aTyr Pharma, Inc. (ATYR) Earnings Call Transcript & Summary

Good afternoon, ladies and gentlemen, and welcome to the aTyr Pharma Topline Results for Phase II Trial of ATYR1923 in COVID-19 Patients Conference Call. [Operator Instructions] As a reminder, this conference is being replayed 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 topline results for our Phase II study of ATYR1923 in hospitalized COVID-19 patients with severe respiratory complications. 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 overview of the top line results, including trial details related to safety and preliminary signal of clinical activity. He will also comment on our ongoing Phase Ib/IIa clinical trial in patients with pulmonary sarcoidosis. We will then open the call up for any questions to Sanjay and Jill. 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 Phase II topline results for ATYR1923 in COVID-19 conference call. I'm pleased to be here today to discuss the topline results of our Phase II clinical trial of our lead therapeutic candidate, ATYR1923 or 1923, in patients with COVID-19 who are hospitalized with severe respiratory complications. We're here today reporting data from a Phase II trial that we initiated, enrolled, completed and analyzed, all within a span of about 6 months. I would like to acknowledge what the aTyr team has done. Along with our partners, clinical sites, investigators and patients, we managed to accomplish quite a bit in this trial, completing this trial, reporting these results in such a short time frame. As we begin, let me remind you of the details of this trial. This was a Phase II randomized, double-blind, placebo-controlled study of 1923 in moderate-to-severe COVID-19 patients with severe respiratory complications who were hospitalized and did not require mechanical ventilation. The trial enrolled 32 patients at hospitals in the U.S. and Puerto Rico. Patients enrolled in the trial were randomized 1:1:1 to a single intravenous or IV dose of either 1 or 3 milligrams per kilogram of 1923 or placebo. Patients were followed for 60 days post treatment. The study was not powered for statistical significance and was designed to evaluate safety and identify preliminary signs of activity of 1923 as compared to placebo. Today, just about an hour ago, we issued a press release summarizing topline results for this trial. I'm pleased to report that the trial met its primary endpoint of safety, demonstrating that a single IV dose of 1923 was generally safe and well tolerated in both the 1 and 3 milligram per kilogram treatment groups with no drug-related serious adverse events. In addition, the study demonstrated a preliminary signal of activity and clinical improvement in the high-dose cohort of 3 milligrams per kilogram through the assessment of 2 key determinants of recovery: time to recovery and the proportion of patients achieving recovery within a week, with recovery in our trial defined as achieving either a WHO ordinal scale score of less than or equal to 3 or hospital discharge with no requirement of supplemental oxygen. Patients who received a single 3 milligram per kilogram dose of 1923 experienced a median time to recovery of 5.5 days compared to 6 days in placebo. Also, 83% of patients who received 3 milligrams per kilogram dose of 1923 achieved recovery by day 6 compared to 56% of patients in the placebo group. Patients in the 1 milligram per kilogram treatment group had a median time to recovery of 7 days. All patients received standard of care treatment at the time of enrollment, which includes remdesivir and/or dexamethasone. Adverse events were mostly mild or moderate in severity and generally assessed as unrelated to the study drug. This is in line with previous safety assessments of 1923, including an interim safety analysis from our ongoing Phase Ib/IIa trial in patients with pulmonary sarcoidosis, a chronic form of interstitial lung disease or ILD. There were 2 deaths observed in the study, both in the 1 milligram per kilogram treatment group, which were deemed not related to 1923 by an independent data safety monitoring board. We're pleased with the results of this study, which continued to demonstrate 1923's favorable safety profile in inflammatory lung conditions. We are very encouraged by the signal of clinical activity seen in the 3 milligram per kilogram cohort of 1923. Compared to other COVID-19 studies, we set a high bar for recovery in that patients had to be discharged from the hospital and also required no supplemental oxygen. The relatively faster time to recovery seen by adding a single dose of 3 milligrams per kilogram of 1923 to standard of care treatment and the greater proportion of patients recovering within a week compared to placebo give us further confidence in this signal. We are pleased that against the backdrop of a rapidly evolving standard of care for COVID-19 patients that we have reaffirmed the positive safety profile of 1923 and elucidated a signal of drug activity from just a single dose of 1923 in this small trial. As a reminder, patients enrolled in the study were acutely ill with moderate-to-severe disease with all patients enrolled having a score of 4 or 5 on the WHO ordinal scale at the time of enrollment. A score of 4 or 5 indicates that these patients were hospitalized and were requiring supplemental oxygen. We wanted to ensure that we saw a balance in our randomization around demographic and baseline characteristics. Key demographic and baseline disease characteristics