Good afternoon, ladies and gentlemen, and welcome to the aTyr Pharma Second Quarter 2021 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. Operator provided instructions. 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, operator, and good afternoon everyone. Thank you for joining us today to discuss aTyr's second quarter 2021 operating results and corporate update. We are joined today by Dr. Sanjay Shukla, our President and CEO; and Ms. Jill Broadfoot, our CFO. On the call, Sanjay will provide an update on our corporate strategy, including our clinical program for ATYR1923; and our research and discovery programs in neuropilin-2, including our preclinical program for ATYR2810. Jill will review the financial results and our current financial positioning 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 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. 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 2021 results conference call. As we make our way through 2021, we continue to make significant progress in our mission to translate novel biological pathways into innovative therapeutics for improved outcomes for patients. Notably, we recently completed the last subject visit in our Phase 1b/2a proof-of-concept study of our lead therapeutic candidate ATYR1923, or 1923, in pulmonary sarcoidosis, our lead interstitial lung disease (ILD) indication. We expect to report results from this important study in mid-September of this year. This is a significant milestone for aTyr and the upcoming readout represents a key inflection point for the 1923 clinical program and the tRNA synthetase biology platform. The clinical proof of mechanism for 1923 established from our Phase 2 study in COVID-19 patients and the favorable safety profile demonstrated to date, along with the preclinical efficacy observed in multiple translational ILD models, support the potential for 1923 as a new therapeutic approach for pulmonary sarcoidosis and possibly other forms of ILD. We believe 1923 could potentially offer an alternative to current treatments, such as steroids, with improved efficacy and fewer side effects. In addition to finishing up the important work for our 1923 clinical program, we've continued to generate new data and publish research related to our preclinical program, further strengthening our pipeline. As we begin today, I'll summarize a few additional highlights. Since we last spoke in May, we hosted a key opinion leader (KOL) event on current treatment options for pulmonary sarcoidosis, featuring Dr. Daniel Culver, Chair of Pulmonary Medicine and Director of Diffuse Parenchymal Lung Disease at the Cleveland Clinic. Kyorin Pharmaceutical Company, our partner for the development and commercialization of 1923 for ILD in Japan, completed a Phase 1 study in healthy Japanese volunteers. We have two abstracts for 1923 accepted for presentation at the upcoming European Respiratory Society (ERS) International Congress. We expanded our research collaboration with Ohio State University (OSU) to deepen the understanding of the immune mechanisms of sarcoid granuloma formation and identify potential biomarkers of efficacy for 1923 for pulmonary sarcoidosis. Dr. Elliott Crouser, Professor of Pulmonology, Critical Care and Sleep Medicine at OSU, will serve as principal investigator. We received a patent grant from the U.S. Patent and Trademark Office covering methods for the use of histidyl tRNA synthetase (HRS) Fc fusion proteins, which includes the use of 1923 for reducing inflammatory response in the lung. We appointed Dr. Sara Zaknoen, a highly accomplished drug development and clinical research executive, to our Board of Directors. Dr. Zaknoen is a hematologist oncologist, who has previously held Chief Medical Officer positions at several biotech companies. She also has a wealth of experience working at large pharmaceutical companies, including Novartis and Schering-Plough (now Merck), where she was involved in supporting the development of a number of important marketed therapies, including Gleevec, Tasigna, Exjade and Temodar. We presented a poster at the Keystone Symposia, 'Cancer Stem Cells: Advances in Biology and Clinical Translation,' related to preclinical research highlighting mechanistic insights into the tumor inhibitory effects of ATYR2810, or 2810, our lead anti-Neuropilin-2 (NRP2) VEGF antibody candidate in preclinical development for cancer. And finally, we presented a poster at the Antibody Engineering and Therapeutics Europe virtual conference related to a second anti-NRP2 antibody, which demonstrated selective blocking of Semaphorin 3F signaling. We made significant progress during the first half of this year and we see the second half of this year shaping up to be equally productive. Let's begin with our clinical program for 1923. We're developing 1923 as a potential treatment for patients with ILD, a group of rare immune-mediated disorders that can cause progressive fibrosis of the lung. There are more than 200 types of ILD, but roughly 80% of these patients fall into four main disease categories: pulmonary sarcoidosis, chronic hypersensitivity pneumonitis, connective tissue disease-associated ILD, and idiopathic pulmonary fibrosis. All of these diseases have limited standard of care with substantial morbidity and mortality. 