Good morning, welcome to the Dianthus Therapeutics conference call. My name is Michelle, and I'll be your operator for today's call. A slide presentation to accompany the call is available on the Investors section of the Dianthus Therapeutics website. Following the company's prepared remarks, we'll move to a Q&A session. Please note that today's call is being recorded. I will now turn the call over to Marino Garcia, CEO of Dianthus Therapeutics. You may begin. Thank you, operator. Good morning, everyone, and thank you for joining us today. Earlier this morning, we issued a press release with our early go decision for the interim responder analysis for our CAPTIVATE trial in CIDP, and we're thrilled to share with you more today on this call. This earlier than anticipated announcement reflects the Dianthus team's commitment and passion for patients suffering from severe neuromuscular diseases. I'd like to take a moment to thank them for their hard work. Specifically, thank you to the clinical development team, to the clinical operations team working on CIDP, and all the supporting players across the organization that are making this exceptional execution possible. I'm very proud and grateful to be part of this team. Just a note before I begin the presentation, we will be making forward-looking statements, and I would refer you to our SEC filings for more information. Next slide, please. I'm joined today by Dr. Simrat Randhawa, our Head of Research and Development, Ryan Savitz, our Chief Financial and Business Officer, and John King, our Chief Commercial Officer. I'll begin with a few introductory remarks about the CAPTIVATE trial and best-in-disease potential we see for claseprubart in CIDP, one of 3 neuromuscular conditions we are pursuing. Simrat will review our interim responder analysis for the CAPTIVATE trial. I'll discuss the opportunity we see for claseprubart in CIDP and upcoming milestones. We'll open up the line for questions. 2 slides forward, please. I'm overjoyed to be here to discuss the planned interim responder analysis and our early go decision to continue the CAPTIVATE trial evaluating claseprubart in CIDP at 300 milligrams, 2 milliliters every 2 weeks. A reminder that CAPTIVATE is an ongoing single 2-part phase 3 pivotal trial, and it's designed to support a BLA in adults with CIDP. Because it is ongoing, we are unable to share specific data and responder rates for Part A at this time, as we must protect the integrity of this pivotal trial. We will aim to provide some color and context, but protecting the patients in this trial is our priority. As a reminder, Part A is open label, where patients who are standard of care naive, stable, or refractory are dosed or switched within 7 days to a single subcutaneous injection of claseprubart at 300 mg, 2 mL every 2 weeks for up to 13 weeks. Only patients that improve by at least 1 point on the NCAT score for 2 visits in a row over their baseline, starting at week 5, can then move on to Part B. Part B is the randomized withdrawal double-blind placebo-controlled part of the trial. Today's announcement is an early go decision based on the planned interim responder analysis and Part A of the trial, which Simrat will speak to in a few minutes. For some of you, CAPTIVATE will look very similar to ADHERE, the trial evaluating efgartigimod in CIDP patients, which resulted in a broad label for the treatment of all adults with CIDP. You know, we generally cannot make cross-trial comparisons, obviously, and in this specific situation, it is even more difficult due to 3 very important differences. Please next slide. The first difference is CAPTIVATE allows patients who are refractory to IVIG or standard care to enter the trial. ADHERE did not. We strongly believe that active C1s inhibition will provide additional benefit above and beyond what IVIG could do for these patients based on the impressive improvements seen with riliprubart in their open label trial. Secondly, ADHERE withdrew IVIG, making patients wash out from their treatment and relapse before allowing them to enter their open label Part A. Patients had to deteriorate in a clinically meaningful way before they were allowed to be dosed with efgartigimod. CAPTIVATE doesn't do that. Like other complement inhibitor trials in CIDP, including riliprubart's proof of concept trial, CAPTIVATE switches refractory or stable patients from their IG treatment within seven days without a washout or making patients relapse. The third key difference is CAPTIVATE Part A defines a responder as a patient that improves above and beyond their baseline. Our goal was to see at least 40%-50% of stable and refractory patients improve by at least 1 point on the NCAT score above and beyond their previous therapeutic regimen, including IVIG, after an immediate switch and without causing a relapse. ADHERE demonstrated a 67% response rate, you need to keep in mind this response rate means only 2/3 of patients were able to recover or approach their baseline scores after they were made to relapse. 