Q2 2021 Enanta Pharmaceuticals Inc Earnings Call

Good afternoon, and welcome to Anantha Pharmaceuticals fiscal second quarter 2021 financial results conference call. At this time all participants are in a listen only mode. There will be a question and answer session at the end of the prepared remarks. Please be advised that this call is being recorded I would now like to turn the.

Operator: Second quarter 2021 Financial Results Conference Call. At this time, all participants are in a listen-only mode. There will be a question and answer session at the end of the prepared remarks. Please be advised that this call is being recorded. I would now like to turn the call over to Jennifer Vieira, Investor Relations. Please go ahead.

Call over to Jennifer Viera Investor Relations. Please go ahead.

Jennifer Viera: Thank you, operator, and thanks to everyone for joining us this afternoon. The news release with our fiscal second quarter financial results was issued this afternoon and is available on our website. On the call today is Dr. J. Lulai, President and Chief Executive Officer, Paul Mellett, our Chief Financial Officer, and other members of the Nantus Senior Management Team. Before we begin with our formal remarks, we want to remind you that we will be making forward-looking statements, which may include our plans and expectations with respect to our research and development pipeline and financial projections, all of which involve certain assumptions and risks beyond our control that could cause our actual developments and results to differ materially from those statements.

Thank you operator, and thanks to everyone for joining us. This afternoon. The news release with our fiscal second quarter financial results was issued this afternoon and is available on our website on the call today is Dr. Jay Lullay, President and Chief Executive Officer, Paul Mellett, Our Chief Financial Officer.

And the other members of the NAV to senior management team.

Before we begin with our formal remarks, we want to remind you that we will be making forward looking statements, which may include our plans and expectations with respect to our research and development pipeline and financial projections on.

All of which involve certain assumptions and risks beyond our control that could cause our actual developments and results to differ materially from those statements. A description of these risks is in our most recent form 10-Q and other periodic reports filed with the SEC and answer does not undertake any.

Jennifer Viera: A description of these risks is in our most recent Form 10Q and other periodic reports filed with the SEC. An answer does not undertake any obligation to update any forward-looking statements made during this call. I'd now like to turn the call over to Dr. J. Luli, President and CEO.

No obligation to update any forward looking statements made during this call I'd now like to turn the call over to Dr. Jay Lown, President and CEO Jay.

Jay R. Luly: Thank you, Jennifer. And good afternoon, everyone.

Thank you Jennifer and good afternoon, everyone.

Jay R. Luly: Our fiscal second quarter marks another productive quarter for the company as we continue to work towards several upcoming catalysts across our pipeline and the remainder of the year. We currently have three active clinical programs across our portfolio, including virology and liver diseases, in which we are conducting seven clinical trials. Starting with Epititis B, we are excited to report preliminary data from one of the two ongoing Phase 1B studies of our core inhibitor, EDP 514, which I will discuss in more detail shortly. Our HPV program also includes ZDP 721, our oral HPV RNA destabilizer, which is set to enter the clinic in the middle of this year.

Our fiscal second quarter marks another productive quarter for the company as we continue to work towards several upcoming catalysts across our pipeline and the remainder of the year.

We currently have reacted clinical programs across our portfolio in virology and liver diseases.

And which we are conducting seven clinical trials.

Starting with hepatitis B, we are excited to report preliminary data from one of the two ongoing phase <unk> studies.

Of our core inhibitor Edp, five one for which I will discuss in more detail shortly.

<unk> HBV program also includes Edp 721, our oral HBV RNA Destabilizer, which is set to enter the clinic in the middle of this year.

Jay R. Luly: Additionally, we have three ongoing studies investigating EDP 938 for respiratory sensational virus, or RSV, and two ongoing clinical studies for two candidates to treat non-alcoholic steatohepatitis, or NET. Furthermore, we continue to progress our viral respiratory discovery initiatives to identify an L-inhibitor for RSV and an inhibitor for human metanumovirus, or HMPV. Finally, we are particularly enthusiastic about the prospects of an oral protease inhibitor specifically designed to target SARS-Cove 2.

Additionally, we have three ongoing studies investigating the edp 938 for respiratory syncytial virus or RSV and two ongoing clinical studies for two candidates to treat non alcoholic hepatitis.

At the tightest for Nash.

Further we continue to progress for viral respiratory discovery initiatives, we identify an L inhibitor for RSV, and then inhibitor for human Metapneumovirus or H M. P D.

Finally, we are particularly enthusiastic about the prospects for an oral protease inhibitor, specifically designed to target Sars COVID-19 two.

Jay R. Luly: With that, I'd like to turn to our robust pipeline, beginning with our HV program, where we are pleased to be able to report today positive data from the first two dose cohorts of part two of our ongoing Phase 1B study of EDP 514 and chronic HB patients treated with a nucleoside reverse transcriptase inhibitor we refer to as nuke suppressed. The data announced today provide critical support for our approach to developing an all-oral functional cure for patients with chronic HPV.

With that I'd like to turn to our robust pipeline beginning with our H P V program.

We are pleased to be able to report today positive data from the first two dose cohorts for part two of our ongoing phase one B study of Edp five one for in chronic HBV patients treated with a nucleoside reverse transcriptase inhibitor, who we've referred to as nuc suppressed.

The data announced a day provide critical support for our approach to developing an all oral functional cure for patients with chronic HBV.

Jay R. Luly: Based on preliminary results of the Phase 1B study, EDP 514 was safe and well-tolerated in nuke-suppressed patients for up to 28 days, and the pharmacokinetic profile is supportive of once-daily dosing, consistent with what was observed in Part 1 in Healthy Subjects. Going a bit deeper into the data, a total of 16 patients, the majority of whom were E-enogen negative, were randomized to receive 200 milligrams of EDP 514, 400 milligrams of EDP 514, or placebo for four weeks.

Based on preliminary results from the Phase <unk> study Edp five one for was safe and well tolerated in nuc suppressed patients for up to 28 days and the pharmacokinetic profile supportive of once daily dosing consistent with what was observed in part one in healthy subjects going on.

A bit deeper into the data for a total of 16 patients the majority of whom were E antigen negative for.

Were randomized to receive 200 milligrams of Edp 501 for 400 milligrams of Edp five one for or placebo for four weeks.

Jay R. Luly: There were no grade three or serious adverse events, and the majority of the treatment emergent adverse events were mild. One patient in the 200 milligram arm had a grade two adverse event that led to study drug discontinuation. There were no liver enzyme elevations or other laboratory abnormalities. EDP 514 exposure increased linearly with dose, with trough concentrations up to 18-fold, the protein-adjusted EC-50, supporting once-daily doses. As expected, the HB DNA assessment did not show any change from baseline because these patients already had suppressed DNA levels from their nuke therapy. Additionally, no virologic failure or breakthrough was observed.

There were no grade three or a serious adverse event and the majority of the treatment emergent adverse events were mild.

One patient in the 200 milligram arm had a grade two adverse events that led to the study drug discontinuation.

There were no liver enzyme elevations or other laboratory abnormalities.

Edp five one for exposure increased linearly with those with trough concentrations up to 18 fold the protein adjusted E. T 50, supporting once daily dosing.

As expected the HBV DNA assessment did not show any change from baseline because these patients already had suppressed DNA levels from their nuc therapy.

Additionally, no virological failure or breakthrough was observed.

Jay R. Luly: Exploratory viral endpoints were also evaluated in this study, and a mean reduction of one log in HBV RNA was observed in patients receiving EDP514 compared to 0.3 log reduction in placebo, consistent with data reported for other core inhibitors after four weeks of treatment. Further, maximum reductions of 2.3 logs in the E. Antigen negative group and 2.8 logs in the E. anogen positive group were observed in patients receiving EDP 514 versus the 1.2 log maximum reduction in the placebo group. The study is ongoing, and we will obtain data on the highest dose group, 800 milligrams, and report final results at a future scientific conference.

Exploratory viral endpoints were also evaluated in this study and a mean reduction of one log in HBV RNA was observed in patients receiving edp five one for compared to 0.3 log reduction in placebo consistent with day to reported for other core inhibitors. After four weeks of treatment.

Further maximum reductions of 2.3 logs in the E antigen negative group and 2.8 logs E antigen positive group.

There have been patients receiving edp five one for versus the 1.2 log maximum reduction on the placebo group.

The study is ongoing and we will obtain data on the highest dose group 800 milligrams and report final results at a future scientific conference.

Jay R. Luly: Later this quarter, we are also expecting preliminary results from our Phase 1B study of chronic HPB infected patients with high viral load who are not currently on treatment, whom we refer to as viremic patients. As in the NUC-suppressed study, preliminary data from viremic patients will include safety, tolerability, and pharmacokinetics, and importantly, the viremic study will give the first indication of EDP-514's effects on viral kinetics when used as a single agent over a 28-day period.

Later this quarter. We are also expecting preliminary results from our phase one b study of chronic HBV infected patients with high viral load who are not currently on treatment, whom we refer to as by remix patients.

Other than the Nuc suppressed study preliminary data in <unk> patients will include safety Tolerability and pharmacokinetics and importantly, the value we're going to study will give the first indication of Edp five one for his effects on viral kinetics when used as a single agent over a 28 day period.

Jay R. Luly: In addition, we're developing EDP 721, our newest HB compound for use in combination with other mechanisms such as Nukes and or EDP 514, with a goal of creating an all-oral functional cure for chronic HB infection. Nukes are the current standard of care for HBV patients and suppress HBV DNA. Core inhibitors such as EDP514 also suppress HBDNA, and in addition, affect several other stages of HBV replication, including uncoding and the nucleosite of the virus, capsid assembly, and recycling.

In addition, we are developing edp 721, our newest HBV compounds for use in combination with other mechanisms such as nukes <unk> Edp five one for with a goal of creating an all oral functional cure for chronic HBV infection.

Nuclear is the current standard of care for HBV patients and suppress HBV DNA core inhibitors, such as Edp five one for all sorts of price HBV DNA. In addition affect several other stages of HBV replication, including on coding and nuclear for imported the virus Capsid Assembly.

