Enanta Pharmaceuticals at Jefferies: Strategic Focus on RSV and Immunology

On Thursday, 05 June 2025, Enanta Pharmaceuticals (NASDAQ:ENTA) presented at the Jefferies Global Healthcare Conference 2025, outlining strategic advancements in their RSV and immunology programs. The company highlighted both promising developments and challenges, focusing on partnerships and clinical data as key drivers for future growth.

Key Takeaways

• Enanta is focusing on zelicapavir, an N protein inhibitor for RSV, with high-risk adult study results expected in late Q3.
• The company is exploring strategic partnerships to advance its RSV treatments, including a potential combination therapy.
• Enanta’s immunology program includes a STAT6 inhibitor, aiming for oral administration benefits similar to Dupixent.
• The company plans to submit an IND for its KIT program as early as next year.
• Enanta’s strategy involves achieving complete target knockdown with its STAT6 inhibitor.

Financial Results

• Royalties from Maverick continue to be a source of income for Enanta.

Operational Updates

Respiratory Virology:

• Zelicapavir is under study for high-risk adults, with data expected in late Q3.
• Pediatric data reported safety, pharmacokinetics, and antiviral activity.
• High-risk adult study involves 180 patients, dosed within 72 hours of symptom onset.
• The primary objective is a meaningful reduction in symptom duration.
• Enanta is considering a partnership to advance zelicapavir and 323, another RSV drug with a best-in-disease profile.

Immunology:

• Enanta is developing wild type KIT and STAT6 inhibitors.
• The KIT program is focused on IND-enabling work, with submission targeted for next year.
• The STAT6 program aims to replicate Dupixent’s benefits through oral administration.
• The company demonstrated strong preclinical results, with plans to select a development candidate later this year.

Future Outlook

• Enanta aims to secure partnerships for its RSV program post-clinical data acquisition.
• The company is open to various commercial strategies, including combination therapy.
• Continued IND-enabling work is planned for the KIT program, with an IND submission expected next year.
• Selection of a development candidate for the STAT6 program is anticipated in the second half of this year.

Q&A Highlights

• Discussions covered the challenges of RSV studies and the importance of patient selection.
• Enanta believes a one-day symptom benefit aligns with historical respiratory drug data.
• The current high-risk study is expected to show significant viral load reduction.
• The company is designing a Phase 1 study for its KIT inhibitor with flexible dosing strategies.
• Enanta is aiming for complete target knockdown with its STAT6 inhibitor, considering strategic decisions before clinical data in symptomatic patients.

For a detailed understanding, readers are encouraged to refer to the full transcript below.

Full transcript - Jefferies Global Healthcare Conference 2025:

Akash Shuari, Pharma and Biotech Analyst, Jefferies: Alright. Good afternoon, everyone. My name is Akash Shuari. I’m a pharma and biotech analyst here at, Jefferies. We have Ananta and Jay.

Always great to talk to you, Jay. Ananta will have a some brief opening slides that will give a bit of a background of what’s going on in the company, and then we’ll get started with q and a. Thank you very much. Go ahead, Jay.

Jay, Unidentified, Enanta: Thank you very much. Here’s the clicker. Before I begin, I’ll 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 our website. For those of you less familiar with Enanta, we’re historically a virology infectious disease company, and more recently have moved into the space of immunology.

So I’ll touch a little bit on respiratory virology and immunology in my opening comments and then we’ll turn it into a fireside chat. So in terms of virology, I wanna just focus on catalysts that are coming up in our program. Recall, zelicapavir is an N protein inhibitor. We reported pediatric data last December. This is one high risk patient population that we’re studying.

The other is a high risk adult, which I’ll talk about in just a second. But to remind you of the peds data that we did, the objectives were to look at safety and PK as a primary objective in part one, and then antiviral activity, and we set out and hit those objectives that were defined. As an exploratory endpoint, we began to look and to begin the validation process on a new tool for observer reported outcome information called Bresolve P and got encouraging early data in that as well. But the data set that is coming is on the high risk adult study. We expect to report that in late Q3.

We recently completed enrollment of that study. It’s about one hundred and eighty patients who are at high risk, either because of their age or because of some other comorbidity. We dose for five days for patients who come into the trial within seventy two hours of symptom onset. So we’re trying to bring people in fairly early for treatment, then we treat them for five days. And the primary objective is a symptomatic endpoint looking at lower respiratory tract disease using a tool that’s been used before, patient reported outcome tool called the RIIQ symptom scale.

