Good afternoon. My name is Catherine and I will be your conference operator today. At this time, I would like to welcome everyone to the Enanta Pharmaceuticals Third Quarter Financial Results Conference Call. All lines have been placed on mute to prevent any background noise. [Operator Instructions] Please note that today’s conference is being recorded.

I will now like to turn the call over to your host Ms. Carol Miceli, Director of Investor Relations. Ma’am, you may begin your conference..

Thank you, Catherine, and thanks for joining us this afternoon. The news release with our financial results for the recent quarter was issued this afternoon and is available on our website. On the call today is Dr. Jay Luly, President and CEO; Paul Mellett, our Chief Financial Officer; and other members of Enanta’s 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 product candidates 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.

A description of these risks is in our most recent Form 10-Q and other periodic reports filed with the SEC. Enanta 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. Jay Luly, President and CEO..

Thank you, Carol. Good afternoon, everyone, and thank you for joining us today. At the end of Enanta’s fiscal third quarter our clinical development programs to treat viral infections and liver diseases have progressed well.

Our pipeline is maturing and we have clinical studies ongoing with three different compounds, all of which have fast track designation. Our most recent achievements were the initiation of a Phase 1 study of EDP-514, our lead candidate for HBV and the announcement of highly statistically significant top line data from our RSV program.

In addition, we and AbbVie our HCV partner recently announced that the European Commission has granted marketing authorization to AbbVie for MAVIRET, to shorten once-daily treatment duration from 12 weeks to 8 weeks in treatment-naïve, chronic HCV patients with compensated cirrhosis and genotype 1, 2, 4, 5, or 6 infection.

I’ll begin my review of our clinical development programs with our most advanced program, EDP-938 for respiratory syncytial virus known as RSV. In June, we announced [Audio Gap] successful completion of this trial was a very exciting milestone for Enanta and yielded some of the most promising data from an RSV challenge study.

Specifically data from this study demonstrated that EDP-938 achieved a highly statistically significant reduction both in viral load and in resolution of clinical symptoms compared to placebo. And remember that highly statistically significant means that the p-value is less than 0.001.

The data on the viral load that we previously reported, namely the number of copies of viral RNA from quantitative RT-PCR is consistent with additional data we now have from cell based infectivity assays using live virus.

The cell based data show an approximately 80% reduction in live RSV virus across subjects in both treatment groups compared to the placebo group. This result was also highly statistically significant.

In addition, EDP-938 demonstrated good pharmacokinetics, mean trough levels of drugs, namely the levels of drug and plasma just before the next dose were maintained at approximately 20 times to 40 times above the in vitro EC90 for RSV infected human cells.

This means that the drug levels achieved in humans were dramatically higher than the amount of drug needed to reduce 90% of the viral RNA and RSV infected cells. Overall EDP-938 was generally well tolerated and demonstrated a favorable safety profile that was comparable to placebo over five days of dosing through day 28 of follow-up.

There were no serious adverse events and no discontinuations of study drug. We expect to present additional details of the challenge study in an upcoming conference.

In summary, the challenge study has shown that we can safely deliver high trough blood levels and get the drug to the target site of infection with concentrations that effectively halt progression of infection.

Also over 250 subjects have now been exposed to EDP-938 for up to seven days and the drug has generally been very well tolerated, has demonstrated favorable safety profile similar to placebo. We are very pleased with this safety profile.

Challenge study’s excellent safety and efficacy data give us confidence to advance EDP-938 into further trials particularly since we have known for some time that EDP-938 is differentiated from fusion inhibitors currently in development.

Because EDP-938 directly targets the viral replication process of RSV and has demonstrated a high-barrier to resistance in vitro. We now aim to show that EDP-938 can demonstrate efficacy in adult outpatients with community acquired RSV infection.

Our goal is to initiate our first Phase 2b study before the end of calendar 2019 and we then anticipate conducting additional studies in pediatric patients than other at-risk populations. Let’s move now to our most – next most advanced program, which is for NASH.