Jay R. Luly: However, high levels of HPVS antigen remain a challenge to achieving a functional cure. EDP 721 is an oral agent that destabilizes HBV viral RNAs, potentially leading to a reduction in HBVS antigen, as well as other viral proteins and patients. We are encouraged by compelling data showing a three-log reduction in antigen levels with EDP721 in a mouse model, which demonstrated equal or superior efficacy to SIRNA-based agents and anti-sense oligo-based agents tested in the same model.

And recycling.

However, higher levels of HBV S antigen remained a challenge to achieving a functional cure.

ETP 72, one is an oral agent for these stabilizes the HBV viral Rnas potentially leading to a reduction in HBV S antigen as well as the other viral proteins from patients.

Whereas we are encouraged by compelling data showing a three log reduction in S antigen levels with ETP 17, one in a mouse model, which demonstrated equal or superior efficacy to S. I RNA based agents and antisense oligo based agents tested in the same model.

Jay R. Luly: We look forward to presenting data on the discovery and characteristics of EDP 721 in a poster presentation at this year's International Liberal Congress, sponsored by EASL, in June, and we are eager to start our phase one trial, VDP721 and mid-year, with initial results expected in the first half of 2022. Moving to RSP, EDP 938, our lead product candidate and the only inhibitor in clinical development today, is currently being evaluated in three ongoing studies.

We look forward to presenting data on the discovery and characteristics of Edp seven to one and a poster presentation at this year's international liver Congress sponsored by easel in June and we are eager to start a phase one trial of <unk> seven to one and mid year with initial results expected in the first half with cash.

'twenty two.

Moving to RSV Edp 938, our lead product candidate and the only N inhibitor in clinical development. Today is currently being evaluated in three ongoing studies.

Jay R. Luly: RSV is a severe respiratory infection associated with significant morbidity and mortality in infants, the elderly, and immune-compromised adults, and a condition for which there is currently no safe and effective therapy. Leveraging our expertise in virology, we designed EDP938 to uniquely target the end protein and block the replication machinery of the virus rather than block viral entry. As we've mentioned previously, RSV, like flu, did not emerge during the usual late fall and winter RSV season in the Northern Hemisphere in the past year due to the continuing COVID-19 mitigation measure. However, once social distancing measures subside, it is likely that RSB will reemerge, as has already been observed in the recent spike of pediatric cases in Australia.

RSV is a severe respiratory infection associated with significant morbidity and mortality in the elderly and immune compromised adults and a condition for which there is currently no safe and effective therapy.

Leveraging our expertise in virology, we designed Edp 938, two uniquely target the <unk> protein and block the replication machinery of the virus rather than blocking viral entry.

As we've mentioned previously our S V like flu.

What emerged during the usual late fall and winter RSV season in the northern hemisphere in the past year due to the continuing COVID-19 mitigation measures. However, once social distancing measures subside likely that RSP will reemerge as has already been observed in the recent spike pediatric cases.

Jay R. Luly: With this in mind, we continue our preparedness efforts to ensure we are ready when RSV reemerges globally, including establishing trial sites in North America, Europe, the Asia Pacific region, and the Southern Hemisphere. These efforts will be key to recruitment in our clinical trial program, which includes RSVP, our Phase 2B study evaluating EDP 938 and adults with community-acquired infection. RSVTX.

Australia.

With this in mind, we continue our preparedness efforts to ensure we are ready when RSV reemergence globally, including establishing trial sites in North America, Europe, The Asia Pacific region, and the southern Hemisphere.

These efforts will be key to recruitment in our clinical trial program, which includes RSVP for our phase <unk> study evaluating edp 938 in adults with community acquired infection.

RSV T X a phase two study evaluating edp nine create an adult hematopoietic cell transplant recipients with acute RSV infection, and sometimes of upper respiratory tract infection.

Jay R. Luly: Phase 2 study evaluating EDP 938, an adult hematopoetic cell transplant recipient with acute RSV infection and symptoms of upper respiratory tract infection. And RSVP, a phase two randomized, double-blind, placebo-controlled, dose ranging study of EDP938 in pediatric RSV patients. The primary objective of the first part of the RSVP study, which we initiated in March, is to evaluate the safety and pharmacokinetics of EDP938 and multiple ascending doses, while the primary objective of the second part of the study will be to evaluate the antiviral activity of EDP 938.

RSV peds, a phase two randomized double blind placebo controlled dose ranging study of Edp 938, and pediatric RSV patients.

The primary objective of the first part of RSV Pea, which we initiated in March is to evaluate the safety and pharmacokinetics of Edp 938 in multiple ascending doses, while the primary objective on the second part of this study will be to evaluate the antiviral activity of Edp 938.

Once RSV becomes prevalent again, we will provide updated guidance for these ongoing clinical studies.

Beyond ADP 93, eight our lead optimization efforts in our RSV L protein inhibitor and human Metapneumovirus inhibitor discovery initiatives continue to progress.

Jay R. Luly: Once RSV becomes prevalent again, we will provide updated guidance for these ongoing clinical studies. Beyond ADP 938, our lead optimization efforts and our RSVL protein inhibitor and human metanumovirus inhibitor discovery initiatives continue to progress. RSVL inhibitors are another drug class, the block replication inhibitors, which could potentially be used alone or in combination with other agents, such as CDP 938, to possibly broaden the addressable treatment window or patient population. For HMPV, we are making progress with lead optimization of potent molecules.

RSV L inhibitors or another drug class the block block replication and can potentially be used alone or in combination with other agents such CDP 93, eight to possibly broaden the addressable treatment window for patient population.

For H M P V.

We are making progress with lead optimization could potent molecules and our most advanced discovery initiative for respiratory viruses like Sars COVID-19, two where our current efforts to develop an oral direct acting anti viral or hope that's focused on protease inhibitors and polymerase.

<unk>.

Building on our virology expertise and success in hepatitis C. We are designing compounds that prevent replication of the virus in human cells versus blocking viral entry and we expect our approach will be effective against emerging spike protein variance, we plan to initiate IND, enabling studies with our lead on.

Jay R. Luly: And our most advanced discovery initiative for respiratory viruses is SARS-Cove 2, where our current efforts to develop an oral, direct-acting antiviral are focused on protease inhibitors and polymerase inhibitors. Building on our virology expertise and success in hepatitis C, we are designing compounds that prevent replication of the virus in human cells versus blocking viral entry.

World Protease inhibitor later this quarter and if all progresses positively we could have a candidate in phase one clinical study in early 2022.

I'll end my pipeline review with a summary of our work in Nash, a liver disease with significant unmet medical need where we were conducting clinical studies of FX or agonists, Edp 305, and Edp 297.

Jay R. Luly: And we expect our approach will be effective against emerging spike protein variance. We plan to initiate I&D enabling studies with our lead oral protease inhibitor later this quarter, and if all progresses positively, we could have a candidate in phase one clinical studies in early 2022. I'll end my pipeline review with a summary of our work in Nash, a liver disease with a significant unmet medical need, where we are conducting clinical studies of FXR agonists EDP-05 and EDP 297. Recruitment and dosing, and Argon 2, our Phase 2B study of EDP-35, approximately 340 patients with biopsy-proven mesh with fibrosis, is ongoing.

Recruitment and dosing in argon two our phase <unk> study of Edp 305, and approximately 340 patients with biopsy proven Nash with fibrosis is ongoing.

Due to the impact and resurgence of COVID-19 rates in Europe and in South America on some of our global clinical sites are internal interim analysis based on 12 weeks of treatment on a subset of patients will now be in the third calendar quarter of 2021, rather than in midyear.

Recruitment and dosing are also ongoing in our phase one for human study on our follow on FX on a candidate Edp 297, and we expect to report data from that study in mid year to build up on compelling preclinical data, suggesting differentiated high potency and tissue targeting characteristics.

Jay R. Luly: Due to the impact and resurgent of COVID-19 rates in Europe and in South America on some of our global clinical sites, our internal interim analysis based on 12 weeks of treatment on a subset of patients will now be in the third calendar quarter of 2021 rather than in mid-year. Recruitment and dosing are also ongoing in our phase one first in human study on our follow-on FXR candidate, EDP 297. We expect to report data from that study in mid-year, building upon compelling preclinical data suggesting differentiated high potency and tissue targeting characteristics compared to other FXR agonists in development.

Compared to other FX or agonists in development.

In aggregate, we anticipate that Edp 297 data and the Edp 305, internal interim analysis will enable us to determine next steps such as potential combination approaches for our Nash program.

Before moving to the financials I'd like to reiterate our upcoming milestones.

In HBV, we expect preliminary results of the phase one B study of Edp free.

Edp five one for and buy remake HBV patients later this quarter.

Look toward the initiation of a clinical trial for <unk> seven to one our oral HBV RNA destabilizer in mid year.

For COVID-19, we expect to begin IND, enabling studies later this quarter for our lead oral Proteasome inhibitor, specifically designed to target Sars COVID-19 two.

Jay R. Luly: In aggregate, we anticipate that EDP 297 data and the EDP 305 internal interim analysis will enable us to determine next steps, such as potential combination approaches for our Nash program. Before moving to the financials, I'd like to reiterate our upcoming milestones. In HPV, we expect preliminary results from the Phase 1B study of EDP 514 and from Remake HPV patients later this quarter, and we look toward the initiation of a clinical trial for EDP721, our oral HPV RNA destabilizer, in mid-year.

For Nash, we look forward to reporting preliminary data from the phase one study.

Our FX, our agonist Edp 297 in the mid and mid year, followed by an internal.

From analysis of argon, two and determination of next steps for this program.

Finally, we are excited by the early prospects coming out of our respiratory virology discovery initiatives and are eager to identify two clinical development candidates out of our COVID-19, RSV and human Metapneumovirus programs by year end.

With that I'll stop here and turn the call over to Paul to discuss our financials for the quarter Paul.

Thank you Jay.

Jay R. Luly: For COVID-19, we expect to begin IND-enabling studies later this quarter for our lead oral protease inhibitor, specifically designed to target SARS-Cove 2. For Nash, we look forward to reporting preliminary data from the phase one study of our FXR agonist, EDP 297 in mid-year, followed by an internal interim analysis of Argon 2 and determination of next steps for this program. Finally, we are excited by the early prospects coming out of our respiratory virology discovery initiatives and are eager to identify two clinical development candidates out of our COVID-19, RSV, and human metanumovirus programs by year-end. With that, I'll stop here and turn the call over to Paul to discuss our financials for the quarter. Paul?