So we’ll be looking at that as well as a number of secondary objectives as well. But how do you benchmark a study like this when there is no approved treatment for RSV? We hope Zelle and our other program will bring some of the first therapies for RSV infection forward. But we really have to kind of look at how is clinically meaningful defined in symptomatic endpoints and registration studies for other respiratory drugs. And so I have on the left of this slide, Tamiflu, sort of in the middle right slide is Zofluzah, otherwise known as Baloxavir, and then on the right hand side, Encitralvir, which is a SARS CoV-two protease inhibitor of Shionogis.

And each of these drugs was proved on a about a day symptom improvement in terms of reduction of of symptom duration. You can also see that these were in registration studies and the n is at the bottom, about five hundred to seven hundred patients in the phase threes that were run. And so these are at least some guidelines that we can use to be thinking about expectations for what is clinically meaningful in an RSV study. So again, RSV HR is about one hundred and eighty patients. We’re aiming to show clinically meaningful reduction duration about a day or more and we’ll also be looking at a lot of other aspects of the study including virology and other symptoms, bronchodilator use, and so forth, so that we’ll get a really complete picture of all of this.

And then once we’ve determined the effect size in this phase two proof of concept study, of course, we would move into a phase three study that would be bit larger and would be powered to show statistical significance on that about a day duration. So that is the plan. We’ve also indicated that our preference is to move this forward in the context of a partnership. We have another RSV drug behind this one called three twenty three, which has probably a best in disease profile if you look at stage for stage of data that even comparing it to Zelle versus any other RSV therapeutic that’s ever gone into clinical trials. So we’re excited about both of these molecules, but this is the next catalyst for us in this program.

Shift gears quickly to immunology, set the stage there. We have two announced programs in immunology. One is in wild type KIT, the other is in stat six inhibition, and I’ll touch on those briefly here. So for KIT, it’s basically this year is focused on IND enabling work. We announced our candidate, our development candidate fourteen twenty one late last year.

It’s an animal molecule. It’s very potent in terms of in vivo activity, highly selective for KIT versus other family kinases and broader based on kinases in general. Doing what Enanta does well, we’ve optimized ADME properties. So it’s a very nice looking molecule right now. Again, we’re scaling up and pushing or knocking down the IND enabling activities this year, and our aim is to get it IND as early next year as possible.

STAT six is a very interesting target. We are focused on oral small molecules here at Enanta. I think everyone’s familiar with the drug Dupixent, which works through the IL-four, IL-thirteen signaling pathway. And STAT6 is the key transducer in the downstream effects of blockade. So our goal is to disrupt at that stage and then basically try to recapitulate the broad clinical benefit that Dupixent has served with, but with an oral agent.

To that end, we have been working very hard in this program, making some very good progress. So we have very good potency and selectivity. Again, we focus on ADME to get these molecules very well behaved into high quality drug candidates. Ultimately, highly selective for stat six, that’s important. There are a lot of other stats that you don’t wanna disrupt and we’ve put out some of that data in our other corporate deck.

You can find more detailed slides in that. But it’s highly selective. We’ve also demonstrated really good target engagement in vivo. In fact, we see rapid and complete inhibition of phosphorylated STAT6 after a single dose in a mouse model. We’ve shown that data and also little bit newer now.

We’ve now demonstrated a good anti inflammatory profile in an ova asthma challenge model. So we are continuing to do a little bit more apple polishing, although we’ve got some great prototypes and our goal, we’re still very much on track to select a development candidate in the second half of this year. Things that we’re demonstrating already, good intrinsic permeability, we’re looking at metabolic stability, clearance, target distribution, and again looking for once daily dosing, low DDIs, etc. And this is ovalbumin asthma model, this is new data that we’re showing, which basically shows that you sensitize the animals with Ovalbumin, come in with the oral inhibitor and then challenge, and you can see in fact a very good reduction in lung phospho stat six activation. And this, if you look at the slide here, is showing the concentrations or the percent activation at Cmin concentrations of the drug.

