Atea Pharmaceuticals Inc (AVIR) Q3 2021 Earnings Call Transcript

Atea Pharmaceuticals Inc (AVIR 0.54%)
Q3 2021 Earnings Call
Nov 11, 2021, 4:30 p.m. ET

Contents:

• Prepared Remarks
• Questions and Answers
• Call Participants

Prepared Remarks:

Operator

Good afternoon, ladies and gentlemen welcome to the Atea Pharmaceuticals third quarter 2021 financial results conference call. [Operator instructions] I would now like to turn the call over to Jonae Barnes, senior vice president of investor relations and corporate communications at Atea Pharmaceuticals. Please proceed.

Jonae Barnes -- Senior Vice President of Investor Relations and Corporate Communications

Thank you, Operator. Good afternoon, everyone, and welcome to Atea Pharmaceuticals' third quarter 2021 financial results conference call. This afternoon, we issued a press release, which outlines the topics we plan to discuss. You can access the press release, as well as the slides that we'll be reviewing today by going to the Investor section of our website at ir.ateapharma.com.

With me today from Atea are chief executive officer and founder, Dr. Jean-Pierre Sommadossi; chief development officer, Dr. Janet Hammond; chief financial officer and executive vice president of legal, Andrea Corcoran; and our chief commercial officer, John Vavricka. They will all be available for the Q and A portion of today's call.

Before we begin the call, as outlined on Slide 2, I would like to remind you that today's discussion will contain forward-looking statements that involve the risks and uncertainties. These risks and uncertainties are outlined in today's press release and in the company's recent filings with the Securities and Exchange Commission, which we encourage you to read. Our actual results may differ materially from what is discussed on today's call. With that, I'll now turn the call over to Jean-Pierre.

Jean-Pierre Sommadossi -- Chief Executive Officer and Founder

Thank you, Jonae. Good afternoon, everyone, and thank you for joining us today. In addition to the financial results, we have a number of updates for AT-527 to review, including an amendment to the phase 3 MORNINGSKY trial protocol and the plan to accelerate its enrollment, quantitative infectious virus assay data from the MOONSONG trial, confirming potent and rapid antiviral activity for AT-527, and new in vitro data for AT-527 demonstrating potent antiviral activity against the major variants of concern or interest, including delta. I will begin on Slide 3.

AT-527, our orally administered product candidate for COVID-19 is a direct-acting antiviral agent derived from our purine nucleotide prodrug platform. AT-527 is designed to protect against disease progression and the development of long COVID complications. Given the evolving dynamics of COVID-19 which is becoming endemic, medical intervention and oral therapeutics, in particular, will be essential in stemming the tide of this pandemic and future surges. AT-527 targets viral RNA polymerase, a highly conserved enzyme critical to viral replication and transcription.

Uniquely, AT-527 has a mechanism with dual targets, it is a chain terminal without introducing new mutations in the virus, and it also inhibits NiRAN, thus, providing the potential to create a high barrier to resistance and antiviral activity across variants as we will share with you in a few minutes. In all studies, AT-527 was shown to be generally safe and well-tolerated. Of particular note, AT-527 is not mitogenic, with no reproductive toxicity, and it's non-teratogenic. We expect the minimal drug-drug interaction since AT-527 is a weak inhibitor of cytochrome P4503A and no dose adjustment is expected for core administration of drug that the CYP3A substrate, which account for the metabolism of more than 50 percent of clinically relevant drugs.

So, this should make our drug candidate prescriber-friendly. On Slide 4, COVID variants of concern continue to create new challenges for treatment and prevention. These variants can also make the execution and evaluation of clinical trial results more challenging because of the impact and differences in viral kinetics, as well as clinical symptoms. Ongoing SARS-CoV-2 genomic surveillance worldwide has improved our ability to rapidly identify such variants.

As you can see on this chart, almost 6,000 variants have been sequenced with an astounding number. The evolution of the virus will make COVID-19 endemic with the ability to continue circulating for years to come. SARS-CoV-2 variants of interest have been associated with increased transmissibility, neutralization resistance, and disease severity. The continuing spread of delta has led to a new subtype called AY.4.2 or Delta Plus, which carries additional mutation.

