Good morning, and welcome to the 26th annual H.C. Wainwright global investment conference. My name is Ed Arce. I'm one of the senior biotech analysts here at H.C. Wainwright, and our next presenting company is Enanta Pharmaceuticals. Very pleased to have with us, representing the company, to my far right is Tara Kieffer, the Chief Product Strategy Officer, and to my immediate left, Jay Luly, the Chief Executive Officer. Welcome. Thank you. Thank you. Thanks for joining us. So maybe I'll start with just a question for perhaps those who are new to Enanta. If you could an overview of the company, your programs, in particular, the RSV, but also immunology. Sure. Well, thanks for the invitation. Before we begin, I want to remind you, I'll be making some forward-looking statements. For a summary of the risks associated with these statements, please see our filings on sec.gov and on our website. For those of you, maybe less acquainted with Enanta, we sort of have a heritage in working in viral infections, treatments for viral infections. And that really got going several years ago in the hepatitis C arena, where we had a certain amount of success working on hepatitis C protease inhibitors. We teamed up ultimately with AbbVie to help bring these forward in late-stage development, commercialization, and to global sales. So, you know, we're very pleased to have participated in two cures for hepatitis C going forward. The lead one is an eight-week cure called Mavyret. It's, you know, it's a commercial story. It's really AbbVie and Gilead that provide the world with cures for hepatitis C today. We continue to receive royalty revenue from that product, and which is, you know, helpful in defraying certain expenses. It is gratifying to have been a part of, you know, curing over a million chronic hep C patients worldwide. That said, we had many approaches in hep C that we eventually dialed back so that we could focus on other wholly owned pipeline. We mined other liver viruses, like hepatitis B. We ultimately wanted to spread out in virology and not be constrained to the liver, and that's when we became interested in the pulmonary compartment first with RSV. Sizing it up as a huge opportunity where there were at the time we got in, there were no vaccines even though people had been trying for vaccines in RSV for over 60 years. There were no therapeutics in RSV, and to this day there still aren't. We saw that as a sizable unmet need that we partook. The pandemic landed at our feet and presented another protease inhibitor opportunity, and so we've worked in SARS-CoV-2. We also worked in human metapneumovirus to some degree. After having mined liver viruses, respiratory viruses, we began to see fewer and fewer really big opportunities in virology, I think, and that became part of the rationale for a few years ago. Internally, we started to make a bit of a migration into a new area, new for us anyway, although some of us had worked in the field in the past, which is in immunology. We sowed the seeds. We got to announced our first entry. Well, we announced our entry into the field and our first program earlier this year. It's a targeted program going after KIT. The indication, at least one of the indications one could think about, is CSU. Our plan is to turn over another card in terms of immunology later this year. But, you know, before that, I would say the big focus now is in RSV. Finally, you know, after the pandemic sort of knocked RSV off its heels, I guess, in a good way, from a global health perspective, but there was very little RSV to be found for a lot of the pandemic. Same with flu, because people were masked up, and importantly, children were not in school. They were staying at home, and the spread just didn't occur, and it was really, really challenging to recruit RSV studies during the pandemic. But that began to change in earnest last fall, when RSV started to reestablish seasonality. There was a pretty robust season that allowed us to enroll the lion's share of our ped study, and we took that down to the Southern Hemisphere in late spring, and we finished it up over the summer down there. So that will be a study that we expect to report data in next quarter. We have another RSV study going on with that same molecule, which is zelicapavir. That's a high-risk adult study, and that is still enrolling in the Southern Hemisphere. It's a study that's about twice the size of our ped study, so will take a little bit longer, but we're hoping to wrap that up in this upcoming Northern Hemisphere season, so that's on the docket. I guess before any of that, and later this month, we expect to have results from our second RSV program in a human challenge study. Great. Thanks. So as investors think about the broader opportunity in RSV, I think it's probably an important question to get addressed upfront. Given the recent launch of RSV vaccines for prophylactics, how does this impact, if at all, your view of the market for treatments? So the prophylaxis approach is definitely part of the solution for RSV. We think that there's still room for treatment, and we've seen that in other respiratory viruses. If you look at the pandemic with COVID, certainly, you know, we were very lucky to have those vaccines come quickly with some of the best efficacy data, but drugs were definitely needed there with Paxlovid. Think about flu, you've got drugs, antiviral drugs there as well. So I think if you look at the different populations that are at high risk for RSV, you have adults older than 65, and there are two vaccines approved in that population. The challenge, I think, with those is going to be uptake. We know for the last Northern Hemisphere season, when they first launched, only about 10%-15% of the eligible population was vaccinated, and you know, hopefully that will increase, but I think, you