So that’s a very conservative way of looking at it. Obviously at Cmax and higher levels than Cmin, you’re gonna see a much more robust robust inhibition than that. But we were looking at c men just to characterize that. We’ve got many other molecules going through this process right now as we zero in for our finalist candidate. This is just a little bit more data from it, showing that you can see lots of other effects in terms of looking at cytokines and chemokines and the bronchial alveolar lavage fluid, as well as inhibition of eosinophil infiltration into the lungs.

So all in all, very robust effects shown with some of our early prototypes here. So I think I’ll just put it there. Here are the key catalysts for the year, which are pretty much what I’ve already gone through. And with that, turn it back to Akash to open things up.

Akash Shuari, Pharma and Biotech Analyst, Jefferies: Alright. Love it. Thank you. So, you know, it’s interesting. You’ve got, you know, RSV, Stat6, Kit.

These are hot targets right now. And so it’s I think it’s gonna be a timely conversation. So let let’s obviously, it’s a tough biotech environment. You guys have royalties from Maverick, but, you know, I think there’s a element of being pragmatic in this space as well. Let’s say okay.

So I wanna be clear. You guys are interested in RSV. I just think with the viral kinetics, running any study is just incredibly difficult because of, you know, how quick how hard it is to identify and get them into that kind of sweet spot. You’re gonna have data, let’s say, that you show a one day benefit. That is probably it doesn’t sound like a statistically significant benefit for what the phase two is powered at.

Would you then go into phase three with a one day benefit, or would you say, you know what? Now I’m going to look at my backup l inhibitor and say it’s actually the combo that I’m more excited about. How do you balance those two decisions?

Jay, Unidentified, Enanta: Yeah. Well, ultimately so it’s a it’s a good question. Ultimately, again,

Akash Shuari, Pharma and Biotech Analyst, Jefferies: our

Jay, Unidentified, Enanta: aim, in this as we’ve started our migration into immunology migration into immunology is to gather these key data sets. We have the first in peds study in our hands, incredibly safe in peds. We showed a great viral load drop. We’re about to come on data here, which if positive is phase three enabling. And I think we would have that conversation in the context of a partnership.

Because again, our goal is ultimately to partner find our commercial partner after these datasets, which, you know, will allow them to progress. We do have three two three, and it’s a great, great molecule. So one could imagine taking zelicapavir forward first, getting it approved, moving into the RSV treatment landscape, and then bringing up three twenty three as a sort of as a next gen molecule. They can also be used in combination. We’ve looked at that at least pre clinically.

They they’re well behaved. You can think of patient populations that are highly immune compromised, for example, that might benefit from two mechanisms rather than one. You can think about prophylaxis with one. So there’s lots of different ways that you could play a commercial portfolio here. But again, our objective was to bring forward two, you know, replication inhibitors, not entry inhibitors, but, you know, bread and butter replication inhibitors, different mechanisms, and then have a portfolio that we can team up and get through the finish line with the first ever treatment for RSV.

Akash Shuari, Pharma and Biotech Analyst, Jefferies: So kind of a pointed question here, but I, you know, I think it’s important to understand. Because, again, this is a large cap development program for RSV. Do you feel like there’s alignment with strategic discussions? Because I’m sure you’re talking about you have to partner this out. Is that day, of symptom benefit a profile that you think a strategic partner they’ve kinda communicated to you, hey.

We’d be excited if that you’re able to deliver that as well.

Jay, Unidentified, Enanta: Yeah. I I won’t talk about business discussions, but, you know, again, what I can say is that, historically, when you look at respiratory drugs that have been approved based on symptoms, the improvement has clinically clinical benefit has been about a day. Yeah. Whether that’s two different flu drugs, COVID, and so I think it’s it’s in line with what you would expect.

Akash Shuari, Pharma and Biotech Analyst, Jefferies: Helpful. And, you know, the previous RSV studies, it was you know, you would assume maybe there were more, elderly patients. In reality, you ended up getting a pretty healthy cohort in in South America. Talk to me about how

Jay, Unidentified, Enanta: I’m sorry. Could could you I’m not tracking.

