Good afternoon, ladies and gentlemen, and welcome to the aTyr Pharma conference call. At this time, all participants are in a listen-only mode. Later, we will conduct a question and answer session, and instructions will be given at that time. As a reminder, this conference is being recorded for replay purposes. It is now my pleasure to hand the conference call over to Ashlee Dunston, aTyr's Senior Director of Investor Relations and Public Affairs. Ms. Dunston, you may begin. Thank you, good afternoon, everyone. Thank you for joining us today to discuss a regulatory and clinical update for our efzofitimod in pulmonary sarcoidosis program. Before we begin, I would like to remind everyone that except for statements of historical facts, the statements made by management and aTyr guests and responses to questions on this conference call are forward-looking statements under the Safe Harbor provision of the Private Securities Litigation Reform Act of 1995. These statements involve risks and uncertainties that can cause actual results to differ materially from those in such forward-looking statements. Please see the forward-looking statement disclaimer in the company's press release issued this afternoon, as well as the risk factors in the company's SEC filings and included in our most recent annual report on Form 10-K and quarterly reports on Form 10-Q. Undue reliance should not be placed on forward-looking statements which speak only as of the date they are made as facts and circumstances underlying these forward-looking statements may change. Except as required by law, aTyr Pharma disclaims any obligation to update these forward-looking statements to reflect future information, events, or circumstances. We are joined today by Dr. Sanjay Shukla, our President and Chief Executive Officer, and Jill Broadfoot, our Chief Financial Officer. On the call, Sanjay will provide an overview of our recent FDA meeting and outline the path forward for efzofitimod in pulmonary sarcoidosis, then we will open the call up to any questions which can be addressed by Sanjay or Jill. I will now turn the call over to Sanjay. Thank you, Ashlee Dunston. Good afternoon, everyone, and thank you for joining us. Earlier today, we issued a press release summarizing the outcome of our recent Type C meeting with the U.S. Food and Drug Administration, or FDA. The purpose of this meeting was to review the results of the recently completed phase III EFZO-FIT study and determine the path forward for efzofitimod in pulmonary sarcoidosis. We held a meeting in mid-April and received the official meeting minutes last week. Based on feedback from the FDA, we are planning to conduct a new phase III study to further evaluate the potential of efzofitimod in pulmonary sarcoidosis. We plan to submit a protocol for the study next month. While EFZO-FIT missed its primary endpoint of steroid reduction, we saw durable benefit for efzofitimod on multiple clinically meaningful pre-specified quality of life measures, including the King's Sarcoidosis Questionnaire or KSQ lung score, the KSQ general health score, and the fatigue assessment score, among others. Therefore, we sought guidance from the FDA regarding the best way to proceed with the program as there remains an urgent need for a safe and effective treatment option for this underserved population. Heading into the meeting, we engaged an expert team of regulatory consultants, including a former FDA division director, the preeminent biostatistician with extensive FDA advisory experience, leading pulmonologists, and patient-reported outcome specialists. This team advised us on our strategy and helped us craft a package for the FDA, ultimately producing the best and most appropriate path forward for efzofitimod. The Type C meeting focused on several key topics. First being endpoints, including forced vital capacity or FVC and the KSQ lung. Critical rationale supporting FVC as an endpoint in the target patient population for a new study. A proposed update to our dosing regimen. A discussion focusing on continued safety monitoring in light of the proposed update to the dosing and the overall benefit risk profile for efzofitimod. Regarding endpoints, the FDA indicated that FVC and KSQ lung are clinically meaningful endpoints in pulmonary sarcoidosis. We will focus on these two endpoints in our next study to assess function and feel in pulmonary sarcoidosis. The FDA indicated FVC to be a direct measure of function, and we note that prior studies have used FVC as an endpoint in this indication and other approved ILD therapies. The FDA also indicated KSQ lung to be a direct measure of how patients feel, as it is the main patient-reported outcome that is used to assess quality of life in sarcoidosis. While the KSQ lung has been validated academically, we've been working closely with the FDA Division of Clinical Outcome Assessment to validate it for regulatory purposes in a clinical trial setting. We've done this work using our data from EFZO-FIT