Study Result

Jul 22, 2025

Hello and welcome to the ABTECT results conference call. At this time, all participants are in a listen-only mode. After the speaker presentation, there will be a question and answer session. To ask a question during the session, you will need to press star 11 on your telephone. You will then hear an automated message advising your hand has been raised. To withdraw your question, please press star 11 again. Please be advised that today's conference is being recorded. It is now my pleasure to introduce Senior Vice President Investor Relations, Pat Molloy. Great. Thank you, operator, and good afternoon and good evening, everyone. I hope you've had a chance to review the press release we issued after market close in the U.S. today announcing the positive top line results of the Phase 3 ABTECT induction trials. Joining me on today's call are our Chief Executive Officer, Marc de Garidel, and our Chief Medical Officer, Dr. Fabio Cataldi. In just a few moments, Marc will provide some opening remarks, and following that, Fabio will take us through the top line results. Following the prepared remarks, we will move to a Q&A session where, in addition to Abivax's management, we are honored to be joined by Dr. David Rubin. Dr. Rubin serves as the Chief of the Section of Gastroenterology, Hepatology and Nutrition, and the Director of the Inflammatory Bowel Disease Center at the University of Chicago. Also, please recognize that we have only had access to this data set for a couple of days, so exhaustive secondary analysis of the data has not been completed. As you will hear from both Marc and Fabio, we are preparing to submit subgroup analysis for presentation at an upcoming international congress. We have held back some subgroup analysis for those purposes. Before I hand the call over to Marc, I'd like to remind you that during today's call we will be making forward-looking statements. A summary of the forward-looking statements is included on slide 4 of this deck and can be referenced in our most recent 6K filing. Now I'd like to turn the call over to our CEO, Marc de Garidel. Marc, please go ahead. Thank you, Pat. Thank you everyone for joining us on today's call. Today marks an exciting day not only for Abivax, but more importantly for the patients and health care providers in the ulcerative colitis community. We are delighted to present to. You the top line results. The ABTECT trials were truly global endeavors, enrolling 1,275 patients over 30 months across 36 countries with participation from over 600 clinical sites. The ABTECT trials included both patients who were naive to advanced therapy and those who had previously experienced an inadequate response to advanced therapies. This comprehensive approach gives us a clear picture of the therapy's effectiveness across a spectrum of disease progression. I'd also like to highlight the fact that ABTECT is one of the largest Phase 3 ulcerative colitis trials ever conducted, which included the largest population of patients. With inadequate response to JAK inhibitor therapy. The results of the eight week induction trial highlight obefazimod's highly efficacious, simple, and safe profile. Finally, and perhaps most importantly, the 50 milligram dose demonstrated highly significant and clinically meaningful efficacy. We observed a robust 16.4% placebo-corrected remission rate with no new safety signals observed throughout the trials. This statistically significant and clinically relevant outcome, coupled with a reassuring safety profile, positions this therapy as a potentially transformative option for patients. Time for Fabio to speak about the. Result of the trials. Thank you Marc. Let's start briefly with the study design. This is the overall ABTECT program consisting of two identical eight-week induction trials studying two doses versus placebo, randomized 2 to 1 to 1 for 50 mg, 25 mg, and placebo, followed by a single 44-week maintenance trial which is randomized 1 to 1 to 1 for 50 mg, 25 mg, versus placebo. I want to remind you that the endpoints for FDA and EMA were different. For FDA, the primary endpoint was clinical remission. A key secondary endpoint were endoscopic improvement, clinical response, and histologic endoscopic mucosal improvement, which are referred to as iMI. Moving forward, for iMI, the co-primary endpoint was endoscopic improvement, asymptomatic remission. A key secondary endpoint were clinical remission, endoscopic improvement, and iMI. We employed innovative study design and execution element based on three simple but distinct pillars that we have been discussing since the beginning of the trials. First, we accelerate enrollment with clinical sites education and expand the presence of global GI counsel. Second, we aim to minimize placebo response with diversification of trial sites, elimination of concomitant use of immunomodulators, and a lower maximum concomitant steroid dose. Third, we aim to enroll a similar patient population in Phase 3 as we did in Phase 2 in