Akash Shuari, Pharma and Biotech Analyst, Jefferies: So your previous study, which is not statistically significant on viral load or symptom reduction, but that was run-in a healthier It was in

Jay, Unidentified, Enanta: a healthy adult population, a young, healthy adult population. So

Akash Shuari, Pharma and Biotech Analyst, Jefferies: how confident are you guys this time that you have the right types of patients to show kind of a delta? And can you kinda compare and contrast the patients that were in that prior study versus the one you have here? Because I’m sure you have some sense of the baseline as well.

Jay, Unidentified, Enanta: Yeah. So in terms of, enrollment criteria, you know, we instead of the, you know, open enrollment to otherwise healthy adults, well, that happened to contract community RSV, we we got them in within forty eight hours of symptom onset. You remember that. Yeah. Know, back in the day.

Absolutely. So because we were like, we have to try to get these people as early as possible. They’re otherwise healthy. And what we found was that wasn’t early enough. You have to get them impossibly early if they’re in a immune competent state.

And even at the forty eight hour time point, by the time we gave them the first dose, their viral loads had already peaked and were coming down. Their symptoms had already peaked and coming down. It’s just impossible to show a drug effect on that tail. In contrast, these are adults who are elderly. You know, they’re at least 65, but we capped the the population that was between 65 and 75 because we didn’t want just, you know, otherwise, healthy adults who were, you know, north of 65.

Akash Shuari, Pharma and Biotech Analyst, Jefferies: And so we skewed it.

Jay, Unidentified, Enanta: You know? We skewed it to, people who were 75, and we skewed it to people with COPD and congestive heart failure and other risk factors. Factors.

Akash Shuari, Pharma and Biotech Analyst, Jefferies: So What percent is that is that of the total population of 75 or with some of these

Jay, Unidentified, Enanta: meaningful comorbidities? Capped people who were just sort of basic asthmatics who were sixty five to seventy five at twenty percent.

Akash Shuari, Pharma and Biotech Analyst, Jefferies: Okay.

Jay, Unidentified, Enanta: So eighty percent of the study is, you know, in a higher risk category. And these are the this is exactly the patient population that the agencies indicated in their guidance that they, you know, should be sought for approval.

Akash Shuari, Pharma and Biotech Analyst, Jefferies: And so tell me about the viral kinetics there because, you know, the other population I know you guys had trouble enrolling the enrolling it was patients post stem cell transplant, like this very niche population where we’ve been more of an orphan drug. But that was one of the only indications like, I think this was the old arrow compound where it was a similar benzo backbone from you guys, but that was one of the rare instances where you were seeing, at least in a subpopulation, a signal with an antiviral. And it took about five to seven days to get to peak viral load. Right? And when you think about the viral kinetics and time to peak load with a immune compromised elderly population versus that kind of niche in hospital stem cell population transplant population, Are they more similar?

Are they different? What has your work suggested?

Jay, Unidentified, Enanta: Well, you know, the stem cell transplant recipients are are very different. And that study Right. You know, RSV TX was our transplant study. I think we, you know, we were trying to recruit that thing in the pandemic. And we had transplant bone marrow transplant recipients who were incredibly I mean, it’s an incredibly cure cautious group anyway.

But in the pandemic, you know, these people are double masked. They’re not going out. Nobody’s seen anybody. And so it was impart it was really, really hard time to recruit that study, and I think we got around a dozen or so participants and decided, you know, we have to really concentrate our efforts and get these two studies that I’m talking about Right. The ped study and the high risk adult.

And we knew that those would be the faster paths to market anyway, so we just doubled down and concentrated on them. In terms of viral kinetics though in a immune, somebody who’s sort of devoid of an immune system is very different. They’re just you know, we had a twenty one day dosing period in there. Probably that’s the place exact place where you would be thinking about using both drugs Yeah. You know, if you had them at your disposal so that you didn’t have time for the virus to make mischief in a immune compromised host, you know, mutation with mutations, etcetera, etcetera.

So it’s hard to really kinda compare that population, but all I can say is that in the adult high risk setting, we tried to skew the risk factor in a very real world way, but also in a way that, you know, tried to capture, concentrate those high risk adults.

Tara, Unidentified, Enanta: Good. And just to add to that, you know, both of those populations, Jay is talking about the high risk, patient population in the current study and the immune compromised, are very, very different in terms of viral kinetics and symptoms as the patient population in RSVP, which were otherwise young, healthy adults. So the viral loads tend to be much higher in these higher risk patients. They What are talking

Akash Shuari, Pharma and Biotech Analyst, Jefferies: about eight, like seven, eight log?

