Thank you for joining Baird's Biotech Discovery Series. I'm Mike Perrone, Baird's Healthcare Specialist, and I'm pleased to be joined by Enanta Pharmaceuticals, CEO Jay Luly and Senior Vice President of Product Strategy and Development Tara Kieffer, as well as my colleague Baird Senior Biotech Analyst Brian Skorney, who will be moderating the discussion today. As a reminder, Baird's Biotech Discovery Series is an opportunity for investors to hear directly from interesting and innovative biotech companies in a fireside chat format. A few quick logistics: if you would like to submit a question, you can do so via the webcast portal or you can email Brian at bskorney@rwbaird.com. Finally, before we begin, I'm required to remind attendees to please refer to the event calendar, published research, or Baird's website for important disclosures regarding the companies discussed during this event. I'll now hand it over to Brian to kick off the discussion. Great. Thanks a lot, Mike. Hello everyone online. Thanks for joining us today. Like Mike said, I'm Brian Skorney, Senior Biotech Analyst here at Baird. Really glad to have with us today the management team from Enanta Pharmaceuticals. I've been following them, I mean, probably more than a decade at this point. I'll let Jay and Tara give a little bit of an intro to themselves and their company before we get into the Q& A session. To start, Jay, would you mind providing a little bit of background on Enanta, including, you know, maybe a brief history of the company's focus on how that plays into today's company strategy? Sure. Thanks, Brian. Before I begin, I want to remind you that 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. Maybe we could pull a slide up here. As you or I know, Brian, well aware, we started several years ago on virology and brought forward a couple of drugs for hepatitis C with AbbVie. We've also focused on other liver viruses and respiratory viruses. A big focus in RSV right now, which I'm sure we'll get into in some detail. We're involved in Covid, and suffice it to say that over time we have migrated our sort of our portfolio into immunology. We found that over time some of the main viruses that we were focused on targeting we had accomplished, and we wanted to move into another area. This has certain adjacencies to virology and would allow us to broaden our reach into many other indications. We moved into immunology a few years ago. We've announced a program focused on KIT inhibition, a program focused on coming up with an oral STAT inhibitor, and we're also planning on, you know, announcing a third program later this year. Again, an initial strong focus in virology building into immunology. We have a good balance sheet. We closed last quarter with just over $193 million in cash. That does not include the over $33 million tax refund we received in April, which, by the way, came in the form of paper checks. I think maybe we flip to the next slide and we can show our pipeline at large and then we can dive in anywhere you want, Brian. I think we. Yeah, on mute, Brian. Sorry, I had you on mute. Maybe focusing on RSV to start, I think you have a pretty near-term catalyst coming up there. Maybe tell us a little bit about your view of the opportunity here. How does this virus work, and where do you see the opportunity for an effective antiviral? What are the current options for preventing or treating RSV, and how are they used today? Sure. RSV has been around for a long time. A lot of people really only heard about it in connection with the pandemic. COVID was running around. Everybody learned SARS-CoV-2 and then RSV, as you know, was repressed during the pandemic, but then it came out afterward. Flu was repressed during the pandemic and then kind of unfurled. Now people talk about the triple demic of COVID, RSV, and flu and so on. In reality, RSV has been around. I think it was first characterized in 1956. In spite of that, and in spite of people trying for a real long time to come up with prophylactic approaches, and we can talk about those, there have been some recent developments there, but nobody has successfully brought forward to completion a therapeutic. Our focus is on therapeutics. We want to try to bring forward the first ever treatment for RSV. The way we're differentiated, I think, from most approaches that have been used in the past: in the past, most people really focused on viral entry. They took an approach where they targeted the fusion protein, the so-called F protein. This is what the antibodies target. This is what vaccines—well, vaccines can target more than that, but fundamentally it's the F protein and prophylaxis that people have used, and small molecules were developed by others in that approach. What was found was a couple of things. It's easy to get really potent molecules, but it was also very easy to generate resistance against those molecules, so it had a super low barrier to resistance. The other thing is we reasoned that when people present with an RSV infection, they've been infected for a few days, the virus has already entered a lot of cells, it's set up replication machinery, and now you have sort of unbridled replication going on. We reasoned rather than trying to block viral entry at a stage when people are already symptomatic and undergoing viral expansion, it was better to try to focus on sort of tried and true mechanisms of direct acting antivirals that would shut down viral