Good afternoon. And welcome to Enanta Pharmaceuticals Fiscal Third Quarter 2021 Financial Results Conference Call. At this time, all participants are in 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 Viera, Investor Relations. Please go ahead.

Thank you, Operator, and thanks to everyone for joining us this afternoon. The news release with our fiscal third quarter financial results was issued this afternoon and is available on our website. On the call today is Dr. Jay Luly, President and Chief Executive Officer; 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 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. 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. With that, I’d now like to turn the call over to Dr. Jay Luly. Jay?

Thank you, Jennifer, and good afternoon, everyone. Our fiscal third quarter was marked by the achievement of several important milestones and continued progress across our clinical portfolio. Starting with COVID-19, we are pleased to announce that we have identified a clinical development candidate EDP-235, an oral protease inhibitor specifically designed to treat SARS-CoV-2 infection and potentially other coronavirus infections. We are eager to progress this program into the clinic and are on track to initiate a Phase 1 study of EDP-235 early next year. In hepatitis B, we are excited by the progress we’ve made with EDP-514 and EDP-721, which we are developing as part of an all-oral combination regimen to achieve a functional cure. We expect to begin dosing in our Phase 1 study of EDP-721, a novel oral HBV RNA destabilizer, this month. Additionally, this quarter, we announced positive Phase 1b 28-day data for our core inhibitor EDP-514 in two important patient populations, chronic HBV patients who have a high viral load, whom we refer to as viremic patients, and chronic HBV patients who are on a treatment with a nucleoside reverse transcriptase inhibitor, whom we referred to as NUC-suppressed patients. The significant progress we’ve made across our HBV program brings us closer to our goal of developing an all-oral functional cure for patients. Moving to the rest of our pipeline, we have three ongoing Phase 2 clinical studies investigating 938 for respiratory syncytial virus or RSV and two ongoing clinical studies for candidates to treat nonalcoholic steatohepatitis or NASH. In addition to our clinical programs, we continued to progress our respiratory virus discovery initiatives to identify an L inhibitor for RSV and an inhibitor for human metapneumovirus or HMPV. With that, I’d like to dive deeper into each of the programs that make up our robust pipeline,…

Thank you, Jay. I’d like to remind everyone that Enanta reports on a September 30th fiscal year schedule. Today, we are reporting results for our third quarter ended June 30, 2021. For the quarter, total revenue was $21.6 million and consisted of royalty revenue earned on AbbVie’s global MAVYRET net product sales. This compares to total revenue of $18.7 million for the same period in 2020. The increase in royalty revenue compared to the same period last year was driven by higher HCV product sales as treated patient volumes have increased compared to the third quarter of last year when the COVID-19 pandemic began. HCV product sales continue to remain below pre-COVID levels as a residual impact from the pandemic continues. Royalty revenue was calculated on 15% of MAVYRET sales at a royalty rate for the quarter of 10%, after adjustments for certain contractual discounts, rebates and set-offs, which are now approximately 2% of AbbVie’s total reported HCV product sales. You can review our royalty tier schedule in our 2020 Form 10-K. Moving on to our expenses, for the three months ended June 30, 2021, research and development expenses totaled $47 million, compared to $34.7 million for the same period in 2020. The increase was primarily due to the timing of our clinical trials year-over-year. General and administrative expense for the quarter was $8.4 million, compared to $6.8 million for the same period in 2020. The increase was due to an increase in headcount and compensation expense. Enanta recorded an income tax benefit of $9.4 million for the three months ended June 30, 2021, compared to an income tax benefit of $7.1 million for the same period of 2020. These income tax benefits were due to the provisions of the CARES Act of 2020, which enables the company through fiscal 2021 to carry back its projected current year tax loss to offset taxable income in prior years. Net loss for the three months ended June 30, 2021, was $24 million or a loss of $1.19 per diluted common share, compared to a net loss of $14.3 million or a loss of $0.71 per diluted common share for the corresponding period of 2020. Enanta ended the quarter with approximately $373 million in cash and marketable securities. We expect that our current cash, cash equivalents and short-term and long-term marketable cash and marketable securities, as well as our ongoing royalty revenue will continue to be sufficient to meet the anticipated cash requirements of our existing business and development programs for at least the next two years. Further financial details are available in our press release and will be available in our quarterly report on Form 10-K when filed. I’d now like to turn the call back to the operator and open up the lines for questions. Operator?

