Good day, and thank you for standing by. Welcome to the Abivax management call to discuss late-breaking abstract at the UEG conference. At this time, all participants are in a listen-only mode. After the speaker's presentation, there will be a question-and-answer session. To ask a question during the session, you will need to press star one one on your telephone. You will then hear an automated message advising your hand is raised. To withdraw your question, please press star one one again. Please be advised that today's conference is being recorded. I would now like to hand the conference over to your speaker today, Pat Malloy. Please go ahead. Great. Thank you, Sandra. And good morning and good afternoon to everybody, and thank you for joining today's call to discuss the results of the late-breaking abstracts presented at this week's UEG meeting in Berlin. Joining me on today's call are our Chief Executive Officer, Marc de Garidel, Chief Medical Officer, Fabio Cataldi, Chief Financial Officer, Didier Blondel, and Head of Medical Affairs, Chris Rabbat. We are also fortunate to have Dr. Marla Dubinsky joining us today to provide an overview of the data presented at UEG Week. Dr. Dubinsky is a Professor of Pediatrics and Medicine and Co-Director of the Susan and Leonard Feinstein IBD Clinical Center at Mount Sinai Hospital. Following Dr. Dubinsky's presentation, we'll move to a Q&A session. Before I hand the call over to Marc to make some opening comments, I'd like to remind you that we will be making some forward-looking statements today. A summary of those forward-looking statements can be found in the slide deck. Now, I'd like to hand the call over to Marc de Garidel. Marc. Thanks, Pat. So we are very excited to share this very fascinating data that shows its first-in-class molecule can work in induction in all types of population, from the naive to the most refractory population. In the next few months, we will continue to update the medical and financial community about the phase III quality of life data, the biomarker data, as well as clinical combination data with other all injectable agents. We thank you for your continued interest in our obefazimod, as our intent is to build a premier IBD company. And now we're going to turn our attention to Marla's presentation. Thanks, Marla. Thank you, Marc. Thank you, everybody, and hello from Berlin, where, again, we're going to go through the ABX data, the phase III program that was presented both yesterday and today, actually, and we'll review both data sets so just as a reminder, in terms of the study design, the phase III program you see. There were two induction trials, and our responders, in essence, would be filtered into a maintenance trial where they were re-randomized into both either the 50 or 25 milligram or placebo, which is important, as we talked about today. We're going to show the week eight data, and Marc talked about other things that will be coming forth in terms of the data, but what we're going to focus on today is the types of patients that actually enrolled in this trial. Just to highlight, you can see by the green boxes, there's a reason why we're sort of highlighting and emphasizing the severity of the population. We've heard a lot about that. We've talked about, even in the press release, noted that we were talking about the most refractory patient population to date, just because of the timing. A lot of people had been exposed or could have been exposed to any therapies, including JAKs, and therefore, for registration, phase III induction. This is the first really looking at this severe population. How do we, as clinicians, define severity? One is endoscopic severity, and the first green boxes really show you the percentage of patients who had the highest endoscopy score, just as a reminder, zero to three, and obviously, the most severe endoscopy sub score is three. And you can see, again, you're looking at about 60% of patients overall when we pooled both the ABX one and two. What I do want to highlight, you can see the green boxes, that there was about a 10% delta between Mayo endoscopic score in ABX one and two, just sort of looking at some subtle differences across the population as we go through the data. Then the other green boxes are really focused on what we define second to severity is number of treatments you failed, really. Essentially, how refractory to prior therapies have you been? And what you can see here, about 50% of patients have seen at least one advanced therapy. And then there's a group that actually received the JAK inhibitor, which is really why I wanted to highlight and note that this is the first registration trial we're seeing this many JAK refractories, meaning failures of JAK inhibitors, which I think is very important when we think about optionality in the clinic. When you have someone who today is getting what we believe to be the therapy for severe refractory ulcerative colitis, the fact that these were included, and I'll show you the data in just a minute, really, as a clinician, sets us up for success with our patient communication that there's hope. Second of all, you can see one through four plus, and you can see the division of how they were divided, and we'll get into clinical response across these categories of exposures in just a moment. Let's move on to the primary outcome metric, which is, at the moment, the primary endpoint, sorry, with both doses showing you a pooled analysis and looking at the 25 milligram and the 50 milligram. But again, what we all look at, and if you've had conversations with me before, you know I'm focused on deltas because it's not the height of the bar per se. It's really the delta between placebo and effective arms. And