replication. To that end, we set about working on a couple of different programs. The first one is our N-protein inhibitor known as zelicaprevir. We also have an L-protein inhibitor called EDP-323. The L-protein is the polymerase. Many people have heard of polymerase inhibitors in connection with antivirals. I think what we've chosen here are two very logical replication inhibitor approaches that again will target viral replication rather than viral entry. We also know that we have high barriers to resistance. Combination of replication, high barrier is where we are, where we are focused. With regards to the prophylactic options that you asked about, there are really two approaches. One is monoclonal antibodies. You may remember years ago there was a monoclonal antibody called Synagis which was the first sort of targeted antibody. It worked to some degree prophylactically in high risk premature babies, but it did not work therapeutically and it was very expensive and it wasn't widely used. There's a follow-on to Synagis called nirsevimab. It's longer acting and I think has been more widely adopted. The problem is that these antibodies just still don't provide lasting immunity. It's only a passive immunity that you get and you really can only use them in the first season, RSV season. If you're born into an RSV season, you might get it. After that you're kind of on your own. The antibody will be gone in a few months and you won't have any lasting or any immunity to the virus until you actually get it. You're destined to have multiple RSV infections just like you ordinarily would. There's been a couple of vaccines that have approved. Pfizer has one that's used in high risk adults. It's also used in maternal vaccination where you vaccinate the mother right before she's due to give birth. Antibodies are generated, transferred transplacentally into the fetus, and then ultimately the child is born with again, some short term immunity, but has the same problem as the others. GSK also has an adult vaccination, but it's only used in adults, not in peds. These vaccines, the uptake has actually been sort of suboptimal and there's basically not a lot of uptake with that vaccine. Punchline is whether people get vaccinated or not, there's still breakthrough infections. Most people aren't vaccinated and none of it's long lasting. What we want to do is again come up with a treatment because that's where the huge unmet need is out there. Maybe I'll pause. Yeah, no, that's a great intro to it. The zelicapavir program, focusing on that specifically, it's seen results in several phase II studies, including a challenge study, seasonal RSV infection study, and a pediatric study. Can you walk us through the learnings that you have from those results? Yeah. So zelicaprevir, formerly known as EDP-938, if you remember that number, it targets the nucleoprotein. This is the only N-protein inhibitor in clinical development today. Currently in phase II, we had great phase I healthy data, safe, well tolerated, good blood levels. The rite of passage in RSV is then to move into a human challenge study. We did that. We got very strong results in that, both from viral load suppression and also symptom suppression. Now where we are is we're currently focused on high risk patients. These are patients that are at one end of the age spectrum or the other. Obviously, very young children are immune naive until they've been infected. Again, they keep having repeated infections as a child, so they're at one level of risk. Elderly people at the other end of the age spectrum start to have that immunity that they built up during their adulthood start to wane. There's immune senescence that jumps in and suddenly they become more vulnerable. There are also adult populations that have high risk, people with respiratory difficulties, asthmatics, people with COPD. Also, congestive heart failure predisposes you for a poor experience in terms of an RSV infection. These are the other high risk patient categories that we're currently studying. In terms of that, taking them in order, the challenge study, again, we saw highly statistically significant reductions in viral load. Symptoms were also very well suppressed over time. It was safe, well tolerated, and the onset was actually pretty quick in terms of that because timing is of the essence when you're dealing with acute respiratory infections. We went from there into a translational study before we got into the high risks. We took people from sort of a similar patient population as the challenge study. These were otherwise healthy adults. We asked the question, what if we caught these people in the real world with community infection, could we get to them in time, did they need to be treated? These were the kinds of questions we asked about a so-called standard risk population. That was a study called RSVP. Unfortunately, what we learned was these patients don't need to be treated. In fact, I would submit that they can't really be effectively treated because even though we recruited patients within 48 hours of symptom onset, which is about as soon as you can possibly do it, and we got, by the time we got drug on board at 48 hours, viral loads had already peaked and were coming down. Symptoms had already peaked and were coming down, so it was just impossible to capture them soon enough. Their immune systems were very much intact. For that population, the so-called standard risk, it's just sort of