Although the original delta variants remain the most dominant on a global basis, this new mutant now accounts for 14 percent of infections in the UK, up from less than four percent just early September, and is more likely contributing to the recent surge of the fifth wave of COVID in Western and Eastern Europe and all the global areas. Preliminary evidence suggests that Delta Plus spread between 12 percent and 15 percent more frequently among household members compared with other delta viruses and will likely become an important strain, including in the U.S. Moving to Slide 6. As you know, we have previously shown that AT-511, the free base of AT-527, is a potent inhibitor of SARS-CoV-2 in vitro.

The average EC90 in primary human airway epithelial cells against the original virus isolated in early 2020 was around 0.5 micromolar with a fivefold assay approximately assay-to-assay variability as you can see in the slide. We recently evaluated our drug candidate against the major variants of concern or interest, including alpha, gamma, epsilon, and more recently, delta. Consistent with its dual mechanism of action, AT-511 maintains its potency against all the variants tested including delta. We believe that these data confirm the key mechanistic advantage of this drug candidate, which target the highly concerned viral RNA polymerase.

In fact, we have analyzed over 3 million SARS-CoV-2 sequences deposited in the database to date and found that less than 0.01 percent with mutation near the active site of the SARS-CoV-2 polymerase. With that, I will now turn the call over to Janet for a more detailed review of our clinical programs.

Janet Hammond -- Chief Development Officer

Thank you, Jean-Pierre. Beginning with Slide 8, as you can see on this slide, our robust clinical program includes six studies of AT-527, which are running in parallel. We are leveraging lessons learned from each of these studies to better quell our patients and updating our program in real time. There are two key updates on this slide, which includes advancing the AT-527 1,100 milligram BID dose in the hospitalized study, and we expect results from the next cohort in the first half of next year.

In addition, we are amending the phase 3 MORNINGSKY trial protocol with a new primary endpoint, a refined patient population, and an increased dosage. And we have a plan to accelerate enrollment completion. I will review the MORNINGSKY updates toward the end of my presentation. Turning to Slide 9.

As COVID-19 has continued to evolve, so have the ways to quantify the virus. After considerable effort, an optimized infectious virus assay is now available to quantify viable infectious virus in addition to the RT-PCR assay, which measures all forms of viral RNA obtained from the sample regardless of whether it is from intact replication virus or from nonviable virus or simply viral fragments. This difference is important because it should be a more accurate assessment of the impact of a direct-acting antiviral on the ongoing infection. I will next review the new viral LERV results for AT-527 from the MOONSONG trial that we have obtained by using this infectious virus assay.

As outlined on Slide 10, our methodology is quantitative and utilize the highly sensitive SARS-CoV-2 live virus assay. Measuring live virus in the nasopharyngeal swab samples from patients has been very challenging for this evolving field, but it is an important advance. Previously, qualitative data from a related type of assay was reported during the development of molnupiravir. In order to assess more specifically the antiviral effects of our drug candidate by using live virus, our CRO, in collaboration with our partner Roche, has developed and optimized highly sensitive and quantitative infectious virus titer assay.

As illustrated in the slide on modified cell line with enhanced susceptibility to SARS-CoV-2 was inoculated with fairly diluted nasopharyngeal samples so that we can determine the type of the virus. After six days of incubation, positively infected cells were detected by SARS-CoV-2-specific immunostaining. This nearly optimized assay has three key advantages. Firstly, it quantifies the infectious virus, thus, eliminating the possibility of noninfectious virus or viral fragments by RT-qPCRs previously reported.

Earlier assays developed with molnupiravir reported an infectious virus assay, which was qualitative, only positive or negative, with no actual viral cated term. Secondly, this is very accurate. And thirdly, it is highly sensitive. The level of quantification of the assay is equivalent to approximately 10 infectious virus particles per millimeter.