I'd like to remind everyone that a natural reports on a September 30 fiscal year schedule.

Today, we are reporting results for our second quarter ended March 31 2021.

For the quarter total revenue was $20 1 million and consisted primarily of royalty revenue earned on add these global Maverick product sales of 415 million.

This compares to total revenue of $27 6 million for the same period in 2020.

The decrease in royalty revenue compared to the same period last year was driven by lower HCV product sales as treated patient volumes have remained below pre COVID-19 levels as reported by Abbvie.

Royalty revenue was calculated on 50% of an average sales at Inc.

Royalty rate for the quarter of 10% and on approximately 30% of the care of seals at a royalty rate of 10%.

Paul J. Mellett: Thank you, Jake. I would like to remind everyone that an answer reports on a September 30th fiscal year schedule. Today, we are reporting results for our second quarter and on March 31, 2021. For the quarter, total revenue was $20.1 million and consisted primarily of royalty revenue earned on Avi's global Maverick product sales of $415 million. This compares to total revenue of $27.6 million for the same period in 2020. The decrease in royalty revenue compared to the same period last year was driven by lower HCV product sales as treated patient volumes have remained below pre-COVID levels, as reported by Abbott.

After adjustments for certain contractual discounts rebates and set offs, which are now approximately 2% average total reported HCV product sales.

As a reminder, our royalties are calculated on a calendar year basis, therefore royalties for our fiscal first quarter ending December 31 were calculated at the highest royalty rate for the year.

And royalties for our fiscal quarter ending March 31 are calculated at 10% our lowest royalty rate tier.

You can review our royalty tier schedule in our 2020 form 10-K.

Moving onto our expenses for the three months ended March 31, 2021 research and development expenses totaled $41 5 million compared to $32 6 million from the same period in 2020.

Paul J. Mellett: Loyalty revenue was calculated on 50% of Mavit sales at a royalty rate for the quarter of 10% and on approximately 30% of the Carasiels at a royalty rate of 10% after adjustments for certain contractual discounts, rebates, and set-offs, which are now approximately 2% of Avey's total reported HCV products sent. As a reminder, our royalties are calculated on a calendar year basis. Therefore, royalties for our fiscal first quarter ending December 31 were calculated at the highest royalty rate for the year, and royalties for our fiscal quarter ending March 31 are calculated at 10%, our lowest royalty rate tier.

The increase was primarily due to the timing of our clinical trials year over year.

General and administrative expenses for the quarter was $8 3 million compared to $6 9 million for the same period in 2020.

The increase was due to additional headcount and related compensation expense.

And then a recorded an income tax benefit of $7 1 million for the three months ended March 31, 2021, compared to an income tax benefit of $3 9 million for the same period in 2020.

The income tax benefit in the current period was due to the Companys pretax loss, which can be carried back under the cares Act of 2020.

Net loss for the three months ended March 31, 2021 was $22 million or a loss of $1 <unk> per diluted common share compared to a net loss of $6 million or a loss of 30 port diluted common share for the corresponding period in 2020.

Paul J. Mellett: You can review our royalty tier schedule in our 2024M10K. Moving on to our expenses, for the three months ended March 31, 2021, research and development expenses totaled 41.5 million compared to 32.6 million for the same period in 2020. The increase was primarily due to the timing of our clinical trials year over year.

And then to ended the quarter with approximately 400 million on cash and marketable securities.

Further financial details are available on our press release and will be available on our quarterly report on form 10-Q when filed.

I'd now like to turn the call back to the operator and open up the lines for questions operator.

Paul J. Mellett: General and Administrative expense for the quarter was 8.3 million compared to 6.9 million for the same period in 2020. The increase was due to additional headcount and related compensation. Anana recorded an income tax benefit of $7.1 million for the three months ended March 31, 2021, compared to an income tax benefit of $3.9 million for the same period in 2020. The income tax benefit in the current period was due to the company's pre-tax loss, which can be carried back under the CARES Act of 2020.

We will now begin our question and answer session to ask a question you will need to press star one on your telephone to withdraw your question press the pound key please standby, while we compile the Q&A roster.

Our first question will come from Brian Abrahams with RBC capital markets. Please proceed with your question.

Hi, there. Thank you for taking my questions and nice to see all the progress across the pipeline.

First question is on a five one for them.

Can you provide a little bit more granularity on maybe some of the differences in or an RNA declines as well as lowest trough concentration that you observed across the two doses and I guess, what you're looking to optimize in this particular study with the higher 800 milligram dose.

Paul J. Mellett: The net loss for the three months ended March 31, 2021, was $22 million, or a loss of $1.9 per diluted common share, compared to a net loss of $0.30 per diluted common share for the corresponding period in 2020. Ananta ended the quarter with approximately $400 million in cash and marketable security. Further financial details are available in our press release and will be available in our quarterly report on Form 10Q when filed. I'd now like to turn the call back to the operator and open up the lines for questions.

Yeah, Hi, Brian This is Jay thanks for the question so.

You know regarding the trough levels.

So the trough levels, you know are basically measure debt at the.

For the 24 hour time point after a given dose and.

We're just really really pleased to see.

The high trough levels as you know, we we bank them on those kinds of attributes with all the product candidates that will make whether its RFP or any of the other viruses.

And.

It's just a very helpful.

Confidence builder when you see that you have such heavy pressure on the virus at the lowest concentration for you'll see.

Operator: We will now begin our question and answer session to ask a question.

During the day, so we we saw.

Operator: session. To ask a question, you will need to press star 1 on your telephone; to withdraw your question, press the pound key. Please stand by when we compile the Q&A roster. Our first question will come from Brian Abrams with RBC Capital Markets. Please proceed with your questions.

Not only are very good.

Profit levels.

400.

Dose group mature about 18 ex U.

On the protein adjusted EPS.

But we also saw very high trough levels that are 200 as well so we'll get all that data.

Out once we put it together with the third and final arm of this study are 800, but I can I can say.

Brian Corey Abrahams: Hey there, thank you for taking my questions and nice to see all the progress across the pipeline. My first question is on 514. Can you provide a little bit more granularity on maybe some of the differences in RNA declines as well as the lowest trough concentration that you observed across the two doses and, I guess, what you're looking to optimize in this particular case?

So far.

Based on on what we're seeing with the.

Even though the two lower doses.

We have very very good.

On exposures for pets.

On a trough concentrations.

And then regarding the viral load reductions.

Brian Corey Abrahams: in this particular study with the higher 800-gram dose?

You know again.

On.

And a nuc suppressed study.

Jay R. Luly: Yeah, hi, Brian, this is Jay. Thanks for the question. Regarding the trough levels, So the trough levels are basically measured at the 24 hour time point after a given dose. We're just really, really pleased to see the high trough levels. As you know, we bank on those kinds of attributes with all the product candidates that we make, whether it's RSV or any of the other viruses.

Such as this you know we've guided all along that.

The study isn't so much about virology as it is now looking at our safety.

Safety and Tolerability in PK levels.

Confirming that we see the same you know good safety and Tolerability.

The exposure that we saw in healthy volunteers.

And we've done that with these sentences.

But importantly, it was on top of a nuc and in HBV patients and going out for you know for 28 day. So all in it's a it's a very strong package the.

Jay R. Luly: And it's just a very helpful confidence builder when you see that you have such heavy pressure on the virus at the lowest concentrations that you'll see during the day. So we saw not only very good trough levels at the 400 dose group, which were about 18X, you know, the protein adjusted EC50, but we also saw very high trough levels at 200 as well. So we'll get all that data out once we put it together with the third and final arm of this study, 800, but I can say, you know, so far, based on what we're seeing with even the two lower doses, we have very, very good exposures at trough concentration.

Again, the DNA he's already suppressed from the nukes, so youre not going to see much there.

Our news or you know are generally lower effects that you see when you see it really kind of.

You know it depends on the exact patient population you have on what their starting the RNA levels, where how far they were also may or may not have been suppressed.

But what we what we saw was.

On what's been typical of.

Our strong RNA response from from core inhibitors.

And I want to underscore it for a week time period.

So which is a short time period in the Grand scheme of some longer trials or ultimately will be run on.

We're looking forward to the partner study of this which I called it by remix studies. So there was you know the patients will have coming on this study will have high.

Jay R. Luly: And then, you know, regarding the viral load reductions, you know, again, in a Nuke-Supresc study such as this, you know, we've guided all along that this study isn't so much about virology as it is, you know, looking at safety and tolerability and these PK levels, you know, confirming that we see the same, you know, good safety and tolerability and exposure that we saw And we've done that with these doses. But importantly, it was on top of a nuke end in HB patients and going out for, you know, for 28 days. So all-in, it's a very strong package.

Viral loads.

Their DNA.

Be elevated and there you'll have a chance to see single agent without a nuc.

Coming in on.

Two to see what you know for.

One for does that dose related manner as a as a single agent.

So.

Again.

So far so good but virology as very strong preclinical assets you know.

Very potent molecule.

It's pan genotypic.

It works incredibly well.

And animal models and now we've got our first patient data that was and I'm very excited about looking forward.

To the next installment which will be by arena.

We would expect to get later this quarter.

Jay R. Luly: Again, the DNA is already suppressed from the nukes, so you're not going to see much there. RNAs are, you know, generally lower effects that you see when you see them really kind of, depending on the exact patient population you have and what their starting RNA levels were, how far they also may or may not have been suppressed. But what we, what we saw was, um, you know, what's been typical of a strong RNA response from core inhibitors at, and I want to emphasize this, over a four-week time period.

Got it and did you guys look for any potential changes in tenofovir concentration and I I know the adverse events appeared.

Pretty mild but I'm just curious did any of those grade one and two side effects.

Were any of them consistent with a potential tenofovir related aes.

You know I'd have to check on that I don't believe so.

I think it was.

Again, no one's will put all the information out of that at a conference when we have the the.

The final cohort in but.