order to get similar results. The baseline characteristics indicate a well-balanced distribution of participants with nearly 50% having prior inadequate response to advanced therapy and nearly 10% who had prior failure with a JAK inhibitor, which is the largest population of JAK failure patients in UC Phase 3 trials to date. Here is the ABTECT-1 primary endpoint for FDA, which delivered high statistically significant difference in both doses related to placebo of 21.4% and 19.3% for the 25 mg and 50 mg dose groups, respectively. The low placebo rate observed is a testament to the high quality of study conduct and design. Here is the co-primary endpoint for EMA, which was met for both doses with highly statistically significant difference for symptomatic remission. Endoscopic improvement, key secondary endpoint of endoscopic improvement, iMI, and clinical response were also met with both doses with highly statistically significant p values in FDA 2. The primary endpoint for FDA of clinical remission was met for the 50 milligram dose with statistically significant difference of 13.4% relative to placebo, but was not met for the 25 milligram dose. Although we do see a positive difference and a clear dose response, we will review results from the population which are positive for both doses. Both doses met the co-primary endpoint for EMA of symptomatic remission and endoscopic improvement with highly statistically significant difference relative to placebo. The 50 milligram dose met all key secondary endpoints including endoscopic improvements, anemia, and clinical response due to testing procedures. P values for the secondary endpoints in the 25 milligram dose are nominal. Notably, we continue to observe a clear dose response across all endpoints in the pre-planned full data analysis. For the FDA primary endpoint of clinical remission, we observe a clear dose response with statistically significant P values and differences of 13.2% and 16.4% for the 25 milligram and 50 milligram doses, respectively. This clearly addresses one of the key questions from the Phase 2B regarding dose responses. We believe the clinical remission rate observed in these induction trials is very competitive, especially considering the shorter duration of the study and the number of treatments currently available. We would like to discuss a few points about the 25 milligram dose. First, as a reminder, the EMA co-primary endpoint was met in both trials with highly statistically significant differences relative to placebo. Second, the pooled analysis shows a clear dose response with statistical significance for both doses. Although we have not shared baseline characteristics by treatment group at this stage, I'd like to highlight that the patient population randomized to the 25 milligram dose in ABTECT 2 was the most difficult to treat population across both ABTECT 1 and ABTECT 2. Based on baseline disease characteristics, we believe this type of patient might require more than eight weeks to achieve clinical remission as evidenced by the difference in clinical response relative to placebo. Lastly, key secondary endpoints were met for clinical response and anemia with statistical significance in ABTECT 1 and nominal significance in ABTECT 2. Reaching gears to safety, the final database lock will not occur until August but is more than 95% complete. We observe an overall favorable safety profile with no new safety concerns. We have low discontinuation rate due to treatment emergent adverse event and serious adverse events, both similar to placebo. Importantly, we observed no signal for malignancy and no signal for serious, severe, or opportunistic infections. Headache was the most common adverse event with lower rates of occurrence and discontinuation than observed in the Phase IIb trial. The headaches occur at the beginning of treatment, were transient, and last a median of less than two weeks. Based on the collective clinical trial experience to date, we do not believe this will be a barrier to treatment. Lastly, I'd like to stress we continue to observe no safety signal indicating the need for pre-initiation testing requirements. Thank you for your attention and I will pass the ball back to Barry. Thank you, Fabio. In summary, we are very pleased to report strong Phase 3 induction results with our first-in-class all year 124 enhancer. We look forward to reporting additional analysis, including efficacy in both advanced treatment-naive and refractory patients and patients that have failed the JAK inhibitor at the future international medical congress. The next significant milestone for the company is the completion of the 44-week Metanos trial if there is no timeline risk and will be read out in Q2 of 2026. Before we move to the Q&A, I would like to sincerely thank the patients who participated in the trials as well as the investigators and staff in approximately 600 sites and 36 countries. Without them, treatment advantages like this will not be possible. Now I would like to turn the call