like a little bit of a bad cold, so not something that needs to be treated nor can be treated. The next study that we did was in a high-risk patient population and that was our first IMPEDE study. The primary endpoints that we were looking for were safety and tolerability. We were dosing babies down to as young as 28 days of age, and so safety is just super, super paramount. We wanted to also look at PK. We had a good handle on our adult dose, but dose in peds at various weights and ages is a different matter. We had to carefully do some dose ranging. The other plan was to demonstrate an antiviral effect and then also symptoms. It would be hard to get a lot of good symptom data in this study, but we wanted to try to capture as much as we could using this proprietary observer-reported outcome tool. The good news was it was safe and well tolerated in peds. We saw very good blood levels even at our low dose. We deemed it to be an effective dose based on what we knew from our challenge study in terms of what we needed, and we demonstrated a good antiviral effect as well. All of those things were the primary measures of the study. We executed on them, and then we even used this proprietary tool that we're building ultimately for registration studies called RESOLVE P. The babies can't self-report, although they do in certain ways. It's hard to have a good tool for crying and other kinds of things, but you have to rely on the observers in order to capture this information. We've been working with physicians, caregivers, FDA, European regulators, et cetera, to build an observer-reported outcome tool that would ultimately be used in registration studies. We got a little bit of that data. I think it was on about a dozen or 15 babies. There was a trend from a symptom improvement, but obviously we need to get more data on that in a bigger study. Those are the studies that have been completed to date and we've got one more coming, obviously. Great. Maybe moving on to that phase II readout that I think we're expecting this quarter in high risk adults. Can you discuss this study design and what in particular we should be looking for on the readout to have confidence in the ability to move forward? Maybe we can. There we go. Let's put up a slide. That's the PEDE studies. Let's see. I think we will go on to the high risk. Here we are. The RSV HR study is a proof of concept study. We have about 180 adults in this study, so it's about twice the size of our PEDE study. These again are all patients that are at high risk for severe outcomes. The populations I just mentioned: elderly, COPD, asthma, and CHF. Also, just so that we didn't enrich a study with otherwise healthy asthmatics or people who are, you know, quote, in our elderly bucket but are 65- 74, you know, they're quote, elderly, but not that elderly, we took those 65- 74 year olds along with the asthmatics and said they can't be more than 20% of the study. 80% are 75 or older for COPD or CHF. It's a larger study, it's enriched for high risk patients, as I just mentioned. We also have a tight window on recruitment. The recruitment window is patients are enrolled within 72 hours of symptom onset. It's really a three day window cut. It's a little tighter than we had, up to five days in our PED study, mainly because we were trying to recruit H RSV positive children so that we could do PK and that sort of thing. The day from symptom onset didn't matter quite as much. We did see that within three days seems to be about the sweet spot in that study, and we're using it in a go forward way here too. Larger study, tighter window. The primary endpoint for reduction here is symptoms. Unlike the peds study where we only had the pediatric tool toward the end of the study to try to capture some information on symptoms, we have a tool called the RIIQ where it's been used previously in studies. We have sort of an understood tool to use, and we will have data on every patient. We'll have a good symptom data set, which is our primary endpoint. I think the next slide. This i s how we're kind of thinking about what to expect. There's not a lot of data symptom wise in terms of looking. What we're looking at is time to symptom resolution. A shortening of the time to resolution, and we want something that's clinically meaningful. Since there aren't any registration studies that have been done in RSV for this age population, what we wanted to do was at least look at other acute respiratory infections. I've got flu here on the left and SARS-CoV-2 on the right. If you look at Tamiflu, which going from left to right are the first two sets of data points, what you can see was in the Tamiflu phase III study, which was 65 and above, they saw about a day shortening in time to resolution of symptoms. This is a phase III study. As you can see at the very bottom there's an N there, it's around, well, just under 500 patients. That proved to be stat sig for one day. The next panel is also Tamiflu, sort of a meta-analysis across a lot of different studies. What you can see is it's also about a day shortening in time to resolution. The third set of data is Baloxavir, which is Shionogi's flu drug. There it was a registration study looking at adults, age 12- 64. All of these are bigger studies, but showed about a day shortening in time to resolution of symptoms. Switching viruses now, this is SARS-CoV-2. This is a phase III that was run in Japan for the Japanese approval on nirmatrelvir, larger