Company Representatives: Sanjay Shukla - President, Chief Executive Officer Jill Broadfoot - Chief Financial Officer

Good afternoon, ladies and gentlemen, and welcome to the aTyr Pharma Second Quarter 2020 conference call. At this time, all participants are in a listen-only mode. As a reminder, this conference is being recorded for replay purposes. It is now my pleasure to hand the conference over to Jill Broadfoot, aTyr’s Chief Financial Officer. Ms. Broadfoot, you may begin.

Thank you, operator and good afternoon everyone. Thank you for joining us today to discuss aTyr's second quarter operating results and corporate update. We are joined today by Dr. Sanjay Shukla, our President and CEO. On the call Sanjay will provide an update on our corporate strategy, including the clinical development of ATYR1923 and our research program in Neuropilin-2 or NRP2 and tRNA synthetase biology. I will then review the financial results and our current financial positioning before handing it back to Sanjay to open the call up 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, Jill. Good afternoon everyone and thank you for joining us for our second quarter 2020 results conference call. As we begin with our second quarter update, I would like to take a moment to acknowledge that as we are now in the second half of the year, we have adapted rather quickly to operate in the new normal due to the COVID-19 global pandemic. I'm extremely proud of the aTyr team, our partners, and all of the physicians and patients who continue to remain responsibly dedicated to our research and development activities, even in light of the urgent and immediate medical care attention and resources required in response to the pandemic. I'm particularly inspired by our research team and collaborators who continue to generate important preclinical and translational findings, resulting in published data despite the current challenges and considerations of working on-site in the lab. And our clinical team who has really worked tirelessly to initiate a new trial on COVID-19 entirely remotely and entirely virtually. It is a testament to the community that we are trying to build here and continue to expand upon even in these trying times. Now let's get started with our quarterly review and corporate update. During the second quarter of 2020 and subsequent period, aTyr continued to progress the development of our lead program ATYR1923. I'm pleased to report that the majority of sites for our trial in pulmonary sarcoidosis have resumed clinical trial activities, and as previously mentioned, we initiated a new trial on COVID-19 patients with severe respiratory complications in June. Additionally, we have continued to drive value and build momentum with our pipeline. We generated valuable preclinical data from our NRP2 antibody program in oncology that validates the high quality and specificity of those antibodies and their potential to be developed for therapeutic applications. Based on these findings, we expect to declare an Investigational New Drug or IND candidate later this year. But we also anticipate the completion of the first phase of our tRNA synthetase research collaboration with CSL Behring early in the fourth quarter. To begin I’ll summarize the key highlights from the second quarter and subsequent period. First off, we progressed our Phase 1b/2a clinical trial of 1923 in patients with pulmonary sarcoidosis. As I mentioned, the majority of sites that had to pause enrollment due to the pandemic have now resumed clinical trial activities. As clinical trial conduct is dependent on COVID-19 activity, we continue to work with each site regarding their institutional policies and procedures in order to ensure the completion of the trial. We initiated a Phase 2 Trial of 1923 in COVID-19 patients with severe respiratory complications. Enrollment is currently ongoing and a pre-planned, blinded, independent data safety review of the first five patients resulted in a recommendation that the trial continue unmodified. We expect to report data from this study in the fourth quarter of this year. Kyorin Pharmaceutical, our partner for the development and commercialization of 1923 for interstitial lung diseases or ILDs in Japan initiated a Phase 1 study to evaluate the safety, pharmacokinetics and immunogenicity of 1923 in Japanese healthy volunteer subjects. We published two abstracts in the American Journal of Respiratory and Critical Care Medicine, characterizing the binding properties of 1923 to NRP2 and the expression of NRP2 in sarcoid granulomas. These findings were also presented as posters at the American Thoracic Society, International Conference Virtual Meeting. We presented preclinical data at the American Association for Cancer Research Virtual Annual Meeting from our NRP2 antibody program, demonstrating tumor inhibitory effects in pre-clinical models of triple-negative breast cancer. And finally, we continued our tRNA synthetase research collaboration and option agreement with CSL Behring, extending work on the first phase of the research program through September 30, 2020. We have accomplished a great deal thus far in 2020, despite the challenges presented by the COVID-19 pandemic, and we continue to make significant progress in the third quarter. Today I'll provide an update on our clinical program, with our lead therapeutic candidate 1923, including the status of our Phase 1b/2a trial in pulmonary sarcoidosis, our Phase 2 trial in COVID-19 patients, and our phase one program with our partner in Japan. I’ll also comment on our ongoing preclinical research and development efforts for our programs in NRP2 and tRNA synthetase biology. Jill will conclude with a review of our financial position. Let's begin with some background on our program for 1923. 1923, the potential first-in-class immunomodulator that downregulates immune response in inflammatory disease states. Inflammatory triggers, whether they are organic, inorganic, infectious or autoimmune in nature can lead to aberrant immune responses in patients, resulting in pathology. 1923’s target receptor NRP2 is upregulated on immune cells in the lungs during this process. Persistent unresolved inflammation in the lung can lead to fibrosis or scarring, which can result in increased morbidity, including impaired lung function and irreversible organ damage and mortality. 