what I really want to congratulate the team on is the control of the placebo rate because we know some recent press releases and what's going to be presented here at UEG Week, sometimes it's hard to control for placebo rate. And what the company did by maximizing 15 milligrams, limiting certain districts, certain areas in certain countries by not over-enrolling, was really important for us to be able to control the placebo rate. But what you're seeing here is a delta of 16% in the 50, I'm rounding approximately, and 13% in the 25. Next slide. This is probably, I think, the most sort of applicable for a clinician, for you all to be understanding how important this is in the clinic. Remember, on a given day, we see patients who are naive to an advanced therapy or have responded in the past but are just not on one now, or they've been exposed to many, at least one. That's what happens the day a drug is approved, right? We have decision-making, and we don't want to be just deciding, "Oh, this drug can only be used in this population," or, "This drug can only be used in that population," as we've experienced with JAK inhibitors, for example, or even S1Ps, to be fair. So the ability to differentiate this drug really comes down to the slide, and Dr. Danese presented it today, and the idea that when you look across endpoints, that yes, there is a difference in naive versus exposed, but that is every drug we have. The point being is that the more refractory you are, you really start to see better deltas between 50 and 25, actually, so that's also to note because dosing may be flexible based on where a patient is in their treatment journey, where their severity is, and everyone loves dosing flexibility, just to let you know, particularly in the U.S., which is why even our IL-23s have dosing flexibility in the U.S. that they may not have in other countries, so emphasizing that across hard endpoint, clinical remission, really understanding the deltas between, and the fact that it made significance, particularly with 50 milligrams. This is a really important talking point for us as clinicians to give hope to our patients who have failed every other therapy, including a JAK. What this does also is looking at the other important endpoint, not just clinical remission, which is always the primary because we remind everybody that clinical remission includes endo improvement as well as clinical symptoms, right, so clinical remission is even a little bit of a higher bar, but the fact that you're seeing endo improvement at rates where you, again, see that in refractory, there's an 18% delta for 50 milligrams in endo improvement, going to a zero or a one, and someone who started at a three, 60% or so, started at a three, which means they had a two-point change, possibly a three-point change, and I'm sure we'll evolve the data Mayo zeros and ones as we evolve over time. But the fact that you had such significance in a very refractory patient population gives me a lot of hope when I talk to my patients about the future and where I put these drugs in my arsenal, and so when you look again, if you look just at clinical response, because we're only focused on clinical response, because just so you know, I know we're all looking at remission and endo improvement, guess what a patient cares about and what a clinician who's going to use this drug is they want to know, is their patient going to be calling them in two weeks to tell them that they're not responding by way of symptoms? We have no endo visualization. We don't talk about endoscopy, so clinical response is really important, and moreover, what I want you to take away from this slide is zero and one look similar. By the way, that's what S1P showed us as well, but what S1P didn't show us is that when you go above one therapy failure, there was no difference from placebo. I think it's really important that we understand the refractory nature, how this is different than S1Ps, very different in terms of refractory nature, and the good news is, as of now, you won't have to fail every biologic on the planet before you can get this drug, which is where the other small molecule, which is Rinvoq, so it's really important that we have a good dialogue and understand the placement of this therapy and how we, as clinicians on the podium, because that's what really matters, what we say at an education conference helps guide treatment, but also be able to have the data to back us up. And of course, you can't talk about efficacy without talking about safety, but I do want to put the box on your radar. You see the JAK inhibitor population, right? So here you're seeing, again, severity. And in a JAK inadequate responder, you see a delta that is that significant to us as clinicians. Again, all looking back, I get it. But this is what we, as clinicians, rely on when we're making treatment decisions. So it's important to note how we look at data when we start talking to patients about the future. All right. You can't talk about efficacy without a fair balance safety discussion. Really, there's not much to see here. And we'll go a little bit further into the thing that everyone wants to talk about is headaches, but we'll get there in a minute. What I wanted to show you here is across the board outside in the 50, which you see probably accounted for more by the headache difference between 25 and placebo. Otherwise, the one malignancy was prostate cancer in a male who was above the age of 50, so that, again, is not thought to be anything that is associated with OB, and so really, you're looking at across the board very similar, and guess what we care about and what clinicians care about? Serious treatment emergent adverse events, and you can see, really, there's