were mostly balanced in the study. However, we did notice some important imbalances in our randomization, including more patients in the 1923 treatment groups over the age of 65, patients with severe hypoxia or patients with baseline comorbidities. Patients over the age of 65 are known to be at higher risk of COVID-19 complications. Our randomization showed an imbalance in this important criteria, as nearly all patients in this demographic were randomized to our 1923 treatment groups. Further, patients with more severe hypoxia and more baseline comorbidities may also be at risk for worse outcomes. These 2 imbalances for these important baseline disease characteristics may have also skewed the patient population between cohorts. These key imbalances suggest that randomization in our treatment groups yielded a sicker cohort of patients compared to our placebo population. We reported that patients in the 1 milligram per kilogram treatment group experienced a median time to recovery of 7 days. As just mentioned, there were notable randomization imbalances seen between treatment and placebo group. We observed an additional important randomization imbalance with the 1 milligram per kilogram treatment group. Patients in the 1 milligram per kilogram treatment group received a single dose of 1923, a median of 5 to 6 days into their hospital stay compared to 3 to 4 days for the placebo in 3 milligram treatment groups. We believe this is also an important confounder, which complicates the interpretation of activity for the 1 milligram per kilogram cohort. Now that we've seen the topline results, we look forward to reviewing the full data set from the study, which will include clinical biomarker data and 60-day safety follow-up. The clinical biomarker data collected during the study when patients' lungs were inflamed may provide additional insight into the COVID-19 disease pathology and the effects of 1923 on key inflammatory biomarkers, including inflammatory cytokines. Of note, the vast majority of patients in our trial received concomitant dexamethasone as part of standard of care. The overwhelming use of dexamethasone, a powerful immunosuppressant, in our study may also impact our biomarker analysis. We believe that even with the availability of vaccines and the current standard of care, additional treatments will be needed for patients who develop severe disease and require hospitalization. We will continue to assess the opportunity and need for effective therapies in the context of evolving standard of care, including additional data expected on the use of dexamethasone, and we will continue to monitor the status of vaccine administration. We have observed in other trials enrolling a similar patient population to ours where background dexamethasone has been used as standard of care, patients tended to recover in 7 to 10 days. This data continues to rapidly evolve, and the severity of those patients does vary. We will be reviewing not only the additional insights from the full data set but also monitoring the evolving standard of care treatment landscape for COVID-19 patients in the near term to best inform our next step planning. As we continue to review the results of this study, we want to highlight data suggesting a preliminary signal of clinical activity in the 3 milligram per kilogram treatment group. This dose is also being investigated in our lead indication for 1923, pulmonary sarcoidosis, one of the most inflammatory forms of interstitial lung disease. This study, this Ib/IIa trial, recently completed enrollment. Current treatment options are limited in this indication and often include treating the inflammation with corticosteroids and other immunosuppressive therapies, which have limited efficacy and serious long-term toxicity. We want to note that this trial administers 6 monthly doses of 1923 compared to the single dose administered in the COVID-19 study. Throughout this COVID-19 study, standard of care evolved to include dexamethasone, a powerful pulsatile steroid. We just reported that the 3 milligram per kilogram dose in that study showed a preliminary signal of clinical activity on top of this steroid. By trial design, the study in pulmonary sarcoidosis reduces steroid use, tapering patients to a low dose of steroid and, if possible, removing steroid completely, while evaluating the 1, 3 and 5 milligram doses of 1923 compared to placebo. We look forward to the results of this study that assess 1923 in pulmonary sarcoidosis which we expect to report in the third quarter of this year. Overall, we are pleased with the results of this Phase II study in patients with COVID-19, which met its primary endpoint and demonstrates 1923's favorable safety profile. We are very encouraged by the preliminary signal of clinical activity seen in the 3 milligram per kilogram dose, showing the potential for a positive impact on clinical improvement through key recovery metrics. We have pointed out some important areas in our randomization that may contribute to the overperformance of our placebo group as compared to other trials, using background dexamethasone. We're excited to see how this signal seen in this trial may relate to our ongoing trial in pulmonary sarcoidosis which we expect to read out in the third quarter of this year. We look forward to reviewing the full data set from this study in COVID-19 and additional insights it may provide to best inform our next steps. We appreciate 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.