[Operator Instructions] Your first question will come from Brian Skorney with Baird. Please proceed.

Hey. Good afternoon, guys. Thanks so much for taking the question. So I really want to talk about EDP-938 and I was wondering if you could kind of give us some compare and contrast on the potency of the protease inhibitor with remdesivir and maybe Pfizer’s PI. And can you do effective serial passage studies with SARS-CoV-2 models and can you comment at all on what sort of resistance you can induce? And then just on the safety front, what sort of room do you have on selectivity index before you start hitting some of the human proteases and seeing cytotoxin? That’s it.

Hi Brian. This is Jay. So I think you meant EDP-235 not EDP-938.

Oh! Sorry. Yeah.

So, anyway, EDP-235, the SARS-CoV-2 protease inhibitor that we announced today, serial passage, I mean, we don’t have the live SARS-CoV-2 virus in-house. So we rely on external providers for some of those kinds of studies. But we do do extensive worth looking in resistance in-house but we use model coronas for that work. And so to that end, the profile that we’ve generated so far internally, it’s very, very nice, and so we’re excited by not only that net attribute, but obviously also the potency that we have there. I think when you look at a candidate, which way we look at a candidate versus others that are out there, just even where we put the mark on the map for what we’re trying to hit, we obviously want to drill down on potency and look at that in lots of different ways. We’ve reported good data in primary human airway epithelial cells, which is a great way to look. We also look at activity against variants and we’re pleased with the profile that we’ve seen there, talked about the serial passages that we’ve done. And then getting on to safety, I think, we’ve -- we look we do sort of extensive safety work prior to taking any of our candidates that we feel very comfortable with the safety package that we’ve put together for this candidate. So I - given the potency and the wide windows, we don’t expect any sort of complications going into our clinical studies with this molecule. But looking beyond that, these are sort of the meat and potato things that we pushed it and looked at even further. As you know, we’re always looking at tissue targeting and social distribution, whether it’s with our FXR, whether it’s with or hepatitis drugs. And SARS-CoV-2 exceptionally, we saw very good tissue distribution and looked at lung levels in rodents, very pleased with that profile. And also having surveyed PK across multiple different species, we feel pretty confident that this is a QD dosing drug. So it’s really the aggregate of all these things put together, you can put a punch those together and check nine of the 10, but we weren’t done until we checked every box we were aiming to do in this candidate. I think the other sort of exciting aspect of this is we have, seeing activity against other coronaviruses with this as well. So there’s the possibility that we could go beyond SARS-CoV-2 here and think about readiness for other pandemic viruses or the coronaviruses. So, all in, it’s a very exciting candidate, and as we’ve mentioned, we’re on track to initiate clinical studies early next year.

Great. Thanks for taking my question Jay.

You’re welcome.

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

Hi. Good evening. This is Swapnil on for Yas. A couple of questions, first is for 721, should we expect to see the 800-milligram cohort data at ASLD and then based upon your internal PKPD modeling work, how much additional HBV DNA knockdown benefit do you expect to see over the reported 200- milligram and 400-milligram doses?

Yeah. I think you’ve got a compound number mixed up too. I think you said EDP-721 and I think you were referring to EDP-514, the...

Yeah. Yeah. That’ right. Sorry. Yeah.

Yeah. No. We have -- I know we have a lot of molecules to keep track of it. So the -- with regards to 514, the 200- milligram and 400-milligram doses, whether we were looking in NUC-suppressed patients or viremic patients, both of them showed a very good performance, not only in terms of safety and PK, which is one of the main things we were looking for, but also in the case of the NUC-suppressed, you can only want to make sure that our molecule behaved well with a NUC, right, because we wanted to set the foundation of a two-drug combo on which to add the other molecule you mentioned 721 to make an all-oral triple. So I think we got -- based on the virology that we saw at the 200 milligrams and 400 milligrams, when you look at DNA or RNA, whether you look at one-third population or the other, we saw good safety and good virology as we would have expected in each of these different patient populations and it definitely sets the stage for moving ahead. I think the 800 milligrams, what will we see there on top of that? We saw such significant exposure at 200 milligrams and 400 milligrams and it’s not clear that any more exposure will give you any more benefit. But of course, we’ll pull that data in and see it, and we’ll put it out at whatever the next appropriate sort of major scientific conferences to do that at. So stay tuned on that front. But, again, I think, we’ve seen what we need to see already to know that 514 has a great antiviral effect a great safety and tolerability profile to assume to date in HBV patients up to 28 days and a good two-drug foundation with the late to set the stage for a triple with EDP-721.