no difference between placebo and even 50 milligrams. If we want to dive into the next slide, which goes into any AE that was at least 1% prevalent and greater than placebo. So pretty well, anything that's literally short of a scratch from stubbing my toe. It sounds like this is what you got on this table. There are no new AEs that are not on this table. So I think, as you can see, across the board, a hodgepodge. I'll get to the headaches in a minute, but the rest of the non-headache stuff. What I want everyone to understand about headaches is the following: that you can see that, yes, headaches are increased. Sure, we know that it was increased compared to placebo, especially in the 50. However, look at the other two lines under headaches, meaning the second and the third. What you can see here is that the average time to onset, you can see, is about one day versus seven. Sorry, my glasses. One day. Starts on day one. Starts on day one. Oh, on day one. So zero to one. That 24-hour period is the point. So within the first 24 hours when they take OB, they will actually get a headache. Okay, but let's look at the next line. How many actually discontinue it due to a headache? And you can see, again, there's no difference across. But what I do want everyone to understand, if this makes sense from a pharmacologic perspective, what happens is that it's believed that the headache is really due to the parent drug. And what happens over the first 10 days, and basically by day 10, there is no parent drug. Around day two, you start to get more of the metabolite, which doesn't cross the blood-brain barrier, overlapping as the parent drug is going out. So it makes sense by day two that that makes sense from a metabolism perspective as for the parent drug, then converting over to the metabolite. So other than that, I'll be honest. I mean, I'll be happy to answer questions. There really isn't something here that is different than what we see in trials. Don't meet even thresholds for anything that is beyond just what we track in clinical trials, including elevations. Great. Well, thank you, Dr. Dubinsky. And operator, we can now move to the Q&A session. Thank you. As a reminder, to ask a question, please press star one one on your telephone and wait for your name to be announced. To withdraw your question, please press star one one again. Please stand by while we compile the Q&A roster. We will now take the first question from the line of Yatin Suneja from Guggenheim. Please go ahead. Thank you, Dr. Dubinsky. That was great. Thank you so much for walking through these data. Two questions for me. First one is on positioning. I think you touched on it a little bit, but given these data, given how severe the patient population is and the efficacy across, I would love to hear from you how do you envision adoption and the positioning across, I would say, the UC treatment spectrum? And then the second one is around maintenance. Could you maybe talk about how should we think about the maintenance data? Any hint in these data that gives you comfort that the maintenance data is going to look similar to the induction or probably better? Thank you. Hi, Yatin. Thank you. So I'm going to take the maintenance because we don't have maintenance data. All we have is from the phase II-B. But what I do want everyone to understand is that what we're doing and what we're going into and the way we think about treatment, and we've seen it across even every drug that has come, if you have a more refractory patient, and we already started to see it in the data at week eight, it is possible that people who have higher endo score at baseline, and we'll start to dig into the data as we start to evolve and have more data, but endo 3, multi-refractory, we know that just based on week eight, 50 performs better than 25. We'll see what the maintenance is. It could be that 25 holds anyone who went from 50- 25 in a rerandomization, but in general, the way our mindset is, as a clinician, typically, for more severe patients, we tend to think more is better than less. That's just the mindset we've taken with 23s. We've taken with TNF. We've taken it with JAK, for God's sake. That's even with the labels and the severity of side effects that people are catastrophizing around. We say to them, "You had a refractory course. You're going to need 30. And the only reason to go to 15 is if you have a side effect that you're not happy with, acne, headache, whatever it will actually be." So I wanted to answer the maintenance side because maintenance is driven often by whether or not a more severe population needed to go back up to 50 if they went down to 25. That's how we evaluated Rinvoq. I'm going to stop there because it is very similar in our mindset on maintenance decision-making. We need the data before we know whether or not 50 can be maintained on 25. If you're in deep remission at 50, you could probably stay on 25. If you're responders but not deep remission, you may need to go to 50. It'll evolve. That's how our clinical practice. Second question about positioning, again, as I sort of hinted, is that what we've been searching for is a drug that we can use first line in naive 5-ASA failure, which, by the way, what I didn't say is what is also unique about this study is 5-ASA failures were not. They couldn't have only failed 5-ASA. They also had to be on conventional or failed steroids, whatever the case may be, which is a unique, what we call naive population, right? So we need to already know that at baseline, we are starting with a more severe population, which we didn't talk about, but I think that's really important in table one as a way to talk about severity. So for us, we thought maybe S1Ps were going to be