1923 binds selectively to neuropilin-2 to downregulate aberrant immune responses, with the goal of resolving inflammation and preventing progressive fibrosis thereby stabilizing lung function and alleviating morbidity and mortality. Our primary development focus for 1923 is to address this substantial unmet medical need in ILDs, a group of chronic, immune mediated lung disorders that can result in progressive fibrosis in the lung, of which our lead clinical indication, pulmonary sarcoidosis is a major form. As data emerged on the underlying disease mechanisms causing severe respiratory complications in COVID-19 patients, it became apparent there was significant overlap with ILD pathology, leading to our decision to investigate 1923 as a possible treatment for these patients. We also believe our findings with 1923 in COVID-19 patients with severe respiratory complications may provide insight into 1923’s potential to treat other acute inflammatory lung disorders. In addition to our clinical efforts, we continue to strengthen our mechanistic understanding of 1923 immunomodulatory properties through NRP2 signaling, supporting its potential use in inflammatory lung disease. Last week we presented two posters at the American Thoracic Society, International Conference Virtual Meeting. Abstracts of these posters were published earlier in the American Journal of Respiratory and Critical Care Medicine. The findings highlight the potentially significant role of NRP2 in serious inflammatory lung disease, and further elucidate the mechanism of action of 1923. These findings report that NRP2 is expressed and readily detectable within the granulomas of lung and skin samples of sarcoidosis patients. Through this research we demonstrated that NRP2 expression can be detected on key immune cells that are known to play an important role in inflammation and granuloma formation. Additional research published demonstrates the 1923 specifically and selectively binds to NRP2 on the cell surface. These findings characterize the molecular basis for 1923’s immunomodulatory properties and indicate that NRP2 could be a novel therapeutic target for immune-mediated lung diseases. Now let's take a moment to discuss our clinical program for 1923. We'll begin with an update on our Phase 1b/2a trial of 1923 in patients with pulmonary sarcoidosis. As a reminder, this is a randomized double-blind placebo controlled multiple ascending dose clinical trial in 36 pulmonary sarcoidosis patients and consists of three cohorts. We previously reported successful results from an interim safety analysis of 15 pulmonary sarcoidosis patients, who received a minimum of one dose of blinded study drug. In addition, during the first quarter our independent data and safety monitoring board completed its second safety review, allowing us to move from our 3 milligram per kilogram dose and test our 5 milligram per kilogram dose in cohort 3 of this study, for the final group of patients in our study. Based on these findings, we progressed to include the third and final cohort of the study. Due to the COVID-19 pandemic, we announced an impact to enrollment and that some, but not all of our investigational sites had to pause enrollment. Last quarter we announced that some of those sites were expected to reopen enrollment in late May or early June. I'm happy to report that we did see that occur in early June and now in fact we've resumed clinical trial activity at the majority of our sites that were paused, where it has been safe for providers and patients to do so. We plan to provide an update on the expected timing of results once the trial has fully completed enrollment. In order to progress our global development strategy for 1923, earlier this year we entered into a collaboration and license agreement with Kyorin Pharmaceutical for the development and commercialization of 1923 for ILDs in Japan. Earlier this week we announced that Kyorin has been cleared by the Japan’s regulatory agency Pharmaceutical and Medical Devices agency or PMDA, to begin clinical development for 1923 in Japan with approval of a clinical trial notification or CTN. The CTN permits the start of a Phase 1 trial, which will be conducted by Kyorin and will evaluate the safety, pharmacokinetics and immunogenicity of 1923 in healthy volunteers in Japan. Establishing safety of a new therapeutic drug candidate in the Japanese population, even when prior safety data is available, is often a requirement by the PMDA. This is an important first step to advance clinical development of 1923 in Japan. For development purposes, 1923 will be referred to as KRP-R120 in Japan. As a reminder, under the terms of the agreement aTyr previously received an $8 million upfront payment and is eligible to receive up to $167 million in the aggregate upon the achievement of certain development regulatory and sales milestones, as well as tiered royalties on the net sales in Japan. Kyorin has the exclusive rights to commercialize 1923 in Japan for all ILDs. Now let's turn to our Phase 2 trial of 1923 in COVID-19 patients. As we already mentioned, inflammatory lung injury may be caused by an infectious agent. While our initial focus has been on chronic lung disease, we believe the mechanisms of action of 1923 may have potential in acute inflammation. We learned early in this crisis that the inflammatory lung injury related to COVID-19 share some remarkable similarities to those observed in ILDs. Many COVID-19 patients with severe disease experienced serious, sometimes fatal, respiratory complications, caused by an excessive inflammatory response in the lung, primarily driven by T-Cells. 