and a third-party content validity study as support. The FDA acknowledged our efforts and suggested additional recommendations, including the inclusion of some specific separate symptom measures, notably cough severity and wheezing, based on further content validation. Our conclusion is that currently FVC is the more appropriate primary endpoint for the next study. When we think about using FVC as a primary endpoint, we must take into consideration that FVC is highly variable in the broad sarcoidosis population due to the heterogeneous lung phenotypes that patients present with. We have to focus on the relevant phenotype when studying FVC as an endpoint. This approach provides us a way to generate a more homogeneous population to study. The main lung phenotypes for sarcoidosis are described by the type of lung impairment that occurs, whether it's restrictive, obstructive or diffusion-limited. The phenotypes also indicate the appropriate pulmonary function test to assess the lung impairment and the relative relevant endpoint to evaluate. When you look at FVC, it is the most relevant endpoint for patients with restrictive lung disease. These patients are typically defined in the literature as having a FVC% predicted between 50 and 80, along with an FEV1 to FVC ratio of greater than or equal to 0.7. This restrictive phenotype is one of the more common forms of lung impairment in sarcoidosis patients. EFZO-FIT enrolled patients with all lung phenotypes, including 44 restrictive patients. When looking more closely at what happened with FVC in those patients, you'll understand our rationale for targeting this patient population in our next study. You may recall that in EFZO-FIT, FVC was largely maintained across treatment groups, which was in line with what we expected in a steroid reduction study. These findings were for all lung phenotypes. Here we group patients from EFZO-FIT by lung phenotype. These groups include those with restrictive disease, defined as I mentioned earlier, and those with non-restrictive disease, meaning all other phenotypes. First, you see that the non-restrictive patients started at a much higher baseline FVC compared to restrictive. When you look at the FVC difference, you see a clinically meaningful difference of 124 milliliters emerge in the change from baseline in FVC between restrictive patients treated with 5 mg of kilogram of efzo versus placebo. This demonstrates that patients with impaired lung function clearly benefited from efzofitimod despite being aggressively tapered from steroids. Our EFZO-FIT data in this functionally impaired population provides the strong clinical rationale needed to prioritize FVC as a primary endpoint in the next study. We believe we've identified the specific patient population that responds robustly to efzofitimod, allowing us to model our next study with precision and confidence. Let's go over the remaining key outcomes from the Type C Meeting. We're also optimizing our dosing to enhance efficacy. In EFZO-FIT, we saw no evidence of any clinically meaningful toxicity in the patients, and our modeling shows that moving to a three-week dosing interval will not only increase drug exposure, but it also provides a wide safety margin, providing patients with the best possible therapeutic benefit. In light of this new proposed dosing regimen, the FDA suggested incorporating some additional risk mitigation strategies in the protocol. One such item was continuing to include safety surveillance for the potential development of anti-synthetase syndrome. Efzofitimod is derived from a splice variant of tRNA synthetase HARS, and patients can develop antibodies to the full-length fragment. This is something we've always monitored in our studies, and we did not see any development of anti-synthetase syndrome in EFZO-FIT. We'll be closely monitoring and prospectively monitoring for anti-synthetase syndrome in the next study, along with having a data monitoring committee in place similar to the EFZO-FIT study. We believe the benefit-risk profile for efzofitimod is strong and with an optimized dosing regimen combined with a target population primed for response, we're moving forward with an excellent development plan. Now let's talk about what the next study would look like. Our go-forward plan is to build on three pillars of strength, switching the endpoint to FVC, focusing on the responsive restrictive patient population, and optimizing to a three-week dosing interval. This design, in our view, is engineered for success. The trial itself is expected to be a global randomized, double-blind, placebo-controlled, one-year study. It will consist of two parallel cohorts randomized equally to either 5 mg of kilogram per efzo or placebo, dosed IV once every three weeks for a total of 17 doses. We intend to roll up to approximately 372 patients. These will be patients with moderate to severe progressive sarcoidosis with restrictive lung disease who are receiving a stable dose of daily oral corticosteroids