1/3 of the patients were not able to recover from their relapse. Why were we targeting approximately 50% responder rates with our Part A? This is based on the impressive precedent data set for active C1s inhibition in CIDP. Next slide, please. This is the proof of concept data I'm referring to with riliprubart, which is currently in Phase 3 for CIDP. This open label trial enrolled CIDP patients that were naive to or stable on a standard of care. As well as patients that were refractory to standard care and switched them within 7 days to riliprubart. In the group on the left, these are patients who are stable on standard care, including IVIG, were switched to riliprubart and 52% did even better than how they were doing before. Again, this is switched within 7 days. In the second group, patients were refractory to standard care and IVIG. These are patients with no real alternatives today to IVIG if it didn't work. Here again, 50% of patients improved when switched to active C1s inhibition. These are the patients that here did not allow into their study. This trial seems to suggest active C1s inhibition may provide a benefit for a significant% of your patients above and beyond what today's standard of care therapy could achieve. The third group on the right are the standard of care naive patients. Not surprisingly, the responder rates there look even more impressive. I will remind you that the dose for riliprubart in this trial and in their phase 3 trials is 600 milligrams, 4 milliliters every week. We are evaluating claseprubart at 300 milligrams, 2 milliliters, half the dose, a single subcutaneous injection every 2 weeks. In other words, they're dosing 4 times more drug than claseprubart, and if delivered in a 2-milliliter auto-injector, it would mean 8 shots a month for riliprubart versus 2 shots a month for claseprubart. How does this data inform our objectives for Part A of the CAPTIVATE trial? Next slide. With Part A of CAPTIVATE, the threshold for the go decision at 300 milligrams, 2 milliliters every 2 weeks was to see a confirmed response in the 50% range with patients or 20 out of the first 40 patients that complete Part A. This target was based on the approximate 50% response rate benchmark we saw with riliprubart in their open-label trial. Next slide. With this, I'll now hand it to Simrat to take you through the update and provide a little more color and context around our early go decision. Simrat? Thank you, Marino. The medical team is very motivated to get their primary results as quickly as possible based on what we have seen in Part A so far. I would like to emphasize that our interim responder definition was a very high bar to meet because it required an improvement in NCAT over baseline, a high efficacy metric to achieve. In addition, this NCAT response needed to be confirmed at 2 consecutive visits, 2 weeks apart, and could not occur prior to study week 7, eliminating therapeutic overlap with discontinued medications. Our go intention targeted an NCAT response rate of 40%-50% in 40 patients who completed Part A based on phase 2 riliprubart CIDP data. This means the upper end of our target was 20 NCAT responders. We hit this target prior to 40 patients completing Part A. On the safety front, we continue to be reassured on the claseprubart safety profile with no concerning safety events recorded, including no clinical symptoms of autoimmune activation, concerning bacterial infections, or study discontinuation for safety or tolerability issues. Next slide. As you can see in these pie charts, the patients studied in CAPTIVATE and the riliprubart phase 2 are quite similar based on treatment bucket. I'll add our results were not driven by a specific patient subgroup such as geography. Next slide. Let's switch gears to how the interim analysis has informed positive changes to the CAPTIVATE study design. Part A remains unchanged. We will continue to evaluate 300 milligrams subQ q 2 weeks. Second, we see no need to evaluate 600 milligrams in part B, so we are dropping that arm and part B will now be a 2-arm blinded RCT evaluating 300 milligram q 2 weeks versus placebo. Third, we are raising our part A responder target from 40% to 50%, which we feel is a comfortable bar to meet. The implication of these changes are a substantial reduction in part B patients needed from 192 to 128, and a greater reduction in part A patients dosed from 480 to 256. Next slide. Finally, we have the revised study schematic showing our updated CAPTIVATE study schematic with a 2-arm part B and a part A responder target increase from 40% to 50%. With that, I'll turn it back to you, Marino. Thank you, Simrat. Now moving to slide 15. Today's update continues to build on the promise of claseprubart as a potential pipeline and a product and best in disease therapy in growing and underserved neuromuscular markets. We announced impressive, robust results in generalized myasthenia gravis with our MaGic trial in September last year. Today, we have a milestone moment with an early go decision for our CAPTIVATE trial in CIDP. We look forward, as Simrat said, to completing this trial as quickly as possible. We will provide guidance for when to expect top-line results sometime later this year. CIDP is a $ multi-billion opportunity for claseprubart because of the significant unmet needs that remain for patients. Next slide, please. The CIDP market is a large and growing $ multi-billion market with an estimated 40,000 patients in the U.S. alone. The unmet needs in CIDP remain high and significant, including the need for more efficacious, better tolerated, and more convenient options. Next slide, please. This conclusion is supported by recent market research we conducted with a survey of 80 neurologists that treat CIDP in the U.S. What we heard clearly from them is they want new therapeutic options that provide 3 things. 