1923 has been shown pre-clinically to downregulate T-Cell responses, thereby dampening the inflammatory cytokine and chemokine signaling, both of which have been implicated in these very severe COVID-19 cases. In addition to these anti-inflammatory properties, 1923 has also been shown to improve lung function in animal models of immune mediated acute lung injury. By targeting aberrant immune responses, we believe that 1923’s mechanism of action has substantial overlap with this disease pathology and presents a very compelling opportunity to potentially treat this subset of COVID-19 patients. As the pandemic has ensued, we continue to learn more about the SARS-CoV-2 virus and the disease pathology and progression of COVID-19. Most notably, a recent article published in the New England Journal of Medicine reported that lung tissue analyzed from patients who die from COVID-19 respiratory failure, showed an increase in the expression of NRP1 and NRP2, suggesting these genes are upregulated in response to SARS-CoV-2 infection. Additionally, two independent labs reported the discovery that SARS-CoV-2 Spike protein 1 directly binds to the b1 domain of Neuropilin receptors on the cell surface, including NRP1 and NRP2. They also show that preventing this binding interaction results in decreased cell infection. Further data is emerging that patients who experience severe respiratory complications from COVID-19 may experience longer hospitalization stays and permanent injury to lung, potentially including pulmonary fibrosis. We believe that by administering 1923 earlier in the progression of COVID-19, it may be able to preserve lung function by normalizing immune system response. Based on the strong scientific rationale, we worked very closely with the FDA to initiate a Phase 2 randomized, double blind, placebo-controlled study in 30 hospitalized COVID-19 positive patients with severe respiratory complications who do not require mechanical ventilation. Patients enrolled in the trial are assigned to one of three cohorts of 10 patients each. Patients will receive a single intravenous dose of either 1 or 3 milligrams per kilogram of 1923 or placebo to be administered in the hospital. Patients will be followed for 60 days post treatment and we plan to enroll at up to 10 centers in the U.S. While the primary endpoint of the study is to assess the safety and tolerability of a single dose of 1923 in this acute setting, we are also focusing on a number of key clinical outcome measures including, but not limited to fever, hypoxia and inflammatory biomarkers. As per our protocol, an independent data and safety monitoring board or DSMB conducted a pre-planned, blinded interim safety analysis after the initial five patients were dosed in this study. A study drug of 1923 or placebo was observed to be generally safe and well tolerated with no drug related serious adverse effects. Based on these findings, which are consistent with previous safety assessments of 1923, the DSMB recommended the trial to continue unmodified. As we are very encouraged by our progress to-date with this COVID-19 trial, given the challenges of conducting clinical trials amidst the current pandemic, enrollment is currently ongoing and we expect to report data from this important study in the fourth quarter. My dogs are excited too about this study as well. Now let's turn to our research and discovery pipeline, including our NRP2 antibody program, which we believe has great potential to create pipeline value and drive meaningful milestones in the areas of oncology and inflammatory disorders. We recently presented pre-clinical data at the American Association for Cancer Research Virtual Annual Meeting from a panel of anti-human NRP2 monoclonal antibodies that we generated from our internal research and discovery program. These antibodies have the potential to be developed for the clinical management of solid tumors. There's a growing body of evidence indicating that the expression of NRP2 is enriched in breast cancer stem cells and that NRP2 signaling is critical for breast cancer stem cell function and resistance development. Specifically, expression of NRP2 has been shown to be high in triple-negative breast cancer and lead to worse patient outcomes. aTyr’s panel of NRP2 antibodies are engineered to target distinct and specific domains of NRP2. Through our collaboration with Dr. Arthur Mercurio, one of our key scientific advisors, and his lab at the University of Massachusetts Medical School, we explored the use of our NRP2 antibodies in triple-negative breast cancer models. The findings demonstrate that one of these antibodies blocked the binding of VEGF-C to Neuropilin-2. VEGF-C is highly expressed in certain breast cancers and is responsible for the mediation of tumor progression. The findings also demonstrated tumor inhibitory effects and increased sensitivity to chemotherapy, suggesting that targeting NRP2 as a therapeutic strategy for breast cancer and potentially other aggressive solid tumors could be useful. We expect that from this panel of antibodies, we will be able to declare an IND candidate later in the year. Finally, our broad portfolio of tRNA synthetase intellectual property provides the opportunity to contribute to our pipeline to our internal discovery programs and external collaborations. Our research collaboration and option agreement with CSL Behring, a leading global Biotherapeutics company provides a framework to identify up to four new IND candidates from our portfolio of tRNA synthetase IP. Due to disruption primarily from the COVID-19 pandemic, we amended the agreement to provide an extension for the first phase of the research collaboration through September 30, 2020. CSL Behring has provided additional funding for research and development activities to accommodate this extension. We plan to provide an update on this collaboration early in the fourth quarter. So overall, we're very pleased with the continued dedication, determination and focus of our employees, which has resulted in the highly encouraging progress we've made to date in 2020. As we look ahead to the remainder of the year, we're excited about the potential that our clinical programs and pipeline hold. Our pulmonary sarcoidosis trial has resumed enrollment and we see forward momentum with the majority of sites now reactivating. The positive outcome from the interim safety analysis of our study in COVID-19 has permitted the Trial to continue enrolling and we expect to report data from this important study in the fourth quarter of this year. Through our partnership with Kyorin, we are advancing clinical development of 1923 in Japan with the initiation of a Phase 1 trial, and due to compelling preclinical data with our NRP2 antibody program, we expect to declare an IND candidate later this year, which serves to strengthen our pipeline and create additional opportunity for value driving catalysts. With that, I'd like to turn it over to our Chief Financial Officer, Jill Broadfoot to review our financial results.