Okay. Great. I had one follow-up question, so for 235, what gating factors are remaining, where are you guys in terms of regulatory pathway before you initiate the Phase 1 trial in 2022?

Yeah. I’d say that, I mean, all the IND-enabling studies are done. So we’re packaging that sort of stuff at. We’re procuring drug supply. We’re doing all those kinds of things in terms of readiness as we prepare for the Phase 1 study, but it’s just sort of routine stuff at this point.

Great. Thanks for taking the question.

Your next question will come from Brian Abrahams with RBC Capital Markets. Please proceed.

Hey, guys. Congrats on the progress. Thanks for taking my question and my congratulations and best of luck to Dr. Adda’s retirement. First question on 235, maybe a bigger picture question, I was wondering if you could maybe talk about how you’re thinking about next steps here, Phase 1 and beyond for the program, what you think the clinical path might look like? And is this something where you might expect a PI alone to be adequate or do you think this could be more akin to HIV or hep C, where you would want to combine this with other classes of direct-acting antivirals like NUCs?

Yeah. It’s a good question, Brian. We -- the answer is nobody really knows, but that said, we’re talking about an acute infection here. So I think we’re pretty encouraged that a single agent could be enough. Now, obviously, when we set up this program at the beginning of the pandemic, we didn’t work just on this mechanism. But we have been and continue to be working on other mechanisms just because you never know what could happen here down the road with regards to variants or anything else. But from what we see, I think, we would be very encouraged to take a produce and see an impact on, hopefully, viral aids and sometimes very quickly with these mechanism sort of or sort of trying through DAA mechanisms and we certainly don’t know yet that we would need to go in with combination therapy as you might expect to do in hepatitis C or certainly in hepatitis B. So, as you know, with RSV we’re looking at short-term treatment with our RSV drug as a moderate agent. But again, for that program, just like with SARS-CoV-2, we’re going to take multiple approaches just because at the end, if we can come up with an even better approach on the line, that would be great if combinations as needed down the line. We want to be in the position to have potentially multiple quality assets and that’s why we continue exploring an RSV now in multiple Phase 3 studies with a very promising agent. Can it help us, for example, get into different patient populations that we might not otherwise be able to get into, but it allow us to treat more severe patients or broaden the treatment window, these are all questions that we can ask in due course.…

Yeah. No. That’s really helpful, Jay. Thanks. And then maybe one more on 938, I know you’ve been continuing to expand and mobilize your sites. I am curious to what degree you’ve been able to take advantage of the recent off-cycle RSV spikes? Is there -- I guess, how much consistency is there regionally with where these spikes are and where your trial sites are and is there any -- are there any changes in the way you might screen or even monitor patients in an off-season RSV surge versus the normal seasonal uptick? Thanks.

Yeah. We’re pretty spread out geographically in the U.S. and globally. You are correct and I saw your note earlier this week that and we’ve been pointing it out, too, that first starting in the Southern Hemisphere, once summer rolled around in the summer. While we were in winter, it was becoming summer in the Southern Hemisphere and the masks started to drop a little bit in Australia and they saw that this huge pediatric spike, interseasonal spike. And then we were quietly thinking, well, that could all happen here, and guess what, it did start to happen, a few weeks ago, the CDC said there has been this big uptick on interseasonal RSV in some spot. It’s been in certain Southern parts of the United States where these things sort of pop up. So we’ve got sites all over the place and so we have seen some upticks and that’s why we are cautiously optimistic that if trends continue and we go into the winter season here, that we should be able to wrap up the RSVP study this season, and if that’s the case, then we would have data in the first half of next year. But what I think we really need to see is are these little interseasonal spikes is going to tamp down? Are they going to tamp down and then come roaring back in the fall, and, again in the one month, two months when RSV is normally prevalent. I mean is every expectation that -- and you start to hear about it on the news, the other -- yet another respiratory virus that people should have on their minds, though, we don’t have enough to think about with COVID. But we’re starting to hear more and more that awareness for RSV is coming back. The testing is coming back. The CDC has recommended that just because somebody has something. Don’t assume that they have SARS. And if they’re SARS-CoV-2 negative, get tested for RSV anyway. So this is the way we’re going to start to figure out where these real patterns are. But we’ve got our catches met on and we’ve got lots of sites around, and so as patients come in, we’ll be ready to grab them.