Please note that the analysis includes the approximately 71 percent of all patients in MOONSONG Cohorts A and B who have positive baseline culture. On Slide 11, today, we are reporting infectious virus stages from the MOONSONG study. You'll see that in Cohort B, in the overall population, including both high- and low-risk patients with the majority being seropositive, AT-527 as 1,100-milligram BID-treated patients demonstrated a rapid and potent reduction of viral load of 0.5 log versus placebo at Day 3. Turning to Slide 12.

We are able to see a treatment affecting the samples of patients with high risk with underlying health conditions and these results reinforce the exploratory analyses in the same population with RT-PCR MOONSONG and the phase 2 study in hospitalized patients. In Cohort B, the actively treated patients administered with 1,100 milligrams BID had a robust viral load reduction of 0.9 of a log at Day 3. These data also share a suggested dose response between Cohorts A Cohort B. Moving to Slide 13.

As I have just outlined, these additional data from the phase 2 MOONSONG trial support the rapid and potent antiviral effective AT-527 as measured by a quantitative highly sensitive infectious virus assay, which detects live virus capable of replication. Leveraging the lessons from MOONSONG as outlined in Slide 14, as well as other recent results, we are submitting amendments to the global phase 3 MORNINGSKY trial. MORNINGSKY is a randomized double-blind, multicenter, placebo-controlled phase 3 trial evaluating the antiviral activity, safety, and pharmacokinetics to AT-527 in approximately 1,600 patients randomized one-to-one to receive AT-527, 1,100 milligrams twice a day or placebo. We, together with Roche, plan to leverage the existing operational global infrastructure from the MORNINGSKY clinical trial sites and expand its footprint with approximately 300 sites in new geographies.

We expect to report the data from this trial in the second half of 2022. Amendments to our MORNINGSKY study include following: changing the trial's primary endpoint to COVID-19-related hospitalization or all-cause mortality. The previous primary endpoint of time to alleviation or improvement of COVID-19 symptoms will become a secondary endpoint. Refining the patient population to include only unvaccinated high-risk individuals.

And lastly, increasing the dose of AT-527 to 1,100 milligrams twice-daily from 550 milligrams BID. Patients enrolled in MORNINGSKY have the option to be enrolled in MEADOWSPRING, a six-month long-term follow-on study conducted in collaboration with Roche to evaluate long COVID in patients who received AT-527 in comparison to placebo in MORNINGSKY. Let's now turn to AT-752, our program for the treatment and prophylaxis of dengue fever on Slide 16. Earlier this year, we initiated a randomized, double-blind, placebo-controlled single and multiple ascending dose phase 1 study to evaluate the safety, tolerability, and pharmacokinetics of AT-752 in healthy subjects.

We have completed Part 1 of this study, the single ascending dose cohort. And in Part 2, the first two cohorts are complete, and the last cohort is ongoing. We expect conclusion of the study by year-end. During the first half of 2022, we expect to initiate our phase 2 study of AT-752 for the treatment of dengue fever in Asia and South America.

In this trial, we will enroll adults with a fever greater than 38 degrees within 48 hours of probable dengue infection and positive result on the NS1 antigen test on RT-PCR assay. The primary endpoint will be changing viral load from baseline. We look forward to keeping you apprised of our progress in this important study next year. With that, I will now turn the call over to Andrea for a review of the financials.

Andrea Corcoran -- Chief Financial Officer and Executive Vice President of Legal

Thank you, Janet. As Jonae mentioned in her introductory remarks, this afternoon, we issued a press release containing our financial results for the third quarter of 2021. The statement of operations and the balance sheet are on Slides 18 and 19. For the third quarter 2021, the increase in R and D expenses in comparison to the third quarter of 2020 was principally driven by an increase in external clinical development and manufacturing expenses incurred primarily in conjunction with the advancement of AT-527 for the treatment of COVID-19.