1923 has the potential to address this unmet need by targeting the aberrant immune responses central to ILD pathology and preventing progression of fibrosis, the key driver of poor outcomes in these patients. We estimate there are over 500,000 ILD patients in the U.S. alone and over 3 million patients globally. While our initial focus for 1923 is pulmonary sarcoidosis, the mechanism of action (MoA) data from preclinical models and demonstrated effects on key inflammatory biomarkers in patients with COVID-19 pneumonia suggests that 1923 could have potential in other ILD indications as well. Our initial ILD indication for 1923 is pulmonary sarcoidosis. A hallmark disease characteristic of pulmonary sarcoidosis is the formation of granulomas, or clumps of immune cells in the lungs. The formation of these granulomas is driven by persistent aberrant inflammation. If left untreated, it can lead to irreversible scarring or fibrosis and diminished lung function, which may lead to respiratory failure or the need for a lung transplant. We estimate the patient population for pulmonary sarcoidosis to be approximately 200,000 patients in the U.S., although estimates do vary. About half of all patients will require some form of systemic therapy, and unfortunately, 30% of all patients will have chronic progressive disease despite available treatments. The current standard of care for pulmonary sarcoidosis typically includes treating the inflammation with corticosteroids and other immunosuppressive therapies. While these treatments can help manage inflammation and alleviate symptoms, such as cough and shortness of breath, they have no demonstrated efficacy on disease progression and can result in serious long-term toxicity. Additionally, many patients do not respond to currently available treatments. So there is a substantial need for a safer, more effective treatment that could reduce or replace the requirement for chronic corticosteroids or other immunosuppressive therapy. This need was recently reinforced by one of the leading experts in the field, Dr. Daniel Culver at the Cleveland Clinic. In June, we hosted a KOL event with Dr. Culver, who discussed limitations with the current standard of care and unmet medical need for treating patients with pulmonary sarcoidosis, including the toxicity burden of chronic steroid use and the need for better steroid-sparing agents. Through this event, we heard firsthand from Dr. Culver about some of the side effects related to steroid use in sarcoidosis, including some staggering statistics related to metabolic complications, quality of life, economic burden and risk of mortality, leading him to believe that there is no safe maintenance dose of corticosteroids in patients with sarcoidosis. If you're unable to attend the event, I encourage you to listen to the replay, which can be found on our website. Now let's talk a bit more about 1923 and why we believe it is a potential first-in-class immunomodulator. For some of the inflammatory lung diseases we've been discussing, including pulmonary sarcoidosis, 1923 is a novel Fc fusion protein based on the naturally occurring splice variant of the lung-enriched tRNA synthetase HARS fragment that downregulates aberrant immune responses in inflammatory disease states. 1923 has been shown preclinically to downregulate inflammatory cytokine and chemokine signaling and reduce inflammation and fibrosis. NRP2 is upregulated on key immune cells known to play a role in inflammation and is enriched in inflamed lung tissue. 1923 selectively binds 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. As a reminder, our ongoing trial in pulmonary sarcoidosis is a Phase 1b/2a randomized, double-blind, placebo-controlled multiple ascending dose clinical trial in 37 pulmonary sarcoidosis patients. The trial consists of three cohorts testing doses of one, three and five milligrams per kilogram of 1923 or placebo dosed intravenously every month for six months. The primary objective of this study is to evaluate the safety and tolerability of multiple ascending doses of 1923. Secondary objectives include assessment of the potential steroid-sparing effects of 1923, in addition to other exploratory assessments of efficacy, such as lung imaging, lung function assessed by pulmonary function tests and relevant serum biomarkers. Based on our trial design, which includes a four-week steroid taper, an integral element of this study is to assess steroid burden in the 1923 treatment groups compared to placebo. As we have discussed here a bit today and reinforced by Dr. Culver, there is a crucial need for alternatives to existing treatment options, including steroids. We look forward to the results of this study, which we expect to report in mid-September this year. While we have advanced our clinical program for 1923, we continue to conduct research to deepen our understanding of 1923's MoA and advance our understanding of sarcoidosis disease pathology. We are pleased to have announced that we have two abstracts for 1923 that have been accepted for presentation at ERS in September. One of these abstracts will present the biomarker data from our Phase 2 study in patients with COVID-19 pneumonia. Earlier this year, we released some findings from this data, which showed substantial anti-inflammatory effects in patients consistent with findings from our animal models. This data provides the first inpatient mechanistic proof of concept for 1923 and we look forward to sharing more details about the data at ERS. A second abstract will present data from a pilot proof-of-concept study conducted in collaboration with Dr. Elliott Crouser, a leader in sarcoidosis research and treatment at OSU, which