Jay R. Luly: So, which is a, you know, short time period in the grand scheme of some longer trials that will ultimately be run. We're looking forward to the partner study of this, which I called the remake study. So there, you know, the patients will have, coming into the study, high viral loads, so their DNA will be elevated. And there you have a chance to see a single agent without a nuke coming along to see what 514 does in a dose-related manner as a single agent.

The east where.

He he's observed for mild.

Got it one more for me if you don't mind, then I'll hop back in the queue.

What are your latest views on what you'd be looking for in the coming months to determine a potential path forward in Nash and and what might those paths forward book like strategically.

Well you know again, we got a we got we have two ongoing.

Jay R. Luly: So, Again, so far, so good. The virology is very strong preclinically, as you know, a very potent molecule. It's pangenotypic. It works incredibly well in animal models, and now we've got our first inpatient data that we're very excited about looking forward to the next installment, which will be Vyamic Data, which we expect to get later this quarter. Got it. And did you guys look for any potential changes in Nalph of your own?

Studies, so we have with two two different compounds.

Edp 297, which is our follow on ethics are.

Obviously, that's a super potent.

Molecule.

It looks like it's the.

You know the most potent.

FX are.

In clinical development today. So that's that's one attribute that we.

Observed.

Certainly pre clinically the other is the tissue targeting of that so.

Think you know we've laid out the the hypothesis.

Brian Corey Abrahams: concentration, and I know the adverse events appeared pretty mild, but I'm just curious, did any of those grade one and

Why and how that could you.

Build to a or.

Brian Corey Abrahams: Of those grade one and two side effects, were any of them consistent with potential tenophir related AEs? You know, I'd have to check on that. I don't believe so.

Better index, if you will from bi.

For me efficacy and target engagement.

Versus tolerability.

Jay R. Luly: I think it was, Again, you know, once we'll put all the information out at a conference when we have the final cohort in, but, you know, the AE's were, any AEs observed were mild. Got it. One more for me, if you don't mind, then I'll hop back in the queue. What are your latest views and what would you be looking for in the coming months to determine a potential path forward

Profile and so we'll let that Ah study.

Run to its conclusion, we're expecting data on that.

You just said mid year.

And then also we're going to have to share alongside with that or to see along with that internally, we're going to have an internal look at.

And the interim analysis on a subset of.

Ah patients in Edp 305, argon two study.

And as you know we've looked at the goalposts doses previously in argon one.

Brian Corey Abrahams: will pass forward in Nash, and what might those paths forward look like strategically. Thanks.

And we're looking at interim doses now so we're having very good calibration.

Jay R. Luly: Well, you know, again, we have two ongoing studies with two different compounds. We have EDP 297, which is our follow-on to FXR. Obviously, that's a super potent molecule.

Point to look at them again, it's all about target engagement slash efficacy versus Tal.

Tolerability, whether it's you know molecule or molecules to be.

We had hoped to have that data on.

On argon two mid year, but since we just stated.

Jay R. Luly: It looks like it's the you know, the most potent FXR in clinical development today. So that's one attribute that we observed certainly preclinically. The other is the tissue targeting of that. So I think, you know, we've laid out the hypothesis of, you know, why and how that could, you know, build to a better index, if you will, from a efficacy and target engagement versus tolerability, profile and so we'll let that study run to its conclusion we're expecting data in that as we just said mid-year and then also we're going to have to share alongside with that or to see alongside with that internally we're going to have an internal look at in the interim analysis on a subset of patients in ADP 305, Argon Tooth Study, And as you know, we've looked at the goal post doses previously in Argonne 1, and we're looking at interim doses now.

COVID-19 has attracted some of our sites and in Europe and in South America, and that's we had hoped to have that.

Around our early August earnings in mid year.

But it looks like that's not going to happen but.

It should be in Q3, so we will look at the aggregate of all of that data.

See what makes the most sense I mean in particular, we're looking for doses of.

A drug that could be very interesting in terms of their targeting engagement and tolerability profile and that could be.

Used.

In combination the goal here is to.

Identify as early as we can this year.

Dose or doses on either or both molecules that could be used in combination and then.

Seek about looking for combination opportunities up here on including possible business development opportunities. So.

Jay R. Luly: So we have a very good calibration point to look at, again, it's all about target engagement slash efficacy versus tolerability, whether it's, you know, molecule A or molecule B. We had hoped to have that data on our gun two by mid-year, but as we just stated, COVID attracted some of our sites in Europe and in South America. And that's, we had hoped to have that around our early August earnings in mid-year. But it looks like that's not going to happen, but it should be in Q3.

Jay tuned on that front, but that's that's the plan.

Makes sense. Thanks, so much Jay.

Youre welcome.

Your next question will come from Yasmin Rahimi with Piper Sandler. Please proceed with your question.

Hi team congrats on the continued progress and update on the two questions for you on maybe the first 20.

Can you help us understand if there were any serological tests on at week, two I guess, what I'm trying to get at is you know on sort of the time dependent.

Jay R. Luly: So we'll look at the aggregate of all that data and see what makes the most sense. I mean, in particular, we're looking for doses of drug that could be very interesting in terms of their target engagement and tolerability profile, and that could be used in combination. You know, the goal here is to identify, as early as we can this year, doses or doses of either or both molecules that could be used in combination, and then, you know, look for combination opportunities, you know, up to and including possible business development opportunities. So stay tuned on that front, but that's the plan. That makes sense. Thanks so much, Jay. You're welcome.

<unk> and viral load or action on and then also like you know whats your dose separation difference between the 200 million.

Ground and 400 and I recognize that the number of patients are really small that's sort of part one.

And then part two was that one AE that led to discontinuation was deemed to be drug related on.

You know when this occurred at the 200 milligram, Jessica and thank you for taking my question.

I'm answering the second question first I guess the AE.

Was.

Possibly drug related.

Scored as possibly so that's you know kind of all you know it's not.

Yasmeen Rahimi: Your next question will come from Yasmin Rahimi with Piper Sandler. Please proceed with your question. Hi, team. Congratulations on the continued progress and updates. Two questions for you.

Definitive but it was standard this is possibly related and debt.

That's a 12 I believe.

With regards to looking at viral.

Yasmeen Rahimi: Maybe the first one is, Can you help us understand if there were any serological tests done at week two? I guess what I'm trying to get at is, you know, sort of the time-dependent change in viral load reductions. And then also, like, you know, was there a dose separation difference between the 200 milligram and 400? And I recognize that the number of patients is really small. That's sort of part one. And then part two, was that one? A.E. What led to discontinuation; was that deemed to be drug-related? You know, and this occurred in the 200-mogram dose group. And thank you for taking my questions.

Loans are kinetics.

You know that's not really what the study you know what.

It's designed to do so.

It was on.

That's sort of data.

In two weeks.

And then we'll get on with.

We put out the day to you and.

You're right that it's a small study.

Again.

It's a it's a small but yet informative study to help us think about combinations how.

How we build them going forward and again.

Looking into the future.

This trial was to set the table if you will for the ultimate.

Adding a 30.

To the to the combination so that we would have a nuke.

Would have a core inhibitor and then we would have a R.

E D. P 721, which is our RNA destabilizer, which should be an oral agent to a target antigen.

Jay R. Luly: Yeah, answering the second question first, I guess the AE was possibly drug-related. So it was scored as possibly, you know, kind of all you know, it's not definitive, but it was stated as possibly related and at the 12, I believe.

So.

Jay R. Luly: With regards to looking at viral loads or kinetics, You know, that's not really what this study, you know, was designed to do. So there wasn't.., that sort of data at two weeks. And then we'll give, You know, we'll put out the data, you're right that it's a small study. Again, it's a small but yet informative study to help us think about combinations how we build them going forward and again, looking into the future, This trial was to set the table, if you will, for the ultimate of adding a third agent to the combination, so that we would have a nuke, we would have a core inhibitor, and then we would have our EDP 721, which is our RNA destabilizer, which should be an oral agent to target S antigen.

Jay R. Luly: And so... That's what we're shooting for, obviously. And that's why this is an incredibly important study, even though it isn't laden with virology. But that will come and do course and end as early as the next study that we'll report out later this quarter.

We're pleased to be able to have the opportunity to present that.

Thank you so much.

Youre welcome.

Yasmeen Rahimi: Thank you so much. And then maybe one last question, I apologize. It's As we head into EASEL, you know, we're very much looking forward to the preclinical data from 7 to 1. Should we be expecting some pre-chronical models where you have done combination studies with 514?

Your next question will come from Eric Joseph with J P. Morgan. Please proceed with your question.

Good evening thanks.

Thanks for taking the questions.

Maybe just a follow up on the five went for a safety can you talk a little bit about the time.

On the onset.

Right.

On the eighties, albeit low grade and how they resolved I'm just curious to know whether you know as you continue to dose escalate or essentially a book to explore longer of course for the treatment. How you think the safety profile Mike Berry.

Jay R. Luly: Um, so I won't comment on an actual presentation until it's finalized. But what we have said is that we have looked at combinations of 721. We've looked at 721 plus core inhibitors and seen addativity to synergistic behavior. We've also added 721 to nuke and observed the same. So we have done those experiments. What shows up on the easel in its final form, you know, will be final. But we're pleased to be able to have the opportunity to present that.

And then in terms of thinking about next steps with these relief for Ace.

B V program, what we hear from Kols is that what we're gonna be a multimodal approach three to four mechanisms perhaps.

Being what it will take to get patients for a functional cure to.

To the extent that you see it similarly, I guess are you strategically thinking it for how are you thinking.

Eric William Joseph: Your next question will come from Eric Joseph with J.P. Morgan. Please proceed with your questions.

Thinking about.

You know combinations with five one for outside of your total portfolio of perhaps a pathology approach on immunotherapy.

Yeah.

I'm, sorry could you repeat the last part of that last question, maybe drifted off how are we thinking strategically about how about what.

Eric William Joseph: Good evening. Thanks for taking the questions. Maybe just a follow-up on 514 and state the, can you talk a little bit about the time of onset of, Well, the AE's, albeit low grade, and how they resolve. I'm just curious to know whether, you know, as you continue to dose escalate or potentially look to explore a longer course of the treatment, how you think the safety profile might vary. And then in terms of thinking about the next day,

Evaluating five one for combination.