EDP-305, our lead FXR agonist has been investigated in two ongoing Phase 2 studies, one for NASH and one for PBC. ARGON-1, our NASH study is a 12-week randomized double-blind placebo-controlled study designed to evaluate the safety, tolerability, pharmacokinetics and efficacy of EDP-305.

Enrollment is complete in the NASH study and we anticipate sharing top line data by the end of this quarter. Directionally, we want to see positive improvements in ALT, C4, and FGF19 among other criteria.

Assuming the aggregate data supported, we plan to initiate a Phase 2b study in the first quarter of calendar 2020 and look to partner the asset prior to Phase 3. This will allow us time both to gain more data on EDP-305 and to explore, which combination assets and partners would be preferred.

We continue to believe that FXR is one of the most promising mechanisms in development today for NASH. In addition to EDP-305, we’ve made good progress with our follow-on program from which we expect to announce a development candidate later this year.

Regarding the INTREPID study of EDP-305 in PBC, we continue to enroll patients who will provide further updates as the study proceeds. Beyond FXR, we also continue our research into other mechanisms for NASH. Let’s shift to HBV. We recently initiated a Phase 1a, 1b clinical study with our novel Class 2 HBV core inhibitor EDP-514.

Part 1 is this randomized double-blind placebo-controlled study is designed to evaluate the safety, tolerability and pharmacokinetics of single ascending doses and multiple ascending doses of EDP-514 in healthy subjects, while Part 2 will explore the antiviral activity of EDP-514 in NUC-suppressed patients with chronic HBV infection.

A steady plan is to enroll approximately 98 subjects and to evaluate up to six dose cohorts with EDP-514 administered orally once-daily. We plan to share data from the healthy volunteer portion and initiate Part 2 of the study, dosing NUC-suppressed HBV patients in the first quarter of calendar 2020.

In addition, we are planning to initiate another Phase 1b study in HBV patients this time and viremic chronic hepatitis B patients not currently on treatment. EDP-514 was selected from our lead series of HBV compounds that are characterized by potent antiviral activity. And our promising preclinical data support our excitement for this mechanism.

Preclinical data demonstrated that EDP-514 is a potent inhibitor of the HBV replication and prevents the de novo formation of new cccDNA in primary human hepatocytes when given early during HBV infection.

In vitro data also show that EDP-514 is pan-genotypic and that combinations of EDP-514 with nucleoside reverse transcriptase inhibitors, which are the current antiviral therapies for HBV or with a Class 1 core inhibitor resulting in additive to synergistic antiviral effects.

In vivo models of EDP-514 demonstrated excellent efficacy with greater than 4 log viral load reduction in HBV infected PXB mice. Based on our preclinical data, we believe EDP-514 may have best-in-class potential for the core inhibitor mechanism.

And I’d like to conclude my remarks by reminding you that we look forward to communicating our progress on all our clinical programs starting with ARGON-1 Phase 2 NASH data by the end of this quarter and then additional updates on our other programs later this year.

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

Paul?.

Thank you, Jay. I’d like to remind everyone that Enanta reports on a September 30 fiscal year schedule. Today, we are reporting results for our third fiscal quarter ended June 30, 2019. For the quarter, total revenue was $44.4 million and consisted entirely of royalty revenue earned on AbbVie’s global HCV net sales of $784 million.

This compares to total revenue of $57.3 million for the same period in 2018. The decrease in royalty revenue is a result of AbbVie’s lower net sales mainly driven by lower treated patient volumes in select international markets.

Royalty revenue was calculated on 50% of MAVYRET sales at a blended royalty rate of 12% and approximately 30% of VIEKIRA sales at a royalty rate of 10%, after adjustments for certain contractual discounts and rebates, which historically have been approximately 1.5% of AbbVie’s total reported HCV sales.

During our third fiscal quarter, our blended royalty rates for MAVYRET encompasses our first three royalty tiers of 10%, 12% and 14%. I will remind everyone that our royalties, which are calculated separately from each product, are determined on the calendar year basis to a tier schedule rising royalty rates.