study, just under 700 patients. The clinically meaningful result was about a day in each of these instances. It's sort of uncanny across influenza, across two different drugs for influenza, across SARS-CoV-2, the message seems to be about a day would be a clinically meaningful input. I think that's even on the next slide. For this proof of concept study, RSV HR has a smaller n. We're only at 180, but I think that's still a decent size proof of concept study. We're looking for about a day shortening in time to resolution. We'll be capturing lots of other secondary endpoints which you can see highlighted below. We'll look at the totality of the shortening and resolution, some of these other secondary endpoints to provide confidence for moving into a larger phase III study which would be sized in a way to confirm with statistical significance the findings from this study. That's the data set. As you mentioned, it's due to come late this quarter. Great. We'll look forward to those results. I know you have a second program in phase II development for RSV, EDP-323. Can you talk about how you see the development of this asset in the context of zelicaprevir development? Do you see different or overlapping opportunities here given the different mechanisms? Yeah. As I mentioned earlier, EDP-323 is an L-protein inhibitor, which is the RNA-dependent RNA polymerase. As I also mentioned, it was zelicaprevir. After a successful phase I, which we had in healthy volunteers, the next rite of passage is to go through the challenge study. We got that data in September, I think last year, and before that, about a year ago, people were asking, you know, what would make you happy, what would be the signs of success in this study? At that point, we were just focused on sort of recapitulating the data that we saw with zelicaprevir. It's a very good—zeli was a great challenge study. We published it in the New England Journal. That was sort of the bar for excitement, if you will, on data. What we were pleased to see was there are even some aspects, I think, that are even maybe more exciting with this molecule. We saw very strong viral loads in the 85%- 87% range in terms of reduction of viral load. AUC, we saw a very good symptom reduction too in terms of AUC reduction of symptoms in the sort of 66%- 78% range. Where I think this really jumped out was if we can pull up the slides on first the viral load by PCR. Let's see, there we go. This is the PCR one. There it is, 85%- 87% reduction. What we did was a high dose and a low dose we explored. They were basically exactly the same because even the low dose gives massive multiples of the protein-adjusted EC90. You can see that on day zero, which is defined as when the first drug is administered, if you look at the y- axis, the viral loads are between two to three logs. What you also see is after the first dose, first little tick mark there is 12 hours time point, it has already altered the course of the infection. Placebo in green. Viral loads keep going higher. Drug treatment, the lines separate. When you look at this, this is a PCR measurement, so you're looking at amplifying live virus, dead virus, viral particles, et cetera, et cetera. If you look at the viral loads by culture, which is on this slide, you can see just how robust this antiviral effect is. Here you see a 97%- 98% reduction in viral load. In fact, 12 hours after the first daily dose, the viral loads are down and then basically just flatline. This is a very, very fast-acting drug. Again, as I mentioned, when you're dealing with acute respiratory viruses, time is of the essence and you need to get a drug on board as quickly as possible. The only thing better than getting a drug on board as fast as possible is to have a drug that works really quickly. So EDP-323 I think may well eclipse zelicaprevir slightly by just the speed of onset. You asked about combinations and positioning. I think, you know, we know preclinically these two drugs play well in combinations. We've explored that, we've looked at the virology of that. There's nothing in the profile of the drug, either drug, that would suggest any DDIs that would be problematic. I think the combinability is very good. The real question is do you need to combine them and if so, in what patient population? Our current thinking is that with a standard patient, sort of a typical RSV patient at either end of the spectrum, monotherapy is probably going to be adequate for an acute virus. It has a high barrier, they're both potent, they're both pretty quick acting and you might not need to do combinations, which is great in my opinion. I mean, we spent a lot of time in the combination world of hepatitis C and hepatitis B. Combination drug development, if you don't have to do it, is, you know, it's always simpler to not have combinations. That said, you know, could there be populations, highly immune suppressed population, so this, in this patient population, if somebody gets infected with RSV, it doesn't behave like an acute respiratory virus because they can't clear it. That's a situation where you need to dose, certainly you probably need to dose longer than just five days. You might also benefit from having, you know, orthogonal approaches going after the virus in a more heavy handed way with two different mechanisms. That's something that we're thinking about. The other is just, you know, when we charted out RSV several years ago, it was with the