in. I'll be honest. Chris and I have had a conversation about S1Ps, so he knows how my feeling is around the fact that the goal was to try and have a drug that was an oral that I can use first line, maybe in a one failure, but not a two failure, but I had Rinvoq, right? That was sort of our mindset around small molecules. And then, of course, the idea that you need to do an EKG, a skin check, maybe an eye check before starting. No one knew, could it be before? Can I do after? Too complicated for a gastroenterologist who is the first line of defense who wants to give an oral but doesn't want to do a lot of work to get someone on an oral, and for me, if all this, as we evolve the story and what we've seen from phase II and we evolve the safety and you could see it already at eight weeks, this could fit anywhere. That's basically my take on the long term, also the durability, by the way. I mean, we studied every time point out to maybe until they were 80 years old, maybe. No, I'm kidding, but we were following them forever until we had this data we were hanging on. And so, I think the durability, the fact that we were able to dose de-escalate to 25 later on, also gives me dosing flexibility so that if there is something that a patient that we need to reduce the dose, we know we can maintain, so I think it's really for us to take the maintenance data next, but to us as clinicians, I don't represent the entire HCP community, but we are looking at this among the chitter-chatter chit-chat amongst ourselves that this gives us a lot of flexibility on where we use these therapies in practice. For those of us who see refractory, we're excited. For those first-line HCPs who make new diagnoses, amazing. They've been looking for a pill. I don't need to do an EKG. I think this is really a nuance that needs to be stressed. Great. Thank you. So operator, let's move to the next question. Thank you. We will now take the next question from the line of Julian Harrison from BTIG. Please go ahead. Hi, good morning, and thank you for taking my questions. I have a related question on maintenance efficacy. I'm just curious if you think it's reasonable, Dr. Dubinsky, to expect a progressive trend in clinical remission rate, especially in advanced treatment, inadequate responders, keeping in mind just how early maybe eight weeks is here, and then also, I'm wondering how you think about the relative importance of induction versus maintenance efficacy when you're considering treatment options for your UC patients. Thank you. Thank you, Julian. So thanks for reminding me about the fact that every other, really, I mean, except for Rinvoq, which was good, but in the S1P and in the IL-23 world, it was a week 10 or week 12 outcome, right? 10 for ozani mod, and then it was 12 for etrasimod and for all the 23. So one thing we did see in the phase II clinical trial program, we saw that things get better over time even. And when we chose an eight-week, obviously, you sort of balance endoscopy versus placebo rate. There's a lot you balance when you choose your endpoint. So here we are almost a month earlier than the current S1P and the current IL-23. So we believe, at least those of us, again, who are interested in this asset or thought about it or excited to see what happens next, is as you follow patients, particularly refractory, you need more time. I'm going to give you a historical lesson. So with Gemini, even vedolizumab, we looked too early. Six weeks was ridiculous to look for Crohn's patient in particular, but we learned. IL-23, in Europe, for example, with Miri, you could give another 12-week induction. With JAK, with Xeljanz, the first thing that came out is refractory people need to take longer. Eight is too early. In refractory, you have to re-induce or give an extended induction. Same with Rinvoq for UC Crohn's, obviously, there was a safety concern about giving longer. But I can tell you, in clinical practice, many people who are refractory need more than eight weeks to get into remission. So I think, in general, this is not how we practice, right? We do not say, "Oh, you're done in eight weeks. You're either a responder or not," particularly in a multi-drug failure. So I think, Julian, the idea that we need maybe to even bake it a little bit longer in the oven, especially in a refractory, I think will be really cool to see. Time to response will also be something everybody looks at when they're choosing induction. So we'll get that later on, which I think in a competitive UC world where time and urgency is of the essence for people who are on steroids and need to stay on the toilet all morning because they can't get up, time to, more than Crohn's, is actually important. So we'll see that later on, obviously, way later on. But Julian was asking, "How do I make decision-making on drugs?" And so I think for me, I can't wait to see what happens also if you look out another eight weeks or another four weeks and match it more closely to what we know as recent week 12 outcomes. And I've already commented on what makes the difference for us in maintenance, and it's all personalized to the patient's severity. Yeah. Great. Great. Operator, we can now move to the next question. Thank you. We will now take the next question from the line of Sam Slutsky from LifeSci Capital. Please go ahead. Hey, thanks for taking the questions. Great work on the presentation. Going back to actually the kinetics of clinical response being a leading indicator for converting to clinical remission, I guess for the Abivax team, do you recall how likely it was for a patient to convert from clinical response and induction to clinical remission and maintenance during the phase II study? Yes. Yeah. Yeah. So yeah, this is