The royalty schedule restarted at our lowest royalty rate of 10% in our quarter ending March 31. This means that the quarter ending March 31 will be at the lowest royalty rate of 10%, and our royalties for the quarter ending December 31 will have the highest royalty rates in our fiscal year.

You can review our royalty tier schedule in our 2018 Form 10-K. Moving on to our expenses. For the three months ended June 30, 2019, research and development expenses totaled $34.5 million compared to $28.5 million for the same period in 2018.

The increase was primarily due to greater clinical costs associated with the progression of our wholly-owned clinical programs at RSV, NASH, PBC and HBV, including our three Phase 2 clinical trials. General and administrative expense for the quarter was $6.2 million, which was consistent with the comparable quarter in 2018.

Enanta recorded an income tax benefit of $0.9 million for the three months ended June 30, 2019 compared to income tax expense of $3.7 million for the same period in 2018. The income tax benefit for the quarter was driven by a federal tax benefit associated with foreign derived royalty income from our AbbVie collaboration agreement.

Enanta’s effective tax rate for the nine months ended June 30, 2019, was less than 1% to 2% compared to approximately 22% for the same period in 2018.

We expect our effective tax rate for fiscal 2019 to be approximately 1%, which reflects the impact of the foreign derived royalty income tax benefit, R&D tax credits, as well as tax benefits from stock award activity.

Net income for the three months ended June 30, 2019, was $7 million or $0.33 per diluted common share compared to net income of $20.3 million or $0.97 per diluted common share for the corresponding period in 2018.

Enanta ended the quarter with approximately $389 million in cash and marketable securities, an increase of approximately $64 million from our 2018 fiscal year-end balance of $325 million.

We expect that these cash resources as well as our continuing royalty revenue will be sufficient to meet our anticipated cash requirements for the foreseeable future. Further financial details are available in our press release and will be available on our Form 10-Q for the quarter when filed.

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

Operator?.

Yes, sir. [Operator Instructions] Our first question comes from the line of Brian Abrahams with RBC..

Hi. Thank you for taking my questions. I guess, first question on 938. It sounds like you’ve been able to do some additional analysis on the data from the positive challenge study.

I’m wondering if you have – were able to get any data with respect to resistance variance as well as the efficacy of the agent relative to when post infection it was given? And then I have a follow-up..

So, no, we don’t have data on resistance variance. We haven’t identified really any patients with them. So it’s challenging. I think one of the things to point out is 938 has an incredibly high barrier to resistance, and we’ve been given in laboratory settings where we’ve tried to force the conditions to allow it. We haven’t been able to really do that.

So we’ve not identified any patient with a breakthrough yet..

Okay, that’s really helpful. And then, you mentioned in addition to the community acquired study that’s about to start, down the line you’d be also looking at potential pediatric study.

And I was just curious what if any additional work would need to be done with respect to dose mapping, formulation, tocs, et cetera, before moving into the pediatric population and what might that study look like? And I’ll hop back in the queue. Thanks..

So there’s always preparatory work for ped studies. I mean, you obviously need to switch up your formulation. You need to do a lot of, basically DMPK work, modeling. You need to – basically a lot of it really results from modeling.

The bioequivalence doses that you look at in adults, you’ve got to translate into children and it’s going to depend on what age group the children are in too because some of them have still developing metabolic hardware, if you will. So there’s still a few extra studies that you want to try to understand in advance to that.

So all that will be going on in parallel with our adult studies, which from a timing perspective is what we want to do anyway. We do want to get as much information as we can in adult population before we go into repeat study. So we can go into it most intelligently. So yes, I think that’s where we’re at..

Your next question comes from the line of Yasmeen Rahimi with Roth Capital Partners..

Hi, team. Thank you for the update. Two questions for you. Question one is on RSV and question two is on NASH. So can you comment on sort of what led to your tremendous success in challenge study? Your infection rate was one of the highest.

And then second that leads into what elements of the Phase 2b challenge study require really thoughtfulness and how do you plan tackling it? And then I have a follow up on NASH..

