Good afternoon, ladies and gentlemen, and welcome to the aTyr Pharma second quarter 2022 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. To ask a question during the session, you'll need to press star one one on your telephone. 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 Director of Investor Relations and Corporate Communications. Ms. Dunston, you may begin. Thank you, and good afternoon, everyone. Thank you for joining us today to discuss aTyr's second quarter 2022 operating results and corporate update. We are joined today by Dr. Sanjay Shukla, our President and CEO, Ms. Jill Broadfoot, our CFO, and Dr. Leslie Nangle, our VP of Research. On the call, Sanjay will provide an update on our corporate strategy, including our clinical program for efzofitimod, and Leslie will go over our research and discovery programs in Neuropilin-2 and our tRNA Synthetase platform. Jill will review the financial results and our current financial position before handing it back to Sanjay to open up the call for any questions. Before we begin, I would like to remind everyone that except for statements of historical facts, the statements made by management 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, subsequently filed quarterly reports on Form 10-Q and in our other SEC filings. 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. I will now turn the call over to Sanjay. Thank you, Ashlee. Good afternoon, everyone, and thank you for joining us for our second quarter 2022 results conference call. We're pleased with the progress we've made in the second quarter as we advance our phase III study of efzofitimod in patients with pulmonary sarcoidosis. This global pivotal study is a major milestone for aTyr and the sarcoidosis community, as it is projected to be the largest interventional study for patients with sarcoidosis to date. I'm happy to report that the study is underway with several centers initiated in the U.S., and importantly, we remain on track to enroll a patient this quarter. As we begin, I'll summarize a few highlights since we last spoke in May. We announced plans to initiate EFZO-FIT, a global pivotal phase III study to evaluate the efficacy and safety of efzofitimod in patients with pulmonary sarcoidosis. We announced fibroblast growth factor receptor four or FGFR4 as the target receptor for a fragment of the alanine tRNA synthetase, which is also known as ARS. We were recently very pleased to receive FDA Fast Track designation for efzofitimod for the treatment of pulmonary sarcoidosis. Since the announcement of the EFZO-FIT study in May 2022, we've rapidly executed a number of operational milestones to advance the study start. Multiple interactions with regulatory authorities in the U.S., E.U., and Japan have occurred, along with the submission of the study protocol and clinical trial applications to regulatory authorities, ethics committees, and institutional review boards. Site selection, qualification, and initiations for several sites have occurred, as well as an investigator meeting for U.S. sites. It's been a highly productive period for aTyr from the point of receiving our FDA green light on the design of the EFZO-FIT study just last quarter to now, and we eagerly anticipate enrolling a patient soon. I'd like to acknowledge our fantastic clinical operations team that has moved at light speed to get our pivotal trial launched so expeditiously. With that said, let's discuss our clinical program for efzofitimod in a bit more detail. As a reminder, efzofitimod is a first-in-class immunomodulator for fibrotic lung disease. Efzofitimod is a novel Fc fusion protein based on the naturally occurring splice variant of the lung-enriched tRNA synthetase HARS fragment that down-regulates aberrant immune responses in inflammatory disease states. Efzofitimod has been shown pre-clinically to down-regulate inflammatory cytokine and chemokine signaling and reduce inflammation and fibrosis. The Neuropilin-2 or NRP2 receptor is upregulated on key immune cells during active inflammation and is enriched in inflamed lung tissue. Efzofitimod binds selectively to NRP2 and therefore has the potential to normalize the immune system, serving to resolve inflammation and prevent progressive fibrosis, thereby stabilizing lung function and alleviating morbidity and mortality. We're developing efzofitimod as a potential treatment for patients with interstitial lung disease or ILD, a group of rare immune-mediated fibrotic lung disorders. Our initial ILD indication for efzofitimod is pulmonary sarcoidosis. Sarcoidosis is the most prevalent ILD and is characterized by the formation of granulomas or clumps of immune cells in one or more organs of the body. Sarcoidosis that affects the lungs is called pulmonary sarcoidosis and occurs in more than 90% of cases. If left untreated, persistent granulomatous inflammation can lead to irreversible scarring or fibrosis, which may lead to respiratory failure and death. We