[Operator Instructions] Our first question comes from the line of Zegbeh Jallah from ROTH Capital Partners.

Congrats on the data. Really, really exciting. And for me, just a few questions here about the balance between the arms. And I think the first one for me is, were patients on dexamethasone balance between the treatment arms? And Sanjay, I apologize if I missed this already.

They were. We saw nearly all patients in this trial receive dexamethasone. I think out of the 32, only 2 did not. So there was a relative balance of dexamethasone use between 1, 3 and placebo.

Okay. And then just for clarity, can you comment on the timing of the dose of the ATYR1923? Was it given after remdesivir had been given for 2 days or something like that? Can you provide any commentary on that?

Yes. All patients had dexamethasone and remdesivir onboard. So there were no instances where, in fact, those therapies were rescuing, if you will, 1923. It was the other way around. 1923 was administered after remdesivir and dexamethasone were on board. The time and the amount of how long these drugs were onboard does vary. We don't see any real suggestion that one group or the other skewed in the amount of time other than the one thing I pointed out in the 1 milligram population, that in this population, it seems that the patients were in the hospital a little bit longer, a couple of days longer compared to the 3 milligram placebo population before they received their 1923 dose. So that was an important highlight that we wanted to mention.

I think it's also helpful that you clarified that neither remdesivir nor dexamethasone was aspiring ATYR1923 -- was kind of -- not aspiring but kind of salvaging ATYR1923 and [ was getting active after ] those had been administered. So that's a really good sign. And then any comments from clinicians working on the study, their impression after the drug was given? Was it ease of use, since it's only a onetime administration? Any kind of comments from them?

Well, we'd always heard anecdotally that they were quite happy with the performance of the patients in this trial. I think overall, we can look at all the patients and say it was quite successful when you compare it to other trials where some of these patients require 7, 8, sometimes 10 days of hospital stay. I think with regards to the ease of use, it's a 1-hour infusion. We did not notice really any concerning adverse events. I think there was quite a bit of interest to continue the trial. I think, in particular, now that we've seen some of the randomization and have noticed that perhaps a slight skew to the more severe and high-risk groups are in our treatment group, that might have explained some of the anecdotal feedback we got where there were some rather sick elderly patients that turned around rather quickly. And now we know that those patients likely received 1923 rather than placebo.

Yes. That's really nice that you're able to tease that out that there was an imbalance with regards to patients over 65 that exhibited severe hypoxia comorbidity. So that's really good. And I guess the question that everybody wants to know is, do you anticipate then that the benefit could move beyond the 0.5 day or -- yes, 0.5 day or 12 hours to something much higher if you mean things are more balanced?

Sure. I mean I think if we had a more balanced population, what you might expect to see is slightly better numbers for our treatment group if some of those sicker patients were in placebo. And placebo would probably more reflect what you've seen in, for example, the baricitinib or tocilizumab trials. Those are trials that had background dexamethasone and you started to see improvement around 7 to 10 days. Though I will point out that those trials also enrolled a milder cohort of patients than we looked at patients who received -- who weren't on oxygen therapy were allowed in those trials. So I think we've learned quite a bit in our trial. And certainly, if we had a few more of those sicker patients, better balance in the placebo population, I think you would have likely seen that number increase. Therefore, the difference would have been greater.