Well, we did have a very high rate of infection in the study. I mean, that always helps that number one just because you can get more data on more patients more quickly.

I think what – the lesson learned and I think it’s probably intuitive from even before we did this study that, in translation to Phase 2b, we need to identify what is the allowable dosing window. And we’re going to have to be very thoughtful about how we approach that.

Just basically really trying to understand for this virus and for this mechanism against this virus, what is the acceptable dosing window? So we’ll look at that over a time window, breaking it down into parts so that we understand what the limits are. Hopefully the broader the window, this identify the better.

For example, with flu, you really have like a 48 hour window in which you have to identify the patients and get drug on board. So, will it be flu like? Will it be a more forgiving than flu? We don’t know that.

No one knows the answer to this question other than intuitively, the earlier that you treat, the better, the likelihood of more impactful outcomes. So, it’s really every step of the way that from our Phase 2b studies that we’re going to be looking at, we’re going to be thinking about – looking at optimizing that dosing window, opportunity.

And we’ll learn more about the drug as we go in terms of what that allowable window is for this mechanism but against this virus.

Is that helpful?.

Yes. Thank you, Jay. And then the question on NASH is, I mean, we’re very eagerly awaiting the ARGON-1 data, but then you continuously remind us that you are going to advance a follow-on FXR clinical candidate, which sort of puts fear in investors, which makes one conclude that maybe EDP-305 optimize and therefore there’s a need for a follow-on.

So can you explain to me, while we’re waiting for the data, why there is such a need for a 2.0 version?.

So again, just to back up a little bit. We don’t work on any program without having follow-on molecule, some backups. Everything we do is done. It’s very common in small molecule drug discovery, a page right out of the – the sort of standard playbook. So there’s nothing mysterious about this program or any of our other programs.

We do this as a matter of course on everything we do. You may remember, in the hep C per use days, we had lots of molecules, thousands of them. We picked pibrentasvir as the first candidate to move forward. But that was going along in clinical trials. You just have a lot of – what should I say, just quiet periods where you’re waiting for data.

In the meantime, it’s just prudent to have ever continuing activities in a mechanism that you feel strongly about just pipeline management and it also affords the opportunity that, even if you have a good molecule at the outset, you may still be able to come up with an even better one. So that’s a worthy ambition to have.

And it’s just prudent practice and it’s just the way an answer to that business, which isn’t quite honestly that different than many other companies that do hardcore small molecule drug discovery and development. So all that said, we look forward to ARGON-1 data at the end of this quarter. We have been working on our follow-on program now for a while.

We’ve been just patiently going through also potential molecules and looking for within the contenders as a follow on. Just basically, we have the beauty contest sort of wrapping up. And we always say, it’s safe to assume that no matter what we do, we’re thinking about optimizing potency, like activity, safety, anything that we can try to tweak. We do.

And so stay tuned on that front, but I think that we’ve made some very good progress on that program. And then we’ll have more to say later in the year..

Thank you, Jay.

And are you able to comment at least what the follow on chemistry? It’s different versus 305 at this point?.

Yes. We’ll roll out a lot of data at the appropriate time. But again, this will make the assumption that is – it’s all about efficacy and safety and DMPK consideration and other kinds of things via distribution. There’s lots of things you can study here. That really focused on what you would look for in a follow on molecule.

So anyway, that’s what I can say right now. We’ll have a lot more to say later in the year..

Thank you. Thanks for taking my question..

Your next question comes from the line of Akash Tewari with Wolfe Research..

Hi, this is [indiscernible] on for Akash. Thank you for taking my question.

The first question is what’s the cost of the potential phase should be for NASH? And my follow-up question will be, what are your expecting on ALT/AST reduction, LDL increase MRI, PDFF and pruritus rate at week 12 for your compound EDP-305?.

Yes. So if I had all the data, I would talk about it. But let me answer your first question first. So the cost of the piece to be, we’re still in the process of mapping out the protocol, what that looks like in terms of powering patient numbers, duration, et cetera, et cetera.