goal of not only having the first RSV drug to the market, but also having, you know, sort of the best portfolio for the long term. To that end, you know, one might imagine zeli h as being potentially the first to market, following it with EDP-323, you know, in a longer term scenario for life cycle management, either as monotherapy or used in combination. That's our current thinking about it. Got it. Great. On your slide you list the RSV programs under BD opportunities for partnership. Pharma has kind of been in and out of antivirals over the years. Can you discuss the level of interest you're seeing on partnerships for the RSV assets, the appetite for antivirals in general, and any question just on the level of confidence and timeline for a partnership? Yeah, I think, let us get our data, we've got some data coming. I probably won't comment too much on sort of detailed business development discussions, but suffice it to say I think there are pharma companies out there that are interested in RSV antivirals. It's a strong, there's just no, there's no approved therapeutic really. Right. You have a market that's just laying there open. Many of the fusion inhibitors, as I've mentioned, have faded away. Gilead had one and it went away. J& J ultimately shut down their program that had a fusion inhibitor in it. Roche had one that they ultimately handed off to Arc Bio. They're developing it. Mostly has been developed in China. Pfizer had a fusion entry inhibitor from ReViral. They dropped that one. I think it's time for replication inhibitors. As I said at the outset, we were very focused on that from day one. We only made fusion inhibitors to benchmark and to demonstrate to ourselves that they had very low barriers to resistance, et cetera, et cetera. We'll see. I think it's time for people to have a therapeutic opportunity for RSV. Great. Maybe shifting gears a little bit, you've started to deploy your medicinal chemistry expertise into the INI space. Maybe talk through a little bit this pursuit and how you think about strategically pursuing targets. Yeah, as I mentioned, we targeted most of the viruses we set out to target and, you know, looked, in fact, until the pandemic came along, we thought we were ready to move to some other things. The pandemic probably deferred that a little bit. Even during the pandemic, we started building for the future in terms of other areas that we could pick. Immunology just surfaced. Some of our virologists had actually trained in immunology and, you know, became virologists. We had the skill sets we thought inside to be able to go after some of this. We just wanted to make careful selections in terms of targets and unmet need and so forth. I think at the beginning of last year we unfurled our first program, which is in KIT inhibition, again going after wild type KIT, going after small molecule approaches. I think the antibodies had sort of paved an interesting path for wild type KIT, small molecules to come in. We also said at the beginning of last year, you know, our goal would be to have a second program by the end of the year announced. We now know that to be STAT6. We've been working on STAT6 actually for some time now, didn't announce it till the end of last year. Similarly, now we have another program announcement that we're aiming for later this year on a third program. We're trying to bring these out with a certain cadence, with a certain critical mass of having explored the targets, explored the markets, thought through clinical trials, thinking for things where there's either clinical validation or good biomarkers or human genetics, looking for things where there's very significant markets, but maybe an opportunity for a small molecule modality to fit in. This is how we've largely selected these things. We're also trying to, at the time of announcement, have assays and models in hand, chemical matter built up, intellectual property underway, et cetera, so that there's a certain level of maturity of these programs when we pull them out. Great. Maybe turn into the first half of the KIT inhibitor, which I think you've nominated a drug now, EPS-1421, if I'm not mistaken. How do you sort of think about the validity so far of KIT as a target and how your approach might be differentiated? Yeah, I've been talking a lot. I think I'll hand this one to Tara, let her chat for a little bit. Sure. Yeah. I think with our KIT inhibitor, in terms of the, we would look at would be urticaria, so either chronic inducible urticaria or chronic spontaneous urticaria. What we know about that disease is that mast cell activation is actually a primary driver of that inflammation in the skin, and it's also implicated in a number of other, multiple, multiple other allergic disease areas. What we're doing with KIT is inhibition of this is directly reducing the quantity of mast cells that are available to cause that pathology by apoptosis and depletion. It's really targeting and addressing a key driver of the disease. The current therapies that are out there are really reducing just the level of activation of mast cells, but KIT inhibitors will directly reduce the quantity of mast cells. We also like the target because there's good clinical validation, as Jay mentioned, with an antibody against this target. This is from Feldex, and they've now shown long-term 52-week data with a phase II study. That efficacy that has been established is some of the best disease efficacy that