will you need to show, like, in, you know, in, like, from a long-term perspective? So I guess if you run the trial, it's twenty-four weeks for the primary, would you Or would you have to run fifty-two weeks or something longer to get chronic dosing? Like, what's the ophthalmology division's kind of view on chronic dosing? Yeah, so we haven't had the meeting yet. Okay. The regulators. We'll ask you again, don't worry. Yeah. But, I mean, I think, having worked in chronic autoimmune diseases- Mm-hmm You would expect your dataset that you demonstrate across what has happened to the dynamic or kinetics of response across the endpoint at certain times will be able to define how you can help a label- Mm-hmm More or less, like, to your point, if the primary efficacy endpoint is at week twenty-four, and we have treated patients all the way to week fifty-two, there are some patients where resolution has already happened earlier. So you could end up with a label that's individualized, that gives the confidence to the prescriber that for patients who still are having- Yeah Signs of inflammation, you can continue for a little bit longer duration with monitoring and seeing whether you are reaching the target that you are aiming for. Got it. Okay. Well, so let's talk about So lonigutamab- Yeah. - covered that. So what's next? So obviously, you know, there was some pruning of the pipeline also with the c-KIT, so we're not moving forward there. But you still have, you know, a fair amount of cash. You've done the restructuring, so you're reducing spend. So, like, you know, you've talked about business development. What's kind of priority other than Lonnie? Like, that's sole focus, but, like, on the peripheral, like, what are you doing in terms of, you know, additional pipeline candidates, and what's attractive to you right now? Yeah, I mean, maybe I'll answer sort of the prioritization piece and then turn it over to Gil on the BD side. I mean, our priority is TED, right? And, you know, our focus is on executing on that program, right? And again, sort of the fundamental principle around the restructuring and some of this prioritization is we wanted to know we had the capital- Mm-hmm right, to go all the way with these trials. And so, you know, we view those, that phase III program is fully funded, right? With additional runway beyond that, and we think that that's really important. So that is absolutely the operational and sort of execution focus. You know, we talked earlier about the fact that we also have uveitis that we're going to be reading out, and we'll make a decision there. You know, and then I'll turn it over to Gil on the BD side, but, you know, for sure, we'll look. Yeah. The only thing I would add, and Mina, nice, had a nice set up, but in our guidance out to 2027, we do have some capital that is reserved for kind of selective business opportunities. I think the bar is going to be high for us. We want to maintain this runway and the fully funded nature of the lonigutamab program that we reset. But we'll continue to look at opportunities that are sort of right-sized and focused for us. Mm-hmm for potential pipeline expansion. That was sort of in the DNA of the company. All our assets- Sure were brought in from the outside, and that's a process we'll continue to focus on. I mean, do you want to stick just with autoimmune, or are you looking maybe at other things? And I guess what stage of development, too? And, you know, I guess the other thing is the environment. Like, are we in an environment- Mm-hmm is things really expensive? Like, what are you, you know- Yeah … how competitive are these, you know, deals right now? Yeah. I think you know, the things that we look at. I mean, the bar is high, but as you mentioned, it's a competitive environment. The things that we look at are leveraging the expertise of our team. Mm-hmm. You know, you know, the stage, catalyst, capital required, those are all things that we put together to, you know, to make decisions around business development. We want a very differentiated asset, of course, and so those are we kind of look at that holistically as we go through decision-making processes and process and review various opportunities, so we'll continue to do that. Yeah. I, I mean, we're going to be super disciplined. Yeah. And I think, you know, the nice thing, frankly, about having the runway that we have- Mm-hmm right, is we can be patient, right? And, you know, keep that bar super high. Got it. Yeah. I guess if we think about the catalyst path here, so we have uveitis. Mm-hmm. And then first quarter, we'll have, you know, TED and TED updates, right? So, after that, it seemingly, like, would be a little bit of a catalyst gap, no? Depending on the uveitis. I guess, again, that's why I'm saying, like, is there some sort of priority to kind of bring something in, in more the near term, almost, to kind of fill that gap? Or you don't really see the need to do that? So, again, I mean, I think that having the runway that we have- Yeah. right? You know, and having a program that's effectively the phase threes funded- Mm-hmm. like, gives us a lot of flexibility, right? You know, to take our time, find the right asset. We will always be opportunistic and look at stuff, right? But, you know, but we're going to keep that bar high, and we've got the flexibility because of our runway. Sure. - to do that. Gotcha. And maybe last question. So VRDN-008 is coming out soon, you know, IV and five infusions versus eight, all this sort of stuff. You think that helps you, hurts you? Like, what How do you view it in terms of the competitive landscape or even de-risking your trials, even though, again, it's IV? But I guess if we can do some crazy math, if it's their IV, their subQs modeled off that IV, then maybe that means their subQ works, that means your subQ, I don't know, like, we're getting wild. But, you know, just what do you think about that data and how it could impact you, is basically the question? I was going to throw that one back at you. I mean, you're the research analyst. That's what I'm doing. I've got all these calculations, so you You know, that's why I'm asking the questions. I don't know. Yeah, I mean, I think the one thing that we think, and Shep touched on this earlier, is we are very fortunate to be doing our dose ranging within TED patients. Sure. Because you kind of get into a second derivative problem when you're looking at, you know, IV, different regimens- Sure and you're going to subQ on modeling. So I think without commenting specifically on their trial. Yeah. We do like that feature of not only the characteristics of lonigutamab, but our ability to play that out in the clinic and really optimize the dose within that window. Sure. You know, we think it's really important, and we've learned things in the clinic. We're continuing, which is why we're- Yeah - You know, making sure we get to the right dose before we launch the phase three. Yeah. Yeah. My comment is, in a patient-centric approach, which is what we're trying, we know fixed dosing works for a few patients, but not every patient. This is not a one-and-done gene therapy treatment, so we still expect patients to be needing more treatment past the week fifteen. Okay. Well, we'll leave it there. Thank you so much. All right. Thank you so much. Thanks for having us.