So until we really finalized all of those inputs, it’s hard for me to give you dollar projection on that. But it wouldn’t be dissimilar from what other people’s similarly structured pays to these. Number two with regards to all of the readouts from our trial. Again, there are a lot of things that we’re looking at in this trial.

And we’ll look at ALT, of course, we’ll look at before FGF19. We have MRI, PDFF as we looked at MRI, PDFF predominantly as an inclusion criteria, because we wanted to since we were bringing patients into the study phenotypically, rather than necessarily having a biopsy proven NASH. We wanted to make sure that the patients were steatotic.

So we just did baseline MRI, PDFF and of course we’ll get that on subjects that at the end of study as well. So we’ll have that kind of data. And so on other biochemical markers, we’ll have elastography, et cetera.

But the punchline is, now what do you want to get from a study like this? This is a 12-week study over mind, you and others that this is a 12-week non-biopsy study that’s aiming to do a few things. We need to learn what is the safety profile in NASH patients? Now we want to confirm activity with our drug in NASH patients.

And also importantly, we want to affirm what our dose selection is for a Phase 2b. So from this we’re going to get directionality from a number of different readouts among the ones that you just mentioned. But for FXRs that work for 12-week endpoint, it’s just not a ton of comparable data out there.

Even for ALT on the 12-week time point, you can think FLINT had – you’re looking at placebo corrected percent change from baseline. On ALT, FLINT had about 20% reduction. And Intercept’s Phase 3 study regenerate had about 15% to 18% reduction.

And really the only other comparison out there on 12-week is, Novartis’s molecule, that’s advancing had about 6% to 9% reduction. That’s the sum total of a 12-week ALT data that you can look at. You look for 12-week MRI PDFF data, you find even less.

I think Novartis was around 6% to 7% depending upon the dose, and Gilead was around 8% to 15% depending upon the dose. So as I mentioned many times before, MRI and PDFF is not predominant, probably for an FXR, that’s not the calling part necessarily at the mechanism, particularly at a 12-week time point.

So people just need to think about it in the context of what other people have seen in 12-week studies. We’re going to look at that. Again, main goal here is to look at the number of different readouts that show proper safety, good target engagement and confirmation of what our Phase 2b dose should be progressing at the next step.

So when we have data, we’ll share it. And as we said in the prepared remarks, and what we’ve said for many quarters now is we expect to have that at the end of this quarter..

Thank you very much..

Your next question comes from the line Jay Olson with Oppenheimer..

Congrats on the progress and thank you for taking my question. I just wanted to follow-up on EDP-305. There was a recent NASH Phase1 2 study that read out in our competitors study, and it missed a primary endpoint of MRI PDFF. But it didn’t hit on important secondary endpoints like ALT reduction.

And you touched on this a little bit, but I was wondering if that study had any impact on your plans for EDP-305 and the designing of Phase 2b study that you plan to initiate in the third quarter, especially with regards to use of MRI PDFF as an end point?.

Yes. I mean, we – again, I think you’re referring to a PPAR mechanism, Alpha Delta. We – they set status for primary, they didn’t see that activity. They did see, I think, they had some ALT reductions from their study. But as I just mentioned, fast reduction isn’t necessarily especially in short time periods, it’s not the hallmark of an FXR.

So we’re going to be looking our next study is going to be histology endpoint study along the lines of, say for example, what a flint type study was. So we would be very cognizant of what’s everybody else is doing, particularly focusing on efficacy that remain for the mechanism that you’re studying in this case FXR..

Okay. Great. Thanks for that color.

And then I was wondering if you could provide any comments from the rationale behind your decision to partner EDP-305 prior to initiating Phase 3?.

Yes. We’ve spoken about that a little bit in the past. Again, I think that we’ve got a lot of things going on in the NASH. We’ve got NASH, we’ve got FB, we’ve got RSV. If I line all those up at one end of the spectrum, NASH is going to be likely in the end, it is going to be a combination therapy. The Phase 3 are going to be big and expensive and global.