So it definitely sounds exciting. The press release didn't have any comments about what the next steps would be. So I know you mentioned having some biomarker data later. And then beyond that, in terms of continuation of clinical analysis, what do you need to see? What is the next step?

So I think you're absolutely right, we have the full results, the 60-day follow-up, the clinical biomarker data. Those findings will be coming in, and we'll be looking at those analysis just to see if we see any trends there in cytokines, for example, that could be really useful for us to pick up. Would have liked to see maybe a little bit less dexamethasone use because that allows us to tease out these biomarker -- this biomarker data a little bit easier. But nonetheless, we will look at that. I also think it's important for us to look at the landscape right now and -- with other trials. There are a number of readouts where dexamethasone has been used a little bit more robustly. We were one of the first trials that when dexamethasone data came out in the summer, many of the investigators started experimenting with it a bit more. I think we're going to learn with regard to some of these other therapies that have had emergency use authorizations, whether or not they really are effective once you start to see a little more dex use. So we come in really improving things better than anything out there on the market right now. We also have a placebo population to compare to. And compared to the drugs that have been approved for emergency use, we look certainly a factor better or even, in some ways, 2 factors better than some of those therapies. So it kind of behooves us to look at some of the data that's also going to be coming out in the next 60 days, see what's happening with this new COVID variant, see what's happening with vaccination. I think all of these things also with the new administration will allow us to maybe engage with the government in a different manner. So lots of things for us to pay attention to over the next couple of months here as we map out next steps.

So it sounds like you're waiting for the next set of data to kind of reengage. So we'll be looking forward to that. But congrats, again, on the data. I think, again, like you said, this is some really exciting expectations for the pulmonary sarc data now that we've seen some clinical efficacy signals.

We absolutely agree. I mean, seeing this signal with just 1 dose really has us feeling good about that trial. And that trial, the design with the steroid-sparing element also sets us up nicely because we won't have this sort of background issue with certainly not a potent steroid like dexamethasone.

Our next question comes from the line of Joe Pantginis from H.C. Wainwright.

Congrats on the data. First, a quick logistical question, and I appreciate all the color you gave with regard to these potential imbalances. So were there any other background therapies that these patients had?

No. No. The only other experimentals were not allowed in our trial. It's really dexamethasone and remdesivir. We did allow convalescent plasma. We just saw, I think, just a handful of patients, maybe 3 patients, get convalescent plasma. But that quickly fell out of favor earlier in the summer, but no other investigational drugs were allowed.

Perfect. And then I guess my -- I guess it's a forward-looking question here because you're waiting on the biomarker data and monitoring the landscape. I think that's important in trying to elucidate your next steps for the drug, which appears to clearly have activity here. And I guess, I'll ask some open questions here, but I'm wondering if there are any additional. So number one, your confidence on the 3-milligram dose? Number two, do you feel you're going after the right population as the landscape is evolving? And number three, again, how -- well, you already addressed the standard of care, basically, but how that could possibly evolve and impact first 2 parts?

Yes. I think certainly seeing a signal in a small trial with 1 dose, we see that as a real positive. And it matches some of the things we saw preclinically, for example, where we thought we had a fairly potent immunomodulator looking at our preclinical data. With regards to next steps in COVID, I think it behooves us to really look at our data and observe what's occurring in the standard of care landscape. Is our signal, as we think it is, an overperformance? What's the scale of overperformance there? So I think we're going to pay attention to some of the additional trials that are coming out there. When you talk about a patient population, clearly, our 3-milligram dose had an uphill battle with more elderly, more hypoxic and sicker patients in that population. Yet, we still improved things in less than a week, in less than 6 days here. I think that's a rather dramatic sign. But when we think about next steps, maybe our therapy ends up looking like a type of therapy that can rescue these kind of patients in the hospital. That's something that we will talk to the PIs with and the investigators to see if there's interest in that kind of a population. So the biomarkers will also guide us because that will provide perhaps more mechanistic understanding on what to really target for, especially when we look at our sarcoidosis trial results. So all in all, I think I'm very happy with -- to put a ball on it, to also having a confirmatory reaffirmation of safety here is, I think, really, really important as well. So we'll be looking forward to mapping out some things here as we see what's occurring in the COVID landscape, but we also are really, really excited that we've got our sarcoidosis trial enrolled and teed up for readouts here later this year.