Thank you, Sanjay. Total revenues were $8.3 million and $0.1 million for the six months ended June 30, 2020 and 2019 respectively. Revenues for 2020 consisted primarily of the $8.0 million upfront payment under the Kyorin Agreement. As previously mentioned, we are eligible for an additional $167 million in payments upon achievement of certain milestones. Now that Kyorin has been cleared to begin clinical development work in Japan, we begin to track towards some of the development milestones which could result in further payment. Revenues for 2019 consisted of license revenue under the CSL agreement. Research and development expenses were $8 million and $6.7 million for the six months ended June 30, 2020 and 2019 respectively. The increase in research and development expenses was due primarily to clinical trial activities for 1923 in pulmonary sarcoidosis and COVID-19. General and administrative expenses were consistent between periods at $4.7 million and $5 million for the six months ended June 30, 2020 and 2019 respectively. As of June 30, 2020 aTyr had $41.4 million in cash, cash equivalents and investments and we continue to expect to end the year with more than $20 million in cash, consistent with prior guidance. In addition, as of June 30, 2020 our term loan balance decreased to $5 million and we intend to fully extinguish this debt in the coming months. Now, I'd like to turn the call back over to Sanjay before we open it up to Q&A.

Thank you, Jill. We appreciate all of your interest and continued support and look forward to providing updates in the future. At this time Jill and I will be happy to take your questions.

Our first question comes from the line of Zegbeh Jallah with ROTH Capital. Your line is open.

Thanks guys and congrats on the progress. Just have two questions; the first one, the ongoing Phase 2 COVID study has a primary outcome of safety. But for the subsequent studies that you are going to do, after which you know what do you think the primary outcome could be? Are you going to be relegated to something that the FDA has predefined as an approval endpoint or do you have some liberty to look at your secondary efficacy outcomes and then kind of decide what to make your primary outcome?

So hi Zegbeh, that’s a very good question. I think one of the things that the FDA is really doing here with a lot of the COVID trials is trying to develop at least a framework, if not a master protocol on what's approvable. On the therapeutic side, they haven't quite come out yet on things that they might be looking for in a Phase 3 trial, but I think what you can see from some of their emergency use authorizations, certainly decreasing hospital stay has led to at least emergency approval for Remdesivir. Mortality of course—well, 30 day mortality is a standard measure we look at here that I'm sure the FDA would also want us to look at in this trial. Normalization of some of those clinical endpoints, this is something that when we put the protocol forward, they like the fact that we're trying to look at hypoxia and seeing if we can normalize things there sooner than later. And then I think some of the metrics around hospitalization, utilization, days in the hospital, avoiding ICU stay, decreasing ICU stay, all of these are being measured in the current trial. My expectation is they will probably prioritize 30 day mortality and certainly if you have any signal on being able to discharge patients sooner rather than later, I think that portends really well as an approvable endpoint.