And to a lesser extent, AT-752, which is being developed for dengue fever. These expenses include our share of costs incurred by Roche and increases in internal spend mostly due to an increase in personnel-related expenses. The increase in general and administrative expenses was primarily due to the expansion of our organization in 2021 and consists principally in an increase in payroll and personnel-related expenses. I am pleased to report that we ended the third quarter with a strong balance sheet to support our clinical development programs.

As of September 30, 2021, cash and cash equivalents were $839.7 million. This includes the $50 million development milestone the company received in July under our license agreement with Roche. I'll now turn the call back over to Jean-Pierre for closing remarks.

Jean-Pierre Sommadossi -- Chief Executive Officer and Founder

Thank you, Andrea. As Janet outlined, the protocol changes we are making to the phase 3 MORNINGSKY study maximize our ability to demonstrate a positive clinical outcome. The updated inclusion criteria, dosing regiments, and primary endpoint should allow execution of a more focused and de-risked trial. Importantly, the encouraging infectious virus data we have disclosed today give us further confidence in AT-527 rapid and potent antiviral activity against COVID-19, which is critical to stopping disease progression and transmission.

We continue to be very excited by the opportunity at Atea to change the course of COVID-19, dengue fever, hepatitis C, and other viral infections. This is an exciting time to be bringing forth what we believe to be groundbreaking technologies, and we look forward to updating you on our progress. As always, we thank you for your continued support as we build the Atea into a global leader in the discovery, development, and commercialization of all therapies that address the unmet medical needs of patients with life-threatening viral diseases. With that, Operator, we will now open the call up to your questions.

Questions & Answers:

Operator

All right. [Operator instructions] First question comes from the line of Eric Joseph from J.P. Morgan. Your line is now open.

Hannah Colgan -- J.P. Morgan -- Analyst

Hi. Good afternoon. This is Hannah on for Eric. Thanks for taking the questions.

Just a few from us. So, first, just wanted to get your thoughts on the feasibility of conducting the phase 3 trial where we have the Pfizer pill, paxlovid, and molnupiravir accessible. How confident are you in the stated timeline that you've given? And then also, with the recently reported remdesivir outpatient trial, PINETREE, which showed a meaningful effect in hospitalization or death despite a minimal or really no effect on viral load. Just wanted to get your take on this dataset.

And then from a theoretical perspective, what other than viral load reduction do you think might translate to an effect on clinical outcomes? Thank you.

Jean-Pierre Sommadossi -- Chief Executive Officer and Founder

Sure. Janet, would you address both questions, please?

Janet Hammond -- Chief Development Officer

Sure. Thank you, yes. So, with regard to the feasibility of conducting the study, we believe that it's still feasible, and in some ways, I think it's unfortunate that it is. But I think that's being rolled out across the world.

While impressive in many places, it's lagging in many others. And I think that, unfortunately, this provides an opportunity for many high-risk patients still to be susceptible to the disease. We have an extensive footprint already and plan to have a still further extensive footprint as we move forward. As I mentioned, we have more than 300 types or thereabout in the trial.

And so, we believe the study ought to be able to be enrolled and completed in the timeframe that we suggested. And then with regard to to remdesivir, I wasn't completely sure that I understood your question. I think that what remdesivir showed very elegantly and in a large study was really that there was no correlation between viral load and clinical effect. And I think that's -- probably, that is true, in general, for the direct-acting antivirals, particularly when measured by RT-PCR.

And I think and really some of what we have attempted to show today is really that in addition to RT-PCR, which seems to be a rather blunt tool and I think is recognized as such, the live virus assay that we have reported on seems to be somewhat more able to discriminate between viral fragments and nonviable virus than actual live virus. And I think we're actually showing quite nicely even suggestion of a dose response in what we're seeing there. And certainly, clinical endpoints are really what it's all about, ultimately, and we have to really care about is whether the patients get better. And if we can prevent hospitalization and find some surrogate endpoint, which is able to help support that and, ultimately, be a useful surrogate endpoint, that would be great.

But I think the remdesivir data actually are supportive of the field, in general, and what others are experiencing, as well as ourselves.