of 5 mg or less and/or a stable dose of background immunosuppressant. All background treatment will remain stable throughout the study. The primary endpoint will be changed from baseline in FVC at week 48. The key secondary endpoint will be changed from baseline in the KSQ lung score also at week 48. Some of the additional key inclusion and exclusion criteria include parameters to ensure these patients are symptomatic with restrictive lung disease, however, not fibrotic. Patients must have a documented history of pulmonary sarcoidosis for at least six months, a dyspnea scale score of greater than or equal to two, KSQ of less than or equal to 60, FVC, as I mentioned, between 50 and 80, while also having an FEV1 to FVC ratio of at least 0.7. As I already mentioned, these patients will be on a stable dose of background treatment. Restrictive patients have impaired lung function whose symptoms may not be adequately managed by steroids or other immunosuppressants. Yet the extent of fibrosis isn't at the stage where they would need or benefit from antifibrotics. Therefore, some of the key exclusion criteria include a HRCT fibrosis score of greater than 20% and treatment within four months with biologic immunomodulators or antifibrotics, among others. We believe by implementing the criteria around the restrictive lung phenotype, we've created a homogeneous patient population to study, looking specifically at that FVC primary endpoint. Let's take a minute to look at the market opportunity for the patient population that we're now targeting in this new study. A recent claims analysis suggests there are nearly 160,000 confirmed diagnosed patients with pulmonary sarcoidosis in the U.S. Approximately 90,000 patients have moderate to severe disease characterized by impaired lung function. The current epidemiology for lung phenotypes suggests that there are around 38,000 patients with restrictive disease without advanced fibrosis. If you also consider approximately 24,000 patients with mixed disease, this is diffusion, mixed diffusion limited disease without advanced fibrosis, this is a group that we believe also can benefit from efzofitimod. We're looking at an initial target population, anywhere between 38,000 to 62,000 patients in the U.S. alone. These patients may still be impaired despite the use of first-line treatments. We believe this target population represents a multi-billion dollar opportunity for efzofitimod in pulmonary sarcoidosis. Finally, we'll discuss our next steps and operational readiness for the study. We're ready to execute. With the protocol expected to be filed next month, we anticipate a rapid start to enrollment by leveraging our existing global network of over 85 centers. We have long-term drug supply on hand and are moving forward in a capital-efficient manner to bring this potential life-changing therapy to patients. We're currently exploring various avenues to finance this phase III effort. Most importantly, we're still the most advanced therapy in the development for this disease. We believe we have an active drug that can significantly improve the lives of pulmonary sarcoidosis patients where they had no new treatments in more than 70 years. With strong support from the community, including pulmonologists, patients, their caregivers, advocacy organizations around the world, we're ready and ready to move this therapy forward. Thank you for your interest. At this time, along with Jill, we're available to take any of your questions. Star one and one on your telephone and wait for your name to be announced. To withdraw your question, please press star one and one again. We'll now go to our first question. One moment please. Our first question today comes from the line of Derek Archila from Wells Fargo. Please go ahead. Hey, good afternoon, and thanks for taking the question. Just a couple from us, Sanjay. I guess first, like, how long do you anticipate enrollment given the more narrow focus to restricted patients? That's our first question. We enrolled the last trial, if you remember, Derek. It took about 20, 21 months to enroll that trial. We are going after a larger N here to ensure that we've got the statistical power in the next trial to firmly hit on this endpoint. It is a smaller, restrictive population. We believe we can enroll this trial in about two years. We haven't guided specifically. That's the ballpark we're thinking about right now. We're looking to firm up those timelines with our CRO partners. Remember, five years ago, the world didn't have a lot of experience with efzofitimod. Many of these centers that we're going to, we're gonna be able to turn the key faster in with regards to site activation and getting all that contract work. We could probably cut three to six months in that regard. I also think there's more interest in efzofitimod than ever before in the SARC community because it's the first and only therapy that's ever improved quality of life and has done so with regard to cough, shortness of