demonstrated the ability of a splice variant of HARS, the active component and portion of 1923, to disrupt sarcoid granuloma formation in vitro. Based on these successful pilot study findings, we announced earlier today that we are expanding our research collaboration with OSU and Dr. Crouser to continue this important work. The collaboration is intended to deepen our understanding of the immune mechanisms of sarcoid granuloma formation and identify potential biomarkers of efficacy for 1923. The study will assess the effect of 1923 on sarcoid granuloma formation in vitro using blood samples taken from sarcoidosis patients. We will also focus on identifying the relevant immune mechanisms triggered in granuloma formation and analyze promising biomarkers predictive of strong granuloma formation in order to assess whether they could be used as a predictive biomarker for treatment selection or treatment response to 1923. We're very excited to continue our work with Dr. Crouser and his lab at OSU. The research generated from this collaboration may help direct us to biomarkers indicative of a population that may be sensitive to treatment with 1923 which could present the opportunity to take a much-needed step forward in managing this disease and lead to improved patient outcomes. To wrap up our discussion on 1923, we're pleased to inform you that Kyorin Pharmaceutical, our partner for the development and commercialization of 1923 for ILD in Japan, has completed its Phase 1 study, which investigated the safety, pharmacokinetics (PK), and immunogenicity of 1923 known as KRP-R120 in Japan in 32 healthy Japanese volunteers. In this study, 1923 was observed to be generally safe and well tolerated with no drug-related serious adverse events and PK findings were consistent with previous studies of 1923. Before we turn to our preclinical program, I want to take a minute to highlight an important business update that occurred in the second quarter. In May, we announced the appointment of Dr. Sara Zaknoen to aTyr's Board of Directors. Dr. Zaknoen, a hematology oncologist by training, is an experienced pharmaceutical drug development and clinical research executive who has previously held Chief Medical Officer positions at several biotech companies. She also has a wealth of experience working at large pharmaceutical companies, including Novartis and Schering-Plough (now Merck), where she was involved in supporting the development of a number of important marketed therapies, including Gleevec, Tasigna, Exjade and Temodar. We believe Dr. Zaknoen's experience in advancing programs at both biotech and large pharma companies is ideally situated to support and guide aTyr as we prepare for the next clinical stage program to emerge from our tRNA synthetase biology platform. I'd like to take a few minutes to discuss our preclinical program, which includes the development of anti-NRP2 antibodies for cancer and inflammation. NRP2 is a compelling therapeutic target in a number of disease areas, including oncology and inflammation. When it comes to cancer, NRP2 is upregulated on a variety of solid tumors and is particularly enriched in highly aggressive tumors, with expression linked to worse patient outcomes in several cancers, which may include drug resistance to current therapies such as chemotherapy or targeted agents. NRP2 is also highly expressed on key immune cells implicated in regulating cancer progression, including tumor-associated macrophages and myeloid-derived suppressor cells, among others. Antibodies that can selectively block different aspects of NRP2 signaling pathways may have therapeutic potential in these aggressive cancers where NRP2 is implicated. Our lead anti-NRP2 antibody and IND candidate is 2810, a fully humanized monoclonal antibody that specifically and functionally blocks the interaction between NRP2 and VEGF. The role of NRP2 and VEGF signaling in the tumor microenvironment and its potential importance in the progression of certain aggressive cancers is becoming increasingly validated. We have generated a body of compelling preclinical data in both patient-derived and animal models demonstrating 2810's blocking ability and tumor inhibitory effects. Notably, we've continued to strengthen our mechanistic understanding of the link between NRP2 and the critical process of epithelial-mesenchymal transition (EMT), which is of great importance in regulating tumor growth, progression and metastasis, as well as being implicated in tumor evasion of the immune system. At a recent Keystone Symposia on cancer stem cells, we presented a poster demonstrating that in a preclinical study, 2810 sensitized certain patient-derived xenograft models of triple-negative breast cancer to chemotherapy. We are actively working to understand the underlying gene signatures that confer responsiveness. These findings build upon our mechanistic understanding of 2810 and demonstrate the molecular basis for selectivity by directly obstructing the VEGF binding site of NRP2. 2810's ability to affect EMT and cancer stem cell properties may be one mechanism by which it mediates the anti-tumor effects we have observed. This work moves us closer to identifying the underlying characteristics within a tumor that may confer responsiveness to treatment with 2810. IND-enabling activities for 2810 to support advancements and clinical trials in cancer in the future are ongoing. I will now turn it over to our Chief Financial Officer, Jill Broadfoot, to review our financial results.