we've seen. We're hoping to replicate that with an oral molecule. The nice thing about this target as well in this disease is that there's really good biomarkers that are available in, for example, serum tryptase, that you can get early signs of as a croupy in the clinic, even in healthy volunteers. You'd asked about differentiation, and I think, for that, we're obviously targeting, as we always do, a best-in-disease efficacy with an oral option, optimizing around things like potency, selectivity, and then DMPK properties as well. The other thing we're thinking a lot about is dosing strategies for this molecule that may enable a more favorable tolerability profile. Great. So maybe just talking a little bit more about development strategy and how you kind of think about the monoclonals out there. Do you see 1421? I mean, is it really just on the oral bioavailability and the oral option that you see as an improvement over the monoclonal, or do you sort of see a chance in any of the characteristics for actual outperformance on efficacy? Absolutely. I mean, certainly oral is an advantage. Many patients will prefer to have an oral option in terms of route of administration, but certainly we're thinking about other differentiation factors as well. I hinted a little bit about that at the end of my last comment talking about different dosing strategies. The one thing about the antibodies has been some on target tolerability in the form of decline in neutrophils and some hair color changes. They seem fairly manageable and many of them are just tolerability issues and not really safety effects. We are thinking a lot about having different dosing strategies that might be able to better thread that needle between efficacy and safety to improve that profile. What I mean specifically about that is, are we able to dose enough to drive down the population of mast cells that would allow for the same clinical efficacy, but that PD effect may outlive the PK in that once you deplete those mast cells, it will take some time for them to repopulate. If you take the drug pressure off, you may be able to see a repopulation of other cell types like neutrophil blood cells that have a more rapid turnover rate. We're thinking a lot about how we might interrogate this in the clinic and optimize further around a better tolerability profile. Got it. Moving on to STAT6, which is your second announced INI target, maybe talk to us a little bit about the validation of this target and INI. I think STAT6 inhibitors have been called the oral dupixent. How does STAT6 fit in the pathway versus IL-13? Yes. Basically, you're dealing with the same sort of signaling pathway. When you look at IL-4/IL-13 signaling, upon receptor engagement, you get JAK activation, JAKs phosphorylate STAT6, and then when you get the phosphorylated STAT6, you get dimerization of STAT6 and translocation into the nucleus and then subsequently transactivation of a number of pro-inflammatory cytokines, basically. It's the same signaling pathway coming through STAT6. We like it because STAT6 is sort of specific to that pathway. Whereas JAKs, people who have entered, you know, JAK kinase inhibitors work well as well, but they're involved in the signaling of a lot of other receptors. You don't get quite the same level of selectivity as you do with STAT6. We like it for the validation that it has mainly through, I mean, there's genetic gain of function and loss of function types of studies that you can look at mechanistically. The ultimate validation of that pathway, I think, is Dupixent, which has obviously been approved in many different indications. That's kind of how we're thinking about it. If we can come up with an oral Dupixent, you would, you know, I think, have a broad opportunity to hit a number of different indications with a single drug, assuming that you can get, you know, very good selectivity. We've demonstrated high levels of potency, high levels of selectivity, not just with, you know, STAT6, but, you know, across the whole STAT family, we've demonstrated good target engagement in in vitro and in vivo models. Our prototypes are looking very, very good where we've got good PK. It's really a little bit of apple polishing that we're doing right now, zeroing in on the exact finalist which we expect to announce here in the second half. Got it. Maybe can you compare and contrast your efforts at targeting STAT6 with some of the other small molecule efforts? In particular, how we should think about sort of direct binding of STAT6 versus degrading STAT6. Tara, you want to take that one? Yeah. We're taking the approach of targeting STAT6 with a small molecule inhibitor. To your point, Brian, there's other companies, Kymera for example, that is protein degradation, which removes the target and the protein entirely. We obviously like small molecule inhibitors. They're a very well understood modality with long-term, robust preclinical and clinical data. We'll have to see as more clinical data come out on these degrader modalities. There aren't any approved to date, so the data is certainly more limited. From a small molecule perspective, we have a lot of learnings that have generally been able to guide a good translation from preclinical models into the clinic. Predictable PK/PD relationships for dose selection, good understanding of the metabolism profile. I think we'll ultimately have to see as the clinical data comes out. Certainly, as Jay said, we're