know, best-case scenario, if you look at flu vaccines in that population, it's still only about 50%-60%, so there'll still be a good chunk of the population that is vulnerable, and even those patients or those people that do get vaccinated, you do see breakthrough. None of the vaccines are 100% efficacious. The pediatric population is a little bit different because those options for prophylaxis are not active vaccines, so they're providing passive immunity, and companies have gone one of two strategies. One is vaccinating the pregnant mother, and so the antibodies are then passed to the child, or just giving the antibody to the baby when they're born. So this doesn't provide any active immunity. It's, it's only, you know, helping the babies until those antibodies are no longer in the system, and so they will ultimately go on to get RSV. We know that it takes multiple infections of RSV for them to build up a robust immunity that you might see in a young, otherwise healthy adult population. So still a need for treatment there as well. The other thing that we are cognizant of with these antibody approaches is that one can see development of resistance. We've seen that obviously with in the COVID space, with the antibodies, but even in RSV, there's been cases where resistance can develop. And so, you know, that is something that is being monitored and, you know, would be important. In that situation, a treatment would be very valuable. Okay. And with your lead program, the mechanism there is also one that is shared by a couple in the broader treatment landscape. Maybe it's helpful to discuss what other competitors are out there right now. Yeah. So maybe I would compare and contrast. If you look at the universe of approaches and therapeutics, I would say there are two major approaches. Mm-hmm. One is to block viral entry. This is where the fusion inhibitor molecules, many of which have progressed in that mechanism, but not yet fully succeeded, right? So, Gilead had a fusion inhibitor very early on that looked to be, you know, one of the best fusion inhibitors, I think, that was ever really made, and it stumbled in phase two studies. J&J used to have a fusion inhibitor, and they wound down that whole program. There's one in phase three that phase three data in China that's sitting in the Chinese regulators for some time. And there's another fusion inhibitor that Pfizer has that they obtained from a small biotech. So those try to block viral entry, and, think of it as, well, they're targeting the fusion, the F protein. This is what the vaccines target. This is what the monoclonals target. It's similar, in SARS-CoV-2 parlance to looking at the spike protein, right? We decided early on that that was not the best approach for us to take in therapeutics because at the time a patient presents to a physician, with an RSV infection, there's active replication going on and huge amplification of the virus. This is why people become symptomatic, and we reasoned that the most important thing you could do is actually to shut down replication, rather than to try to block viral entry. But, a certain amount of viral entry has already occurred, and it's gonna be harder to stop the viral entry from this expanding, rapidly expanding universe of viral particles. So, instead, we go in and shut down replication, and this is replication inhibitors have been used in hep C, and hep B, and HIV, and all the classic viruses. And so, we felt RSV could profit from having replication. So our approach is only replication inhibitors. Our N inhibitor is a replication inhibitor, and our L inhibitor, the polymerase, also a replication inhibitor. So we're hoping, again, to bring forward good data sets with maybe a new approach that will hit this virus hard. It's a traditional approach on the one hand, but it hasn't been extensively mined in RSV simply because most people went after fusion inhibitors and tried to block viral entry. Okay. So your next upcoming data readout would be from your phase II trial in pediatric patients in the fourth quarter of this year, and so just wondering if you could expand on what data sets investors can expect? Yep. That is the next one for zelicapavir. It is in Q4, and it's the peds data set. Even before that, but with our earlier molecule, we'll have a challenge study data readout later this month. Recall that zelicapavir successfully made it through the challenge study. It's reported in the New England Journal of Medicine. It set probably a high water mark or high bar for any other molecules. If you look at the whole landscape of fusion or of challenge studies that have been run, zelicapavir's is right up there at the top. But we're hoping to replicate that success with our second molecule coming forward. In that study, we'll be looking at virology, and we'll be looking at symptoms. It's a very similar trial design to the one we ran for zeli. So if you're familiar with that study, and I think that data is even in our current corporate deck, just so it's out there, people can stare at the study we've run and, you know, to see the kind of data that we'll hopefully be bringing forward, with our second molecule. And then the peds study, which is the lead asset, next quarter, we'll have readouts in virology. It's a smaller study. It's our first in peds study. It's about 90 patients. We'll glean anything in symptoms that we can, although, you know, the study wasn't powered to do that. In order to get statistical power on that front, it would have been a much larger study. And the goal here is to, you know, get those directional readouts, both from virology and anything in symptoms that we can glean, to figure out the right registrational study that would be run subsequent to that. And that one would be larger, powered, et cetera, et cetera, you know, in the peds arena. So those are the two