All right. Good morning, everybody. Welcome, Jay and Tara from Enanta Pharmaceuticals. Thank you so much for joining us. We've got a couple of different topics to get through today, but I would love to start with you, Jay. Just wanted you to kick us off and tell us what we should be thinking about as we finish out the year and head into 2026. Sure. Before I begin, I want to remind you I'll be making some forward-looking statements, and for a summary of the risks associated with them, please see our filings on SEC.gov and on our website, so, yeah, we had a really interesting year with lots of activity, so, you know, starting with RSV, we brought forward what we're envisioning as the first-ever treatment for RSV infection. We have two molecules there, and the more advanced of the two, zelicapavir, reported out a really compelling phase II-B data set in high-risk adults, so that was a good part of the year, and then separately, and I'm sure we'll get into all these different topics, we've been building out beyond virology and getting into areas of immunology and inflammation, and to that end, early last year, we announced our first program in KIT inhibition going after mast cell-driven disease. We announced a development candidate for that, and more recently nominated the clinical candidate, the one that will actually be going into the clinic, called EDP-978. We're on track for an IND there in Q1 of 2026, and then basically at the beginning of this year, we talked about a new program called STAT6 for us. There we're targeting an oral Dupixent-like profile, and we also nominated a development candidate for that and expect to file an IND on that in the second half of next year, and then in the coming weeks, we plan to announce yet a third immunology target, so it's been a very interesting year. Let's start with the RSV data before we transition into immunology. The big question here, I think from the market's perspective, is what is large pharma's view of the infectious disease space in general? What's their appetite for direct-acting antivirals? And what's the development future for a drug like this? Yeah, so I think virology is here to stay. I think there's all kinds of different curveballs viruses can throw at you at different times, most notably in the pandemic in recent years, but there's other pesky little viruses that have been around for a long, long time, and RSV is one of them. I think it was first characterized in 1956, and to this day, there's no approved treatment for RSV, so it comes every year, except during the pandemic when it didn't for a little while, but it's back, and it comes every year. It affects the young people who have no immunity. It affects high-risk adults where immunity has waned. It affects immune-compromised people, so we think it's a really good target that has compelling effects on the healthcare system at large. And pharmas, you know, I think there are not as many pharmas that have been involved in infectious disease as there has been in the past, but there are clearly those who are committed and those companies of other types that are looking for just really interesting, potentially large market opportunities where you have the opportunity to be first in a disease. We've got a second molecule that could be a potential next- gen. And so we believe there are indeed companies out there still very interested in infectious disease. Let's talk a little bit about the data. Obviously, you had a positive result. You saw a reduction in symptom time, symptom resolution in the efficacy population as well as in the high-risk HR3 subpopulation. Can you talk to us about the difference in those markets and what we might expect from a potential effort to penetrate in those places? Yeah, the difference that, you want to talk about the markets, Tara? Sure. So I think, you know, this is a significant opportunity. As Jay mentioned, there is no currently approved drug for RSV. And the CDC estimates up to 6.5 million outpatient visits for this infection annually. And the majority of those are going to be in the high-risk population, so in pediatrics and then the high-risk adults. In our study in the HR3 population, as you mentioned, that would include patients that are older than 75, those with COPD, and those with congestive heart failure. In that population, we showed about a week reduction in symptoms, also a reduction in hospitalization. So providing, potential to provide significant benefit for these patients and an opportunity there. Coming into the data, we talked a lot about the different components of that high-risk population of folks who might be high risk for different reasons, some of whom have more severe disease burden than others. So can you talk about what an expected treatment paradigm would be like? Who would docs prefer to be treating if they had something like this on the shelf and who might skate by without getting treated? Yeah, so the patients that are considered high- risk for severe outcomes of RSV include the very young, so pediatric patients, say under three years old, and then adults that are older than 65, 75, and then have other comorbidities. So in our study, we looked at those chronic lung and heart diseases. There's other comorbidities, kidney disease, diabetes that also predispose. So those are things that could also be studied down the road. Okay. And based on the results in the phase II-B, what would it take in a phase III to push this over the