back over to Pat. Thank you, Marc. As we move towards Q&A session, I'd like to remind everyone that top line data only became available to us a couple of days ago, and therefore exhaustive secondary analysis of the data has yet to be completed. Also, as Marc pointed out, we're looking forward to presenting several subgroup analyses and complementary data sets at upcoming congresses. Before handing the call back to the operator for the Q&A session, I know that Dr. Rubin would like to say a couple words regarding the data presented today. Hi everybody. Thank you very much for letting me be here. As you heard at the introduction, I am a gastroenterologist and an inflammatory bowel disease expert at the University of Chicago, where I direct our center. I am happy to be here to discuss these positive results and to share with you a couple of insights into the uniqueness of both the mechanism and the delivery system, as well as to highlight the clinical significance of this finding for this important induction trial. First thing I want to make sure everyone understands about obefazimod is that this is a first-in-class new mechanism for the management of moderately to severely active ulcerative colitis. We have no other therapies in our field that treat the disease the way this mechanism is believed to work. In fact, the way I like to explain it is that rather than targeting specific active inflammation, it shuts it off at the source, resetting a balance of the immune system. That may not be as important to you, but I can guarantee you that to my clinician colleagues and to our patients, it will be a very important message and something that I think will be very quickly embraced. The second thing I want to highlight is that it is a small molecule. That means it's oral. Many of our monoclonal antibodies face a distinct challenge in ulcerative colitis because they are protein and proteins leak from active colons. That's a unique challenge we face that the dermatologists and rheumatologists do not have to deal with. Oral small molecules have a very favorable and predictable pharmacokinetic absorption and profile that avoids those challenges. That is also a very important message about this unique therapy. Third thing I do want to highlight is that this is a very positive study. While it is important, as you heard, to wait for maintenance results, in general, when we see such striking and clinically and statistically significant induction results, the maintenance follow-up, and if you look at their phase 2 results that had long-term follow-up, is something that I think is fairly predictable and will likely be equally impressive. Lastly, of course, is understanding safety and tolerability. I think that this overall has been a very positive study from a safety point of view as well, with no surprising or new concerns. I am very optimistic and enthusiastic about this for the people who live with ulcerative colitis and my colleagues who have to treat them. Thank you for your attention. Great. Thank you, Dr. Rubin and Andrew. Let's proceed with the Q and A session. Certainly. As a reminder to ask a question, please press star 11 on your telephone and wait for your name to be announced. To withdraw your question, please press star 11 again. Our first question comes from the line of Allison Bratzel with Piper Sandler & Co. Hey, good afternoon team and a big congratulations on this data set. Thanks for taking my questions. Maybe just first on differences in ABTECT 1 versus 2, could you just refresh us on differences in enrollment or baseline characteristics or geography between the two Phase 3s? That just might explain some of the differences across efficacy measures, just particularly for the placebo arms and the 25 mg dose group across trials. Maybe bigger picture on read through to maintenance. Could you just talk to your views on how this induction data could potentially read through to your maintenance readout in Q2 of next year as it compares to your Phase IIb experience. Thank you. Hey Allie, thanks for your question. Good to hear from you. Maybe we'll have Fabio take that one. Thank you, Pat. Hi Holly. The two studies, as I said, they begin with two sister trials. Basically, they're identical. Very minimal differences between countries. Japan was one of the drivers and I think probably the most noticeable thing that we observed in this past couple days looking at the data when we are blinded. As I mentioned at the beginning, we have not disclosed this information. If the information regarding the 25 milligram group in 106 was clearly more severe than any other of the groups, that could be maybe the reason why we feel a bit of a difference in the way that the two studies from an FAQ standpoint reminded that both studies, the 50 milligram port, was highly statistically significant. We met the Mea Primarium point for both studies. That's another good news. Of course, we are going to dive a little bit more and dissect the data in the days to come to better understand