Great. Thanks again.

You’re welcome.

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

Hi. Great. Thanks for taking the question. Had a couple on 235, I guess, so the structure of Pfizer’s lead oral inhibitors out there. I am just curious if you guys did any side-by-side comparisons in view of potential differences between assays and if you have a side-by-side comparison of the potency? And then can you tell us if 235 is covalent, is it reversible and a follow-up.

Yeah. No. I know exactly the kinds of questions you’re asking. It’s not the kind of questions I usually answer until we’re ready to answer them. But it’s fair to assume that we do extensive benchmarking across all kinds of parameters with every molecule that we can lay our hands on. And we’ve done that with 235.

Okay. And then kind of along the same lines, are you going to present or publish either preclinical or chemical data before the Phase 1 results or are the Phase 1 result is going to be the first we’re going to see data?

So there might be -- we’ll see -- you’re talking about putting up preclinical data of some sort?

Right. As opposed to paper, right?

Yeah. Yeah. We’re working on that strategy internally. I think on the one hand, it’s deciding to put these kinds of bits of information out in various public for a. But we’re really focused on mobilizing and pushing ahead to get ourselves into the clinic and then ultimately get into clinical -- later-stage clinical studies as fast as we can, so that the data will come out in due course.

Okay. Got it. And I had a few on 721, looking at the clinicaltrials.gov record, I see the one site in New Zealand, I guess that there are going to be additional sites added. And I didn’t see any breakdown of the number of patients in the viremic and the NUC -suppressed groups. Can you give us a sense of what that target breakdown is, if there is one and then I have a few more questions?

Yeah. So right now we’re -- as we sort of had in our prepared remarks and the release, the 721 study has been initiated. We’re screening now. We’re expecting to dose this month. So let us do the study and we’ll report more details on our clinical trial design on how we’re going to put this triple combo together, et cetera, et cetera. We’ll have more details on that at a later time.

Okay. Fair enough. You probably won’t answer my other questions either, but I didn’t see you have the combo with 514 in the trial design, so that’s exciting. Sorry, I guess, I’ll ask…

Yeah.

… one last question on a different topic, so NASH not the current programs, but you guys have talked about a novel mechanism for some time. I am just curious when you might disclose the target or the pathway, just any news there? Thanks.

Yeah. So we obviously haven’t prepared to disclose that target and program this quarter. But I think it’s fair to say we’ve just got a lot in NASH all coming together here in the next little bit. And I think this quarter we will be really interesting for us as we’re pulling in our internal interim read on ARGON-2. We’ll have Phase 1 data on our other FXR agonist, EDP-721. With the ARGON-2 IA, our hope is to figure out what are the appropriate doses that we can peel off then and entertain a combination studies with perhaps in the context of a partnership, et cetera, et cetera. So suffice it to say, we’re thinking about this quarter in NASH and a big picture sort of way. Even if we were thinking of ultimately teaming up in some sort of a partnership, would we do that even with our earlier stage program? These are questions that we haven’t completely sorted out, but we’re thinking through right now. But with regards to your very specific question about what is the target, we’re not [Technical Difficulty]

Talk a little bit about as we prepare for RSVP, what specifically we should be looking for in the data to -- and to make an assessment?

Sure. Maybe I’ll pull this question over to Nathalie to comment on further. But maybe I’ll just go and preface it by saying, you recall our human challenge study where human volunteers were infected with the virus, you wait around, you constantly monitor their viral loads and once the viral load puts a certain threshold, you began dosing and when the people begin to receive drug, they were also symptomatic with at least a symptom of sorts. And what we saw was, number one, a very nice set of viral kinetics as one of the key things we were looking for in that study. Very different than placebo, as soon as we started dosing drug, the course of the infection completely changed. People with placebo continued to get worse and people on drug got better. That was -- you could look at that in the form of viral loads. You could look at it in parallel with the same time course with people’s symptoms. I think in the outpatient setting, we’re not able to get the same frequency of viral loads. I think we were doing -- when they’re in the challenge study, you’re able to take swabs twice a day. I think we were doing over the course of the whole study. That’s just not feasible in an outpatient study. So but it’s not to say that we won’t get any virology, but what we are tracking is at least symptoms. Some have sometimes, some we’ll have virology, as I said of readouts. But, Nathalie, do you want to comment any further?