1, greater efficacy with more consistent, sustained symptom control. 2, safer and better tolerated options with no box warning or REMS. Finally, more convenient, easier to use, ideally a self-administered therapy. Next slide. IVIG is still considered the most effective therapy on the market today for CIDP patients. Yet, when we specifically asked these neurologists how they felt about IVIG, we found that 3 quarters of neurologists surveyed told us they need therapies that can help patients that are refractory to IVIG, as they don't have any effective options for these patients available today. More than half told us that their patients on IVIG experience waning efficacy before their next dose, suffer a high treatment burden due to frequent and time-consuming infusions, and that they are concerned about IVIG's boxed warnings. These overall needs are what claseprubart aims to address effectively. Next slide, please. The target product profile for claseprubart in CIDP aims to be a potentially best-in-disease therapeutic. Our goals are to achieve efficacy that compares favorably to current standard of care therapies like IVIG, with a safety and tolerability label similar to the first generation C1s inhibitor, sutimlimab, or Enjaymo, which has no boxed warning of REMS. Finally, with a Dupixent-like convenience of a one-click, self-administered, fast auto-injector dose once every two weeks. Next slide, please. With today's update, we're well on our way to building a powerhouse neuromuscular franchise where claseprubart can compete effectively as a first-line biologic in 3 growing markets with over 150,000 patients in the U.S. alone. As I mentioned earlier, we have reached 2 important milestones in building our position in MG and CIDP, our next step is to read out our phase 2 MMN trial in the second half of this year. Next slide. Looking ahead, this will continue to be a catalyst-rich year for Dianthus. We announced this morning we plan to initiate our phase 3 trial in MG in mid-2026, evaluating 300 milligrams every two weeks, as well as 300 milligrams once a month versus placebo. Top-line results are expected in the second half of 2028. We continue to expect, as I mentioned, top-line phase 2 data from our MoMeNtum trial in MMN in the second half of this year. We also look forward to our GENESIS phase 3 results for Zilucoplan in MMN later this year, which should have very positive read-through to us. For DNTH212, our new clinical stage bifunctional fusion protein targeting BDCA2 and BAFF/APRIL, we expect to announce indications we will be prioritizing in the first half of this year, and then announce top-line results from our phase 1 healthy volunteer study in the second half of this year as well. As a reminder, we have a very strong balance sheet with cash balance of approximately $514 million as of December 31st to fund operations into 2028. Please turn to slide 22. With that, let me close with this one comment. Today's announcement is a double upside scenario for us. Not only did we hit our target number of responders much earlier than expected, and hence the reason we are here with you today ahead of our already accelerated guidance of Q2 this year. I want to point out that moving our baseline conservative assumption of responders required in part A from 40% to 50% is a huge change and a signal of our confidence in the data we are seeing. We went into this trial assuming success with a 40% ratio in part A, expecting to see similar efficacy to riliprubart. The fact that we are changing it to 256 patients or a 50% ratio on top of a go decision signals very strong confidence in the data we're seeing. With that in mind, thank you, and let's open it up for questions. Thank you. If you'd like to ask a question, please press star one one. If your question has been answered and you'd like to remove yourself from the queue, press star one one again. Our first question comes from Yatin Suneja with Guggenheim. Your line is open. Hey, guys. Thank you for taking my questions, and congratulations on the data. Really good results in our perspective. Two-part question. First is, I mean, when you are showing that the patient population is very similar to riliprubart, and despite that you're able to produce, or it seems like the efficacy is better than riliprubart. Could you talk about what your hypothesis is? What is driving the superior data relative to riliprubart? You know, you just made a comment on change in this percentage to 50% now. I know you cannot disclose the data, could you articulate, like, if you see, let's say, something in the 40-55% responder rate, would you have changed that? Does that need to be meaningful higher than your assumption for you to make that 50% change? Thank you. Thank you, Yatin. On the first question, let me hand it to Simrat to provide his perspective. To summarize the question was, you know, why do we think we're seeing data that