Thank you, Sanjay. Cash, cash equivalents and investments as of June 30, 2021 were $44.1 million; research and development expenses were $7.7 million for the second quarter of 2021, which consisted primarily of 1923 and 2810 program costs, including increased manufacturing costs. General and administrative expenses were $2.8 million for the second quarter of 2021. We do expect expenses to continue to increase throughout 2021 as research and development of 1923 and 2810 progress, including additional manufacturing costs for both 1923 and 2810, to prepare for future clinical trials. However, we have sufficient capital to take us through the readout of our trial in pulmonary sarcoidosis and initiate a patient trial in cancer for 2810. Common shares outstanding were 16.9 million and fully diluted shares were 18.7 million as of August 9, 2021. Now I'd like to turn the call back over to Sanjay before we open it up to Q&A.

Thank you, Jill. We're highly encouraged by what we've been able to accomplish in the first half of 2021, and we are looking forward to the upcoming readout for our proof-of-concept study for 1923. We've taken a very methodical approach to the development for 1923. When you look at 1923's MoA, we've shown that 1923 downregulates innate and adaptive immune responses during active inflammation. We've shown 1923 binds selectively to neuropilin-2, a receptor that we've shown is upregulated on key immune cells during inflammation, including sarcoid granulomas. And now, based on data we will present at ERS, we've shown that the active portion of 1923 has the ability to disrupt sarcoid granuloma formation in vitro. We've established a library of data demonstrating 1923's favorable clinical safety profile, which has consistently shown that 1923 is safe and generally well tolerated with no serious drug-related adverse events. This now includes data from two Phase 1 studies in healthy volunteers, a Phase 2 study in COVID-19 patients and two independent data safety monitoring board reviews from our current study in pulmonary sarcoidosis patients. And finally, we've demonstrated potential efficacy which includes a robust portfolio of translational work demonstrating 1923's anti-inflammatory and anti-fibrotic effects in multiple preclinical models of ILD and clinical proof-of-mechanism from our Phase 2 study in COVID-19, with biomarker data showing that 1923 reduced inflammatory cytokine levels in patients consistent with preclinical models, including cytokines that are directly implicated in sarcoidosis and other forms of ILD. Based on the totality of this data, we believe 1923 has the potential to be a transformative alternative to steroids and other available treatments with improved outcomes in patients with pulmonary sarcoidosis. This upcoming readout represents years of hard work and dedication to developing and advancing our tRNA synthetase biology platform to one that can generate new therapeutic targets and from which we can develop a new class of medicine. We look forward to sharing the results from this important study with you in mid-September. We appreciate your interest and continued support. At this time, Jill and I will be happy to take your questions.