estimate that there are close to 200,000 patients with pulmonary sarcoidosis in the U.S., around 150,000 in major European markets, and another 20,000 in Japan. Up to 75% of patients require treatment for their disease. Approximately half of these will progressively progress disease despite treatment, and around one in five of all patients will go on to develop lung fibrosis. Indication for treatment of sarcoidosis is twofold, to avoid danger to an organ or to improve quality of life. First line treatment is typically corticosteroids, which may effectively control symptoms but are associated with severe debilitating side effects, particularly with chronic treatment. Second and third-line treatments are anti-metabolite immunosuppressants such as methotrexate and biologic immunomodulators such as infliximab. These drugs are also known to cause serious side effects. Outside of prednisone and other glucocorticoids approved in the 1950s, none of these therapies are approved for the treatment of sarcoidosis, and all are used based on limited clinical evidence. We believe the initial target population for efzofitimod will be patients whose disease is progressing despite steroid treatment. However, even patients who are able to control their symptoms with steroids often experience such debilitating side effects that they are forced to choose between living with the burden of disease or the toxic effects of steroid treatment. Therefore, we also see an upside opportunity for efzofitimod as a steroid-sparing agent in patients who are responsive but unable to tolerate their steroid treatment. Combined, these populations represent an addressable market of roughly 150-200,000 patients in major markets. Even with conservative market penetration and pricing assumptions, this represents a significant peak sales opportunity in sarcoidosis alone. Because this is an orphan disease and treatment options are limited, the FDA granted orphan drug designation for efzofitimod for the treatment of sarcoidosis. Additionally, we recently announced that FDA has also granted Fast Track designation for efzofitimod for the treatment of pulmonary sarcoidosis. The FDA's Fast Track designation helps facilitate development and expedite the review of drugs that treat serious or life-threatening diseases with unmet medical needs. Fast Track designation provides certain benefits, including more frequent interactions with the FDA throughout the development program, as well as eligibility for accelerated approval, priority review, and rolling review. This Fast Track designation underscores the significant need for a new therapy that provides clinically meaningful outcomes for patients living with pulmonary sarcoidosis and reinforces the potential of efzofitimod to be a transformative disease-modifying therapy and address a major unmet medical need. We see further upside potential for efzofitimod in other forms of ILD, where immunomodulatory treatment is the current standard of care. This includes indications such as scleroderma-related ILD, other connective tissue disease-related ILDs, and chronic hypersensitivity pneumonitis, among others. These diseases share overlapping immune pathology with sarcoidosis and are currently treated with similar drugs. Additionally, efzofitimod has been shown to be effective in animal models of these diseases. Taken collectively, the opportunity for efzofitimod in sarcoidosis and other ILDs represent $2 billion-$3 billion in peak sales. Let's take a moment to go over the data we generated for efzofitimod and some of the details around the current EFZO-FIT study. As a reminder, last September, we reported clinical proof of concept for efzofitimod based on positive results from my phase I-B/II-A study in pulmonary sarcoidosis. The study, which included a forced steroid taper, demonstrated safety, tolerability, and a consistent dose response for efzofitimod on key efficacy endpoints and improvements compared to placebo, including measures of steroid reduction, lung function, sarcoidosis symptom measures, and inflammatory biomarkers. According to medical experts, this is the first randomized placebo-controlled trial of any therapy for pulmonary sarcoidosis that demonstrates effects on physiologic and quality-of-life measures concurrent with steroid reduction. Based on findings from the phase I-B/II-A study and feedback from the FDA, in May of this year, we announced plans to initiate the EFZO-FIT study. This is a global pivotal phase III randomized double-blind placebo-controlled study to evaluate the efficacy and safety of efzofitimod in patients with pulmonary sarcoidosis. This is a 52-week study consisting of three parallel cohorts randomized equally to either 3 mg per kg or 5 mg per kg of efzofitimod or placebo, dosed intravenously once a month for a total of 12 doses. The study intends to enroll 264 patients with pulmonary sarcoidosis at multiple centers in North America, Europe, and Japan. The trial