With.

Agents outside of your portfolio potentially with them all ago, like messenger, RNA or NAV, so or with immunotherapy.

Got it.

So and again with regards to any aes.

Again, which were.

Which we're all.

Mild except for the one that we.

Noted.

You know, they're just scattered throughout the study and in a different.

Eric William Joseph: I've been thinking about it.

Eric William Joseph: from KOLs, is that likely going to be a multimodal approach, three to four mechanisms perhaps, seeing what it will take to get patients to a functional cure, to the extent that you see it similarly, I guess, are you strategically thinking, or how are you strategically thinking?

Doses over different periods of times, and so on and so forth. So there's just nothing to really a point.

Point out that this time.

Mary.

On.

You know sort of just like any any sort of a study like this whether it's a phase one study or anything like that its when you see on the remarkable safety findings.

Eric William Joseph: just thinking about

Eric William Joseph: you know, combinations with 514 outside of your internal portfolio, perhaps with an oligal approach or immunotherapies.

Scattered so we'll have again, a summary of all of that but there was nothing.

Concerning with regards to how we're looking at anything going forward.

Eric William Joseph: or immunotherapy.

Actually agree.

Eric William Joseph: I'm sorry, could you repeat the last part of that last question? You drifted off.

Unremarkable.

While with with no real pattern.

With regards to <unk>.

Eric William Joseph: How are we thinking strategically about what? evaluating 514 combinations with agents outside of your portfolio, potentially with an oligo, like an S-R-N-A or an A-ISO, or with immunotherapy.

The the strategy so.

It wasn't so long ago that people on the community, where we're wondering you know quote a core inhibitor plus a nuc lead to a functional cure and.

Jay R. Luly: So, and again, with regard to any AEs, which were, um, which were all mild except for the one that we noted. You know, they're just scattered throughout the study and at different doses over different periods of time and so on and so forth. So there's just nothing to really point out at this time. It looked very, you know, sort of just like any sort of study like this, whether it's a phase one study or any study like this, when you see unremarkable safety findings, they're just sort of scattered. So we'll have, again, a summary of all of that, but there was nothing concerning with regard to how we're looking at anything going forward. It was actually a very unremarkable profile with no real pattern.

In theory, nobody really still knows the answer for that although.

Some of the work that.

Others have done suggest that that may not be enough, even though we had a core inhibitor. We've had a core inhibitor for many years now and we're obviously planning for this study for a long time that we just announced today, which was the first such a combination of a nuc plus of course, we were never is.

Assuming that that would be enough if it if it were to be enough.

We would be delighted because it's five one for US you know amongst the.

The finest core inhibitors, we believe but we were we were that would be an exciting upside, but we were always planning for the future assuming that that wouldn't be the case.

Now.

Jay R. Luly: With regard to the strategy. So, you know, it wasn't so long ago that people in the community were wondering, you know, could a core inhibitor plus a nuke lead to a functional cure. And I guess in theory, nobody really still knows the answer to that, although some of the work that others have done suggests that that may not be enough. Even though we had a core inhibitor, we've had a core inhibitor for many years now, and we've obviously been planning for the study for a long time that we just announced today, which was the first such combination of a nuke plus the core, we were never assuming that that would be enough

What you now know 71.

Our molecule that is oral and goes after S antigen.

As the result of our continued pursuit down the line of of you know we will keep going until we know we have enough agents and ideally we're going to try to harvest all those agents in house.

I see right now we've shown comparative data.

Of 72 one.

You know versus S. I Rnas and antisense Oligos, we put a slide comparison of that on the same animal model.

Jay R. Luly: If it were to be enough, we would be delighted, because 514 is, you know, amongst the, uh, the finest core inhibitors, we believe. But we were, that would be an exciting upside, but we were always planning for the future, assuming that that wouldn't be the case.

That's been reported and setting.

Two one turns up.

You know very well against them.

So could that be a third agent.

Moving to one plus our core inhibitor five on core plus a nuc could that'd be enough.

It certainly gives you a stronger chance on a nuc plus a core alone.

Jay R. Luly: So now, what you now know is 721, our molecule that is oral and goes after as an antigen. It is the result of our, you know, continued pursuit down the line of, you know, we will keep going until we know we have enough agents. And ideally, we're going to try to harvest all those agents in-house. I see right now that we've shown comparative data of 721, you know, versus fir-r- I mean, we've got a slide comparison of that in the same animal model that's been reported.

We're hopeful that it could be but it might or it might not we'll find that out as the propel down into next year, and hopefully get triple combinations going on but suffice it to say.

We hope that it could be but we want a rest and in terms of looking at other kinds of things thinking about other mechanisms until we're sure we have enough together.

A functional cure and hopefully one that's an all oral one.

You know could we.

Could we find an asset outside that we could combine with on top of our triple.

Possibly it could be generate something in the house there could be combinable on top of a or triple if you count the nuke again I think that's another possibility so but our strategy to be clear is to keep them aggregating as many mechanisms as we need to provide the same.

Jay R. Luly: 721 stands up, you know, very well against them. You know, so could that be a third agent? 721 plus our core inhibitor 514 plus a nuke. Could that be enough? It certainly gives you a stronger chance than a nuke plus a core alone.

Jay R. Luly: We're hopeful that it could be, but it might or it might not. We'll find that out as we propel down into next year and hopefully get triple combinations going. But suffice it to say, um, we hope that it could be, but we won't rest in terms of looking at other kinds of things, thinking about other mechanisms until we're sure we have enough to give a functional cure, and hopefully one that's an all oral one.

Really the same.

Quality.

Cure.

That we've been able to offer hepatitis C patients and that's our that's our goal on the and our dream to do that.

Okay. Thanks for taking the question.

Youre welcome.

Your next question will come from Roy Buchanan with JMP Securities. Please proceed with your question.

Hi, Thanks for taking the questions and congrats on the phase one results for five one for first question on that can you just remind us on that.

Jay R. Luly: Um, you know, could we, um, could we find an asset outside that we could combine with on top of our triple? Possibly, could we generate something in the house that could be combinable on top of our triple if you count the newk again? I think that's another possibility, but our strategy to be clear is to keep aggregating as many mechanisms as we need to provide the same, ideally the same quality that we've been able to offer hepatitis B patients. That's our goal and our dream to do.

Like you're stopping at 800 milligrams at how you how you chose that.

Cut off.

Yeah.

So we you know we modeled them.

All of these doses were just modeled based on you know phase one work for you had done in healthy and you know to that end we.

Pay particular attention to pharmacokinetics.

Exposure overall, but importantly, you know that.

Eric William Joseph: Thanks for taking the question. You're welcome.

The C 20 for concentrations.

Make sure we have.

Douglas Royal Buchanan: Your next question will come from Roy Buchanan with JMP Securities. Please proceed with your question. Thank you for taking the questions and congratulations on the phase one results for 514. First question on that, can you just remind us? It sounds like you're stopping at 800 milligrams. How did you choose that?

Good pressure on the virus.

So it's it's really a combination of PK.

PK PD safety information that we get from our phase one.

A healthy portion.

To to help establish the doses that we that we did on.

And it's played out quite well.

Think again.

Jay R. Luly: Yeah, so we modeled, um, all of these doses were just modeled based on phase one work we had done in Healthies. And, you know, to that end, we pay particular attention to pharmacokinetics, you know, the exposure overall, but importantly, you know, the C-24 concentrations, you know, to make sure we have good pressure on the virus. And so it's really a combination of PKD safety information that we get from phase one.

204 hundred both give.

Very nice exposures.

And to.

To remind everyone. We we did a we.

We did put out the.

A study in healthy volunteers.

As usual.

Back at the virtual easily beating last year.

But for reference too.

Okay, Great and then for the Sars Cov two inhibitor area. I mean, you guys are clear that is specific for Sars cov. Two I'm. Just curious if you have any sense of the pan coronavirus potential IV, specifically looked at it.

And then do you think that your preliminary inhibitor might be close behind on development such that you might have a potential combination treatment option in the not too distant future.

Jay R. Luly: A, the healthy portion to help establish the doses that we did. And, you know, it's played out quite well, I think, again, uh, 200 and 400 both give very, very nice exposure. And to mind everyone, we did put out the study in healthy volunteers at Easeel, you know, back at the virtual easel meeting last year. That's there for reference, too.

Well so starting.

So the preliminaries program as a non.

Not as far along as the protein.

I'm, sorry, you know and the way Science Guy was.

Some things are catch up other things like behind.

But you know the goal ultimately will be compressed down on on both of these mechanisms bring them forward and hopefully the.

Douglas Royal Buchanan: Okay, great. And then for the SARS-CoV-2 inhibitor, I mean, you guys are clear that it's specific to SARS-CoV-2. I'm just curious if you have any sense of the pan-coronavirus potential, or have you specifically looked at it? And then do you think that your polymerase inhibitor might be close behind in development such that you might have a potential combination treatment option in the not-too-

You know the two pads are able to cross if we need them to cross.

You know to ultimately build combinations. So let's all hope for the World that you know one agent will be enough.

And then with regards to Sars Cov, two I mean, we.

We you know we design a protease inhibitors to targeted we do look at other corona viruses as well so.

Jay R. Luly: Well, so the Plymeries program is not as far along as the protease, so I, you know, and the way science goes, some things catch up, other things, you know, like behind. But, you know, the goal ultimately will be to press down on both of these mechanisms, bring them forward, and hopefully, the two paths are able to cross if we need them to cross, you know, to ultimately build combinations. Let's all hope for the world that, you know, one agent will be enough.

I think you know, we'll have more to say on that ultimately, but there is the possibility.

Debt, whereas we didn't want.

Something.

You know we are well on the back up you know as you know earlier in the in our process. We did scan through libraries of compounds and so on and so forth just to see if there couldn't be and expedient.

Start by by catching our elite earlier, and you know, whereas we did find molecules that had activity against the virus.