Tara, Unidentified, Enanta: Yeah. It depends on, you know, the exact assay that you use and when you catch them. But they’re definitely higher. And more importantly, they’re more prolonged. So they don’t come down as quickly.

Akash Shuari, Pharma and Biotech Analyst, Jefferies: Yeah. That seems like the angle because I don’t like, I have a hard time believing that an elderly person is like, again, time to symptoms, I don’t think it’s gonna be particularly different. So you’re still probably gonna be catching these patients within two to three days of them having symptoms, and then it’s like, okay. It’s really getting bad. We have to go to the hospital.

So my guess is you’re still probably cash catching them as they are either approaching or at peak viral load. It seems like that’s gonna be hard, you know, to do. But the angle here is that the clearance

Tara, Unidentified, Enanta: Mhmm. Much

Akash Shuari, Pharma and Biotech Analyst, Jefferies: longer. Is gonna be more prolonged, and that’s where you see the dose

Jay, Unidentified, Enanta: window to try to

Akash Shuari, Pharma and Biotech Analyst, Jefferies: make Is that way to think about it? Yes.

Tara, Unidentified, Enanta: Absolutely.

Akash Shuari, Pharma and Biotech Analyst, Jefferies: That’s really interesting. I’ve always asked you guys this question. Like, you know, some of the issue sometimes the issue with the NANCHE is, like, do you have a study that’s powered to hit stats on? You know, that’s what a lot of investors are gonna ask. What is your level of confidence that you are and and and I’ll let’s put it this way.

What is the primary endpoint? And is it viral load reduction? Is it symptom reduction? I just wanna be clear. And then number two, are you powered?

Is if you show a one day benefit, is that statistically significant? I just wanna make sure.

Jay, Unidentified, Enanta: Yeah. In in a study of this size, a one day is likely not. I mean, you’d have to see you’d have to see what the placebo looked like at

Akash Shuari, Pharma and Biotech Analyst, Jefferies: the

Jay, Unidentified, Enanta: source, but the placebo would have to be incredibly short. You can see in these phase three studies where they were powered to show a day, there were around five hundred to seven hundred patients, whether it was flu, two different sponsors with flu, a different class with COVID. I think to see stat sig on a day, you know, that’s the kind of phase three range

Akash Shuari, Pharma and Biotech Analyst, Jefferies: of 500. But reasonable for a phase three. And then also on the

Jay, Unidentified, Enanta: But down here Yeah. Just the last bullet point on on this slide. And so you’ll define the effect at at a 80. I mean, we could have done 500, seven hundred patients, but we know, it’d take us a few more seasons. Right?

Akash Shuari, Pharma and Biotech Analyst, Jefferies: Right.

Jay, Unidentified, Enanta: And the key here is get the proof of concept, get the directional thing, see, you know, if you can find about a day, may not be stat sig on a 80 patients, but you look at it in the context of did you see virology lineup? Did you shorten the time to symptom improvement?

Akash Shuari, Pharma and Biotech Analyst, Jefferies: What about viral load reduction? What are you guys expecting there?

Tara, Unidentified, Enanta: Yeah. And so, you know, again, I think viral load in these patient populations is being compared to placebo, which is also declining. And so in our ped study, we saw about a log over a log at the end of treatment. And so that’s something reasonable.

Jay, Unidentified, Enanta: And COVID drugs, again, people it took me a while to get my head around it because I was coming from the hep c world where you see five, seven log reductions. But in these acute infections, as Tara mentioned, the placebos are coming down. Paxlovid and SARS CoV-two protease inhibitors, when they show an antiviral load, it’s or antiviral drop, it’s about point eight logs, maybe a log, something like that. Yes.

Tara, Unidentified, Enanta: And I mean, just they are. You know, for this study, the point of it was twofold. We wanted to get confidence around the compound and moving forward in this program. And we’ll get that with the many endpoints that we’re looking at. And then also to see what a treatment effect size might be to enable powering a larger phase three.

Akash Shuari, Pharma and Biotech Analyst, Jefferies: Lastly, RSV, and then I actually we definitely wanna hit on the other stuff. On the L inhibitor, you mentioned that they’re doing you’re seeing something that you haven’t seen with previous compounds. Talk to me about what you’re seeing, in terms of speed of onset of viral load reduction.