design incorporates a forced steroid taper design, with the primary endpoint of the study being steroid reduction. Secondary endpoints include measures of lung function and sarcoidosis symptoms. The trial design for EFZO-FIT is based on key learnings from the phase I-B/II-A trial that we believe sets up this study for clinical and regulatory success. This includes takeaways from the forced steroid taper and results for steroid reduction in the post-taper period. In the 1-B/II-A study, which was a six-month trial, patients underwent a forced steroid taper to 5 mg with the option to be titrated to zero at week 16 based on symptoms. We learned that patients could generally handle the forced taper, and even though an 8-week taper was aggressive, we found that those patients on efzofitimod were able to taper more successfully. To be able to best evaluate the efficacy of efzofitimod compared to placebo, in EFZO-FIT, patients will be forced to fully taper their steroids to zero mg, though over 12 weeks instead of eight. We believe that by providing more time for the taper and tapering steroids completely, and finally, by following patients for an additional 24 weeks compared to the prior study, we expect more patients receiving placebo to experience worsening symptoms requiring increased steroids compared to patients receiving efzofitimod. We also have adjusted the entry criteria for background steroids from a minimum of 10 mg in the I-B/II-A study to a minimum of 7.5 mg of prednisone per day in the phase III. This aligns with feedback from physicians, but there are many patients who require a bit less than 10 mg of daily steroids to maintain their symptoms and could really benefit from a reduction. Even a reduction of 2 mg or 2.5 mg of daily steroids for these patients over the course of time could be very impactful. On the whole, we believe these adjustments will enrich the study and build upon the positive findings from phase IB/II-A trial. Again, EFZO-FIT is the largest interventional study for patients with sarcoidosis to date. With this study, efzofitimod is positioned to be the first disease-modifying therapy to market for patients with this debilitating disease, and based on data to date, we believe one that could reduce steroid burden, maintain lung function, and improve symptoms. I'll now turn the call over to Leslie Nangle, our VP of Research, to discuss our preclinical and discovery programs and our tRNA synthetase platform. Thank you, Sanjay. While our primary focus is on advancing our clinical program for efzofitimod, we also have a number of exciting opportunities emerging in research. Our lead preclinical candidate is ATYR2810, or 2810, a fully humanized monoclonal antibody that selectively and functionally blocks the interaction between NRP-2, a cell surface receptor that is upregulated on a variety of solid tumors and particularly expressed in many aggressive cancers, and VEGF, one of its primary ligands. VEGF is a validated mediator of tumor survival and growth and correlates with tumor invasiveness and metastasis. Current therapies that directly target the classic VEGF receptor signaling do not block the NRP-2/VEGF receptor signaling. Preclinical data suggests that by blocking the interaction between VEGF and NRP-2, 2810 may be an effective novel therapeutic that combats resistance and reduces invasion and metastasis by downregulating master drivers of lineage plasticity, such as ZEB1, to serve as a differentiated approach to targeting aggressive cancers. Our current work for 2810 is focused on designing and refining our clinical strategy. We are focusing on resistant and highly aggressive solid tumors where NRP-2 is implicated. We are prioritizing tumors based on scientific rationale backed by our preclinical data and support from external literature, and then incorporating the clinical development path for each to generate a list of top target tumor types. This approach provides us with data-driven methodology to select indications to target our first clinical study for 2810 with neuroendocrine tumors, including pancreatic neuroendocrine tumors and neuroendocrine prostate cancer, renal cell carcinoma, and triple-negative breast cancer all scoring high using this algorithm. As we continue to hone in on the target indications where 2810 may be the most effective, we are on track to initiate a phase I study in cancer patients in the fourth quarter of 2022. At this point, I want to take some time to highlight our tRNA synthetase platform, which is the science that aTyr is founded upon and we expect to be a defining part of our future. Our approach to drug discovery and development is rooted in our deep understanding of this family of proteins and the extracellular pathways they regulate. It is our mission to generate therapeutics targeting these pathways in order to improve patient outcomes. We have built an intellectual property estate of over 200 issued patents to date that creates a strategic