Thank you. And then the follow-up one here is, for this study which is clinically focused on safety, you did say that you're not enrolling patients that are on ventilators, but are you thinking that you may narrow the patient population a little bit more and would you be using what we’re seeing with some other studies, the WHO scale to kind of define that patient population?

Yeah, I mean I think it’s two-pronged here. Number one, our biology of our drug unlike some of those other drugs being used in pre-ventilated patients, we think we are differentiated in that our drug works better potentially when you administer it early in the inflammatory response, directly interfacing and modulating the T-cells before you get into some of that cytokine storm. So I think that's first of all part of the attraction of going into an earlier population. If in fact we are successful with this trial, much as you've seen some of those later phase drugs potentially being used upstream in milder patients, you could see our drug potentially being used in the ICU setting. In that case, yes, we'll have to look at those ordinal scales that you highlighted there. We didn’t have to follow that so much here, because we're not focusing on those patients. So I actually think that if we show activity in this trial, given the nature of how dynamic COVID-19 is right now, my expectation is doctors will want to use it even for those ventilated patients just because of the nature that we're trying to find good drugs in the tool kit right now to help these folks.

And I think that makes sense based on what you said with regard to still seeing NRP2 upregulated in those patients. It could be attractive even in some of those later patients as well, that could be interesting. And then I guess I have one final one actually. Just wondering if you're going to have another pre-planned DSMB analysis? It was nice to see that you guys made it past the first one. Was there another one planned before the study reads out?

This is the only one that was required and pre-planned by the FDA. It doesn't mean that we’ll, as this is a safety study, continue to actively monitor safety, and we have the ability to of course reach out to our DSMB as much as we'd like in this study. But as per our protocol and discussions with the FDA, given that there wasn't specific experience with our drug in this population, they asked for a quick look here, which we did with the first five patients.

Thank you. Glad to see that you’re making progress on both of these studies.

Thank you.

Thank you. Our next question comes from the line of Hartaj Singh with Oppenheimer. Your line is open.

Great, thank you. Thanks for the updates Sanjay and Jill. Just a couple of questions; one is, to follow up on the questions from the previous analyst. The cocktail antibodies from Regeneron for example are being tried in patients in a preventative fashion, and both in an acute setting, so patients don’t have the disease. With your work with 1923, do you think that it could actually go from the ICU maybe into the ER or maybe even in a preventive study. I know that you need a lot of data to get there, but could you see that progression similar to what’s happening in the cocktail antibodies and I just got a couple of follow-ups.

Yes, we do think that if you show activity in this cohort of patients, the potential to go upstream or downstream in the progression of COVID-19 is certainly on the table. In particular, upstream patients that are maybe in the ER, you want to make sure that you're not interfering with their normal host immune response, because probably 80% of folks can get through this infection either asymptomatically or with mild symptoms staying at home. But yes, the ER setting could be an area where, especially when hospitals are really full of hospital bed, you're seeing a lot of patients who typically wouldn’t have been discharged in the past, now being asked to convalesce at home, sometimes even with a little bit of oxygen at home. So certainly that's an avenue for us once we demonstrate activity here, and then downstream as a combo therapy, I think doctors are right now searching for any and all things in the tool kit here to basically address morbidity or mortality in an effort to kind of get this crisis under control. Once we establish safety and selectivity in this trial, I believe both of those avenues open up for us.

Great! And then on the pulmonary sarcoidosis trial, I had a question on—as you’re getting the sites back up and if you've gotten a lot more information from the sites you had to get back up and patients that you were tracking to finish this study. Do you think that between now and the trial readout, you might have to make some protocol adjustments or amendments, based on changes from COVID-19? Do you think you could pretty much finish the trial under the current protocol and read it out without changes to it?

That's a great question. At this time I don't expect any major protocol changes. I also think we're pretty late in the game right now to have another amendment. I think one thing to keep in mind when you work in respiratory trials, and because this is a respiratory infection, a lot of hospitals have protocols in place around very vigorous pulmonary function testing, because these patients are exhaling forcefully. So we're working with those centers in the sense that there could be some modifications there in the capture of some of those PFTs, if in fact they don't want these patients using the sort of spirometry tool they have in the hospital. So that might be the only tweak, I would say is important for folks to understand that. We may have to use slightly different spirometry tools depending on what the hospital wants to do.