really what is really, if there is a difference between the two. We were able to keep the placebo under control in both studies. It's almost unprecedented to see a 2.5 in 105 and also very, very low in 106. Clearly, they tell you that the study conduct was optimal. Really an excellent execution of the trial and great. I think the follow up question was a read through to the maintenance so often. To say always the induction is really a prediction of what we are seeing, what we're going to see in the maintenance. If we are looking at our maintenance data or long term data in Phase II. Right. That is still ongoing, you see really an increasing efficacy. We know impact on safety. The safety stays really well under control in long term for what we have seen in the Phase IIb. The other thing that we are expecting, which is typical what we see clinically. Right. The patients with a high response, with a pretty high response in both studies, probably will translate in remission. We are probably going to see a much higher rate of remission in the maintenance study coming from both because the number of patients responding even in 106 in a 25 mg is pretty high. We are assuming to see basically to replicate probably what we have seen in the long term of the Phase IIb in 107, which is our maintenance time. Great, operator. Let's move to the next question. Certainly, our next question comes from the line of Julian Harrison with BTIG. Hi, thank you for taking my questions. Congratulations on these very impressive results. First, are you able to quantitatively or qualitatively comment on the activity of obefazimod in advanced treatment experience? Are you seeing resilient activity? In that subset, consistent studies? Second, how are you thinking about the. Read through to Crohn's disease? Finally, Dr. Rubin, I'm curious. How you think the rates of headache. Compared to 5-ASAs in your experience. Hi Julian. I'll respond to the first part of the question. As we indicated, we want to preserve the ability of the company to present at International Congress, you know, the split between biologic performance and bio-experienced. What I would say about the bio-experienced population is when you look at the combination of, let's say, clinical remission and clinical response, it gives us a lot of hope that this treatment indeed will have a great maintenance outcome for patients. We'll disclose more in a few months, but it's very encouraging. To be sure, I respond to your question. You're asking what is the prediction for Crohn's based on this data? Correct. That was my second question. Yes. Yeah. Typically what we have observed over the years is that every compound, every drug that has been tested in both UC and Crohn's, typically we see a very good effect if one indication works in the other as well. Right. There's been almost every single drug study approved to this date. We have mainly reason to believe that the drug will work mechanistically. You know, now that we know the doses, we believe that actually we did a good job in dosing. The study has been very well designed. It's at the beginning, so it's a little bit difficult to say anything about efficacy. We stay very, very optimistic that actually we are going to see very good results in Crohn's. As well. I'll address the headache question, but I'm going to start by addressing the other ones as well, if that's okay. For the experienced analysts on the call, you know that one of the challenges in managing inflammatory bowel disease and interpreting trial results is when we treat patients who have had prior treatments that didn't work or in which they were intolerant, so-called inadequate responders. I want to just clarify that traditionally those were biologic inadequate responders. I've already mentioned to you why. The mechanism and delivery system of this therapy I believe is going to bypass some of that. I also want to highlight for you that we're not talking only about biologic inadequate responders. With these two Phase 3 trials, it included the largest number to date of JAK inhibitor inadequate responders as well. That's a very important point for you because as this makes its way hopefully to our patients, we're going to think about it in both earlier phase management as well as in patients who maybe have already been on multiple other therapies including a JAK inhibitor. This therapy worked well in those more resistant patients and still had statistical significance in those breakdown sub analyses. I think that that's very positive. To understand my second comment about whether this may work equally well in Crohn's, of course we need to show that and Crohn's studies have some additional complexity. In terms of the mechanism, there's no reason not to think it's going to work in Crohn's as well. There's nothing unique about the active immune system in ulcerative colitis or in Crohn's of the colon especially and of the ileum as well that would make us think this isn't going to be something we should be actively pursuing and