breath, fatigue, muscle ache, all the things they've ever wanted out of a therapy. With the interest, with the fact that we already executed successfully a phase III trial, with some of the timelines that we'll shave off by starting fast with these centers, you know, we think that the target early is to try to get this trial enrolled around two years. As we fine-tune some of those numbers, we'll come back to update everyone. Understood. Just a follow-up here. I guess you kind of changed the dosing schedule, and you talked about kind of exposure. Was there, you know, patients that were not getting enough drug in EFZO-FIT and that's kind of why you're moving? Like, what data did you see to get more confident, or at least to make the move to Q3W dosing versus the monthly? Looking a little bit more specifically at some of the clinical pharmacology, and efzofitimod obviously provided us a lot more PK and clinical pharmacology data that we could more robustly model off of. It was the discussion within the team from a clinical pharmacology perspective that, look, we might be able to enhance some of the exposure here, in particular, to look at C trough levels. By going to Q3, we're gonna get more exposure on board, while at the same time, not really pumping up Cmax here, which would run into some of the nice safety margin that we've already established. It's an effective strategy for us to get more drug on board. We already like the effects we've seen with FVC in the restrictive phenotype. It's just a function of looking at some of the modeling. Then we had a really nice discussion with the FDA, with their clinical pharmacology group, and we think this is a nice win for us to get more firepower out of the drug and patients getting more benefit without conversely having safety risk in our opinion. Understood. Last one from us. Just an update on efzo's SSc-ILD trial that's ongoing and when we could get updated data there. Thanks. Yeah. We previously have guided that we're looking to finish enrollment in the first half of this year. We're still on track for that. That is a trial that would read out, approximately you know, I'd say seven months after we get that last patient. Stay tuned for us to finish up enrollment there, and then we'd be looking to get that SSc data out, as I said, you know, probably about seven months after that last patient enters the trial. Great. Thanks, Sanjay. Sure. Thank you. Your next question today comes from the line of Yasmeen Rahimi from Piper Sandler. Please go ahead. Thank you. you. Thanks team for all the updates and getting the, you know, the study design all to figure it out and coming back. Just a couple questions. One is, do you need to show a statistical separation in the KSQ score, given it's a key secondary as well? Or is the study deemed, you know, fileable based on FVC? That's question number one. Then question number two is, how large is this restrictive population versus, you know, the broad population that you had in EFZO-FIT? Like, what is the market opportunity and market size, and do they represent phenotypically different that you could talk about? Then maybe the third question is just thinking about the cash and the how to fund this phase III and what the capital needs would be. Sure. I'll break those questions up. You know, going back to the first point around the relative size of the trial, we were aiming for the primary endpoint to size it to make sure that we're powered to hit stat sig on FVC. It's KSQ is gonna be a key secondary here, but the trial is really powered and sized for improvement in FVC. As it turns out, we're relatively in the same ballpark with 372 patients to also be more than adequately powered for FVC as well. I wanna highlight here, it's not a co-primary. It's a clear secondary here that would be part of the hierarchy. The goal here is to hit on FVC, and we feel like based on what we've seen with other approved therapies, that's gonna be very much down the fairway, when you think about approving therapies for interstitial lung disease. Your next question was really around market size. Comparatively speaking, the restrictive phenotype represents a smaller subset of the broader, say, steroid-dependent population. EFZO-FIT is doing, I think, It's really causing a bit of a shockwave throughout the SARC world in the sense that we proved something that had never been proven before, that you can treat these patients on significantly less steroids. What you're seeing now is, I think, a larger group of patients in the front line get steroids and methotrexate. That being said, those therapies don't really touch or help these restrictive patients. Now looking at the restrictive patients, you might be aiming to, as I said, at a minimum, somewhere around that $35,000-$40,000 range. We may have some upside here if you look at patients who have mixed disease. These are patients with, I would say, a greater unmet need. These are patients that are morbidly sick. Steroids and methotrexate don't