Jay R. Luly: And then with regard to SARS-Cove 2, I mean, we, you know, we design protease inhibitors to target it. And we do look at other coronaviruses as well. So, um, I think, you know, we'll have more to say on that ultimately, but there is the possibility that, you know, whereas we didn't want something like that, well, let me back up. You know, as you know, earlier in our process, we did scan through libraries of compounds and so on and so forth, just to see if there couldn't be an expedient start by catching a lead earlier.

Jay R. Luly: And, you know, whereas we did find molecules that had activity against the virus, we weren't satisfied with the degree of potency and other characteristics that we saw with them. So, in parallel, and kind of leaving nothing to chance, you know, we were doing more of a design approach. And we did look, and we have paneled against multiple different coronaviruses, including SARS-Cove 2, but to be clear, this was very targeted to make sure, more than anything, that we had molecules that worked really well against SARS-Cope, too.

Jay R. Luly: I do believe now we're building up a stable of molecules with multiple different chemical classes and other kinds of properties that will be able to hit multiple different coronas, and that'll put us, been a great position, you know, to the extent there's ever, God forbid, another such beast as SARS-Cove 2 to be in a position to really harvest a much more targeted library that we know hits coronaviruses versus, you know, what we had prior to our efforts here.

Bit lower than we were expecting and I you know I understand the first quarter seasonality.

Dynamics, but was there anything else that you guys can communicate that.

Have impacted the sales on the first quarter. Thanks.

Yeah, No I I would I would take your input for me I'd be on that and.

And they said what you know what Gilead is also noted there's still a COVID-19 impact.

Douglas Royal Buchanan: Okay, great. And then one last one. Actually, on Maverid, I know you guys are not marketing that drug yourself, but the, you know, AbV sales came in quite a bit lower than we were expecting and, you know, understand the first quarter seasonality dynamics, but was there anything else that you guys could communicate that, um, might have impacted the sales in the first quarter. Yeah, no, I would take

Okay. Thank you.

Yep you're welcome.

Your next question will come from Brian Scorning with Bird. Please proceed with your question.

Yeah. Good afternoon, guys. Thanks for taking my question start on E. D. P 721, I mean, it sounds like you either have or or just about to submit 90. So I was just wondering how should kind of think about the clinical development program. Here. I mean, you know can you can start with traditional sad Mad and healthier and then how early.

Douglas Royal Buchanan: Yeah, no, I would take your input from Abby on that, and they said what Gilead has also noted, there's still a COVID impact. Okay, thank you. Yeah, you're welcome. Your next question will come from Brian Scornie with Bayard. Please proceed with your question. Hey, good afternoon, guys.

Can you get into patience and and what sort of the the the the goal in terms of initial proof of concept day, though I mean, obviously, it's not an anti virals, who wouldn't be looking necessarily for D. N a.

Or on a [laughter].

Impact. So I mean is the comps here really kind of the army I based therapeutics were were you know what's important is to look at the Santa general doctrines or what other sort of Biomarkers for me kind of considering here for for non stop.

Brian Peter Skorney: Thanks for taking the question. Start on EDP 721. I mean, it sounds like they either have or are just about to submit an I&D. So I was just wondering how we should kind of think about the clinical development program here. Start with traditional sad, mad, and healthies, and then how early can you get into patients? And what's sort of the goal in terms of initial proof of concept data? I mean, obviously, it's not an antiviral who wouldn't necessarily be looking necessarily for DNA or RNA impact, so I mean, are the comps here really kind of RNA-based therapeutics? important to look at.

Yeah, I I think that'll be you know somewhat similar to the past five one for you know first of all do sad Mad healthy as as you point out that will get into H P. B patience.

And you know we might.

You'll be able to look at.

By Reman can nuke patients.

For a period of time, but but clearly with this one we're going to be also looking at a sandwich on levels right. So that's will be one of the one.

One of the key reasons. In addition to obviously D N, a and RNA, which some other other mechanisms they'll take care of so.

Brian Peter Skorney: The assay antigen reductions or what other sort of biomarkers should be used

You know hopefully being able to get.

Jay R. Luly: Yeah, I think it'll be, you know, somewhat similar to the path of 514. First, we'll do sad, mad healthies, as you point out. And we'll get into HPV, you know, patients. And, you know, we might be able to look at Vyremic and NUC patients for a period of time, but clearly, with this one, we're also going to be looking at us and engine levels, right? So that's will be one of the key reads in addition to obviously DNA and RNA, which some of our other mechanisms will take care of.

Is it really a read as we as we can on that.

And it's gonna be patients will be will be clearly one of our aims and getting the you know the triple together.

Jay R. Luly: So, you know, hopefully being able to get as early a read as we can on that and HPB patients will be clearly one of our aims and getting the triple together as expeditiously as we can. So stay tuned on that, Ron. I think we'll have more to say as we... As we take that in to Healthies, again, we're aiming to do that mid-year, have the results from that in the first half of next year, but also be, you know, getting on to other, other studies as quickly as we can, kind of like 514.

Jay R. Luly: I mean, with 514, we had the healthy stuff done. We saw the dose information, and then we were on to the next studies because we saw what we knew we had to see in order to propel it. So I think as we get the healthy data and we're embarking upon the patient studies, we have a very detailed outline to share in terms of how we're going to prosecute that. Great, and on the SARS-Cove 2 produce inhibitor program, I mean, I don't know if you...

About sort of.

Use of antiviral monotherapy without really walk characterize barrier to resistance and.

How do we think about that in the context of a protease inhibitor.

Brian Peter Skorney: Be comfortable sharing specific data on your leader; I just want to talk kind of generally about what we know.

Yes.

Good news is we're talking about.

Hope hopefully short period of treatment for rich right.

Brian Peter Skorney: about the potential selection pressure and, you know, potential conservation of important binding proteins, proteates inhibitors and the ability to drive resistance, then I think there's a bit of a, I guess, remorse for the utilization of MAB monotherapy and potential selection pressure. I guess we're regulators, hesitant at all about sort of the use of an antiviral monotherapy without a really well-characterized barrier to How do we think about that in Yeah, well, you know, the good news is we're talking about a, you know, a hopefully short period of treatment duration, right? You know, a correlate that one might think about is looking at our RSE program and thinking about, you know, drug dosing durations of maybe five days or something like that.

Correlate that one might think about us.

Looking at our RSV.

Program and thinking about drug dosing durations of maybe five days or something like that so.

That's number one thing that's good the other is debt.

We're not going after.

We're not going after spike protein and <unk>.

Doug we're going after.

Highly.

Conserve targets with conserve the binding pockets that are key for the survival of the virus. So.

I think the the opportunity to go in and go in.

And.

And inhibits these.

Sort of concern.

And he says conserve targets.

It would be.

About the best strategy, you could take if you're trying to minimize these sorts of challenges so.

Jay R. Luly: So that's the number one thing that's good. The other is that, you know, we're not going after spike protein. Instead, we're going after highly conserved targets with conserved binding pockets that are key to the survival of the virus. So I think the opportunity to go in and go in and inhibit these, you know, sort of conserved regions that conserve targets would be about the best strategy you could take if you're trying to minimize these sorts of challenges.

I think that's.

That's what we're on the Mark for.

And so.

So far so good day again, we're excited to be.

Pushing them.

For first protease inhibitor against this target into IND, enabling studies soon and if those go well.

Hope to be.

In our phase one study early.

Early next year.

Great. Thanks, Jeff.

Youre welcome.

Your next question will come from our cash Tomorrow with Wolfe Research. Please proceed with your question.

Jay R. Luly: So I think that's... That's what we're on the mark for. And, you know, so far, so good. Again, we're excited to be pushing our first protease inhibitor against this target into INABELIN studies soon. And if those go well, we hope to be in our phase one study early next year. Great, thanks, Jeff. You're welcome.

Hi, This is an add on for a cash. Thank you for taking our questions I think starting with silent for I think the first question. We have is that we noticed you mentioned the kitchen 90 to one log reduction of RNA did you notice any like dose response between the.

Tosh Tawari: Tosh Tawari with Wolf Research, please proceed with your questions. Hi, this is Leo with Akash. Thank you for taking our questions.

200, Megabits per 100, Meg and reducing the RNA level and the second on the Colgate program. Previously you mentioned about the protease inhibitor as well as preliminary thinking about Europe being a very interesting targets from COVID-19. So on the now you have more forward debt protease inhibitor, so I'll, let andre.

Tosh Tawari: I think starting with 514, I think the first question we have is, we noticed you mentioned the treatment led to a one-lock reduction of RNA. Did you notice any, like, dose response between the 200-MEC versus 400-MEC in reducing the RNA level? And the second, on the COVID program, previously you mentioned both protease inhibitors as well as polymer inhibitors being a very interesting target for

Is there any like posed on call comparing these two different targets and clothing 10 months in terms of efficacy safety and do plan to test both molecules uptick from analyzing that clinic.

And the last question is more related to the RFP.

Tosh Tawari: COVID, so now you have moved forward with a protease inhibitor.

Tosh Tawari: Are there any pros and cons in comparing these two different targets in terms of efficacy as well as safety? And do you plan to test both molecules of different MOAs in the clinic? I think the last question is more related to the RSE regulatory pathway. Maybe we'll just pause there with the questions so we can keep up with it. So, um, I think, I mean, this is a very small study in 514. And we, again, Um,

Hey, Michael this is only possible. If you will just maybe it will just pause there. Okay. A question for so we can.

Keep up with it so.

I think I mean, this is a very small study and five one for.

And we are again.

The dose response from I'm not.

Sure.

Not only do you want to comment on on any dose response.

Jay R. Luly: The dose response, I'm not sure we Natalie, do you want to comment on any dose?

Sure.

So I think just to complete maybe what Jay was starting to say Oh do you see a smaller number of patients in each of them does book.

Natalie: Sure, hello. So I think just to complete maybe what Jay was starting to say, obviously, as you have noticed, we have a small number of patients in each of our dose groups. It is not totally clear that we can see a dose response, but I don't think, you know, I would have expected that clearly in the NUXAWRES patients. Now, if we look at E-plus versus in-HEC patients, we could maybe say that the 400 milligrams may have a little bit more decreased in the RNA, but again, we're talking with a very small sample. You deal with the ability of So I think once we get all the very unique data and we compile all the data together, the three doses will make better sense.