And importantly, the commercial enterprise that takes on this new field, this new indication to the marketplace, I think needs to require a certain degree of sophistication and strength. And this is where we’ve seen it before, I mean, I would put the same thing, If we were looking at AbbVie today, ourselves again, we’re similarly situated.

There’s no question that having an AbbVie alongside us when they ran 12 or 15 Phase 3s and that’s suggesting what we would be involved here but that would be huge Phase 3 program, it was global. It required sophisticated commercial launch strategy.

There’s no way that, I think, a smaller company like Enanta could maximize the asset like we could if we’re teamed up with somebody who was powerful at that late stage. And not the least to it’s a very expensive undertaking. We know that in the c case. So I think we would aim to do that with the other part of this, there’s strategic partnering too.

Because as I mentioned, there’s combination therapy likelihood here.

And if you’re thinking to the future about where the wind could ultimately be perhaps with other combination ingredients that we don’t have today, you could team up in a way that we have strategic value by partner A bringing one asset, partner B bringing another asset and going after that way.

So, I think you just increase your overall chances of success in this indication from many different perspectives. I guess that could always change, but for now, we’ve been – that’s why we’ve been thinking and the way we’ve been thinking about it for a number of quarters.

I would contrast that with RSV, where we’re hopeful that given our mechanism, given the fact that we’ve got a super high barrier to resistance, we may not need to combine it with other anti-virals from an efficacy perspective or to prevent resistance.

We may be able to proceed with a single agent into a little bit more of a defined area of RSV infection, something that’s very easily and readily diagnosed, and an area, where practitioners, who have been looking forever for a successful RSV therapeutic, I think it would be an easy one for us to get a message out and ultimately, to have the opportunity to push forward with that one all the way ourselves.

So, we don’t anticipate sort of a big global type of partnership on RSV like we might, well contemplate on NASH Program..

All right. That’s super helpful. Thank you so much for all the color..

You’re welcome..

Your next question comes from the line of Eric Joseph with JPMorgan..

Hi, this is [indiscernible] for Eric. Thanks for taking the question. Just one on EDP-514 and thinking about the Phase 1b and potential viral load reduction.

I’m curious what we viewed as clinically differentiated to some of the other novel core inhibitors or rather one parameters would you look to establish differentiation to the other core inhibitors in development and what would you be – and what would be viewed as meaningful advantage on that front? Thank you..

A little hard to hear you.

Basically what – just juncture, what we’ve done, we’ve created a molecule, EDP-514 that’s as far as we could tell has one of the best preclinical profiles of any core inhibitor that’s been reported, now looking at the totality of the in vitro data that we’ve generated and the in vivo data that we’ve done in some very, very challenging animal models.

So, I think the preclinical profile, it looks good. We’ve also done a lot of work on DMPK. And so the molecule EDP-514 swings to go into the clinic.

Phase – the early studies were going to be really looking at safe DMPK confirmation and healthies that we’ve got just like we’ve had with many other candidates, where we’ve designed the molecules, hopefully well, taking them into Phase 1.

Hopefully, we’ll have a nice safety profile that will give very good exposures after acuity administration; none will rapidly be going into the 1b portion of this study part two. And looking at viral activity of the molecule, especially, once we get into the treatment naive patients by remix patients that will be the other Phase 1b.

So, we’ve got two Phase 1b’s coming up to start next year. The first 1b study, which will be in nuke-suppressed is assuming Phase 1b and healthies finishes when we expect it to. We would roll right into the nuke-suppressed on 1b. and then that would be in the first quarter of 2020 calendar quarter.

And then we would aim to get into the viremic patients sometime in the first half. So, stay tuned on that finetuning of that timing. The goal is really to get the molecule as quickly as possible into a variety of HPV patients and to start to confirm and in fact that patients be very good results that we’ve seen preclinically..

Got it. Thanks.

Sorry if – is this line better now?.

Yes. Sounds a little better..

Okay. Yes. No, sorry. I was asking specifically in thinking about the viral load reduction in the Phase 1b, what would be viewed as clinically differentiated to some of the other novel core inhibitors that are currently in development? Thanks..