boundary around our proprietary library of extracellular tRNA synthetase protein fragments. This library covers fragments from all 20 tRNA synthetases, placing particular emphasis on those that have the highest likelihood of being therapeutically viable. Our experience with bringing efzofitimod from discovery all the way to clinical proof of concept has paved the way to develop additional molecules from this gene family and has educated us on the most efficient ways to translate these discovery findings into therapeutic potential. Recent innovations enabling rapid target cell and receptor identification, in addition to phenotypic screening efforts, have become hallmarks of our research program. We are currently accelerating research efforts to mine this library for potential new therapies. As an example, in June, in a poster presented at the Keystone Symposia on Tissue Fibrosis and Repair, we announced the discovery of a target receptor for one tRNA synthetase fragment from alanine tRNA synthetase, or ARS, to be FGFR4. This receptor is involved in many cellular processes, including cell proliferation, differentiation, and tissue repair. FGFR4 is known to play a role in diseases related to inflammation and fibrosis, including conditions where unchecked fibrosis can precede the development of certain cancers. We look forward to further interrogating this interaction between this fragment of ours and FGFR4, exploring the implications for this synthetase fragment as a potential new therapeutic. Moreover, the methods utilized to identify this receptor can be further employed to identify and validate new molecular targets from our tRNA synthetase platform, which we believe holds great value that we aim to continue to unlock. I will now turn it over to our Chief Financial Officer, Jill Broadfoot, to review our financial results. Thank you, Leslie. I'm happy to report that we ended the second quarter 2022 with $89.3 million in cash, restricted cash equivalents, and investments. Research and development expenses were $9.1 million for the second quarter 2022, which consisted of product development and manufacturing costs for the efzofitimod and ATYR2810 programs, as well as start-up costs for the phase III EFZO-FIT study. General and administrative expenses were $3.4 million for the second quarter 2022. Common shares outstanding were approximately 28.1 million, and fully diluted shares were 33.1 million as of June 30th, 2022. While we are taking important steps to advance our clinical, preclinical, and discovery programs, we believe we are tracking well with our capital utilization. We continue to implement a data-driven approach to determine capital allocation for programs that warrant further exploration. We believe our current cash position, along with the opportunity for additional milestone payments from our partner, Kyorin Pharmaceutical, supports this approach. Now, I'd like to turn the call back over to Sanjay before we open it up to Q&A. Thank you, Jill. As we've discussed here today, we've really had a highly productive quarter, particularly for our efzofitimod clinical program. While we focus on advancing efzofitimod, we've continued to capitalize on our intellectual property portfolio by unlocking new ways to create therapeutics from this novel biology through the discovery of molecular targets for tRNA synthetases and the exploration of their role in disease. We believe we're in a strong position financially, and with the launch of the EFZO-FIT study, we're looking forward to entering the next phase for the company. We appreciate your support and look forward to providing additional updates this quarter. We now open it up to questions. Thank you. As a reminder, to ask a question, you will need to press star one one on your telephone. Please stand by while we compile the Q&A roster. Our first question comes from Gregory Renza with RBC Capital Markets. You may proceed. Hey, good afternoon, Sanjay and team. Congratulations on all the progress to date, and thanks for taking my questions. Sanjay, maybe I can just start with respect to the regulatory progress outside of the U.S.. I know you had some points at the top there. Just to build on that maybe a little further, I'm just curious how we would think about the level of regulatory alignment in ex-U.S. countries just regarding steroid-sparing as the primary endpoint, and maybe just touching on the strategy for an ex-U.S. approval and even launch. Maybe I'll just ask more broadly if I may, as you speak to getting the sites set up and getting a patient on drug for third quarter. I'm just curious if you could comment a bit on what you see as just some of the broader challenges and risks to that, the timeline as you build alignment with the centers and get patients on trial. Thank you so much. Thanks for the questions, Greg. First off, with regard to, you know, regulatory interactions, what I can say is they've been very productive, and frankly, the