It is not a tiny peer that you can see a dose response, but I don't think we would have expected debt clearly.

<unk> suppressed patients now if we look at it price versus E make patient.

Please maybe say that discipline interest many from man, but he didn't do it.

More on decreasing the RNA, but again you know we're taking we've been very small income for size.

Many of you, saying my empathy for someone.

So for science, So I think once we get all the value that Oh, we compile all of that together caused this free disease and other bigger things.

Yeah. So.

And again I think the viremia data.

Natalie: Yeah, so, and again, I think that Vyremic data We'll probably be dealing with a much more elevated DNA to start with, obviously, a greater opportunity to see those responses. Again, we've only got two doses then, not the third. The changes that you're going to see in this new suppressed population are going to be very small RNA changes if you see them typically. And usually they're larger in eanogen positive patients, and they were the minority of patients in this study.

We will probably be dealing with a much more elevated.

<unk> DNA test to start with obviously greater opportunity to see those responses again, we've only got two of the doses and not the third.

The changes that Youre going to see you on this nuc suppressed population are going to be a very small.

RNA changes, if you see them typically and usually they're larger.

And E antigen positive patients and they were the minority of patients in this study from some other studies have selected to get the E.

Natalie: Some other studies have chosen to get the, you know, eanigen positive patients selected. We didn't do that. So, you know, we have E-Nig and E-Pont. Regarding your question about PI and polymerase, you know, we're prosecuting both targets, and was your question if we were successful? Where would we take them into the clinic, as I understand it?

E antigen positive.

Patients are selected.

We didn't do that so you know we'll be seeing again in the past.

Regarding your.

Question about a P I.

Preliminaries.

We're prosecuting both targets and like what's your question. If we're successful there would we take them into the clinic, but I understand your question right.

Jay R. Luly: Yes, and also just high level, like, what do you think of the pros and cons in terms of both efficacy and safety between these two targets? Yeah, I think no one knows the pros and cons yet; there's just no data really to speak of broadly across these different classes other than to say, you know, either or both have a compelling rationale to work.

Yes, and also just any high level like in Germany, like do think of the pros and cons in terms on both efficacy and safety here between these two.

I think no one knows.

Pros and cons, yet Theres, just no data really to speak of a broadly across these different classes other than to say you know.

Either or both is a compelling rationale to work.

Jay R. Luly: You know, within protease inhibitors versus polymerases, you can have, with polymerases, either nukes or non-nukes. Sometimes nukes can have safety challenges over non-nukes, but, you know, it really just comes down to an individual molecule. So, again, I think both of them, we wouldn't be working on both mechanisms if we didn't think that they were compelling ones to try. That said, you know, we need to let the field mature a little bit, get these molecules with some clinical data sets that are, you know, um, that are analyzable so that people will understand what these therapeutics can do. We're obviously very bullish on the need to have these beyond vaccines for obvious reasons.

Within our protease inhibitors are versus polymer aces, who couldn't be with polymer races, we can have either nukes or non nukes, sometimes nukes.

Can have safety challenges over non nukes, but you know it really just depends it comes down to an individual molecules. So again I think both we wouldn't be working on mechanisms. If we didn't think that they were.

On a compelling.

Ones to try that said you.

We need to let the field mature a little bit debt. These molecules for some clinical datasets that are.

Our analyzable, so that people will understand what these therapeutics can do.

We're obviously very bullish on the.

The need to have these beyond vaccines.

Tosh Tawari: Got it, thank you. I think my last question is about the RSV regulatory pathway. I wonder, based on your discussion with FDA, do you have any thoughts on the disease?

For obvious reasons.

Got it. Thank you I think my last question is from a balance to RSV regulatory pathway I Wonder had based on your discussion with FDA and does it have any thoughts on the design for the pivotal trials.

Tosh Tawari: for the pivotal trials, specifically on endpoint selection.

Tosh Tawari: selections and specific outcomes selection. For example, it could be a percentage of progression to lower spatteral infection or maybe time to hospitalization.

Typically on the endpoint selection and especially thank all Com selection for example, it could be a percentage on a question to another specially infection or maybe tend to have sensation.

Yeah, sorry, I think we need to finalize for phase two B program, then will have these.

Jay R. Luly: Yeah, so I think we need to finalize our Phase 2B program, then we'll have these discussions with the agency over registration endpoints. It's, uh, It's, you know, it's not appropriate to comment on that until you've had that discussion. Okay. Thank you very much.

These discussions with the agency over registration endpoints.

No.

But are.

You know you, it's not appropriate to comment on that until you've had that discussion.

Got it thank you very much.

Your next question will come from <unk> <unk> with Roth Capital Capital Partners. Please proceed with your question.

Operator: Your next question will come

Hey, guys. Thanks for taking my question and congrats on all the progress.

Zegbe Jala: from Zegbe Jala with Roth Capital Partners. Please proceed with their

Zegbe Jala: Proceed with their questions.

Zegbe Jala: Hi guys, thanks for taking my question and congratulations on all the progress. I just have a few quick ones for you. I think the first day is just trying to clarify that you will not be moving forward towards approval if you don't have something that could perhaps produce a cure with your HBV program. Even if you get to a triple and you don't have a cure, you're not going to move forward with that.

For a few quick ones for me I don't know.

First off let's just trying to clarify on still will not be moving on towards.

What approval if you don't have something that could perhaps but just to clear on what the HBV program. Even if he gets on a triple a and you don't have a clear are you not.

And on the phone with that.

No it's.

Did I.

So I I don't believe on you said that.

Jay R. Luly: No, did I, so I don't believe I said that. You have to keep going. I think what I was trying to say, well, if two mechanisms aren't enough, you add a third, and if a third isn't enough, you know, maybe you need to add a fourth, or maybe you need a longer duration of treatment or, you know, what have you. Maybe there's certain patient populations that you need to explore further. So, no, I think it's really premature to know what a triple therapy will look like in this, especially given one that hits so many different cylinders. I think we're, you know, for us.

You have to keep.

I think what I was trying to say what if a two two mechanisms isn't enough you've added a third I don't know if a third isn't enough.

Maybe you need to add a fourth or maybe you need a longer duration of treatment or other.

You know what have you maybe there's certain patient populations that.

But you need to explore further so.

No I I think.

You know, it's it's a it's really premature to know what the triple therapy.

<unk> therapy will look like.

This, especially given one that hits so many different cylinders I think were.

Jay R. Luly: You know, core inhibitors do a lot of things in addition to pushing on DNA like Nukes do, but they have a number of other points of mechanistic interest against the virus, but what a nuke and a core, a nuke plus, you know, a lot of other mechanisms don't have is the ability to robustly affect S-anogen. And that's something that we really are anxious to get brought into this mechanism. You can affect the S-anogen, which obviously, among other things, is sort of a foil to the immune system being able to fully, you know, take on the virus.

For us.

You know a core inhibitors do a lot of things in addition to.

Pushing on DNA like nukes to but they have on a number of other.

Points of a mechanistic interest against the virus, but what.

What a nuke kind of core or nuc, plus you know a lot of other mechanisms don't have.

Is the ability to to robustly effect S antigen on and that's something that we are we really.

We're anxious to.

Get brought into this mechanism.

Can affect the S antigen, which are obviously among other things is it's sort of a foil to the immune systems being able to fully.

Jay R. Luly: If you can knock that down, along with the other mechanisms that we're adding, we're quite hopeful that we'll be able to, you know, have a major impact. But like I said, it's more of a we're not going to, We're not going to say we're finished until we're done. If we need, ultimately, to add another mechanism, whether it's an immune stimulation mechanism or something else, you know, we'll continue to explore that. And if we can, we want to try to keep on our track of having an all-oral regimen.

Pick on the virus.

If you can if you can knock that down.

Along with the other mechanisms that we're adding we're we're quite hopeful that we'll be able to.

You don't have a major impact.

But like I said, it's more of a day.

We're not going to.

We're not going to say we're finished until we're done.

If we need ultimately to add another mechanism, whether it's abuse and stimulation mechanism or or something else.

You know, we'll continue to explore that and.

And if we can we want to try to keep on our on our track of having an all oral regimen because right now the three agents that we're talking about for our triple.

Jay R. Luly: Because right now, the three agents that we're talking about for our triple do represent an oral opportunity, which is, you know, fairly rare in the landscape of HPV treatments. So I think what we want to do is to continue to build on that. Yeah. Obviously, there could be other things out there that could give you an immune boost. I mean, an easy thing to look at, and others are doing it too, is to attack on, you know, an interferon arm to see what it could do.

Do represent.

On an all oral opportunity for which as you know fairly.

Fairly rare in a landscape of HBV treatment. So.

I think what we wanted to do is if we can continue to build on that.

Obviously, there could be other things out there that could give you an immune boost for me in an easy thing to look at and others are doing it to us to tack on you know an interferon arm to see what it could do so there's easy ways to build the quad.

Jay R. Luly: So there are easy ways to build a quad, if you want to do that in part with your arms. We're obviously thinking about all kinds of things right now. But to be very clear, I think we're very bullish going into the possibility of having our all oral triple.

If you want to do that and part of your arms, we're obviously thinking about all kinds of things right now so.

But to be very clear I think we're.

We're very bullish going into.

Zegbe Jala: Thank you, and just to pull up to that. I was just kind of wondering.

Possibility of having our oral triple.

Thanks, and just a follow up to that.

Zegbe Jala: And this is a difficult one, but I was just kind of wondering.

Just kind of on lending.

Zegbe Jala: Is that what we should be looking for, especially with the vermic data coming up, you know, in terms of signals as to perhaps, you know, combining this with your other agents could perhaps, you know, lead to that care with perhaps a longer duration of treatment or whatnot. But just, you know, what should investors and analysts be looking towards? Is it the law difference or, you know, what should we keep our eyes on?

For the difficult for him is that just kind of wondering what it is that we should be looking for it especially with that for them at data coming up you know in terms of signals as to perhaps you know combining this with your other agents to perhaps you know lead to that came with perhaps on the duration of treatment or whatnot, but just you know what should investors on.

Unless they're looking for like as if the law defense or you know what should we keep our eyes on.