Yes. Again, I’m – I think we’ll have to wait. Why don’t we pause on that one until we see more data at AASLD? I think, right now, we’ve only seen a minimal amount of data in terms of what cores can do in that environment. And I think we’ll have a more complete data set from a larger group of potential competitors after AASLD in November.

So, I think we’re still – it’s very early days to see, with that log drop is – and it’s not just the log drop of course, that’s a – that’s one piece along the road, you’re really looking into other pieces of information, in terms of getting into functional cures.

So I mean, core inhibitor is even with a poor core inhibitor, some of the earliest ones that went into the clinic showed some significant, viral load reductions. But that’s obviously necessary, but not sufficient.

And so I would expect based on the high potency of EDP-514 that we would see a very good draw, but more importantly, it’s going to be, how does it perform in combination with the new and how do you get to a functional cure. right now, we have no reason to think that, EDP-514 is less than any other compound from a potential perspective out there.

We just need to generate that data..

Great. Thank you. Sorry about the line..

Your next question comes from the line of Liisa Bayko with the JMP Securities..

Hi, Jon, on for Lisa. Thanks for taking the questions and for the updates.

just the quick one on NASH, Jay, when you’re mentioning AASLD, I’m wondering it’s the goal to have the NASH data late this core and then hopefully have some additional presentation at AASLD will have timing workout do you think?.

Yes, I’d say that would be beyond – probably beyond likely – but who knows, I can’t commit to say on that. What’s a – okay, well let’s get to the data first and then we’ll roll out a top-line data first. And then we’ll look to ultimately get it into as soon as reasonable conference that we can get into..

Okay. And then just one last one on RSV came in as of the size and design of the phase 2b you’re expecting to kick off here. Thanks..

No. The outpatient study of the size, so protocols being put together sort of as we speak. So, we’ll be discussing that soon enough, but we don’t have the final ends “worked out” looking at powering and other considerations. I don’t want to put a number out until the team’s had a chance to finalize the protocols..

Your next question comes from the line of Patrick Trucchio with Berenberg Capital..

Hi, good afternoon. I have a follow-up on EDP-938 and also on EDP-305. just first on EDP-938, Jay, you alluded earlier to determining acceptable dosing window for EDP-938 for RSV. And we know with the influence of drugs this windows within 48 hours, that’s the best case we can get with these drugs.

So, I’m wondering if with RSV, assuming the results of this acceptable dosing window in the phase 2b study, is there a definitive way to understand whether or not a patient is actually in that optimal dosing window or is it more based on how long the patient’s demonstrated RSV symptoms with that being perhaps just a key part of the inclusion criteria?.

I think it’s the ladder. Yes. We’ll be looking at time from symptoms. And we’ll be able to analyze the data based on that. So, yes, I think it’s a – it’s the ladder..

And then in ARGON-1, specifically on safety and tolerability of EDP-305 in this study, can you tell us what we should anticipate in terms of impact on LDL-C and pruritus at each dose compared to placebo? If this data will be included in the data release, that’s expected at the end of the third quarter, or if it would be provided a later date.

And then finally, what would you want to see demonstrated by this data or other data to give you confidence that EDP-305 has best-in-class safety and tolerability attributes?.

So, literally, lipid data will be included in this analysis. And again, I think as I was sort of saying before with all the efficacy parameters, I think we’ll be looking at the safety parameters in the same way, getting the gestalt at what our doses do. And what that sort of “therapeutic window”, defined as for a go-forward dose.

So, it’s just going to – it’ll be data that we’ll put into context, just like all the efficacy parameters, but we should have that included in the data set at the end of the quarter..

That’s helpful. Thank you very much..

You’re welcome..

It looks no further questions. I’d like to turn the call back over to Carol Miceli for any closing comments..

Thank you everyone for joining us. If you have any additional questions, feel free to give us a call back in the office. Thank you..

Okay. Ladies and gentlemen, this concludes today’s conference call. You may now disconnect..