alignment has been 100% regarding the primary endpoint. I think it speaks to the fact that steroid reduction now universally is being viewed quite favorably as an approvable endpoint. You've seen other companies start to, of course, in other indications, receive approvals based on steroid reduction. Our plan is I think a really crisp and well-thought-out plan that not only FDA, not only Japanese regulators, but the larger European regulators continue to support. Frankly, the back and forths have been very easy. I think it also helps that we have buy-in from probably upwards to 60 experts worldwide. Folks have been waiting a long time for a sarcoidosis program to get into phase III. To my knowledge, we're the only one ever to kind of get you know to this point. I do think that there's a really strong desire to get a drug approved. I think we've smartly advanced the program, and now it's really set up well for success. When you think about some operational challenges, you always have to think about planning ahead of time to really mobilize sites and get things moving. Having some of the launch activities at ATS, where we started to bring people together, show them our data, this has been rather fast. The fact that we've been able to basically from one quarter, flip the switch here and are close to enrolling a patient, I think it speaks to not only our clinical operations team, which is, I would say, two standard deviations better than anybody out there in the industry. They've demonstrated that they can get a trial done through COVID, a respiratory pandemic, and we finished a respiratory trial in a very grave population here. I think we have a great team, but also the patient and provider community have been so excited to get involved with this trial. We wanna keep that excitement and that sort of acceleration that's occurred from our phase II data and continue to build upon that as we go into this trial so that we can move as quickly as we can. Patients don't wanna wait. We don't wanna wait to get the results out. We know it's a longer trial, but thus far, I would say we're in a fast start here. That's great, Sanjay. I appreciate the color, and congratulations again. Thanks, Greg. Thank you. One moment for questions. Our next question comes from Joseph Pantginis with H.C. Wainwright. You may proceed. Everybody, good afternoon. Thanks for taking the question. Sanjay, first, a logistical question on EFZO-FIT. What do we need to see to be able to get Kyorin into enrolling patients in the study? Yeah, I think it's just a matter of you know, Kyorin itself being its own company. They're operationalizing in Japan. Thus far, I can tell you that we have no hiccups from a regulatory point of view with Japan. I think it's just a matter of now opening sites and getting patients dosed over there. We are focusing on the U.S. first, and I would expect the first patient to be enrolled in the U.S.. Then I think you know, in the following months, you know, we'll look for Japan and Europe to start to enroll as well. What I can tell you is it's hard to guide to exactly when a patient might be enrolled in Japan, but we're tracking really well over there. Thus far, there's nothing in the timeline that is slowing us down. Got it. You know, when you talked about EFZO-FIT and, you know, looking at certain inclusion criteria, I was wondering if you can describe a little bit of the exclusion criteria. Because if I'm looking at some of the differences between the earlier study and EFZO-FIT, you know, look at some differences with regard to the initial fibrosis level, as well as what appears to be differences in the imaging that I think could potentially broaden the population. Yeah, I'm glad you brought that up. Let's first address the imaging. The field has moved back into HRCT as being the appropriate imaging metric. Now, it's not an endpoint. It's not a validated endpoint that the regulators would approve. We are using it to enrich, I would say to de-risk in a way, patients that are too fibrotic. We know our drug works best when there's active inflammation. Therefore, we wanna make sure that we have patients that are not too fibrotic. Now, in previous studies, I think we had the opportunity to exclude based on PET scan. As I said, HRCT is now the sort of more acceptable way of delineating fibrosis and inflammation. I do think our cutoff being at 20% aligns with some of the other therapies you've seen. Tocilizumab and nintedanib in the Scleroderma trials have that as a cutoff. What do I expect to happen? The toughest patients to treat with efzofitimod, I expect that we will be able to frankly exclude some of those patients. We may end up with more patients with some mixed disease, but still enough inflammation that we can move their disease and modify it. I think it does two things for us. Number one, those patients that may be too far gone to do well with efzofitimod, we think we'll exclude those patients. We also think we'll