kind of beat our expectations, which were largely based around what we saw with riliprubart's data? I think there are two possible explanations. One is, I think we're seeing that the hypothesis of classical complement pathway inhibition upstream seems to be real. Now we've seen it twice. we know that the mechanism is behaving well in this patient population. Of course, we know that we are a far more potent product, which means that we are probably delivering more upstream inhibition than they're able to. That's one hypothesis. The other hypothesis, again, is I just wanna caution everybody, like we are releasing an interim analysis. This is in a meaty but a small number of people. We designed an interim at a time when we thought it would be informative to the study. Again, that should mean something. Again, it is in a relatively small number of people. It is, So, you know, I just wanna make sure that that is also well understood. Yeah, on your second question, I think what you're asking is, if the response rates we had seen were somewhere in the 40%-55% range, would we have changed it to 50%? No. We needed to see a substantially higher response rate than that to move that 50%. That 50% assume is a conservative number to make sure that we absolutely don't risk under enrolling Part B. Next question. Thank you. Our next question comes from Alex Thompson with Stifel. Your line is open. Hey, great. Congrats on the data. I guess for the subpopulations here, maybe could you comment on whether you're seeing response rates that are sort of consistent with what you would expect based on the riliprubart Phase 2? Then could you also comment on sort of what it is to, you know, define a responder in your study versus the riliprubart Phase 2 and how that might be more rigorous or not? Thanks. Surely. I think what we've suggested is that the overall response rate that we're seeing seems to be higher than what was seen previously. What that would imply is that in each of the buckets, the response rate was somewhat higher, and that is true. In terms of consistency between where we expect the response rates to be highest, I would say yes, that's largely true, and we wanna see that. In those patient populations where you would expect a slightly higher response rate, that's exactly what we see. If we didn't see that, we'd actually be concerned about our dataset. We're actually pleased to see that. The second point around the rigor of the actual endpoint. The NCAT is a relatively high efficacy metric to move. If you look at the possible different efficacy metrics in CIDP you can approach, right? There's the NCAT, there's the I-RODS, there's the MRC, or the MRC Sum Score, there's grip strength. Those are generally the ones that you think about. Of those, the hardest one to move is really the NCAT. It takes the most improvement to move it. In of itself, it's pretty rigorous, and that's what was used in the riliprubart trials as well. In our specific case, because this is a registrational study and not just a single open label study, we really tried to make sure that the responses we were seeing are valid because of course, we want to have a positive Part B, not just a pleasing Part A. What that means is we required confirmation of the NCAT at a subsequent visit, and that confirmation could not happen prior to week 7. What that means is that if you came in at week 5 and you were an NCAT responder, you had to confirm that response at week 7. You could not simply revert back to baseline and then confirm the response at a later visit. It had to be on 2 consecutive visits. The other thing, of course, as a medical team, you know, we took great pains to make sure that what we were seeing on the NCAT was actually consistent with what was happening on the other efficacy metrics. We didn't just sort of checkbox off an NCAT responder and say, "Great." We looked and made sure that whatever the patient said they improved on was reflected on what the physician saw in their physical exam. All right. Next question please. Thank you, Alex. Thank you. Our next question comes from Pete Stavropoulos with Cantor Fitzgerald. Your line is open. Yeah. Good morning, Hi, Pete. How are you? Good morning, Marino, Simrat, Ryan and team. Congratulations on the outcomes. One question that I have is the dosing window for Part A is up to 13 weeks of treatment. Will you miss some of the patients and therefore reduce the reported responder rate when Part A is completed? The reason I ask is, you know, when you look at the riliprubart data, there is continued deepening of benefit and some patients, you know, had not crossed the one-point threshold on the NCAT by week 12 and 16. Pete, that's a great question. Look, I'll ask Simrat to add some comments there. Yeah, it was a higher hurdle. We would not count anyone obviously after 13 weeks. We are only counting responders who respond 2 weeks in a row starting at week 5 to week 7 and so on. Yeah, if someone needed 15 weeks, 16 weeks to respond, they weren't counted as responder in our analysis. Yeah, I don't have much more to add to Marino outside of saying that this was something we paid attention to during the course of the study. On the table was always extending Part A if we thought that that was needed. Fortunately