coming, one later this month, one next quarter. And then, hopefully, well, I'm not gonna hope for a robust RSV season in the northern hemisphere, but were that to happen, it would greatly facilitate conclusion of our high-risk adult study. Right. ... which again, will be coming up. Right now, we're in places like Argentina and Brazil, New Zealand, Australia, South Africa, and the season is winding down there. We're still getting the occasional patient- Right. But it is, the virus is in transition. So in the next few weeks, probably before the election, we will have RSV in the Northern Hemisphere, and we aim to wrap up that other high-risk adult study up here. Yeah. Okay, and you mentioned EDP-323, the next compound. Yep. With the data coming later this month, what data, in terms of a challenge study, can we expect from that readout, and how is 323 differentiated from zelicapavir? Yeah, well, as I mentioned, they're both direct-acting antivirals. They're sort of orthogonal mechanisms. So one's a polymerase inhibitor, one's an N inhibitor. So one could imagine, were you to use them in combination in, say, certain patient populations, they would have the benefit of not... you know, the virus couldn't mutate, try to mutate against both of them at the same time, or said another way, it'd be incredibly hard to do that, and the way this study is run, it allows fantastic ability to capture good information early, so it allows you, since you're taking healthy volunteers, number one, you're not at the mercy of an RSV season. You can inoculate people with the virus any time of year. Then you can study them. They're domiciled, so they're carefully studied in patient, in an inpatient setting, and you can watch them over the course of a couple of weeks. So after a few days, the viral loads start to come up, you know, it might be three days or four days for one person and five days for another person. But once those viral loads come up, and we're watching by RT-PCR, twice a day, they'll hit a threshold, and then 12 hours later, they get dosed. And so what that allows is, you know, regardless of when you got infected relative to the presentation of virus and early symptoms, you get dosed at the same time as your comrades in the trial, and allows for a wonderful data set accumulation. And then that allows us to look at viral loads, twice a day, symptom scores three times a day, and to number one, establish that we've got a safe and good antiviral effect in a human with a real virus. And number two, it's a de-risking opportunity from the standpoint of making sure you've selected the right dose. Because you know, you can try different dosing schemes in that arena very easily, which we've done in the past and are doing now. That gives great confidence in terms of subsequent studies, that you're number one, have an antiviral on your hands, and number two, you've selected the right dose to show it in other people. Great. Great. All right, so, with the time remaining we have, I wanted to quickly switch to, immunology, and have you talk a bit about what CSU is and, what the unmet need is in that disease? Sure. So CSU is chronic spontaneous urticaria, which essentially is a very severe skin inflammatory disease. It can also so it creates wheals that are very itchy for patients on their skin, and then also angioedema, which is deep tissue swelling. There's also other associated symptoms, like sleep disturbances, anxiety, depression, so it's really, you know, quite severe for these patients, and it can affect up to 1% of the population. There's quite an unmet need for an efficacious agent here. The standard of care is antihistamines that can be dosed up to four times the standard dose. But unfortunately, it only really alleviates symptoms in about half of the patients. There's one available biologic, although very few patients go on to take that, so there is an unmet need here. We are looking at this disease through a mechanism of KIT inhibition. So KIT is a signaling molecule that is basically required for survival of mast cells, and we know that mast cells drive the pathology in CSU. It's the activation of the mast cells and the release of all the downstream mediators and histamines that create this inflammatory disease. So by blocking KIT, you're essentially reducing the number of mast cells that are available to create that pathology. So we like the mechanism. We also are aware of the fact that there's clinical validation through an antibody against this target, and they have shown efficacy that is some of the best we've seen in this disease from a phase II study. I think the other thing that's important to point out is that because you're targeting mast cells, this mechanism could be very useful in other indications that are driven by mast cells. So the antibodies are looking at a host of diseases outside of CSU, EoE, for example, PN. People are thinking about asthma, atopic dermatitis, so there's a number of diseases where it might be useful. Okay, great. One final quick question. What is your current cash balance and runway, and which milestones would that cover? Yeah. So, we ended the last quarter with about $270 million. Our runway is into the third quarter of 2027, fiscal 2027. And, that also contemplates a tax refund of on the order of $30 million that we're due. So, that's in the mix. And that should allow us to, you know, progress our RSV program with a phase III trial in peds, as well as bring up immunology programs. We also continue to receive, you know, hepatitis C royalty. Even though we monetized just over half last spring for $200 million, we still receive royalty revenue on just under half of the hepatitis C sales. Okay ... or royalties that we were- I'm not- ... previously due. Yeah. Right. Great. Yep. Thank you both so much. Appreciate it. Thanks. You're welcome. Thank you.