So I'll use your word rescue and go off of that. So even if you were to keep the same patient population going forward, if I heard you correctly, it appears that an area of low-hanging fruit is to be able to get the drug faster to the patients because if I heard you for the 3 mg dose, they got it within 3 to 4 days of hospitalization in 5 to 6 days for the 1 mg group. So if they were to get it early, even a couple of days could make a major difference.

Correct. I think any time you can actually administer an immunomodulator that is viewed safe earlier, that's better. You want to prevent those sort of secondary morbidities that might occur in the hospital or even progressing to becoming ventilated, things like that. So absolutely. I think there's a balance. I think what we're going to learn is how remdesivir and dexamethasone help certain patients, but there's going to be some patients that clearly are going to be refractory to those therapies, too. So you may see an opening there that that's where our drug best fits in. Absolutely, Joe.

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

Congratulations. I think this is a tough patient population. And with that background standard of care, a really, really high hurdle that you had to get over. Just a couple of questions. One is that what -- could there be some additional insights that you glean from the data you're going to get in the next 60 days, the biomarker data, the follow-up data that could then kind of get you to go meet the regulators and want to move into another trial, maybe a Phase IIb kind of trial? Is there anything that you're looking for that could change how you engage with investigators to maybe follow this up with a larger trial, which, again, I imagine is nontrivial in this patient population?

Yes, Hartaj, good question. I think when you think about, for example, COVID long-haul disease, what we don't know is 30, 60 days out when people have recovered, how much disability do they have, do they have any limitations, for example, in their quality of life 60 days out. So there might be something for us to look at there between 1923-treated and placebo population. So even if you did recover, do you have any long-lasting damage? We know our drug is built really well to address that sort of chronic inflammation and maybe even prevent some of that progression of fibrosis. So I think that's something you're going to see in a cadre of COVID patients, and many of the interstitial lung disease experts have asked us quite a bit about tracking some of that. It's a small trial. So we'll see what we glean with that 60-day look there. But I think that might be probably the most important thing to pay attention to outside of the biomarkers.

Okay. And then, Sanjay, when I saw you have -- the patients in the high-dose arm had a median time to recovery of 5.5 days versus 6 days of placebo arm. All these patients are on dexamethasone and remdesivir. But then you also had 83 patients -- 83% of patients on high-dose arm achieving recovery by day 6. So it seemed like you had some patients that did very well on 1923 and maybe there were some that just did not and kind of brought you back closer to the placebo arm. Is that the right way to think about it? I mean did you have some kind of really good responders in there? And then a majority of that maybe were closer to placebo and that's why your median time to recovery got closer between the 2 arms?

Well, I mean, it's a median. So I think the way -- the better way to look at this is how true are these signals. And we clearly pointed out some reasons in randomization where the placebo might have just overperformed. But I'll also point you to something else we've learned, and that's really the confidence intervals here, and we haven't gotten into that too much. But confidence interval for our 5.5 median time to recovery was 3 to 6. So it's a pretty tight range there. We saw a lot of improvement, a tightness there. The confidence interval went up all the way to 12 in the placebo population. So it's a less 30 signal. And I think I know why. I think it has to do with a lot of the background randomization. So what we're seeing is a tightness of improvement in the 3-milligram population, which is why there's a trueness of that value that we really like. And then you start looking at the placebo population, and you can maybe explain why you've got overperformance here. And then you compare it to also what's out there in the literature. It would be a rather remarkable overperformance. I mean I think if that number is true, remdesivir, baricitinib, some of these other drugs will probably get an EUA rescinded, and they should probably send that money back to people as well. But that's just my view.