Hannah Colgan -- J.P. Morgan -- Analyst

OK. Great. That's helpful. Thanks for taking the questions.

Operator

Next one on the queue is Jonathan Miller from Evercore ISI. Your line is now open.

Jonathan Miller -- Evercore ISI -- Analyst

Thanks so much for taking the questions, guys. I have a couple of maybe more detailed ones on some of the data you released today. You mentioned that your phase 2 cohort is majority seropositive. I think you said 71 percent seropositive at baseline.

How different are the results there between seropositive and negative patients at baseline for one? Then secondly and sort of falling on the last question, it seems like the majority of the patients on the 1.1-gram arm in phase 2 were high-risk. And just trying to back out, I believe I talk to you with my head on log scale, but is it fair to say that the viral load impact in low-risk patients is really pretty modest? And the falling on that prior question, you know, if you think that there's not a good read-through some viral load to clinical efficacy, do you expect that direct-acting antivirals, maybe broadly, will have a meaningful clinical impact in low-risk patients? And I'll -- I guess I'll pause there. It's a lot -- 

Jean-Pierre Sommadossi -- Chief Executive Officer and Founder

Janet.

Jonathan Miller -- Evercore ISI -- Analyst

[Inaudible] stuff there .

Jean-Pierre Sommadossi -- Chief Executive Officer and Founder

Janet?

Janet Hammond -- Chief Development Officer

Sure. Thanks, Jean. So, firstly, in regard to your question around the seropositivity. Yes, the seropositive was actually very high and perhaps not surprisingly increased, I think, as the study went on.

We were still awaiting some of the final -- and serology data from Cohort A. But certainly, in Cohort B, 87 percent of the treated patients were seropositive and I think 80 percent in the placebo group. So, really high numbers. And I think that does blunt what you're able to see, perhaps a glance at less, I think, in the high-risk patients than in the other ones.

But I think, essentially, what we're seeing and I think it touched on to -- sort of your second question, too, around the viral load impact in the low-risk patients. I think, clearly, if you're a low-risk, you're able to cure the virus perhaps more effectively yourself without the need for a direct-acting antiviral. But I think if you're able to prevent hospitalization and, you know, I think as others have demonstrated preventing hospitalizations and deaths in high-risk patients, you have to believe that you're having a similar effect, although it's harder to measure in patients who are at no or more modest risk for those types of outcomes. But nevertheless, I'm certain that you're probably shortening the duration of symptoms, and it's something that we have been hoping to demonstrate in our phase 3 trial.

But it seems that these harder endpoints are certainly easier to document. And I think that points us to the -- in how we're going in the direction that we are with MORNINGSKY. But I think that if you're showing the types of benefits of high-risk patients, we need to refine the tools in which we demonstrate that in order to protect high-risk patients, you're clearly also shown benefit in low-risk patients, albeit viral load, particularly, by RT-PCR isn't the perfect measure. But I think you can see that there are reductions in viral load across the board.

I think just the high-risk patients, perhaps less surprisingly, also do tend to start off with higher load. And clearly, you need to have a bigger delta to be able to demonstrate something. So, I think it all tells us -- tells the same story quite cohesively. I hope that answered the question.

Jonathan Miller -- Evercore ISI -- Analyst

Yes, somewhat. And then I guess one final one. How are you defining high-risk in the new criteria?

Janet Hammond -- Chief Development Officer

So, I think it's -- I think the definition is pretty standard in terms of patients being elderly, obese, diabetic, immunosuppressed. And I think also, potentially, asthmatic patients with underlying renal disease, underlying tumors, and so forth.

Jean-Pierre Sommadossi -- Chief Executive Officer and Founder

And hypertension.

Janet Hammond -- Chief Development Officer

And hypertension, yes. Cardiovascular disease.

Jonathan Miller -- Evercore ISI -- Analyst

Thanks very much, guys.

Operator

All right. So, for the next question, we do have Tim Lugo from William Blair. Your line is now open.