targeting a best-in-class molecule. Certainly as we've seen with other targets and with other indications, if you can get a small molecule inhibitor that can achieve exposure levels that are above your EC90 or your measure of preclinical potency, they should be able to completely inhibit the protein without removing it. We've shown this actually preclinically with our prototype. Great. As you look at additional immunology programs, and I know you're saying there's probably an announcement before the end of the year on a third program, what sort of informs your decision making process here? Do you select a target and try to design a chemistry around it? How does biological validation and competition come into play when you're determining where to go next? Yeah, you want to take that? Yeah, yeah. We're really focusing on areas where there's a good understanding of the underlying biology, disease pathology, and where the target has some level of validation, you know, whether that's genetic or clinical validation, that's ideal. We're obviously looking for indications where there's a clear development path, well-defined populations, and ideally, if there's biomarkers available for those early signals of efficacy, that's helpful as well to de-risk the program early on. We're looking for areas where there's really a large unmet medical need and a good opportunity there and where, you know, maybe the target is either not currently drugged with a small molecule or suboptimally drugged. Those are ideal targets for us. We have a really good preclinical kind of drug discovery process in house and good expertise in that area. Great. Maybe just last question I really have is you continue to receive royalties on the AbbVie Hep C combo, Mavyret. Can you tell us a little bit about your view of the stability there, durability, and what you currently get in terms of economics? Yeah. You know, we first got royalties on paritaprevir, which was the first protease inhibitor that was ultimately surpassed by glecaprevir, our second protease, which is best in class. That has been in Mavyret now since, I guess, the U.S. approval was in 2017, 2018. We've been getting royalties, double-digit royalties on glecaprevir, which is half of MAVIRET, for several years now. I think AbbVie's analysts have revenues going out into 2033 in their models. We have been participating in that now. It's interesting, the HCV market changed during the pandemic. It was really strange for both Gilead and for AbbVie. They're basically the two companies that sell hepatitis C drugs now. As we came out on the other side of the tunnel, the overall sales were down versus before the pandemic. It's still, you know, AbbVie's selling north of $1 billion a year on MAVIRET, and we expect that to continue for a good long while. A couple things have come up. Just a few weeks ago, we got the first ever label for acute hepatitis C. We had chronic, but we didn't have acute. What that is going to allow is for people to basically be treated just at the acute phase. If you get a positive test for HCV, you don't need to wait around for it to become chronic. You can treat early, and we think that's obviously an advantage. The earlier you can treat, always better. Gilead and AbbVie both have the indication for chronic, but we'll hopefully pick up a lot of patients at the acute phase before they even have a chance to become chronic. It's nice to have that label. That's also eight weeks. We have the only eight-week cure for now, acute and chronic Hep C across all genotypes. We monetized a little over half the royalty two years ago for $200 million. Our royalties now are on the other 45.5% of that royalty, which will continue until 2032, after which point 100% of the royalties will revert to us. It's been good to have that cash flow through these years. Great. I think you mentioned at the top you had a little less than $200 million in cash at the close of March. $34 million on top of that. How does that kind of look versus your burn, and how much of your operating expenses are covered by the AbbVie royalty right now? Yeah, it certainly contributes to our operating expenses. With the cash on hand, the paper checks that we got from the IRS for $33.8 million, you know, we've got cash runway into fiscal 2028. So reasonably good on cash. That allows phase I, phase II study in KIT, getting our STAT6 into the clinic, and progression of a third program into the clinic as well. That's without any assumptions on RSV partnerships. I think, you know, overall it's. It’s pretty sound great with that. That’s basically all my questions. I’d love to give you the opportunity if there’s something that you think I missed that you’d like to mention about Enanta, please feel free. I think you hit everything on the head. Big data set coming and new catalysts emerging in immunology. Great. Jay, Tara, always a pleasure to talk to the two of you all. Great. Hand it back to Mike to close. Thank you so much, Jay and Tara. Just for the investors out there, do know that Enanta is going to be coming to Baird's Global Healthcare Conference. That is going to be Tuesday and Wednesday, September 9th and 10th, in New York. They'll be there on the 10th. If you'd like to connect with them, we'd be happy to set it up there. If you're more interested in catching up earlier, please let us know and we'd be happy to make the connection. Thanks everybody for joining and have a great day. Thank you. Thank you.