finish line? How big a trial do you think it would need to be? We think for a phase III trial, we'd probably focus on symptoms as a primary endpoint, looking at hospitalization as well, of course, but it would probably be in sort of the 500, 600, 700 range. Is that something that you've had a discussion with the agency about? Yeah, so we're in the process of getting all of that underway and we'll be discussing with the FDA. Great. Well, let's spend the bulk of our remaining time on the immunology, the building out of immunology pipeline. Jay, you mentioned a couple of different targets there and one more coming down the pipe soon. Let's start with the broad question about target selection and what areas of immunology, obviously huge space, that you're most interested in. Yeah, so as we made this shift, you know, we were looking at, I don't want to say we ran out of interesting viruses, but there were fewer and fewer really compelling ones to go after where we felt there was major unsatisfied patient needs, and RSV clearly ticked that list, but looking beyond that, you know, the immunology space, which is one that a lot of the company had worked on in previous career opportunities and just an expanding universe of different kinds of targets, approaches, disease indications, some of them are really, really large, they're competitive for that reason, so our eyes are wide open on that, but I think we always tend to gravitate toward disease areas where we think there's an unmet need or an area where we could at least be a vibrant participant, Hep C used to be wildly competitive. And then gradually it contracted down. And my belief, even at the very beginning of Hep C, was as long as we can be a strong contender and be in the winner's circle, even if we're among others in good markets, then a small company like Enanta will do very, very well. So we tend to look for good markets. We tend to look for areas where we think we can understand disease pathology pretty well and then, if possible, nail down a specific target that makes a tremendous amount of sense with regards to that. Also, anytime you can find clinical validation, you put it in your back pocket and use that. And so, you know, I wouldn't say that everything that we've done or will do satisfies all of those, but we try to check off as many of those boxes as we can when we're selecting these. And some of our targets, they're reasonably served with monoclonal antibodies, but not completely served. And we're very adept at building high-quality small molecule drug candidates that are oral, have good drug-like properties, can be dosed typically once a day, safe, easy to use. And so in some of these instances, whether it be going after mast cell-driven disease approaching KIT or whether it's going after an oral Dupixent, we're coming in with the angle of just having a really convenient dosing form as well. Let's start with STAT6 since you mentioned competitive landscapes. You mentioned things that are maybe not completely served, but are reasonably served with other modalities. Obviously, STAT6 has multiple competitors there with a wide variety of different modalities. So can you talk about how that fits into that paradigm that you just said? What is the unmet need in the current STAT6 landscape that you can help? Dupixent's the big one out there, right? It did on the order of $15 billion last year. It continues to add. A second drug. Yeah, it continues to add other indications. There isn't an oral STAT6 available that would basically be a counterbalance to Dupixent. I think the degraders, there are some companies out there working on degraders, so that's an interesting approach where you're just trying to take the protein out. You know, that's one way to do it, but in most drug arenas, you don't necessarily have to remove the actual protein if you can come up with good ways of inhibiting it. And I think the reason degraders became popular in STAT6 was because for many, many years, STATs were thought to be really, really hard to drug targets. And they were. I was working on STATs in the early 1990s, and they were hard to drug, and they were hard to get selective, and you had, but I think some of the structural biology, some of the other insights have come along the way in terms of really elucidating how you might go about that. And it's a little bit like rock climbing, right? You got to get your hand in the right crevices, and then you can build on that and then ultimately scale that STAT mountain, I guess. But, so we believe we've found a way to come up with small molecule inhibitors that completely inhibit the target. And we've talked about that. We can hammer STAT6 over a 24-hour period. And it's now shown good activity. Our candidate we just announced two weeks ago has demonstrated good activity in an animal model of atopic dermatitis and also one in asthma after, again, oral dosing. So very excited about that, on track to now having the candidate in hand and have IND on that in the second half. One of the things that jumped out at me when we looked at the data that you, preclinical data that you said you just showed, was the selectivity of the molecule for STAT6 versus other STAT isoforms versus other targets in the area. How does that dovetail in with what you just said about hammering the target over a 24-hour period when we compare your molecule to other small molecules that are modulating the pathway? You compared in your deck to the