Tim Lugo -- William Blair -- Analyst

Thanks for the question and the additional data. I'd like to -- maybe a broader question on, you know, given the recent impressive protease inhibitor data. I just want to hear your update thoughts from targeting the RNA polymerase directly versus the protease. You know, we, I guess, previously were thinking the correlation between HCV and HIV and other more chronic diseases would suggest the RNA polymerase was the correct targets for, you know, minimizing resistance.

But is that so the case? And can we really extrapolate those diseases with the SARS-CoV-2 and COVID-19?

Jean-Pierre Sommadossi -- Chief Executive Officer and Founder

Sure. Well, look, first, we welcome, really, all progress in developing treatments as a part of our multipronged approach and to come back on COVID-19 pandemic. And as there is several vaccines, we believe that multiple treatment options would be needed. So, regarding -- I don't think that one target is going to be better than the other one.

You've seen the data just mentioned about the remdesivir in the outpatient. Unfortunately, the drug can be given only IV, and obviously, we know the limitations. I think we have not seen from Pfizer or the detailed analysis of the data talking about viral load, talking about potential emergence of resistance. And what I believe -- what we believe is that it's going to be a very different, I would say, situation in the real world than in clinical trials with protease inhibitors potentially used in immunocompromised patients used in arm.

So, in -- it was maybe issues on taking all the doses at the right time. And so, we have to see -- let's not forget that any drug -- any antiviral drug with one-point mutation will very likely lead to resistance. When Tamiflu was launched in 2008, 2009, there was absolutely no resist at all. Just one year later, it was the majority of the flu strains were resistant to Tamiflu.

So, I don't want to picture a future -- negative picture on protease inhibitors. But I think we have to be -- we can celebrate today, we should celebrate. But in the same time, we need to see the reality for the future. As Janet indicated, we are going to have an endemic situation that is going to be new strains.

And I believe that -- I would not be surprised that we are going to talk about combination therapies as, you know, to -- with a potentially -- the combination of two different classes in [Inaudible] have been shown in the past to be a very interesting combination. So, I think what we have learned over the last 12 to 18 months is what we know today may be different in six months and surely, in twelve months to come. So, I would be cautious there.

Tim Lugo -- William Blair -- Analyst

OK. That's -- understood and I agree. I think we're all looking toward the first combination that's going to be incredibly interesting. But, I guess, generally, when we look across the oral trials and even remdesivir as well, you know, the patient numbers that have been enrolled on the other trials have just been so much higher.

I know MOONSONG took a while to get underway.

Jean-Pierre Sommadossi -- Chief Executive Officer and Founder

Yeah.

Tim Lugo -- William Blair -- Analyst

Can you just maybe comment on how, you know, MORNINGSKY will be different in terms of patient enrollment, in really pushing patient enrollment? Because it did take a long time to get those patients for MOONSONG.

Jean-Pierre Sommadossi -- Chief Executive Officer and Founder

You're absolutely right, Tim. We are very aware of it. Janet, would you share, basically, what we are putting in place and how we foresee to accelerate the the MORNINGSKY enrollment after we will have basically file and finalize the amendments with the regulatory authorities?

Janet Hammond -- Chief Development Officer

Sure. I think we have increased the sample size somewhat, but we certainly have, I think, really doubled down on the geographical footprint, particularly looking at areas where we're likely to be able to enroll patients who are unvaccinated. And I think with that footprint, and also I think with the potential for conducting an interim analysis, and so forth similar to what others have been able to do, we believe that we should be able to meet the timelines that we are committing to and end up confident that this is something which is still possible. I -- we realize that the window is going to close as more people become vaccinated, and also therapies become more accessible.

But we're certainly committed to doing this and really believe that we can.

Tim Lugo -- William Blair -- Analyst

OK. Got it. That's understood and maybe another. Well, just how many patients have been enrolled in MORNINGSKY by, you know, when you file the protocol amendments? And I, you know, if I recall, I think the higher dose had a bit of a nausea signal.

Are you going to be allowing antiemetic in MORNINGSKY. And I guess also could you maybe give us some more details on this additional cohort of MOONSONG that we'll be expecting early next year?