capture some patients and maybe even this has relevance to a larger market opportunity, with patients who have mixed findings, but still enough inflammation so that we can impact and reduce their steroids. Remember, these are patients that also, if you start to have fibrosis, steroids can make your fibrosis worse. They're in a tricky situation. I think this points to our ability to enroll better, enroll smarter, and probably long term, have a much larger footprint of market potential here with patients with mixed disease. Got it. That's helpful. Thanks. Just real quick, if you don't mind. With regard to ATYR2810, are you willing to share either a, let's call it an initial communication strategy subject to change, obviously, about, you know, how would you look to release news from the upcoming phase I study? Do you have a, you know, proverbial magic number of patients that you'd wanna see a couple responses first or a critical mass of patients before you release news? 'Cause obviously these are gonna be, you know, a tough patient population. Yeah. I think the first step is, and then Leslie alluded to it, we have a number of, you know, top target tumor types. We've outlined based on, I think, smartly looking at literature, looking at our data, talking to experts. We're gonna be able to enrich right off the bat. I think first understanding what the trial exactly looks like, and the expectation here is I will come back to you and the rest of the public to basically outline what that clinical protocol looks like. You're gonna be able to get into when are you gonna have batches of data available? Is it gonna be at the end or iteratively? Given that it's an early trial, it's a safety trial, the expectation here is, we could probably have a more steady flow of information, first starting with safety, but then also looking at pockets of response, in these early trials, similar to how most cancer studies are set up, where you at least wanna check the box there early on some safety work. Then you can start to dig into, okay, from these enriched tumor types, where are you seeing the best effects? Then that's gonna further define what the next steps for that program are going to be. I'm really proud of the work the research team has done here to, again, really be data-driven. I would say we are one of the most data-driven biotech companies out there. We're not, you know. Our goal is to set up these experiments for success, learn along the way, you know, shut down the valves of things that aren't really working well, but then really focus on what's working well. Stay tuned for that, Joe. I'm anxious to get those details out soon as well. Got it. Thanks a lot, Sanjay. Thank you. One moment for questions. Our next question comes from Hartaj Singh with Oppenheimer. You may proceed. Great. Thank you. Thanks for the couple of questions and really nice update, Sanjay and team. Sanjay, you know, you described the taper in the EFZO-FIT study. I believe going from like, you know, you'd start steroid taper at about two weeks and going to about 12 weeks as you're recruiting these patients. That's pretty. I mean, maybe aggressive relative to the previous study, right? I mean, is that a good sign that you're feeling confident you can take these patients off more quickly on steroids and try to get them to as low, you know, a steroid level as possible? So that's the first question. You know, how did that impact enrollment, you know, for the EFZO-FIT study, that taper? Secondly, you know, you talked about how your clinical team is now starting to really kind of come together. You know, if you have an IND for 2810 in the fourth quarter, second project in the clinic. What are the main differences you're seeing, you know, in developing your targeted therapies between oncology and inflammation? Back to the question. I'll break this into parts. First is the taper itself. I'll start maybe with enrollment. The fact that we saw patients get to zero in the last trial was really an outstanding finding and really unexpected in such a fast manner. In a six-month trial to see in that last cohort you know three out of nine patients get to zero, that was really unexpected. It also has, I think, lit a fire around the patients, the providers, the internal team here to say, "Let's really try to actually see if this drug could have even more steroid sparing effects, maybe a steroid replacement, type of effect for certain patients." That's actually helping us with enrollment and some early projections, because patients now look with that data that we produced and say, "This I might have an opportunity here to get off steroids if I participate in this trial." I think in many ways, the design is gonna help us enroll better. Now, with that in mind, we have to be a little bit more careful about how we taper. We had an eight-week taper that brought folks down from anywhere to 10 mg- 25 mg of prednisone down to five over eight weeks. We have to go. Now