JAK, STATs, and obviously those are much less selective molecules. Yeah, so JAKs, you know, we're not focused on JAKs. I mean, they have selectivity challenges. I mean, they can be incredibly efficacious, but with some selectivity baggage. I'm not sure I'm fully understanding your question, but when you look at the signaling through Dupixent, it channels down through this JAK and STAT6 pathway very selectively. So we targeted the key STAT that was involved. And I think how much of the efficacy is really due, say, with JAK inhibitors to that lack of selectivity, that's one question that could be asked. I think it's more likely that there's more safety issues that surround that than efficacy issues. And Dupixent, you know. Dupixent's obviously selective. Shows it very well, so. Okay. In our last couple of minutes, let's move on to the KIT inhibitor and the mast cell-driven diseases. So can we talk a little bit about your process for candidate selection here, how you might differentiate from others in the space? Tara, you want to take that? Sure, yeah. I think what we're trying to do with the oral KIT inhibitor is to be able to replicate some of the efficacy that the antibodies are seeing in their later- stage trials, which in CSU, which is chronic spontaneous urticaria, where they're being studied, has shown some of the best efficacy in the disease. So if we can replicate that efficacy with an oral small molecule, potentially improve the safety profile, that is our goal. So we've optimized preclinically for a molecule. We have EDP-978 as our candidate. It has shown nanomolar potency, actually subnanomolar potency in an animal model, good selectivity here for kinase inhibitor as well, and then good ADME properties. So both in vitro and in vivo, we've seen good PK across preclinical species, potential for daily dosing. So we're excited about that candidate. Here again, selectivity is a key feature that you mentioned. Can you talk a little bit about the liabilities of less selective molecules relative to what you're looking for in a development candidate? Yeah, I think it's particularly important with kinase inhibitors to have really good selectivity. And so something that we've spent a lot of time optimizing around and characterizing. And I'm very happy with the current profile that we have, but it's important, obviously, to be able to selectively inhibit KIT and not have any potential kind of off-target effects. As we look forward to potentially initial clinical data, maybe the end of next year or thereabouts, obviously TBD, but what sort of things should we be looking for to nail that differentiation home? For clinical trials? Yeah, yeah. What would you just said translate into a clinical setting? Sure, yeah. I think taking a look in phase I at safety, obviously, will be key, and then we'll be looking at all the PK profiles as well as biomarkers that you can measure in healthy volunteers, so serum tryptase is a really good biomarker for CSU so we can get to understand a little bit about the activity that we'll have in patients. Are there key safety features that you're hoping to observe or key tolerability issues that you're hoping to avoid? So I think there's known on-target tolerability things that have come up for the antibodies with KIT. We are thinking about different dosing strategies where we may be able to mitigate that rather than kind of hitting the target very hard for very long periods of time. Might you be able to modulate that with different dosing schemes, whether you have more intermittent dosing or sort of a lowering dose and the maintenance dose? Those are all things that we're thinking about where you might be able to maintain that efficacy but have a better tolerability profile. Are those dosing regimen differences things you're planning on exploring in phase I, things we can see in an initial readout? Yeah, I think we'll have to think about how we would do that either in healthy volunteers or patients. Obviously, patients are probably an environment where you'd get a little bit more information. Maybe in our last minute, the mystery third immunology candidate, Jay, is there anything you can tell us about the sorts of places you've been looking or what areas you're excited to explore further? Not today, probably. I think it fits within the realm of what I was talking about earlier in terms of looking for approaches that you could target, basically areas where there's good unmet need, maybe a countervailing approach to things that other people have done or that you might be working on so that you've got different shots on goal. All right, well, we look forward to hearing in a few weeks when you announce it. Maybe last thoughts on the catalyst path from here. You mentioned the IND for KIT coming, but just remind us when we could start seeing data from some of these immunology programs. Yeah, so we're excited, again, getting KIT IND in Q1. We'll be rolling out, as Tara just mentioned, some of the things that we'll be looking at. I think the nice thing is you can learn a lot in phase I with these molecules and approaches because there are surrogates that you can be looking at and markers. And that's true in STAT6 as well. So a phase I study in STAT6 healthies can give you an incredible amount of confidence-building information. With good translatability to a patient study down the road. Exactly. Excellent. All right, well, thank you so much, Jay, for joining us. Thank you. Thank you.