Operator instruction: To ask a question, please press star 1 on your telephone keypad. Your first question comes from the line of Prakhar Agrawal of Jones Trading.

On 1923, I had a couple on the healthy volunteer trial update from Kyorin. Could you expand on what has been seen in the safety database? I understand there are no drug-related serious adverse events, but on other adverse events, how did that compare with what has been seen with 1923 previously? Was there anything new? Secondly, as we think about the September readout, what data will be disclosed at the time of the press release? What exploratory efficacy endpoints might we see and what endpoints might we need to wait for? And then I had a follow up.

Sure. Thanks, Prakhar. So with respect to our partner's trial, as I mentioned, this trial is complete. 1923 tracked well, very consistent to what we saw in our trial. No serious adverse events related to the drug effect, and generally safe and well tolerated. So very much consistent with the findings we saw several years ago with our Phase 1 trial. Those are the details that I can share with you about that trial. With regard to your second question around the readouts in September, we expect to not only report the primary objective, which is safety and tolerability of the trial, but we will be focusing on those key exploratory endpoints, namely around steroids, steroid burden, looking at pulmonary function tests, imaging, and inflammatory biomarkers. So really, we're looking at the totality of all of that data, in an attempt to get it all out at once. I do not expect things to trickle in after that. We're looking to report all of the primary and secondary objectives of the trial.

Good. I think same question on NRP2, the antibody — the secondary antibody that blocks NRP2 interaction with Semaphorin and Plexin. Could you expand on how this could play a different role than 2810? And what are the potential next steps for this antibody? Thank you.

Yes. This is an early opportunity for us. 2810 emerged out of this suite of specific antibodies that block different epitopes of neuropilin-2. Our 2810 blocks VEGF signaling; this is the next opportunity that we're looking at blocking Semaphorin signaling. With regards to how tuning neuropilin biology could be different, it could be useful in some instances in cancer; we are seeing some effects, rather early on, with 2810. With regard to Semaphorin, those pathways are broadly implicated a bit more with inflammation. So we now want to look at how that signaling could be useful either in cancer or inflammation. The idea here is by tuning neuropilin biology, our suite of antibodies could be useful not only in cancer, but also potentially as a more targeted anti-inflammatory, when you think about Semaphorin biology. But again, the first thing we did there was to make sure that it's a good strong blocking antibody; we have observed that, and now we'll start to tease out a little more of our mechanistic understanding of that next-generation antibody.

Your next question comes from the line of Emanuela Branchetti of H.C. Wainwright.

A couple for me. So with regards to the upcoming Phase 1b/2a readout, obviously, we are excited to see the potential for steroid targeting with 1923. But in this regard, do you expect a certain level of variability in patient responses based, for example, on the length of treatment with steroids? And also, I guess, what would be the main drivers of this variability?

Okay. So your question is really about duration of prior steroid therapy, Emanuela? That's right. And most of these patients can sometimes be on steroids for years. So this will be an important element for us to look at closely in our trial. What we understand from the experts, however, is once you progress to meeting at least 10 milligrams of prednisone a day, upwards to 25, that's really what we've enrolled in our trial. You now have moderate disease and in many ways, these patients are similar, whether they've received therapy for six months or sometimes for several years. But it is going to be an important characteristic for us to look at to determine whether or not duration of steroid burden contributed to any of the responsiveness. But I think that's an open question. I will say though, one of the things we really looked to do is to eliminate folks who self-resolve. This is why we focused in on a population receiving a moderate to high dose of steroids in our trial to create a bit more homogeneity amongst the patients enrolled, but that will be important for us to look at for sure.

Got it. Thank you, that's very helpful. And also, it's nice to see the update on Kyorin Phase 1. In this regard, I was wondering if you can provide more color on the strategy for the development of ATYR1923 with Kyorin. Should ATYR1923 move to pivotal, should we expect Kyorin to participate in a parallel development in sarcoidosis or would they focus on other ILDs?

So the plan at this moment is for Kyorin, as our partner, to potentially join our next trial if we are advancing this program forward. In addition, there is also the ability to move into other interstitial lung diseases with Kyorin, something that we will sit down and map out strategically. Kyorin has the ability to look at interstitial lung disease in Japan independently or together with us. So I think these readouts are going to solidify a little bit more of the strategy. But at this point, our aim here is to conduct potentially a worldwide trial next in which Kyorin can hopefully support us with Japanese experts and trial sites.

Your next question comes from the line of Hartaj Singh of Oppenheimer.