Chris. Yeah. It was a little over 50% of patients that responded ended up in remission at week 48. Yeah. So then they continued to climb from there. Okay. And was that on top? Was that on top of the remission patients already? Could you repeat that? Oh, yeah. That 50% conversion, was that on top of patients who were already in clinical remission after induction? Yes. Yes. So I just want to add also what's interesting in phase II-B is 40% of the patients who were not responding at eight weeks did end up in remission at one year. Yeah. So we put that all up together. And this is why the open label extension, again, it was open label extension for some caveats to this. We ended up with 66% of the patients being in remission at one year, which is indeed way above where we were at eight weeks and three months. Yes. 100%. So that's why I think, and especially you had a very refractory population also in remission. It wasn't like these are naive dominant patients. So again, I think our rush to sort of not understand that that severity will tell us over time that people take a little bit longer. I think hopefully we'll show it again in the III, like what we saw in the II-B. Yeah. Great. Sam, did you have another question? I guess just on the, and you may have answered this to start, but you have that one figure of clinical response based on number of prior advanced therapies. I guess just have you looked at clinical remission too or other endpoints as well as this and kind of how that looked if so? Yeah. We certainly looked at it. There's just not enough room to fit all the data in one presentation. So we'll be presenting that at a later congress. Yeah. I mean, Sam's asking because the depth of the remission can we get is it even more remarkable to be able to communicate to patients, not just response, but there's also endo other outcomes that we want to make decision-making just as I noted why response is so important because that's the first thing we want to tell patients, especially refractory. But Sam's right. We've made all of our decisions on durability of these drugs based on deeper endpoints. So I think that will be important as well. Great. Great. Thanks, Sam. Operator, let's move to the next question. Thank you. The next question is from Jason Butler from Citizens JMP. Please go ahead. Hi. Thanks for taking the questions and appreciate the detailed presentation today. I guess, Dr. Dubinsky, you talked about those considerations in the maintenance phase, but when you think about starting this drug, can you just kind of talk us through the pushes and pulls of whether you would start a patient on 25 versus 50, given the tolerability profile and the remission data, how you think about that with the less and more advanced patients? And I guess, why would you not start all patients with the higher dose? And then just the second question, how do you think these data translate through to the potential for the drug in Crohn's disease? Thanks. Great. So thanks for the question. The first one is really important. When you say it's funny because we always say that we'll never go wrong if we use the higher dose. There's never, honestly, I mean, you look at we don't have as much dosing optionality for induction. Actually, it's usually in maintenance where we have dose flexibility. There's Rinvoq at 45. Velsipity is two milligrams. It's not like I have dosing flexibility. However, what you said is correct. We, as a community, feel more is always better, no matter what, as long as there's not a safety hit. 100%. Look at Rinvoq, 45 - 16, right? We went all in because we knew that you need more for a refractory population. So you're right. Unless headache tolerance is different than day one and then gone by day two or three, unless we see that differentially, that could be the only, based on what we see today, the only reason why we would lower the dose. Or if someone has, I don't know, a baseline of severe migraines, would we make a decision? I'm making this up on the fly, by the way, because I'm thinking about the patient tomorrow. Would I ever make a decision on 25 when I see this data? And right now, the answer would be no. There's no need. You give more in induction, just like why combo story is why we think combo is better in induction than it is in maintenance, because you want to hit them as hard as you can upfront because that makes a difference of if you don't get them there with induction, how do you maintain them in maintenance? So I think you're right. I think that most of the time it will be 50 will be where we're going to go. Was we through in the organization? Oh. But yeah. I mean, listen, what I'm excited about is when you look at the MOA, so I'm not looking at the name of the drug, whether it's oral, IV, the Th17 aspect. Today, if you look at IL-23 just for a minute to say that's within the same framework of how we impact the immune system, Th17 pathways, they're better in Crohn's than they are in UC. We can use, and this is the fact that this looks refractory in UC. I just want everyone to understand that with our 23s, we do not walk away thinking that 23 is great in refractory population for UC. Crohn's, we can use it refractory or we can use it naive, so the fact that we are seeing a distinction here is already better than our 23s because we walk away with 23 thinking this is a naive play. I'm talking IV subQ 23 in UC. But in Crohn's, we're like, whatever, bring it on. It's a great asset and it's a great target. So I think as we evolve the story, I think mechanistically, I would guess that it should look like other IL-23. So I'm excited to see how it evolves in Crohn's because right now, we think 23 is good for naive and refractory for Crohn's, but not for