Right. And then just last question for me, Sanjay, which is that there -- as we get -- as the treatment paradigm for COVID-19 disease kind of evolves, just like with any other disease, there's probably a few patients -- there might be quite a few patients that don't tolerate remdesivir or dexamethasone or for whatever reason don't qualify for either one of those. Could those patients become sort of candidates for 1923 going forward? Because you did see the signal over both of those, and again, that's a pretty big hurdle to get over. So meaning that if there are patients that might not be candidates for either/or, or both, could those patients be patients for a trial of 1923?

Absolutely, I mean if you're talking about could our drug be useful in a refractory population, whether you're refractory because you can't get those therapies or you're not tolerant to those therapies, when you talk about, for example, an elderly patient, they may not tolerate pulsatile dexamethasone really well with all the sort of acute toxicity that comes with that. Our therapy being a safe therapy that also has been able to demonstrate this signal of activity, absolutely. If there ever was a paradigm where there was a second-line therapy, I think we would be right at the front of that line for sure.

Yes. And is there -- I mean is there -- you think regulators might get more amenable to those kinds of trials? I mean it happens in every other disease. Or is that kind of a to be determined kind of...

I think if you expand it broadly beyond just even COVID and look at acute interstitial pneumonias, I mean, there's a lot of literature out there showing that steroids maybe don't work as well there. It's controversial. And we know that steroid toxicity, especially once you're talking about 70, 75-year-olds, there's not much that you can reach for. So our therapy becomes, I think, very, very relevant in that kind of a population, whether it's a COVID pneumonia or any other form of acute interstitial pneumonia. Absolutely. I think you're talking about an inclusion criteria that starts to really get specific where our therapy could be very, very attractive.

Our next question comes from the line of Jason McCarthy from Maxim Group.

Congrats on the data. I know it's early, but it looks impressive so far, especially considering that the aTyr group has the sickest and highest risk patients. So looking at the data, I'd like to follow up a bit because it's interesting that you saw the relatively large increase in the patients recovering by day 6 compared to the reduction in median time to recovery. So would this actually potentially suggest that rather than speeding up the course of the disease across the board, 1923 is primarily stopping the progression to more severe disease, at least when it's used in combination with drugs like remdesivir and dexamethasone?

Yes. Jason, that's a very good point. I think both things can be true. I think you could be looking at a situation where we are blunting some of those more severe complications. I think in our population, we had clearly more of an uphill battle. We had no patients in the placebo arm who had baseline hypoxia in the 60s or 70s or low 80s. So we really turned around those patients rather dramatically. We had 0 of these patients with those sort of low hypoxic entry criteria. And with the risk factors pointing to more of a severe population, yes, I think it is something that you could say that we could blunt some of the more severe complications. I think that's an open question, and I think it's a fair way of looking at our drug that even its performance in a tough cohort of patients, we ended up doing quite well here with the 3-milligram dose.

All right. And then -- so as a follow-up, mortality reduction has been a particularly tough target to hit with COVID. But based on the number of patients that you're seeing recovering at that sixth day mark, would it be fair to expect that this could potentially translate to a mortality reduction? And would this be something you potentially look at in a future trial?

Yes. If we had a larger trial, a Phase III trial with that kind of signal, I think that would be universally sort of celebrated because if you're able to get people out of the hospital a greater proportion, we're talking about almost a 50% relative increase in getting people out the door, there's going to be less complications, that will absolutely impact your mortality numbers on more of a population scale. So in a larger trial, when you look at endpoints like that, yes, I think we're set up really well there to demonstrate that kind of benefit on mortality.

All right. And then I'd like to actually just follow up on the potential future trial. Would it be possible to have a sort of steroid tapering in a future trial? Because it seems like pretty much across the board the emerging standard of care in a changing therapeutic landscape, and COVID has impacted some treatments, which initially looked really promising, like, what we saw with cell therapy. And also, I mean, in a future trial, realistically, how much would you expect to be able to reduce hospitalization in these patients? They're already very sick. So how quickly best case can you get them out of the hospital?