do anything for them. These are sicker patients, who as you can see, responded quite well to efzofitimod. Based on preliminary pricing work, we know that some of our pricing estimates now need to be revised upwards because we're talking about a sicker population. Again, I feel very confident that this is again, a multi-billion dollar opportunity. Now you're looking just at a tighter population, but a population that you'd probably get more penetration because these patients have more of a desire, more of a need to get a second line agent with the potential efficacy profile of efzofitimod. You know, your last point, as I said, we're evaluating right now how we think about funding this next opportunity, we wanna be capital efficient here. Right now that's TBD as we start to work through what's the best pathway to, as I said, build upon this successful and positive FDA meeting. Thank you. Thank you. Your next question today comes from the line of Joe Pantginis from H.C. Wainwright. Please go ahead. Hey, everybody. Good afternoon. Thanks for the updates. Glad you had some productive feedback. A couple questions, if you don't mind, Sanjay. With regard to the regulatory path going forward to potential filing, this is a single phase III. Any conversations whether EFZO-FIT could be part of a filing, or do you think you would need an additional phase III? In my mind, Joe, good question there. I can't necessarily get into the specific heads of the FDA. Maybe you can better than I can, but I think we've run a phase III and garnered some real outstanding data with regards to quality of life. This one would, of course, be much more focused on function. In my mind, those are two phase IIIs with a lot of also safety data. This is why that benefit risk discussion is important. In our mind, we view this as a registrational trial. Again, that will be something that upon readout, let's see what where the FDA's head is at. You've seen obviously a lot of things publicly around a single and well adequately controlled trial. That's what we're aiming for here. Much of the leadership there is shifting, and I think all of the groups there are, I would say, learning what the, what the sort of new remit is for the FDA. The way we consider this trial is we have a signal here, a large signal in this restricted population. Most of our KOLs firmly look at that and say, "That's quite impressive." That would be something that clearly, they would then, look to use a therapy if we were to hit on that in the next study. That's how we're approaching this in this one single study. Got it. About the study itself, maybe endpoint-wise and inclusion criteria-wise. Inclusion criteria, can you discuss maybe the background of, or variability, the variability of background therapies on these patients, number one. Number two, can you give some early thoughts on benchmarking, the improvement you would wanna see in FVC? Thanks. Sure. Much less variability now that we're going into a more homogeneous population. FVC, if you remember in our last trial, I mean, we enrolled many of the patients with normal FVC. It's a really wide range of FVC or for that matter, even FEV1. We're taking all comers. Moving now into a restrictive phenotype, you can have a tighter standard deviation with FVC. It's gonna reduce statistical noise in the next trial. With the signal that we've seen, greater than 120 milliliter difference, approved therapies for ILD, typically you need, if you look recently, 50 milliliters, 60 milliliters is what's getting approved. We would of course maybe not need to aim as high as 120 milliliters and also not as low as 60 milliliters. This is what we're fine-tuning right now with our power assumptions. But again, with less variability and with a rather large signal, we could perhaps go somewhere in the middle and have a very well-powered trial with an N of 372. The idea here is to hit stat sig. What I'd like to be powering for is to hit stat sig with multiple zeros after the decimal point, so that there's really no question with regards to the utility of efzofitimod. That's the goal, and I'll fine-tune some of those sample size assumptions really here in the coming weeks. Thank you. Thank you. Your next question today comes from the line of Brian Abrahams from RBC Capital Markets. Please go ahead. Hi, everyone. This is Nevin on for Brian. I was just curious if you could break down the subgroup analysis a little bit more. Wondering what the split of those who were on the 5 mg dose versus placebo was in the restrictive cohort. I was also wondering if maybe the KSQ questionnaire was. Environment, this is where FVC to see, you could see improvements. The fact that more or less we were flat in the last trial in this restrictive population is really surprising and also very promising to really look at that large difference closely. Thanks. Just a quick follow-up for the planned phase III. Is there any plan to look at an interim to enable kind of an earlier look? Not at this time. You