we're trying to go to zero, which essentially is a similar population, 7.5-25. We gotta give it a little bit more time. We've added four weeks. I think in my mind and the expert's mind, we've designed this very closely with people like Robert Baughman, Daniel Culver, some of the experts that were involved in the last trial. We feel bullish with the goal here to get to zero. Patients want to actually try to, you know, go to zero, and we're allowing for a little bit more time, four more weeks. That's also not gonna hurt us in our analysis 'cause you're really now looking at a full, basically a year trial. We're adding, you know, another 20-24 weeks of therapy here. I think all in all, this is gonna, you know, provide us, I think, a lift from enrollment. It is something that I think we're gonna challenge the norms here. It's why I think the market opportunity is closer to $3 billion, when you talk about what efzofitimod could do for patients, not only in sarcoidosis, but in a number of interstitial lung diseases. We think as time goes on, hopefully the investment community picks up on the fact that what's staring you in the face and hitting you in the mouth here is a transformative multi-billion dollar therapy. We hope people start to pay attention to that. The patients and providers already have. The regulators have. I think this is something that people need to wake up and see the kinds of impact we can make here. Yep. No, that makes sense. Just the broader question, Sanjay, on as you're going from developing, you know, in inflammation to oncology. I think this is one of the actually very unique things for me, for aTyr, is that, you know, you've got some pathways that you don't really encounter with a lot of other companies. There's a, I imagine, a scarcity value, but then what does that do to your discussion with the regulators, you know, as you're looking at NRP2 synthetases, et cetera? Yeah. Okay. That's the important follow-up here. I think first and foremost, validating the platform is what efzofitimod did. That's also given. We've always had comfort in that, but externally, there's a lot better comfort. We produced some data already from a safety perspective. Now, understand the modality there is different. It's an antibody, so it's a bit more straightforward. But the approach is still for us to basically say, "Yes, we are playing outside of the norms of most drugs in oncology, and we are breaking ground on a new area in oncology." Again, it's really guided around understanding of inflammation and fibrosis, and we've used that term quite a bit. Both are mechanisms that play a huge role in oncology as well. I think what we've done here is smartly designed, again, a plan. Regulators, I think, are becoming more understanding around our biology. It's making those kind of interactions easier. It's speeding things up. But at the same time, we're going to really, you know, create really cogent clinical strategies, because again, I think our goal here is to run smart experiments that we believe will succeed, and we'll do that even early on. In oncology, you have to do that really, really early on, because in many ways the market expects to see response even in those early patient trials. You don't do healthy volunteer work. You go straight into patients, for example. We will incorporate a, I would say, a more accelerated way of demonstrating effects, for ATYR2810. Lastly, I'll just say even the FGFR findings, again, we're now anchoring, and we feel really, really good around the process that we have here. That's a receptor that is better understood than Neuropilin-2, and clearly has more implications with regard to liver fibrosis, liver cancer, kidney fibrosis, a lot of literature there. We're gonna be hitting it from a different angle, and our angle has already produced the most really fantastic findings in sarcoidosis since the fifties. I think there's something to be said around the process that Leslie's also developed here with the research team, so that we create a steady stream of de-risked and potentially really transformative pipeline candidates. Yeah. Thanks, Sanjay, for the questions and all the comments. Really appreciate it. Thank you. As a reminder, to ask a question, you will need to press star one one on your telephone. Our next question comes from Yale Jen with Laidlaw & Co. You may proceed. Good afternoon, and thanks for taking the questions. My first question is that, Sanjay, you have mentioned that the last time that the enrollment till data release is roughly two to 2.5 years, I guess. Whether this timeline still holds? Yeah. Hi, Yale. Absolutely. I mean, we're just getting started. I will. You know, allow me to update guidance depending on how enrollment goes. Give me. Let's get the 70 centers up. Let's start to see some data. I think it's fair to say that this data, you know, we'll be looking at that, you know, that timeline that you've laid out there. I mean, as we get closer to, you