for us is, you know, we saw a very hefty responder rate, we didn't feel the need to do it. I think, you know, obviously if we extended out to 24 weeks, any rational human being would assume that our response rates would go up a little bit. Yeah. Look, part of why we thought 13 weeks was enough and felt like that higher hurdle was not a problem for us is the data we saw in MG. I mean, it's just very rapid, robust, quick response in patients with neuromuscular conditions. The data that we're seeing in CIDP is consistent. All right. Thank you. Thank you, Pete. Thank you. Uh- Thank you. next question, please. Our next question comes from Gavin Clark-Gartner with Evercore ISI. Your line is open. Hey, guys. Congrats on the great outcome. I just wanted to make sure I heard you correctly on safety. There was no drug-induced lupus, no autoimmune symptoms, including lupus, and I think no other signs of autoimmune activation. Just quickly on the sample size. For Part B, was there any consideration to lower the sample size below 256, or was this really the lowest you wanted to go? Thanks. Yeah. Sorry, Gavin, you're talking about you said Group B, but 256 is Group A. Which one are you referring to? The 128 in B or the 256 in Part A? The 128 in B. Sorry. Yeah. I'll ask Tim to comment on on those. The safety remains very pleasing, right? In terms of what we saw clinically in MG, a very clean study, and that remains true now in CIDP as well. Of course, as you start to get more and more experience with the drug and a greater number of people now across two indications, you know, we feel more and more confident on what the ultimate safety profile of this drug is. Yes, I will confirm there were 0 indications of anything that would lead somebody to believe in any autoimmune activation, let alone DIL, right? Very, very clean from that standpoint. In terms of going lower in Part B, I think, you know, I think it's a registrational study, right? Sponsors always kind of tend to become very, very conservative in their assumptions because you've got one shot at getting this done correctly, and you wanna make sure that in trying to reduce sample size, you don't somehow end up with a study that fails. It's my way of telling you that, yes, if we, if we look deeply, probably, you know, you could shave some numbers off here or there based on common sense, but I think it's a small price to pay to over-enroll a little bit to make sure that the molecule is allowed to show exactly what it needs to do. Thank you, Gavin. Let's go to the next question. Thank you. Our next question comes from Yaron Werber with TD Cowen. Your line is open. Hey, congrats, as well from me really for the terrific results. 2 questions. One is just a follow-up on Gavin's question. For the phase 3 gMG study starting mid-year, can you... It sounds like you've been in discussions with FDA about whether you need to do ANA monitoring, and you can exclude patients with baseline ANA titers. Can you give us an update on that? Secondly, it sounds like in Q2, we're gonna get an update on DNTH212 and potential indications. I think you've talked in the past about cutaneous lupus nephritis, SLE, dermatomyositis and Sjögren's. How should we think about? Would you only prioritize one? Would you run 2 phase 2s, 2 different indications at the same time? You know, any thoughts would be great. Thank you. Yeah. Thank you, Yaron. On the MG trial, yeah, we had a very, very productive, very fast, very short meeting with the FDA. We're just waiting for the minutes to come in, they're imminent, and make sure that we have everything that we agreed to in black and white. We'll provide more details and updates on the MG trial in the very near future, near term. On the second question. Oh, 2 and 2, yeah. Well, no, I mean, you named the 6 indications that were made the short list. You should expect that we're gonna announce 3 that we're interested in pursuing as quickly as possible. Then at some point later this year, potentially, you know, what exactly is gonna be the rollout, what phase, et cetera, et cetera. Yeah, we're gonna mention three that we prioritize from those six. Does that answer your question, Yaron? Thank you. I'm assuming, yes. Our next question comes from Rami Katkhuda with LifeSci Capital. Your line is open. Hey, guys. Wanted to pass along Mike's congrats on the update as well. I guess any hypothesis as to why you've been able to accelerate enrollment of your CIDP study while Canopy has announced delays? Go ahead, Rami. Finish up. I was gonna say, based on the results in MG and now CIDP, do you also expect to drop the 600 mg dose of claseprubart in MMN, or is there a need for greater complement inhibition in that disease? All right, great. Thank you, Rami. One thing, on your question about... Look, they're having delays with their recruitment. They say it's because of recruitment. We're not seeing that issue. I think there's two things I've mentioned to investors that I think were very helpful. One is, you know, we designed this trial for multiple reasons, and one of them was that we knew that it would be very competitive out there. CIDP is a rare disease, and yet there are multiple pivotal trials going on with multiple sponsors. The idea was: How could we make our trial