Jay, Unidentified, Enanta: It’s it’s, so we didn’t

Akash Shuari, Pharma and Biotech Analyst, Jefferies: in the abbreviated

Jay, Unidentified, Enanta: deck, we don’t have that slide. And even in our current corporate deck, which, we have on our website, it you go you have to go back to the challenge study dataset where we’ve got all the slides in there. But what you will see, is it is incredibly fast at knocking down infectious virus. So if you look at, not just viral load reduction, which looks, it’s PCR driven assay, so you’re looking at live and dead virus Yeah. Fragments and stuff.

It looks very good there. But when you look at cultured virus, within twelve hours after the first dose, I think all but two patients in the study had were the virus was gone. And so that you know, Zelle was good and and we’ve seen other challenge studies that were, you know, not bad, but nothing knocked it down like three two three. So imagine if you can take that virus down about a day faster, even if you’re getting, you know, whatever it is

Akash Shuari, Pharma and Biotech Analyst, Jefferies: Wait. So did you overlay the challenge curves and said one I remember you used to give me grief on that, on the n inhibitor, and you’re like, oh, you shouldn’t be looking at this. Are you saying that now maybe that is the

Jay, Unidentified, Enanta: what you’re saying? Again, you can’t

Akash Shuari, Pharma and Biotech Analyst, Jefferies: I’m kidding. I’m kidding.

Jay, Unidentified, Enanta: But You were you were pointing to a a toxic, molecule that got ultimately

Akash Shuari, Pharma and Biotech Analyst, Jefferies: But it was lumasitabine. Development. Right. Right.

Jay, Unidentified, Enanta: Yeah. Was a nuke. We’re a non nuke. We don’t wanna get into the nuke preliminary scheme, but it’s a nuke. It’s super potent.

Akash Shuari, Pharma and Biotech Analyst, Jefferies: I’m interested in seeing that, and I think there is an angle there for sure. Okay. Maybe stepping back to Kit. You know, obviously, one of your your peers was recently acquired. Here’s the thing, the way I kinda think about it.

There are games you can play in terms of, knockdown on trip days, and you can say 80% is actually a %. There are error bars in terms of some of these heme markers, and and and you can have high baseline hemoglobin. You can have males versus females. And so to me, I’m skeptical that any of these compounds are not gonna have on target heme toxicity, frankly. And all these top compounds are relatively, selective as well.

So when I think about what would differentiate any of these drugs, I think it’s the it’s the clinical development plan that actually doubles down on it being oral. And so I would almost imagine, like, a very, very clever titration scheme where you get to certain levels of tryptase reduction and then stop, and then you look at where your kind of heme markers are. And if you can have something clean there, that that can really help in terms of strategic decisions going forward. How would you design knowing what blue you know, what what some of your peers have done, how do you design a phase one study that is generating more useful data to make a more informed decision? And, again, do you how how would you design it differently than some of your peers?

Jay, Unidentified, Enanta: Well, I think and I’ll let Tara comment on it too. But I I mean, we’re trying to distinguish ourselves certainly from antibodies, so Celdex and Jasper with really long half lives that become tricky even if you try to have a shorter half life antibody, it’s still multiple days. Right? And in this area, I think you’re you’re right. It’s about how do you come up with very clever dosing strategy that allows either, you know, sort of a knockdown and then a maintenance or intermittent dosing or, you know, basically figuring out what is the most titratable scheme that you can come up with.

And suffice it to say, we imagined our program with that in mind. So some of the characteristics of, fourteen twenty one, I think, are gonna allow for, some very interesting flexible dosing design.

Akash Shuari, Pharma and Biotech Analyst, Jefferies: Do you think, maybe too long of a half life is a bad idea. Right? So, like, when when is a half life too long when it comes to a daily oral?

Jay, Unidentified, Enanta: You know, we’ll have to it’s hard to know. Multiple days too long.

Akash Shuari, Pharma and Biotech Analyst, Jefferies: Yeah. Forty?