UC. Interesting. You learned something. I did. Thanks. All right. Thanks, Jason, for your question. And operator, we can move to the next question. Thank you. The next question is from the line of Thomas Smith from Leerink Partners. Please go ahead. Hey, guys. Congrats on the stellar data. Thanks for taking our questions. First, for Dr. Dubinsky, could you just elaborate a little bit on your expectations for the maintenance data we're going to get next year? And I guess based on everything we've seen now with the phase III induction experience, how do you expect the maintenance data to evolve relative to the phase II? Are there reasons for thinking that it could improve or anything that you would be concerned about potential degradation, I guess, from the phase II experience? And then a second question, if I could, for the Abivax team, could you just provide a little bit more color on the lipase increases that were seen at the 50-milligram dose level? Realize these were relatively low rates, but how elevated were the lipase levels? Were there any clinically relevant sequelae? And did these lead to any treatment discontinuations? Thanks so much, guys. Thanks, Thomas. I'm just going to have Fabio talk to the lipase, and I'll come back to the maintenance process. Yeah. Thank you, Marla. So if you're looking at the elevation of the pancreatic enzyme, in this case, the lipase, it's way below what we see typically in inflammatory bowel. They're more or less equivalent by group. So we feel that it's within the disease threshold, actually way below the disease threshold. We are monitoring the pancreatic enzymes, which is something we don't do typically in practice. Not many physicians do that because we observe elevation of enzymes in the pancreas all the time in this patient. So it's something that we really don't do. The important thing to note, to close the answer fully to your question, is that we don't see abdominal pain. So this elevation does not translate in acute pancreatitis. We have really just less than a handful of cases in pancreatitis, which is divided by group. And Thomas, in follow-up, I also asked the team because not only abdominal pain, but there's nausea, vomiting, other things. There was no pattern, meaning those are randomly, irregardless of lipase levels. So there's not evidence of clinical changes that match the lipase, right, Fabio? No. Absolutely not. Yeah. All right. So the second question on, again, when you're evaluating eight weeks, what do you know about maintenance? I mean, again, I think the biggest question is going to be, does it get better with time? That's number one. Even people who are on 50 who dose de-escalate by randomization to 25, can we maintain them? And my guess is, like every other drug, that there's a certain phenotype of patients that you could de-escalate after week 8- 25, and then there's going to be a group of people who you need to stay at 50. That is a rinse and repeat for every clinical trial where we've had a re-randomization, particularly where you're giving them a low potential, you've got de-escalated based on randomization. And like I said, it is usually the case that in retro, we look back and we're like, listen, Mayo score ≥ 3, if you failed at least two, you should be on 50 the whole way. Maybe that is different. We will see at how many people needed to fall out of the 25 and go into open label for 50. That's how we knew about Rinvoq. That is exactly how we knew that someone who's refractory should stay at 30, and we don't de-escalate to 15, as I noted before, unless they have acne. That is the only reason we de-escalate because we know what got you to the party is what you need to stay right on, particularly in endo three and refractory, and I would guess a JAK refractory patient, that's even going to be more meaningful, so outside of being in the lack of prediction business, I would say, why would this be different? That would be my first question, and the only thing that's unique is the growing increase of potential people who go from responder at week 8 who are in remission have the endoscopy at the week 12 or 16. That I think is going to be up for interesting investigation. Yeah. Great. Thanks, Tom. Operator, let's move to the next question. Thank you. The next question is from the line of Judah Frommer from Morgan Stanley. Please go ahead. Yeah. Hi, guys. Congrats on the update. Thanks for taking the questions. Maybe one, I guess, fairly high level. Can you give us an idea of maybe improved recognition or awareness of obefazimod at this point at UEG, maybe relative to prior to the top-line data, kind of awareness of the drug and the mechanism and how the differentiated mechanism is resonating with clinicians when compared to just the efficacy and safety data? And then maybe secondarily, any, I guess, catalyst timelines you can point us to on those additional data updates you'll be giving outside of the maintenance data over the next year. Thanks. Thank you. So I'll talk just about the enthusiasm because that's what we're in the audience. And I think, one, okay, so we know we've maxed IL-23s are out. We know there's somewhere down the line TL1As, and we don't have anything in between. And the idea that we're going to have an oral sooner than waiting for the next big revolution of TL1As, we need something now. So I think the excitement was around the proximity to getting the maintenance data, bringing the drug to market, and having something that is oral that I can use across the spectrum of patients. And that was the sentiment after the presentation yesterday. And then when you showed the advanced therapy stuff, everyone was like, well, this is really exciting. So I gave a lunch symposium today, and I could