Jean-Pierre Sommadossi -- Chief Executive Officer and Founder

Janet?

Janet Hammond -- Chief Development Officer

So, in fact, the -- with regard to the number of patients, it's not something that we've disclosed. And secondly, with regard to the use of antiemetics, we are going to educate positions on the fact that there has been some GI signal. We don't believe that it's a particularly significant one at the moment, but it's certainly something that we are actively managing and also setting up studies to assess how best to address it in terms of potential food effects and protecting patients from feeding these symptoms and something that we're actively working on. But we don't actually believe yet that we fully understand the significance of it as there were some peculiarities with the patients where the adverse events were experienced.

In particular, all of the adverse events that resulted in discontinuation or came from the same site, which is somewhat unusual. And so, we're still trying to really understand that and work out how best to manage it. We will allow the use of antiemetics and make those available. But on the other hand, we don't want to encourage and, you know, allow people to believe that this is something that they don't experience because it is something which I think is susceptible to some autodigestion.

So, it's quite a tricky one to manage, and we're actively thinking our way through that at the moment. And then lastly, in regard to your question around MOONSONG, we're not planning to enroll any further cohorts in MOONSONG, at least at the moment.

Tim Lugo -- William Blair -- Analyst

OK. Thank you for all the granularity and all the answers. Best of luck.

Jean-Pierre Sommadossi -- Chief Executive Officer and Founder

Thank you, Tim. Thank you.

Operator

Next one on the queue is Roanna Ruiz from SVB Leerink. Your line is now open.

Roanna Ruiz -- SVB Leerink -- Analyst

Hi. Thanks for taking the question. A couple regarding MORNINGSKY. I was curious in your protocol amendment plan, would you possibly explore going for an even shorter time period than five days in symptom onset as I believe, I think, Pfizer's interim had less than three days of symptom onset or less?

Jean-Pierre Sommadossi -- Chief Executive Officer and Founder

Janet?

Janet Hammond -- Chief Development Officer

Sure. I -- so, Roanna, we were working to allow patients in who have had symptoms for five days or less. I think we will certainly try to ascertain whether their symptom duration were short than that and we could certainly analyze by shorter duration and see whether that has an impact. There was a small impact, I think, in the Pfizer study, but it actually was surprisingly difficult, I thought.

I mean, I think it was 87 percent versus 89 percent. So, shorter is obviously better, but I don't think it made as much of a difference as I was expecting.

Roanna Ruiz -- SVB Leerink -- Analyst

OK. Makes sense. And I was also curious, in the remarks, it sounded like you will run the new MORNINGSKY protocol by the FDA. So, does that mean that you're taking steps toward opening some trial sites in the U.S.? Or could you just give an -- us an update on where that stands right now? That'll be great right.

Janet Hammond -- Chief Development Officer

All right. I can give you a broad update which is that we continue to engage with the FDA, and we will be sharing with them the protocol. And we have ongoing positive dialogue, and we do hope that we will be enrolling patients in the U.S. in this study.

But I think that's about what I can say.

Roanna Ruiz -- SVB Leerink -- Analyst

OK. Fair. Thanks.

Operator

And there are no further questions on the queue. I will now turn the call over back to the presenters.

Jean-Pierre Sommadossi -- Chief Executive Officer and Founder

So, again, thank you very much for your participation. And we'd like to thank everyone, and thank you again. Goodnight.

Operator

[Operator signoff]

Duration: 40 minutes

Call participants:

Jonae Barnes -- Senior Vice President of Investor Relations and Corporate Communications

Jean-Pierre Sommadossi -- Chief Executive Officer and Founder

Janet Hammond -- Chief Development Officer

Andrea Corcoran -- Chief Financial Officer and Executive Vice President of Legal

Hannah Colgan -- J.P. Morgan -- Analyst

Jonathan Miller -- Evercore ISI -- Analyst

Tim Lugo -- William Blair -- Analyst

Roanna Ruiz -- SVB Leerink -- Analyst

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