expect some nice results as well. The headache is a unique point that I am glad you brought up. It was in a small number of people, smaller than we saw with the earlier phase studies, and was not durable. It lasts for a short period of time in the first few days or week of treatment and goes away. We don't see that with 5-ASA in answer to your question. I don't anticipate that this is a therapy that's going to replace aminosalicylates in ulcerative colitis. This is a therapy that if everything goes as we hope and anticipate, would be positioned after aminosalicylates and earlier in the treatment algorithm before getting to injectable or infeasible therapies. I hope that addresses it for you. I was specifically interested in that and was pleased to see these results in that regard. Excellent. Very helpful all around. Congratulations again, operator. Let's move to the next call question. Our next question comes from the line of Thomas Smith with Leerink Partners. Hey guys, good afternoon. Thanks for taking our questions and congrats. On the really stellar data here. Asia for Dr. Rubin. I was wondering if you could just. Expand on your comments and how you're thinking about the induction results here relative to some of the other oral treatment options. How important is the prospect of being able to start obefazimod without specifically screening for ocular cardiac issues? Can you just talk about what. Proportion of your moderate to advanced UC patients you think would be an ideal candidate for a drug with obefazimod's profile here? Thank you for the question. I would start by just reminding the group that the S1P receptor modulators, ozanimod and etrasimod, that have been available now for some time for moderate to severe UC have unfortunately carried the concern by folks that there can be cardiac arrhythmias or macular edema. That's been somewhat misinterpreted. Sometimes perception is reality. It has to do with an asymptomatic, self-limited sinus bradycardia with those S1Ps. The S1P mechanism does have a rare event of macular edema, so that's led to people being hesitant to use them even though they're very good treatment options and safe otherwise. The JAK inhibitors, I'm sure that most here are familiar with the concerns as well as the fact that they had been labeled to be used after anti-TNF in the U.S. due in part to the concern about major adverse cardiovascular events and venous thromboembolic events that occurred in a Phase 4 rheumatoid arthritis safety study in high-risk patients. This therapy does not have either of those concerns. What I have advised the company and have been discussing is that as my colleagues in the GI world are learning about small molecules, they need to help them understand the differences in mechanism and not lump them all together. I think that they're going to be able to do that well and that this is going to have a clean signal when it comes to those prior concerns. We don't have to worry about that and we want to distinguish this mechanism as unique but also safe. Got it. That is super helpful, and maybe just a question for the company. I know you're still going through some. Of the subgroup analyses, I was just wondering if you could comment either quantitatively or qualitatively about some of the differences in efficacy from a regional basis. Was the efficacy in the North American subgroup consistent with the overall top line results? Was there any one specific region that was driving the treatment effect there? Thanks, Tom. Good to hear from you. Maybe we'll have Chris Rabat, Head of Medical Affairs, take that one. Hi there. The data is really fresh. We're still analyzing it, and today we've shared the relevant top line data. We'll have further disclosures at upcoming medical conferences, including looking at regional sub analysis. Good question. Got it. That makes sense. If I could just sneak in one last follow up. I know you've generated some initial data in combination with an S1P. Can you just talk about how you're thinking about potential combination strategies now that you have these really strong Phase 3 induction data and a really clean safety profile? Thanks so much. Yes, Tom, maybe we'll have Marc take that. Just how we're thinking about the combination given this, the profile of the drug that we're seeing right now. Yeah, we all know, and Dr. Rubin can actually speak better about that. I can do that. The future of ulcerative colitis treatment may also involve combination therapy, just like what happened in oncology. Two years ago, when we basically built our strategic plan, we really wanted to address this challenge up front. We are in the process of testing a number of compounds in preclinical experiments. We have to indicate that. However, those experiments are a bit hard to conduct because the technicalities of finding the right models where each individual drug works and then you can obviously test the combination is somewhat difficult given the story of some of the compounds. I would say more recently