Great, thank you for the questions and nice update, Sanjay — looking forward to September. Just a couple of questions from my end. One is, when I look at the secondary outcome measures on ClinicalTrials.gov, they're listed as total cumulative steroid dose, results in a number of patients who achieve and maintain the tapered dose. Which of these would you consider more important? Is it trying to get the patient down to that targeted tapered dose? Is it total cumulative dose? I know also during Dr. Culver's presentation he had some opinions there. Just your thoughts, and then I have a couple of follow-ups.

Yes, great question, Hartaj. I think the way to think about this is we really are looking at steroid burden a couple of ways. First off, we want to be able to evaluate whether or not folks were able to maintain a response and response being able to be on five milligrams or less in our trial. I think that is a subtherapeutic dose, and if patients do well on our therapy and are able to maintain that kind of dose—remember, these are patients that have had a very difficult time even dropping one milligram, they've sort of landed somewhere between 10 milligrams to 25 milligrams sometimes for several years—so that's number one. Number two is looking at the total steroid dose over time during the six months with regard to what Dr. Culver talked about; this could obviously have a big impact on that toxic burden over time. And if we can show some differences between placebo and treated populations there, that could also be a nice win for us. So I think those are the ways we're looking at this trial. Of course, we have the ability that if a patient was able to even taper to zero, I think Dr. Culver highlighted that; that would be an outstanding finding if we were able to do that even in the short trial. These patients at the end of the day want to get off steroids or be on their way to getting off steroids. And if we're able to observe anything like that, I think that would be a tremendous finding. With regard to some of the secondary endpoints, I think right now we really are looking closely at some of those inflammatory biomarkers in addition to some of those other endpoints that you see on ClinicalTrials.gov. Biomarkers have become really important, in particular, after we demonstrated some nice improvement in COVID-19 patients.

Yes, that's very helpful. It would be great to show these effects in a 24-week trial — that's not very long. The other question I had was, assuming you had a positive readout in mid-September, what would be the next step with regulators and the timing on that? And then related, how important would your OSU collaboration be in looking at what could be a potential diagnostic or predictive strategy — how important would that be to interactions with regulators?

Sure. So obviously, we would want to move really quickly here. These are rare disease patients; they can't wait. So after these readouts, we would look to have an aggressive timeline to get back to the FDA. Some of that will also involve us sitting down with the investigators of our trial and really mapping out their thoughts. But we would want to quickly engage with the FDA so that we could start a — what's hopefully a single pivotal trial next year. Again, that's pending some of that FDA dialogue, but our approach here would be that in rare disease, these patients can't wait, and our approach would be to move forward with an aggressive regulatory strategy. With regard to your question around the OSU collaboration, absolutely, this could be an avenue for us to develop an ex vivo assay which can effectively identify patients sensitive to 1923 prior to even dosing these patients. So I think as a companion predictive diagnostic, this would be something that we would work towards and potentially use to, at a minimum, enrich our target patient population for the next trial. So I think it sets us up nicely to create even more homogeneity around those patients that respond to 1923.

Great, thank you, Sanjay.

Your next question comes from the line of Yale Jen of Laidlaw and Company.

Good afternoon and thanks for taking the question. My first question is a follow-up with the previous one: in terms of the Japan study versus the study you have done in healthy volunteers, was there any PK differences between the Japanese and, I guess, Americas or was there not much? And then I have other follow-ups.

Yes, hi, Yale. No, we saw consistent findings on half-life of our drug; it's somewhere around eight to nine days, and those PK findings tracked in the Japanese population as well. So we were more or less in the same ballpark, which is one of the reasons you conduct this trial because there sometimes can be differences in PK between populations.

Okay, great. And the second question is that in terms of the readout in mid-September, by what venue do you think you will communicate to investors? Would that be an analyst or investor call or other means, or just a press release?

We would plan to have a call, certainly. This is an important inflection point for us, so we'll want to get everybody on the line and go through the data with each of you.

Okay. And then maybe two more quick ones. First, on ClinicalTrials.gov, one secondary outcome measure is listed as incidence and titers of anti-Jo-1 antibodies. Could you give a little more color on what that is and why it's being monitored?