tell you that that was a very interesting topic where people wanted to know more about this because they're like, forget five years from now. I want to know what. Tell me more about the way that obefazimod will be integrated into your practice. Same questions you're asking me. The audience wants to know how do the academic guys view this and where will we put it into our practice? So that's what I can tell you on the side of the awareness here. And then, of course, whatever your PR does thereafter. Marc, maybe you can comment on awareness and MOA stuff. Yeah. I think in general, what I think is fantastic for Abivax here is the fact that we got two late breakers, two sessions. This is extremely rare for such events. And when you heard the presentation from the response to questions from the top KOLs like Marla, when you hear them saying, "This is incredible. This drug can work anywhere." These are compliments that you rarely get in the space. So you could tell the enthusiasm in the room was packed. There were several hundred people in the room for Abivax compared to UC a year ago. This is a different world. And then we met also in parallel with a number of doctors here with Fabio and the team. And I can assure you, whether you have been exposed to the drug or not, there is a lot of interest on obefazimod. So I think everyone is excited and looking forward to the maintenance. But in terms of next announcements, I think the next thing on the phase III is going to be a top-line on quality of life. We have measured up to eight different things in our PRO, including things that are very important to patients like fatigue, like bowel movement, particularly at night. So we're going to come up, I think, with very, very exciting data because it's important obviously that the medical community is excited about the compound. But at the end of the day, the patients have to note a change in their quality of life. And I just want to remind you, these patients are diagnosed at the age of 35. In our study, they were 42 years old. So this is a working population. This is a population that has a miserable life thanks to the unfortunate history of this condition. So I think we'll deliver top-line data in November. We'll release at ECCO. On top of that, the richness of our phase III will allow us to also publish more data on biomarkers for obefazimod compared to DDW. And as I told you in the introduction, we want to be at Abivax a premier IBD company. So scientifically speaking, we're going to continue with the year of 33s and 50s here to dominate the segment because we want to show that this drug would have the potential to be the reference treatment for IBD in the years to come. Great. Great. Thanks, Marc. And thanks, Judah, for your question. Operator, let's move to the next question. Thank you. Next question is from the line of Sebastiaan van der Schoot from Kempen. Please go ahead. Thank you, Doctor. Thank Doctor. Thank you for the excellent presentation. This is my question. I'm wondering whether you can talk a little bit about the growing use of advanced therapies in patients with maybe less severe disease, seeing also both researchers were suggesting positioning of obefazimod prior to advanced therapies. If so, could you maybe indicate what type of patients with maybe less active disease you would use obefazimod for over immunosuppression? Thank you. Sure. Thanks for the question, Sebastiaan. So a lot of the movement that's happening in our world is we're all accepting that 5-ASAs, which are approved for mild to moderate disease, do not, if they were tested in today's regulatory environment, may not even be approved for UC because symptoms are not enough, right? So that was endo, the full Mayo before, and physician you're talking, in my opinion, you're talking a different environment completely. And there are so many people that are walking around using nightly suppositories because their doctor said, "Well, if you don't want to do these pills, I'm going to give you an IV or an injection," and they walk away saying, "Thank you very much. I'll go do my own thing. I'll change my diet." And they're suffering. And that's why those like bowel urgency, fecal incontinence, all the things that Marc was sort of getting at, that's a fine burden. And we are unfortunately looking at a point in time for people what their disease activity is. We do not take into account the burden, the urgency, wearing a diaper. I mean, it's ridiculous. And so part of the safety fears of physicians was they didn't want to give drugs that were perceived as, maybe in their own opinion, weren't as safe as 5-ASAs. Well, if we could show that the headache rate is the same as doctors do when you give Lialda, which is a 5-ASA, and your patient will need to wear a diaper or use suppositories, you should be using this therapy. It reminds you of the safety of the 5-ASA, but has the efficacy across our portfolio. So to me, honestly, and this is a PSA to everybody in my room with me here, is to make sure that no patient is suffering unnecessarily when there is an oral that has the safety profile of a mesalamine. It is unacceptable. So I'm really passionate about this question, Sebastiaan, but what I'm saying is we as a community have the responsibility of making sure people get drugs that actually heal their colon, literally, not just on a commercial that says visible colon lining, but actually the burden of the disease for patients. So I think it should be applied everywhere, and that is the responsibility of all of us in this room and whoever and advocacy groups that to tell them that there's something that can help them early or late. Now, again, we're going to be approved for moderate to severe. One of the questions