Sure. Hi, Liisa [ph]. Thank you for your question. So let me just add to what Jay was saying. I think there’s -- I would make a few additions to that. Obviously, we want to confirm the selected dose, the 800 milligrams that was assessed in the challenge study. There were 600 milligrams, but through this year, we had to increase it. So I think it’s going to be important to at least have a good assessment and confirm that our selected dose is the one for the patient savings. That’s one thing. And we’ll confirm then to important primary endpoint, which is the status quo. We want, obviously, to get out of that study, understanding that the translation from the challenge study in a more, I would say, artificial savings is confirmed in an outpatient saving and we want to show that as you treat patients within a very short window, that we can allow the patient to not progress to a more severe disease and they will be translating into more symptom, this is where it’s going to be for to look at our primary endpoints. We have well-powered dose study to be able to do that without. We believe that the effect size was assessed for the four of the study is appropriate and then we benchmark that to the challenge study, but we were very conservative when we -- for our RSVP study. So I think we will be able to confirm the translation on the challenge to the allocation state.

Okay. Great. And then, Jay, if you could talk a little bit about kind of your different, I guess, potential path we could take with the NASH program and what you’re looking from the data kind of go down those different paths? What -- maybe you can summarize how you’re thinking about it ahead of data coming out? Thanks.

Yeah. Well, I -- we’ve always -- for years now, I think, actually, we’ve said that with regards to NASH, we don’t aspire to be a commercial stage NASH company. We don’t aspire to be a Phase 3 NASH company. Instead we want to do Phase 2 work, get appropriate Phase 2 data point and then team up with another party. And so I think that’s really how we’re thinking about it, the focus on that, I think ultimately, FX in the right doses can still make a big impact, I think, in the form of combinations. And so we’ll be -- again, that’s why the IA that we’re going to be getting here soon is really appropriate. You recall from our ARGON-1 study, we looked at 1 milligram and 2.5 milligrams. We saw unacceptable pruritus at 2.5 milligrams. It’s sort of like an intercept, now looked at 10 milligrams and 25 milligrams, right? We looked at 1 milligrams and 2.5 milligrams. And so ARGON-2 now is, as you know, and I know we’ve had discussions on this in the past, ARGON-2 has gone down between those two doses. Just to see is there another dose other than the 1 milligram where we did see significant target engagement. So even at one milligram, we saw it, but we felt like we could be leaving some efficacy on the table. So can we tweak it a little further, extract more efficacy without pushing pruritus button, whatever mysterious button that is and so that’s what we’ll get. We’re going to get that data. Again, we already know the 1 milligram. We know the 2.5 milligrams. We’re looking to be it in three nodes point and that will give us dosing information, again for which we can peel off and do seek certain combination possibilities. So and we would aim to do that in the context of a partnership. Again,

Okay. Great. Thank you.

You’re welcome.

[Operator Instructions] Your next question will come from Jay Olson with Oppenheimer. Please proceed.

Hi. This is Matt [ph] on for Jay. Thanks for taking our question. The first thing I wanted to ask was since HBV is a large global opportunity, what are your thoughts for a potential partnership there, especially ex-U.S.? And also since a potential partner would be likely to seek a role in clinical development, at what point would you consider potentially identifying a potential partner in HBV? Thanks.

Sure. Those are great questions. Well, since actually, we just talked about partnering and NASH, I’ve also spoken about partnering in HBV. And there is a little bit different than NASH and it’s -- and that in turn is a little bit different than our human respiratory program. But let’s talk about HBV and I’ll contrast it to HCV. When we did our HCV deal with Abbott, which became AbbVie several years ago, we had a protease inhibitor and they had other assets, but neither of us had the combination that we needed to put together to create the all-oral cure. This is a little different. We do have possibly anyway, we’re assembling the agents that we hope to be sufficient for an all-oral cure, right? We have mixes of standard-of-care. Everybody sort of gets a NUC for free. That our core inhibitor. We’ve now put out two good data sets on that, including the 2-drug combination with the NUC and now we’ve got 721 getting ready to be dosed here very soon, which will be the third part of that potential all-oral triple. So I think what we’re going to have is, is that enough and we’ll be doing the experiments, clinical trials that will help us sort out whether or not that is enough. We’re very excited by the possibility because if we do, it’s a highly differentiated product profile with an all-oral therapy. All-oral will always win out over a mixture of injectable and oral therapies, all things being equal. And so with the -- now with the advent of 721, which we announced just this year, we announced it in the context of a candidate and the short runway into the clinic and a punitive effect on S antigen reduction, we think we may have all…