Jay, Unidentified, Enanta: You know? So once a

Akash Shuari, Pharma and Biotech Analyst, Jefferies: day Forty might be too

Jay, Unidentified, Enanta: long. Possible. Are you going for shorter than are

Akash Shuari, Pharma and Biotech Analyst, Jefferies: you thinking about 20 like, let’s put it this way. When you think about a daily oral, is it maybe a mistake to have over forty hours of half life because you get kind of a steady state drug accumulation?

Jay, Unidentified, Enanta: Yeah. And the key is about being able to turn it off.

Akash Shuari, Pharma and Biotech Analyst, Jefferies: Right? Right.

Jay, Unidentified, Enanta: It’s one thing about turning it on, and you do get accumulation, and then there’s a longer tail and so on and so forth. It’s impossible to know the answer, Akash, in terms of what is too long. All I know is historically, we’ve just tried to find the right sweet spot for dosing, And, you know, it may not be having a super long half life as an advantage.

Akash Shuari, Pharma and Biotech Analyst, Jefferies: Got it. And as we think, there have been compounds that have shown liver toxicity here. I think generally speaking, you know, if you can avoid the Dilly rule of two or should, you know, are you confident that you can get to, let’s say, 80 to 90% IC coverage at a dose that’s below a hundred mix?

Jay, Unidentified, Enanta: Yeah. I can’t answer that today.

Akash Shuari, Pharma and Biotech Analyst, Jefferies: Okay. Stat six. I thought there was some really encouraging data. I don’t know how to interpret it, to be honest with you, but I do think in terms of knockdown, you’re seeing stuff that I have not consistently seen with a degrader. When you think about an inhibitor and you think about differentiation like, because here’s here’s kind of my worry.

I don’t understand stat six in terms of its correlation on clinical endpoints. I don’t think anyone does. And when I look at the story of Entyvio, when I look at the story of even Dupi, like, it’s not just receptor occupancy or IC coverage. There’s frankly efficacy that’s going there’s a dose response with some of these drugs that are well beyond simply, like, pocket fit. Right?

Like, you’re getting complete target receptor occupancy. So when you think about stat six and amplification downstream because it’s an it is an upstream target, how important is it to be hyper potent? Right? So not just 90% knockdown, but a % or more knockdown. And do you think you’re gonna be able to deliver that with an inhibitor program?

Jay, Unidentified, Enanta: Yes.

Akash Shuari, Pharma and Biotech Analyst, Jefferies: Okay. Do you think you’re gonna be able to get levels of in of of target knockdown or steady state inhibition that is meaningfully higher than a degrader?

Jay, Unidentified, Enanta: Well, I think you don’t need to be meaningfully higher than the degrader. I mean, you need to knock it all down. And as long as you can as long as you’re operating within a PK range where, you know, trough concentrations ultimately give you the knockdown you need, then you’re fine. I mean, it doesn’t and so I I I feel very comfortable and confident in small molecule here.

Akash Shuari, Pharma and Biotech Analyst, Jefferies: Yeah. How and then maybe lastly, because you are in a more constrained cash position right now, but you have programs that could be theoretically quite valuable a strategic partner or for you guys internally. How’s would your team be willing to make a strategic decision on the stat six program before you have clinical data in, like, in in symptomatic patients? Like, do you think if you can do something like healthy volunteer PKPD, do you feel like that’s a really meaningful card flip for you guys?

Jay, Unidentified, Enanta: Well, we I think we saw this week that phase one data in healthies can be a big value creator.

Akash Shuari, Pharma and Biotech Analyst, Jefferies: How soon do you think we can get that ’20 like, end of twenty six?

Jay, Unidentified, Enanta: So let us we haven’t guided that far out on SAT six yet other than DC in the second half of this year, but we’ll refine that when we Okay.

Akash Shuari, Pharma and Biotech Analyst, Jefferies: Alright. Manoj wants to

Jay, Unidentified, Enanta: be in the trial. Combination. Sorry?

Akash Shuari, Pharma and Biotech Analyst, Jefferies: Manoj wants to be the We’ll do primary research. We’ll enroll ourselves if

Jay, Unidentified, Enanta: you want. Okay. There you go. Sounds good.

Akash Shuari, Pharma and Biotech Analyst, Jefferies: Alright. Thank you. Really appreciate it. See you guys.

Jay, Unidentified, Enanta: Bye now.

This article was generated with the support of AI and reviewed by an editor. For more information see our T&C.