for the team would be, is there a mild to moderate for a later development plan? But I'm saying that we need to show that moderate, you don't have to wait till you're severe. Moderate actually straddles mild to moderate and moderate to severe. So let's focus on digging into who were the more moderate patients in the population and showing how much their lives improved. So it is a bigger question than what you asked because our definitions are changing, and our international organizations are redeveloping what is important as a target for patients, and it goes beyond what 5-ASAs have ever been able to show. So I think it's really important that the field keeps up and we start to continue to educate patients that they don't need to suffer anymore. There's no new normal you have to accept. What you have to accept is we have tools that can actually get you to work, all the things that Marc was saying, and you don't need to suffer. Great. Thanks. All right. Operator, let's move to the next question. Thank you. The next question, based on the line of Yale Jen from Laidlaw & Co. Please go ahead. Good morning. Thanks for taking the questions and congrats on the data. Just got two here. The first one is in terms of the JAK inhibitor resistant patients, most of those patients have been treated with Rinvoq, or what percentage have been treated with Rinvoq beforehand? And the second question is for Dr. Dubinsky that even we're still waiting for the maintenance data, and the drugs currently have shown to be very effective in treatment naive patients. So what is your thought or criteria for patients if you want to prescribe this drug to treatment naive or treatment without the advanced therapy patients? And thanks. Let Chris answer the JAK one. For context, what was the dominant JAK, Chris? Yeah. So most of the JAK failures were tofacitinib. There were a few who had upadacitinib, but dominantly tofacitinib. So most were Xeljanz, very few were Rinvoq, just to give you that background on the JAK. So if I understand correctly, it was how I'm going to is it a dosing question you were asking for maintenance? I just want to make sure I'm - No. I'm just saying that based on the induction data, what kind of patient you would if you want to use it in treatment naive patients, would there be any criteria or thoughts you will put into that to make that decision? Okay. So when we talk about treatment-naive, we really talk divided into 5-ASA failures only, which is a different population than this population, which was they could have seen 5-ASAs, but they had their failed steroids or immunomodulators. So this is even the next level of conventional therapy failure. So I was just sort of going on, standing on my soapbox, telling you that there's so many people who are deemed 5-ASA eligible only because in their minds, the patient doesn't meet the moderate criteria, which is complete nonsense, which is why I say what we view this as is, for me, who doesn't it says conventional therapy failure. I could do whatever I believe to be conventional therapy failure. If I believe a patient needs a drug that actually has a deep remission and/or an objective endpoint and not just symptom change, I'm going to use this drug instead of a 5-ASA. That's my own clinical opinion about how I will use this drug. So as long as they're moderate to severe for people in this room, from a regulatory perspective, that's what we're studying. But moderate is in the eye of the beholder. What we have to stop doing is what the regulators are asking us to do, which is define severity based on a single point in time. And so the minute my patient, who may look like a Mayo 1 on endoscopy, but is wearing a diaper, do you think I'm going to say, "Oh, the only drug for you is 5-ASA?" It doesn't. It's illogical. So what happens after the drug gets approved and it's in our hands the day a drug gets approved, we actually use it because this shows that I can use it in advanced therapy-naive patients as well as even severe refractory. So to me, it gives me optionality across the spectrum of moderate to severe. Yeah. And relying on also Marla's thoughts, we did a market research just after the data in August. And this was a U.S.-only with 70 physicians. One of them, there were two learnings about that market research. One is overall, there was a lot of enthusiasm from those doctors. They said 33% market share potentially in the refractory population, 15% in the naive. But also what they said is exactly on what Marla indicated. There are some patients today who are on 5-ASA, who are not necessarily doing well. But because of the current treatment landscape, physicians do not move them yet into advanced therapy, and to give you an idea, and we are going to do a more extensive market research now in the U.S. and a few European countries. We think potentially in the U.S., this could be up to 100,000 patients in the U.S. out of the 600,000 who are on current conventional therapy, so this could expand the market considerably for obefazimod, so again, stay tuned. We're going to do market research. We'll get back to you probably by JP Morgan. Great. Great. Thank you, Operator. Thank you. There are no further questions at this time. I would like to turn the conference back to Pat Malloy for closing remarks. Okay. Great. Thank you, Operator, well, thank you, everybody, for joining today's call, and thank you to Dr. Dubinsky for making herself available for the call itself. Look forward to continuing to keep everybody updated. We have posted an updated corporate deck on the IR section of our website, and with that, we will close the call. Have a good day. This concludes today's conference call. Thank you for participating. You may now disconnect.