Okay. Got it. Yeah. That’s awesome. Really helpful. Thank you. And then the last question we had was just on EDP-938 and so for the pediatrics and adult studies that you recently initiated. Just curious what you’re hoping to see in the data there also when we could expect to see data and kind of how you’re thinking about the market opportunities for each, that would be great? Thank you.

Yeah. Well, PEDs is the biggest, I’ll tell you that. The PEDs is a very large market. Transplant is a very important market also. I mean, these folks who are immune compromised, if they get an RSV infection, it can just be catastrophic and so it’s a really important other patient population. But PEDs is definitely a larger population. Now the transplant study, we just got going at the end of last year in the PED study, we just got going in March. And also, I’ll remind you too, in the PED study, the first part of it is really safety and PK and then the second part of it is when we’ll get into other aspects of the RSV infection. But so those things are necessarily tracking behind a study RSVP, which we already had ongoing and partially enrolled. So it’s a bit early for us to give any sense of timing on those two studies, are they going to be further out. I think this upcoming season will be very telling in each of them, allow us -- once we get this next season under our belts, I think, we’ll lever a much better idea where we stand.

Okay. Got it. That makes sense. Really helpful. Thanks again for taking my question.

You’re welcome.

Your next question will come from Zegbeh Jallah with ROTH Capital Markets. Please proceed.

Hi. Thanks for taking my question. Just had a quick one really about your COVID program, I was just wondering if you’re considering any unique treatment strategies in light of other drugs being approved or vaccines being approved, I know this is quite different as a treatment. But I was just wondering because Regeneron did also get their drug approved as a prophylactic after exposure. So I was just wondering if you’re thinking about anything unique in terms of when treatment will be delivered?

Yeah. Well, there’s -- treatment of any start would be a major milestone. But I do believe you could also consider prophylactic consistent study. So that’s among the things that we’re thinking about and chewing on. But straightforward treatment is clearly where the most urgent need is right now. So let’s assume that we’ll do that and it’s true here. I mean the antibodies, I think, that are out there played an important role, particularly early in the pandemic and prior to vaccines. Vaccines have kind of helped an enormous amount. It could obviously be helping even more. But I think, ultimately, the missing piece here and the piece that will be durable long-term are going to be the small molecule antiviral molecules, a direct-acting antiviral, of which, obviously, 235 is. And there will be multiple generations there to assume that people are going to be out there doing it. I mean when we were going into hep C, Enanta wasn’t the first protease inhibitor, but we were the best. So and even our first protease inhibitor, even though it was better than the prior ones that had been looked at, we came up with an even better one than that later on, which ultimately did become best in class with of glecaprevir. So I think 235 is a very strong entrant. We feel very good about it and we’ll let the data speak.

Thanks, Jay. And just a quick follow-up in terms of the dosing, what’s the dosing regimen or what are you hoping to achieve with that?

We think we can -- again, we’re -- we always aim for QD dosing. Once daily is always best and we pretty much always have hit that mark. Our preclinical studies suggest that that’s likely to be the case here. I mean we usually hit that mark in the clinic because we’re very good at modeling that pre-clinically across multiple different species. And so spent a lot of time sort of engineering that time sort of engineering that attribute as well and I think people who know this landscape know that it’s not necessarily given that you can achieve that. So, again, we’ll have to prove that in the clinic, but we feel very good about the kinetics that we’ve seen pre-clinically. And then beyond that, again, it’s an acute infection. We would expect normal people who have generally competent immune systems. We could do a short-term dosing, probably, it wouldn’t be unreasonable to assume it’s something like a five-day dosing regimen just like you do in RSV. But we’ll see, it could be -- it’s going to be short relatively speaking to some protracted dose enlargement.

Thanks, Jay. Looking forward for more about the program.

You’re welcome.

And at this time, there are no further questions. I would now like to turn the call back over to Jennifer Viera for closing remarks.

Thank you, everyone, for joining us today. If you have any additional questions, please feel free to contact us by email or call us in the office. Thanks and have a good night.

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