know, we wanna make sure that we really power this well and not really, I mean, a futility here probably is not appropriate. You know, really at this time, I think any kind of interim or futility analysis is not currently planned. Thanks so much. Thank you. We will now go to the next question. Your next question comes from the line of Boris Peaker from JonesTrading. Please go ahead. Great. Thanks for taking my question. I don't know if I may have missed it 'cause I lost sound here for a few seconds. What specific signal, FVC signal assumption are you making for the pivotal study? I know you showed 124 mil in the subgroup of patient with restrictive disease, but now you're also gonna be going to a slightly higher dosing than before. I'm just curious, you're assuming that the FVC is gonna remain at about 120 mil. You think it might go a little bit higher? Or are you assuming a little bit lower for a margin of safety? How are you thinking about that? Yeah. I would likely set the bar slightly lower. I think we can actually improve on that in the sense that we are gonna be able to get more exposure from the drug. I'd rather be conservative in some of our statistical assumptions. I would anticipate that we wouldn't aim so high to be at 120 milliliters. Remember, drugs have been approved, more or less in that 50 milliliters, 60 milliliters delta. I also wanna make sure that this is viewed as statistically important. I think I would anticipate it might end up being somewhere in the, say, 80 milliliter range. That's, you know, to be finalized here with our statistical assumptions. That would be a large signal, a clinically meaningful signal. We wanna be clinically meaningful, but we also wanna make sure that we give ourselves some statistical padding, so that we can hit the P value in the next trial. Great. Just one more question. I mean, the trial includes enhanced monitoring for anti-synthetase syndrome. Yeah. I'm just curious, was this a specific FDA mandate or proactive move by you guys, or how did that come up? This has always been part of our program because our efzofitimod is built on a fragment of histidyl-tRNA synthetase. There's always been a potential theoretical risk of developing anti-synthetase syndrome. We have not seen any production of antibodies going back to our animal work, even in any of our early phase trials or this trial. This is something that, from a theoretical risk standpoint, we will have to monitor. We agreed with the FDA that we'll continue to monitor it. We did not see any Jo-1 antibody production in the last trial. This is just simply a continuation of the safety surveillance that we'll conduct in the next trial. Great. Thanks for taking my questions. Sure. Thank you. Your next question comes from the line of Dev Prasad from Lucid Capital Markets. Please go ahead. Hi. Congrats on the update, and thank you for taking our question. I have a couple of question. One is, how do you expect the placebo patient to perform on FVC in this more respective population, when you look at the data in EFZO-FIT? Second is, given you will be increasing that dosage to Q3W, and that might result in higher cumulative drug exposure, did FDA request any specific safety monitoring? Thank you. To your second point, Dev, some of the specifics were just really, of course, a little bit more around the anti-synthetase syndrome that I mentioned. We may obviously, with Q3, we may get a little bit more frequent with some of those assays that we have for Jo-1. You know, this is outlined and to be expected with what I said before. What was your first question was about, remind me again. Sorry. My first question was, how do you expect placebo- Ah, placebo- Patient to perform? In the context of a steroid reduction trial, we expected to see, you know, 2%-5% declines, and that's exactly what happened with the placebo population. In the next trial where steroids are kept stable with the immunosuppressants, we might expect the placebo to behave flat to slightly decreased. If you look at historically the infliximab trial or some of the golimumab trials that were run previously where steroids were fixed, they saw flat to slightly decreased placebo. That's gonna be part of our modeling. We have much better natural history to model off of with the placebo population, and coupled with what we saw in EFZO-FIT, this is how we wanna organize the next trial to hit stat sig on FVC. Okay. Great. Thank you. Thank you. Your next question today comes from the line of Liang Cheng from Jefferies. Please go ahead. Hey, this is Liang Cheng. I'm for Roger Song. I have two questions. One is, Now you've limited the population to the restricted disease. How do you expect that to your enrollment pace? Second is, during your discussion with at FDA, does FDA mention anything about FVC as a clinical significance? Thank you. Yeah. FVC is clearly seen as the most significant functional measure. In particular, that's why we needed to have a rationale for the restricted population. Now, a