Yes. So I'll answer the first question about steroid-sparing. I think in the acute setting, you throw everything at these patients. And I think it's very, very difficult to really talk about steroid-sparing in an acute ICU type of indication. I think you deal with the toxicity of the steroid use if it's an elderly patient. Conversely, this is why I think our design in the sarcoidosis study is really, really smartly laid out now because we have the ability to pull back on steroids. And those are patients that are on steroids for months, sometimes years. So they want to get off these therapies. But I think in the acute environment, you really can't run a trial like that. I think what you could do is you can look at patients that maybe haven't resolved after, say, 5 or 7 days of dex therapy. If they're still hanging out in the hospital, dexamethasone hasn't been able to actually improve them, then you could be looking at our therapy as an add-on. And in many cases, that's kind of how the patients in our trial, how they sort of presented. They were on dex, remdesivir for 3, 5, 7 days, and they really weren't improving. So they add in 1923. So I see it more as a -- if folks are not responding to steroids, this could be useful. And then there could be a small subset of patients that steroids or remdesivir or any other therapy is prohibited, especially when I think about that elderly population. So I think that's kind of the way I think about some of these approaches. I think with the signal that we see and with the design that we have set up in sarcoidosis, I think it helps sort of address both of those questions in some ways.

Our next question comes from the line of Jeff Swarz from M.M. Dillon.

Congratulations, Sanjay. Considering that there's almost 3,000 deaths a day now with COVID, over 350,000 total deaths, 20 million infections and doctors screaming publicly and in the New England Journal of Medicine for new therapy, have you had any discussions, if you plan to have any discussions with the FDA, where they have in the past given emergency use to therapies with data far inferior to yours? Now that was early days, admittedly, and now there is remdesivir and dex. But the vaccine rollout has been a mess, and you just constantly read every day how doctors are desperate for anything. And the drug has shown good indications, shown benefits, strong benefits. Even though it's a small trial, all of that is admitted. But have you had any discussions with the FDA perhaps to get emergency use for the drug rather than have to do 1,000 patients, 6-month trial, 9-month trial? It seems to be that in this situation, there isn't really time for that. What's your thoughts?

Well, thanks, Jeff. I think those are some really important thoughts. We've just read out the data. So we have -- just read that out. I do agree with you, however, that in the current environment, look, we haven't seen a drug improve time to recovery under 6 or 7 days like our drug has. And certainly, if you've seen that, it's been in open label trials. So I think it's entirely appropriate to have these sort of discussions. We will be, as I said, looking for some of the other signals in our trial with a full data set. But absolutely, I think with the kind of data that we have, we will have to have some discussions with the government given the current crisis that is still ongoing. We think we have a good data set here to discuss for sure.

Remdesivir was approved with an improvement from 15 days to 10 days. Admittedly, that was back in September when the data came out in New England Journal of Medicine, but remdesivir was not an impressive drug in a larger study, but they gave them approval and people are using it. It's good to think -- it's good to know that you're thinking about it because I think the FDA would have to take it seriously. There's a lot of data that you still need, and a Phase III study would be fantastic. I just don't think there's time to do that in this pandemic. So it's interesting to know what the FDA says.

Yes, I don't disagree with your thoughts and approach, and I think it makes a lot of sense for sure. And I think it's something that, given -- it's not as though we saw our half-day improvement, for example, of going from 9.5 days -- 10 days to 9.5 days. I think, as I said, it's a sturdy signal of activity. And I do think that there will be some dialogue that we will have to have with the government about our data.

At this time, I am showing no further questions. I would like to turn the call back over to Sanjay Shukla for closing remarks.

Well, thank you, everyone, for your interest, your questions, great questions today. As I mentioned, this is a top line analysis that we wanted to quickly get out to the public. Appreciate the interest, and we will be reaching back out in the near future. Thank you, again.

Ladies and gentlemen, this concludes today's conference call. Thanks for participating. You may now disconnect.