Great! And then the last question I had is just on the NRP2 antibody candidate that you’re going to declare for oncology later this year. What are your sort of publications that you can expect to see from that, from a pre-clinical setting over the next six to 18 months?

So as we just put out really our initial efficacy data, which is rather promising in this triple negative breast cancer model, we want to be able to explore other models, other solid tumor models. So I think I expect to see more publications, looking a little bit more closely at breast cancer of course, but then in other areas where NRP2 expression in the literature has been shown to be upregulated in pancreatic, prostate, glioblastoma, areas like that. That's where our discovery teams will be looking at those tumor models, because that will allow us to not only declare an IND candidate, but then to basically focus in on for example which two or three tumor settings provide the most rational approach to advance to an IND.

Great! Thank you Sanjay, thanks for all the questions.

Thanks Hartaj.

Thank you. Our next question comes from the line of Joe Pantginis with H.C. Wainwright. Your line is open.

Sanjay and Jill, thanks for taking the question. Hope you are all well and your families. Two questions, really just focusing on trial logistics. So first for the Phase 1b/2a, maybe just a little more detail about sites being resumed. Do you need to get any sort of re-IRB approvals or what are some of the logistical rate limiting steps there?

Hi Joe, good question. No, we do not need to go back to the IRB from the standpoint of restarting at that point. So that would certainly be an administrative rate limiting step that we're not hindered by. I think the main thing here is given that we were recruiting at a vigorous clip prior to COVID-19, what's rate limiting here is understanding how many patients will come back into the clinic, what's the density? While a center can be opened, some centers will be 100% and other center might just say, we only want 50% of the sarcoidosis patients that we would typically have coming back in. So we're going to have to observe here the rate of screening and enrollment. As you can imagine, just like anything else, whether it's a school or restaurant or hospital, all of these institutions are working with their local health departments and monitoring their local COVID incidents in determining how aggressive or not they want to reopen. So that's something that is the next step here, but I think it's a great sign that now the lights are on at a majority of our centers. Now it's a matter of observing what happens here, so that we can complete enrollment.

That's very helpful, thanks. And then regarding the Phase 2 COVID study, a lot of questions you’ve obviously been asked. So it's really surrounding the conduct of the study and just curious, obviously we're talking about different lines before potentially, are we sort of going more into the ER for example. But I guess for the current study, what are the plans on how you look at concomitant therapies, like with regard to maybe a patient getting remdesivir or some other steroids or anything to treat the inflammatory syndrome?

Yes, so the key clarifications we have is really around remdesivir, which as an antiviral works very, very differently and frankly probably works better like most antivirals if you administer quite early to interfere with replication. So remdesivir is allowed in our study, and it’s sort of background standard of care right now at a number of centers. Because we have a placebo arm in our trial, we have to allow what is currently background standard of care. Dexamethasone is being used also here and there in a pulsatile manner as a background therapy, but dexamethasone is not something that you can blast a patient with for a long period of time. So those are the two I would say standard of care drugs that are used. Some of those other monoclonals that are being used more in the ICU when a patient spikes a certain cytokine, we were not really playing in that space. So I don’t see a lot of interference and certainly the recent data from the IL-6 antagonists have clearly indicated that those drugs are not working really well. So lot less competition than there was maybe a few months ago, and I think a better clarity here. One thing that’s come out of our trial is as patients and doctors have been able to manage this infection a little bit better, we are seeing folks being more conservative about putting them on the ventilator. We’ve heard this nationwide. So what's happening is, there is a greater proportion of patients that are hospitalized and not on mechanical ventilation. So I think the key thing right now is also these hospitalization stays which can be quite long in these patients; survival and mortality benefit is certainly being observed, if you keep people off the vent, but you still see these patients staying in the hospital quite a bit of time with significant amounts of inflammation. We think that sets us up really well to be an attractive therapy as we get into COVID next year.

Great, thanks a lot.

Thank you. At this time I would like to turn the call back over to Sanjay for closing remarks.

Well, thanks everyone. Again to reiterate, I really appreciate the interest. Lots of updates today and great questions from our analysts. We will be in touch in the future. Thank you again, everyone.

Ladies and gentlemen, this concludes today's conference. Thank you for your participation, you may now disconnect.