restricted population with regards to enrollment, in my mind, is going to be in many ways more motivated to participate in the trial. These patients, as I said, are trundling down with their lung impairment, and steroids and methotrexate aren't cutting it. The number one reason for screen failure in the last trial was actually the steroid dose criteria, so we will not have that in this next trial. We know the whole population around the world following the EFZO-FIT data is now tapering patients off steroids as we speak. One of the experts said to me as soon as she left Amsterdam and our presentation, she went back to her clinic, in the U.S. and started to cut everyone's steroid in half the next day. What we know in the next trial is not having a steroid threshold criteria of 7.5 - 25, this is gonna make it easier for us to enroll restricted patients also, in my view and the expert's view, who, you know, motivated to participate because they have really morbid disease. These are sick patients, and efzofitimod, of course, showed the ability to help these sick patients and also feel much better. These patients are unfortunately resigned to getting a lot of off-label therapy. Infliximab, leflunomide, azathioprine, all of those drugs also come with toxicity. We believe that there's a large opportunity here to address an unmet, a motivated population that frankly needs a much better second-line agent. Thank you. Thank you. We will now take our final question for today, and the final question comes from the line of Julian Harrison from BTIG. Please go ahead. Hi. Thank you for taking the questions and providing this comprehensive update. First, I'm wondering if you could talk about how the addressable market for efzofitimod could potentially be expanded to mixed phenotype patients, along with the fusion-limited patients. Would that likely involve an additional trial? Sorry if I missed it, I was also wondering if you plan to pursue a Special Protocol Assessment with the FDA for your upcoming trial in restricted patients. Could that be useful in some respect or likely not worthwhile? Thank you. Yeah. I think a SPA is, Julian, typically used in more, I would say, classic regulatory scenarios where you may have more validated endpoints. I mean, in many ways, we were trying to treat this Type C Meeting to also get a lot of feedback on a potential next protocol. We did get a assessment, if you will, on what a protocol would look like, and that's why we're coming out with this update. Beyond just saying the program is a green light to move forward, here's how it would move forward exactly. I think that's, you know, generally the way we think about, we approach this Type C Meeting. Did I answer both of your you had I'm sorry. I'm tailing off here at the end with the questions. Oh, yeah. No worries at all. My first question was with respect to the upside opportunity. Oh, the upside. Yeah. Yeah. Right. Yeah. I mean, we have key opinion leaders now that would like us to potentially expand the protocol into those groups. The issue you get there is you create more variability, and I really wanna make sure the drug is successful in a tight population. Now to that point, would you be restricted from a label point of view? Our regulatory experts do not think so. These are natural groups that we feel as though efzofitimod, and we have data that we could support moving into these these other adjacencies, if you will, to restricted patients. I think the important thing here is for the next trial to really hit on the primary endpoint with FVC. I wanna keep the population as tight as possible. You could potentially look at, you know, after approval scenarios where in phase IV you look, for example, in these sorts of populations. For me right now, I wanna be able to focus in on a less variable, more homogeneous population. That's the restricted population. I think theoretically, there's gonna be a lot of use and utility in some of those other groups. I don't, I don't at this point see the potential to be restricted from a label perspective. If we were, that would be something that you'd move into those phenotypes. Very rarely do you see these ILDs sliced and diced when it comes to phenotypes. If you look at the, for example, the IPF and the ILD drugs that have been approved, they only went after more or less restrictive patients, but they have broad labels. We're following that playbook. Excellent. Very helpful. Appreciate it. Yep. Thank you. This concludes the question and answer session. I will now hand the call to Sanjay for closing remarks. Great. Thanks, everybody. Lots of great questions, interest out there. We're excited with this productive meeting and also of some of the outputs that have come out of it and being able to really hone in on the next step protocol. Appreciate everyone's interest. We will be in touch. Thank you again. Thank you, everyone. Thank you. This concludes today's conference call. Thanks for participating. You may now disconnect.