Sure. As we are working with a class of medicines coming from the tRNA synthetase world, there is an ultra-rare condition called antisynthetase syndrome. In this condition, patients sometimes develop antibodies to a protein fragment of full-length histidyl tRNA synthetase. As we are working in the same class, part of our safety monitoring is to ensure that we do not induce any autoimmunity. These Jo-1 antibodies are something that we are required to watch for. However, I will tell you that antisynthetase patients who develop antibodies to histidyl tRNA synthetase develop interstitial lung disease. So in many ways, we're dealing with patients that already have interstitial lung disease. Another way to think about this is that patients where you perturb this clinical pathway around tRNA biology demonstrate that this is an important pathway; this protein fragment is involved in regulating the development of interstitial lung disease. But as we are working with this class, the FDA, from a safety perspective, requires us to monitor Jo-1 antibodies because we are a tRNA synthetase platform company.

Okay, great. Maybe the last question is a housekeeping one. In terms of the licensing and collaboration agreement revenues for the remainder of 2021, do you see any potential revenue in this timeframe or how should we think about that piece of the line?

We haven't disclosed the timing for each milestone. The majority of the remaining $165 million referenced in the agreement is geared towards development, but we did receive a $2 million milestone upon the last patient in for a partner trial. So you can basically think of that as what we received from a Phase 1 perspective. The next milestone would come in that next stage of development, which would not begin this year.

Okay. But the 'last patient in' was not the one you completed the enrollment, right — completed treatment reported earlier this year?

Right. They had the last patient in in December of last year, and we re-opened it in the first quarter of this year.

Your next question comes from the line of Zegbeh Jallah of ROTH Capital Partners.

Hi, thanks for taking my question. Just a few. The first one is: how many patients were in the biomarker data set for the COVID-19 study? And since it will be presented before the pulmonary sarcoidosis data readout, how should investors interpret that data readout relative to the sarcoid readout?

Sure, thanks, Zegbeh. So this was data we presented earlier this year. There were 32 patients in that COVID-19 mechanistic proof-of-concept trial we ran. Previously we reported that roughly 82% of those inflammatory markers substantially declined when 1923 was used on top of dexamethasone. So this is a poster which brings that data together. There isn't exactly new information coming from that; we previously released it publicly, but we thought it would be useful for the medical community to see this in a conference setting. Previously, we've highlighted this data with interferon gamma, IL-6, MCP-1, showing significant knockdown in those COVID pneumonia patients. These are the same biomarkers that we saw move significantly in our animal studies. So this poster essentially consolidates the information we presented back in Q1 and is being presented at ERS, which happens to be shortly before we're about to announce data from sarcoidosis.

Thanks, Sanjay. And then a follow-up regarding the pulmonary sarcoidosis data coming next month: will it be highlights or will it be full patient-by-patient detail?

We'd like to be as detailed as possible. There's no top-line or interim data; we're aiming for full results, being able to look at not only all of the safety endpoints, but even those exploratory efficacy endpoints that we've highlighted.

Thank you. With the small sample size, are there any data points where you would expect to see variability and how do you plan to tackle that or leverage all the data points to determine the go-forward strategy?

I think Dr. Culver highlighted that pulmonary function tests (PFTs) can be somewhat variable in this population. The way we look at it is we may be able to look at PFTs and stratify based on response; we may learn something there. Our current trial did not create a stratification or inclusion criteria around forced vital capacity because the experts advised that PFT endpoints can be variable, so we left it alone. With regard to some of the lung imaging, some of the newer imaging biomarkers such as PET scans are not fully validated; so we're going to learn — that's why these are exploratory endpoints. I think what we are really prioritizing is safety, looking at steroid-sparing effect and looking at those biomarkers. Patient-reported outcomes are also going to be very important here. Cough, fatigue, shortness of breath are all areas that, if patients are doing well and we're also able to see improvement in tapering their steroids, then I think those pharmacodynamic markers going in the same direction, as Dr. Culver pointed out, could be really impactful.

Thanks, Sanjay. Looking forward to the readout.

Thank you.

There are no further questions at this time. I will now turn the call over to Sanjay Shukla for closing remarks.

Great. Well, we thank everyone for their interest and for the great questions today. We're looking forward to getting back to everyone very soon in the near future. So thank you, everybody. Have a great day.

This concludes today's conference call. Thank you for participating. You may now disconnect. Presenters, please stay on the line.