we have turned our attention to see two compounds that could be of interest. One of them is obviously the IL23, which has gained some momentum with FH2B. We are also looking at the Alpha 4 beta 7. We hope that by the end of this year we'll be able to report preclinical outcome of this combination. Great. Got it. That makes sense. Thanks for taking the questions. All right. You bet, Tom. Let's go to the next caller. Our next question comes from the line of Sam Slutsky with LifeSci Capital. Hey, good evening, everyone. Congrats on these great results and thanks for taking the questions. Got two for Dr. Rubin. I guess just when interpreting clinical trial data in ulcerative colitis, could you just talk about the relevance of induction data versus maintenance for determining how you might think about when to use a treatment like obefazimod? This next one, maybe you answered a little bit. Just as you think about new patient starts versus switches, kind of where might obefazimod play into that whole scheme based on its genius profile. Thanks for the question, Sam. I'll start with just thinking about induction versus maintenance. The traditional teaching and trial design that was essentially developed because of biological therapies and the absence of other options was that whatever worked in induction we would continue into maintenance, both because the mechanism was working, the so-called sequential monotherapy approach, and because we didn't really have much else. In biological therapies with anti-TNF, we early on learned that if you tried using it intermittently or episodically, patients developed immunity to the drug and had hypersensitivity reactions. With small molecules, we can challenge that assertion and that approach and think about whether a therapy could be used for induction only and then transition to something else in maintenance. In general, that is predicated on two things. Number one is the safety in maintenance, which is always the long-term safety concern considerations. Number two, it's based on understanding what else you can use with it or what you would transition to. The idea that we can induce with a single therapy, withdraw it, and then treat the patient with something else is of great interest. We do that with steroids, for example, but it's not proven and it would be a paradigm shift in thinking about how to do these types of treatments. The clinical trial designs are just like you see here. Even the ongoing other trials similarly pursue induction and maintenance. As you all appreciate, I'm sure, committing to maintenance therapy is also where there's more money to be made in the long term. That's another incentive for industry to develop these types of trials. Frankly, that's okay if it's working and again if it's safe. Safety becomes more important when you're in stable maintenance of remission. In regards to the second question you had, which was about where we would position it, I believe I would say to you that it's going to be the usual story, which is that people use what they know. There are the early adopters and then there are the people who are stuck because other treatments aren't working and they're going to throw this on as the caboose on their train of options that they've tried for a patient. I think it's going to remain to be seen whenever there's a new molecule and a new mechanism. There's a lot of the usual challenges that we face in educating people. When you have results that are this strong, it doesn't take that long for somebody to treat one or two patients. When that translates to their clinical practice, they become believers and then they start using it more. I think that we can predict that if this does what we hope in maintenance, that's going to be the story. There will be a little bit of a lag as people learn about it. Some of those who are hesitant and want to see longer term follow up, but we do have the phase 2 long term follow up to lean on for now. You'll see people starting to adopt this as an easier drug to use and something that they want to position early in their management strategies. I hope that gets to it. I know it's a little bit of a long answer for you. I guess just for a quick follow up in terms of, you know, the maintenance while we await those data. Obviously the Phase II data were strong. I guess if that's replicated, how big of a deal is that, the magnitude of benefit they showed in maintenance for Phase II in terms of, again, thinking of how it might be used in practice? You can understand even if you don't have colitis and don't treat people with colitis, that a once a day oral therapy that has a favorable safety profile and a very stable disease control would be a very attractive maintenance option. Even if you look at mesalamine, our old standby that we use for milder disease, those patients in maintenance are on usually two or four pills a day, large pills, because of how it's delivered. If you think about even our safest biologics strategies, IL23s and vedolizumab and Entyvio, we