Jay R. Luly: Yeah, I

Jay R. Luly: Yeah, I would say, you know, it's the, you know, so we've looked at safety, tolerability, and pharmacokinetics and healthies. We've looked at safety, and tolerability in pharmacokinetics now in HB patients and on top of a nuke. And now we're in this next study, we're going to just back out the nuke.

Yeah, I would say you know it's it's the you know so we've looked at safety Tolerability and pharmacokinetics in healthy.

We've looked at safety.

Tolerability and pharmacokinetics now in HBV patients and on top of on Nuke and now we're in this next study we're going to just back out the nuke.

Jay R. Luly: These will be patients that have higher viral loads, particularly on the DNA side. And so what we want to see is just a very solid, you know, reduction in viral DNA. And probably, again, to a lesser extent, you should hopefully see some effect on RNA. But the RNA changes are never as much as the DNA changes that you can usually see in these types of studies.

These will be patients that have higher viral loads, particularly on the D&A side.

So what what we want to see is just a very solid.

No reduction in viral DNA, and and probably again to a lesser extent you should hopefully see some effect on RNA you know they aren't any changes are never as much as the DNA changes that you can usually see a then these types of studies. So you know a good a couple of solid in the law.

Jay R. Luly: So, you know, a good couple solid logs of viral load reduction, seeing good trough levels of 28 days, some good safety and tolerability. These will all be things that give us the Green light, green light, green light, in terms of moving ahead into more advanced studies with 514. It's really helpful to, again, help define the optimal dose in terms of, you know, dose selection for future studies. That's what we would be looking for.

Sort of a viral load reduction seen good trough levels at 28 days.

Good safety and Tolerability. These will all be things that give us a.

Green Light Green light Green light in terms of moving ahead.

And two.

Two more advanced studies with <unk>.

Five one for it's really helpful to again help define the optimal dose.

And in terms of.

Dose selection for future use.

So.

That's that's what we would.

Jay R. Luly: I think, you know, today's sort of a good prequel in terms of the kinds of information we get. I think, just in addition, we should be able to get information on the HPBG. You're not going to see if that's on antigens, you know, in a 28-day period.

I think you know today's.

Sort of a good prequel in terms of.

The kinds of information. We go on I think are just in addition, we should be able to get information on the HBV DNA.

You're not going to see if things on antigen. So you know on a 28 day period.

Zegbe Jala: Understandable. I think people are just getting excited, me included, with the teaser from the ATPV, but moving on to the RSV program, GSK, similar to you, they noted, you know, finding really difficult-to-find regions where there are high RSV cases, but I'm just wondering, you know, even when those cases do return with, you know, Sanofi talking about perhaps falling.

Understandable I think people are just getting excited me included with that teaser for the HBV about moving on to that as the program and you know GSK seemingly on like you didn't know that you know find it really difficult to find regions are where they're high honestly Keith is but I'm. Just wondering you know even when those cases do return.

And with that you know Sanofi talking about perhaps filing on their.

Jay R. Luly: pediatric use, you know, sometime in 2022. I'm just wondering for your later studies, for pediatrics at least, how you think that may affect it. Yeah, I think, well, I mean, people are looking for a more potent version of synergist, you know, which is a monoclonal antibody that historically has been used prophylactically in high-risk premature births and which, when used therapeutically, did not work. Now they've got a longer-acting version of that.

They are jobs for pediatric use you know sometime in 2022 I'm just wondering for you on later studies for pediatric at least you know how you would think of that may affect them.

Yeah, I think well I mean people theyre looking for a more potent version of Synagis, which is a.

Thank you for monoclonal antibody that historically, it's been used prophylactic Lee in high risk premature births.

When used therapeutically did not work.

Now they've got on longer acting a version of that.

Zegbe Jala: And so you just have to wait and see, you know, how A, it might work, and then B, to the extent it has efficacy, in the target patient populations. You know, one of the things I think you're gonna see then is that children get RSV. They need to get RSV repeatedly when they're children to sort of build up a, a, you know, sort of a partial natural immunity to it.

And so you just have to wait and see you know how you know a how it might work.

And then B you.

You know to the extent it Uh huh.

Has efficacy.

On the AR and the target patient populations.

One other things I think youre going to see them as it's a.

Children get RSV, they need get RSV.

Repeatedly when there for children to sort of build up.

Hum.

Sort of a partial on natural immunity to it.

Zegbe Jala: And if they're not getting exposed to the virus, in some ways, you're kicking the can down the road. So I suspect if these antibodies go in and start treating younger children, especially in their first year of life, the first season that they're exposed to, would otherwise be exposed to, and they're being treated prophylactically with a monoclonal antibody, you're just setting them up to get their first RSV infection the next season that they're not on a prophylactic antibody, right? So I think it's, um, It's just a question of what age group of people our drug is going to treat. But there will be a lot of pediatric artists out there.

And if they're not.

They're not getting exposed.

Expose to the virus and in some ways you're kicking the can down the road sorry, I suspect if these antibodies go on and start treating.

Young or children, especially you know on their first year of life. The first season that they're expose what would otherwise be exposed to them, there and they're being treated prophylactic or with a with a monoclonal antibody you you're just setting them up to be to get their first [laughter] there for.

As Darius V infection and.

The next season that they're not on a prophylactic antibody right. So I think it's.

It's going to stay.

Depending on what age group of people, our drug is going to ultimately treat.

But there will be a lot of pediatric RSV.

Zegbe Jala: Thanks again, just the last one year for me. Regarding the NASH program, again, don't want to put words in your mouth, but just wanted clarification of whether or not you'll be looking at 305 as a single agent or as a combination used when you do get the data and you're thinking about moving forward. And then last bit year, I thought the data for 305 and 297 would be coming at the same time, but it seems like 305 might be a little delayed. I don't know about 207, but I was just wondering if you're going to wait to have both of the data sets in hand before making a decision to move forward. Yeah, I want to do it.

Up there.

Thanks, Dan just a last one for me regarding the Nash program again don't want to put words in your mouth, but just wanted clarification on.

Whether or not you'll be looking at three O five as a single agent.

Oh as combat use when you do get the data you are thinking about moving from it and then the last but you know I thought the data for three five and 297 will be coming at the same time, but it seems like you might be on litter domain I didn't know back to Kevin, but I was just wondering if you're going to wait to have perfect does that exact in hand, before making a decision to move from it.

Yeah. It was I think I think the answer.

I mean, we can't make a decision.

Jay R. Luly: Yeah, I think the answer We can't make a decision relating to 305 until we have the data on 305. So I think we will need to, uh, you know, wait to look at that data, you know, to put it into the mix clearly.

Relating to three or five until we have the data on 305, So I think we will need to.

You know its way to look at that day to you now.

Put it into the mix clearly, but I think you know ultimately.

I see.

You know FX ours and the other.

Drug classes against Nash, you know all of them.

Jay R. Luly: But I think, you know, ultimately, I see... FXRs and other drug classes against Nash, you know, all of them, the ones that have efficacy anyway are going to do something, right? But they're not going to be treating patients optimally. And I do believe that optimal treatment for patients is only going to come by way of combos. And I think the sooner you get on with the combos and start running combo trials, Um, you know, I think the better, just because we'll be getting more relevant data sets that have a higher chance of higher impact.

The ones that debt that have efficacy anyway are gonna do something right and but they're not going to be treating patients optimally and I do believe that optical optimal treatment for patients as the only gonna come by way of combos.

And I think the sooner you get on with the combos and start running combo trials.

You know I think the better just because you'll be getting more relevant data sets that have a higher chance of higher.

Impact on.

And again as.

Jay R. Luly: And again, as we've stated previously, our ultimate goal here is to partner up and Nash find a partner for our FXR program, certainly before, Phase 3s, and any time as soon as a data set supports doing a combination, so that's what we're doing. But we just need to harvest the data.

As we've stated previously our ultimate goal here is to.

To partner up and and she find a partner.

For our XR program.

Certainly before a phase.

These phase threes and anytime soon.

As soon as the data supports datasets supports doing a combination potentially so that's that's what we're thinking about but we just need the harvest for the data.

Zegbe Jala: Thanks, and I was just wondering if you're waiting for the data from 305 before making a decision on 297, but it doesn't sound like that's the case. And then your last comment sounds like 297; it's definitely up for consideration also as a combo.

And I was just I was just wondering if you're waiting for the data from I think it will fly it before making a decision on 297 and it doesn't sound like that's the case and then I on your last comment it sounds like you know 297, it's definitely off a consideration also hasn't come down.

Jay R. Luly: I think all the FXRs will be up for consideration and combinations. Again, I think we won't be able to make a complete analysis of our FXR purpose and strategy, you know, which includes two different molecules until we see the totality of the data.

I think all day FX ours will.

It will be up for consideration and combos right again, I think we won't be able to make a complete analysis on our ethics are per fan.

On the strategy you know, which includes two different molecules until we see the totality of the data.

Zegbe Jala: Perfect. Thanks. I appreciate it.

Perfect.

Zegbe Jala: Welcome. At this time, we will do one final call for questions. If you would like to ask a question, please press Star 1 on your telephone keypad.

Yeah.

Yep you're welcome.

At this time, we will do one final call for questions. If he would like to ask a question. Please press star one on your telephone keypad.

Operator: question, please press star 1 on your telephone keypad. And at this time, there appears to be no further questions in Q.

And at this time there appears to be no further questions in queue I would now like to turn the call back over to Jennifer Viera for <unk>.

Jennifer Viera: Questions in Q. I would now like to turn the call back over to Jennifer Vieer for closing remarks at this time.

Operator: Thank you everyone for joining us this afternoon. If you have additional questions, please do not hesitate to reach out to us. Thanks so much. Bye-bye.

Closing remarks at this time.

Yeah.

Thank you everyone for joining us. This afternoon. If you have additional questions. Please do not hesitate to reach out to us. Thanks, So much bye bye.

Operator: includes today's conference call. Thank you for participating. You may now discuss Music

This concludes today's conference call. Thank you for participating you may now disconnect.

[music].

Operator: and so on the way. Thank you, and I'm going to be able to be. And so on in the world.