know, into 2023, 2024, you know, we're gonna know then once that last patient gets enrolled. I think based on our assumptions and current projections, that timeline, you know, is correct. Okay, great. That's very helpful. You actually mentioned earlier in your answer that you could have some mixed type of patient other than the sarcoidosis lesions in the lung. My question to you is that if so, would you also start to analyze the, I guess, symptom relief or other aspects of those mixed patients on, you know, other sarcoidosis in other tissues and start to get some insight into whether, you know, how potentially expand it to other indications? I think what you're getting at is the extent of fibrosis. Let's understand all of these patients have some fibrosis. You know, it's you know, some might have just 1 or 2%, others may have 15 or 16%, but they all may have cough, shortness of breath, and be on a significant amount of prednisone. To your point, do we have any baked in stratification to look at more than 10%, more than 15%? Not necessarily. I mean, these are gonna be tertiary endpoints in the end. What we do know is neuropilin, targeting neuropilin seems to be a potent anti-inflammatory and anti-fibrotic. We have focused on the anti-inflammatory effects. In a longer trial, we may start to see that we're bending things from a fibrotic perspective. We're just gonna be prepared to look at that. I think when you think about efzofitimod as an anti-fibrotic, in the end, that's really what we're trying to do here. We're trying to prevent fibrosis from taking hold in these patients. It's also why I think experts in other areas like even IPF are really intrigued about wanting to try efzofitimod over there because nothing can really change and disease modify. We've seen therapies in development now that have billion-dollar valuations and not show dose response, for example. There's a lot of hope, I think, in IPF to see anti-fibrotic effects. We're going to interrogate that in our trial because sarcoidosis is certainly in the same family as IPF. Being more inflammatory, that's what we are prioritizing. That's why steroid reduction is our primary endpoint. To your point, I do think that the larger market opportunity, again I'm gonna stress here, is several billion dollars because we have a unique offering that, frankly, sits outside those approved therapies. The fact that we see symptom improvement is something that no therapy in fibrotic lung disease has really shown. I think this is where there's a lot of excitement. We're gonna keep our eyes on the prize, execute well on the sarcoidosis trial, but there is significant interest, yes, in even some of those other fibrotic conditions. Okay, great. Maybe last one here is that, well, on ATYR2810, I know you're gonna start a phase I study in fourth quarter. Should we just assume some of the typical cancer study, so dose ranging study design maybe such as a three-plus-three, maybe a multiple or a single dose ascending? Lastly was what might be the PD readout you may have? So what kind of biomarker you might also look for? Thanks. I'm gonna hold off on the biomarker part 'cause that's gonna have a lot to do also with the tumor type that we pick. What I can tell you is it will have some elements. We try, we pride ourselves on being real cutting-edge drug developers here. I think we're going to have an expedited adaptive type of approach. Yes, I think we know in cancer there are certain boxes you have to check with regards to, you know, overall safety, cohorts and then, you know, potentially then looking at efficacy in certain tumor types. It will have some classic elements because we wanna get the IND approved, but I also think there's gonna be some opportunities here to again enrich the risk and try to get an early signal, once I actually know, for example, if it's triple-negative breast that we're focusing a little bit more on or neuroendocrine, we can then kind of get into a cadre of PD biomarkers to start to look at. We think we have a very differentiated opportunity mechanistically, and we're quite bullish on that program as well, as we set it up. Okay, great. Thanks a lot and best luck and congrats on all the progress this far. Thanks, Yale. Thank you. I'm not showing any further questions at this time. I would now like to turn the call back over to Sanjay Shukla for any closing remarks. Thanks everybody for tuning in today. Obviously a lot of operational progress, maybe not the sexiest updates as we've had in the past where we're putting out clinical data. Certainly a quick turnaround here from last quarter, and I'm really proud of the work the team has done to really get this study launched, basically in a quarter here from the green light. Appreciate everyone's interest, continued support, and we'll look forward to talking to you in the future. Thank you. Thank you. This concludes today's conference call. Thank you for participating. You may now disconnect.