have to rely on injections or infusions. There is something very compelling about this, and obviously we want to be thoughtful about what we can expect with maintenance, but I think that this will deliver something that people are anxious to have and then we'll have the opportunity to learn more about it as we move forward. Great. Thank you, Dr. Rubin. I know we have a few more in the queue for questions and I want to be respectful of Dr. Rubin's time. If you can hold your questions to just one so that we can get through everybody, operator could you go to the next caller? Absolutely. Our next question comes from the line of Jason Butler with Citizens JMP. Hi, thanks for taking the questions and let me add my congratulations on the results. Just in terms of the two doses, was there any hierarchical analysis included in the statistical analysis plan between the two doses? Given the strength of the overall data set, do you plan on pursuing approval for both doses? Yep. Yeah, this is Chris. There was hierarchical. I know you guys have been asking that question for months now. I can tell you that we did test the 50 milligram dose first and all key secondary endpoints on the 50 milligram after that, and then we move to the 25 and then key secondaries after the 25. That's for the FDA testing strategy. We hit both primary and all key secondaries with the 50 milligram in both trials. As you know, 25 hit primary and key secondary in one trial for FDA. In the other trial it missed on the primary for FDA, but it hit on the co-primary for EMA. We think both doses are viable. We think both doses are important. Once you see additional data, you'll see why we think that both of. These doses should be taken forward. Great. If I could just squeeze in a real quick follow up. Do you have a final, at least rough estimate of enrollment in the maintenance study? Yes, the study is fully enrolled for maintenance. The patients are ongoing in the study and we are on target, as we say, for mid year next year for end of study results end of next year. I'm obviously not on the advisory committee for the FDA and we're not at that stage yet. I'll just make a general comment, which is that the FDA over the last number of years with our available JAK inhibitor is a good example. Also, our IL23s that have been approved in the IBD space have adopted the phased approach of understanding that more intense therapy seems to be better in induction, but dose flexibility is available in maintenance so that people can identify the lowest effective dose. We'll see what maintenance looks like. I think that these results are strong regardless of how you decide to slice them. I would just predict that perhaps the FDA is going to be interested in making sure we don't underdose in the induction interpretations anyway and maybe if I. Could just add and perhaps clarify. The maintenance data is on track to read out in Q2 2026, and we had 678 patients that moved on or that were eligible to go into the maintenance study. Great, thanks. Again, congrats again on the results. I always say the best predictor of maintenance is successful induction. That's my clinical message and my teaching. Expect the same in a trial. All right, our next question comes from the line of Judah Frommer with Morgan Stanley. Hi, guys. Let me add my congratulations to the results here. Maybe just kind of more of a planning question. Just curious how you're thinking about further. Funding the company with these results in hand, I'd imagine there were several scenarios you had kind of kicking around internally, but funding through the maintenance trial versus the combo trials that you've talked about, any color you can provide on that front. Hi, Judith. Didier Blondel, CFO speaking. Yes, we're still on the same line. Of course, we know we need to raise money in the short term. Our cash runway goes into Q4. We're refining our plans. What we want to do at minimum is to be able to fund the company until the maintenance that I read out Q2 2026, plus a. Bit of a buffer. We're talking about around $200 million for the rest. We'll see. All right. Thank you, Didier and operator. If we could move to the next caller. Certainly. Our next question comes from the line of Yatin Suneja with Guggenheim Securities. Hey, guys, let me add my congratulations as well, and I apologize if you addressed this question earlier because I got dropped twice. The question is on between the 50 and the 25 milligram dose. Did you prospectively or how is the hierarchy? Was the 50 milligram predefined as the first analysis that you do? If you have already answered that, the next question is, can you maybe help us understand what your expectation would be for effect in naive versus experience? Should we maintain, should we expect a similar delta being maintained? Generally, the placebo tends to be lower for experience. Just curious how you are articulating maybe. Final question, if I squeeze in, how transient were the headaches? Thank you, Chris. You want to take that? Yeah. Hey, Yatn. We did answer the hierarchical question just a moment ago. There was a hierarchy. We tested the 5% first for FDA for both trials. It was positive in both trials, and for EMA, it was a co-primary and both trials were positive on both doses. The second question, we have not disclosed that yet. We are holding some data back for some presentations at upcoming medical conferences. I won't comment further on that. The headaches were transient. You'll see on the slide deck that was presented. The median duration was actually less than a week across the board. We do not believe that these headaches are going to be limiting for. The upcoming of the therapy. Great, thanks Chris. Operator, if we can move to the next call. Our next question comes from the line of Sebastian van der Schans with Van Lanschot Kempen. Hi, good evening everyone and congrats on the stellar data set. Really great execution. I was wondering whether Dr. Rubin, maybe you could talk a little bit about the treatment adherence that we saw in the previous studies and how you will put that into context. I was wondering for the company whether they could already give some qualitative statements regarding treatment adherence in the maintenance part of the Phase 3 study. Whether you can say something qualitative about that. Thank you. The question is about adherence, and whenever you have a patient self-administering their therapy and they're feeling well, it's a natural tendency to potentially skip doses or be non-adherent. It's a well-described phenomenon in our field. It's something we educate about to remind people that if they're in remission and they skip a dose of their medicine, they will still be in remission. That's the point of remission. It will accumulate over time the more that happens, and then they'll have a much higher risk of relapse. It does require education. It also will require some better understanding later about the durability of effect if people have an interruption in treatment. All of those things are real-world considerations that we have to deal with right now with our JAK inhibitors, our S1Ps, our 5-ASAs, and frankly with our injectables. I hear you. This is always an issue with chronic conditions. It does require education and additional information and other ways to monitor people so that we know they're taking their meds. That's all part of a future plan I would hope and expect. It's a good question, but I can't say more than that right now. In a clinical trial, of course we're counting pills and we know what people are doing. Thank you. Or we think we do. I should say our next question comes from the line of Yale Jin with Laidlaw and Company. Good afternoon and my congratulations as well. Just two quick ones. The first one is that you guys mentioned that both 25 milligrams and 50 milligrams make you move forward. A specific question is that do you anticipate both movements forward to United States as well as in Europe, or one or two might be, or any difference? The second question here is that in terms of this drug, given the current data, although still need to see the maintenance outcome, what % of patients, at least in your practice or your understanding, might immediately benefit from this drug at this moment? Thanks. To answer the first question, yes, we are planning as we stand today to elaborate and consider bringing both doses for approval according to the data set for induction. Of course, we need to see what's happening in the maintenance. From a safety standpoint, there was a question before; the safety continues to stay very similar to what we've seen in induction and maintenance in a branded fashion. Regarding the subpopulation, I think you were asking about that. It seems like both doses of the drug work in both sides of the disease, so for both severe patients and naive. Again, we have not disclosed more information on that, but that's our preliminary answer to that question. Thank you. I'll now hand the call back over to CEO Marc de Garidel for any closing remarks. Thank you, operator. In conclusion, I would like to highlight that those results give us a lot of hope for patients with ulcerative colitis. We still have to reach the next stage, which is the maintenance study. As indicated before, this will be in Q2 2026. Finally, I'd like to thank all the Abivax team for the fantastic execution work done. Also, with 1,270 patients, 30 months to recruit, outstanding placebo results, execution which was changed, I think, a few months ago. I think this team deserves a lot of credit. Thanks to them, we see. Thanks to all the participants in the trial. Thank you very much, ladies and gentlemen. This does conclude today. Before we close, operator, I just want to thank Dr. Rubin for making himself available for today's call. I'm sure the audience found it quite valuable and just didn't want to let the call go without doing that. Thank you, ladies and gentlemen. Thank you for participating. This does conclude today's program, and you may now disconnect.