more attractive for patients? How could we make it the ideal type of trial for patients to enroll into? When we saw the results of the ADHERE trial and we saw the results of their label, getting a broad population across all adults with CIDP, despite, for example, not having any refractory patients in their trial, we thought this would make the best sense. If you're a CIDP patient looking at multiple trials and trying to decide which one you want to go into if you're eligible, most trials you go in, you're blinded right from the start. You could get placebo. You could continue on IVIG, which obviously you're motivated to get off of, and that's why you're going to clinical trial. You might get a drug that you don't know if you're even gonna respond to it. Versus with us, it's just open label. You just come in, and you only have to come in every 2 weeks as opposed to every week, for example, with Riliprubart. You get 1 shot, and we you see exactly what's happening. Only if you get better above and beyond your baseline, then you get randomized. Yes, there's a chance you get placebo there, but even then, you know, we watch you like a hawk, and the moment you relapse, we pull you out, rescue you, and you get a chance to go back on the drug that you know you responded to in Part A and get that for up to 2 years for free. It's just a much more patient-friendly study, so I think that has a little bit to do with it. I'll let Simrat to maybe add anything. Clearly our team is just executing at a really impressive level. They're doing it across all programs in the company, not just CIDP. Do you wanna add anything or? Yeah, I don't have anything to add to what you said on the first question. On the second question, which regards the 600 milligram arm in MMN. I think that, you know, first of all, I think the CIDP data, because of the nature of the two diseases, right, which seem to be more upstream complement driven than perhaps others. I think the CIDP results really magnify the probability of success in the MMN study, frankly. Regarding the dosing, intuitively, we've dropped 600 in MG. We've now dropped it in CIDP. It would seem to make sense to drop it in MMN. The issues are there are a couple of issues there. Number one is we're already well advanced in that study, right? We didn't have a lot of people randomized in CIDP, so we could go ahead and drop the arm. In MMN, we're well advanced in that study. Number 2, out of all 3 indications that were in with DNTH103, MMN is the most underserved. There are actually no targeted options. Like, I don't consider IVIG a targeted option for an autoimmune disorder, so there are no targeted biologic options in MMN. This is the one shot that we have to just make sure that we deliver the very best efficacy possible, and we don't know enough about MMN. We have no data there. There's just scant data available, period. The medical team has really decided actually a while back that we'd like to proceed with both arms in MMN. Thank you. Thank you, Rami. Let's go to the next question. Thank you. Our next question comes from Maury Raycroft with Jefferies LLC. Your line is open. Hi, good morning. congrats on the update, and thanks for taking my question. wondering how many patients you estimate could be enrolled by the end of this year and what type of guidance you'll be able to provide for Part B at that point? will you be able to announce when you've achieved the 128 responders needed to complete Part B? Thank you, Maury. We're not gonna give any guidance right now on what our targets are for this year. Suffice it to say that every target we set for this trial, we keep beating, which is a nice situation to be in. Sometime later this year, we'll provide guidance on when exactly we expect top-line results for the entire trial. I mean, frankly, for myself, and I think for Simrat, we'd wanna see at least 100 patients in part complete Part A before we really got comfortable with our estimate so that we don't, you know, sandbag or overpromise on when we expect top-line results. The other thing I'll add there is, you know, we didn't hold back on this study whatsoever, right? We took a very global approach to where we're gonna go. We were not at all conservative in terms of the number of countries or the number of sites that we wanted to approach because we knew how many patients would be required, especially when we still had the 600 arm in play, and we knew how competitive the market was and that CIDP patients aren't a dime a dozen either, right? We went pretty broad. What that means is that when you go broad, different countries have very different startup times. Part of the reason why we're not giving you guidance is, frankly, we still have some very meaty geographies that are just opening up this week. We haven't really had time to let them enroll and see what they're able to do. Until we do that, it's hard for us to come out and just give you a date. Was there another part to your question? No. Respond. No. Yeah, that was it. That was helpful. Thank you. That's it? All right. Thank you. Next question, please. Thank you. Our next question comes from Danielle Brill with Truist Securities. Your line is open. Hey, guys. Good morning. big congrats on these incredible results. I have a question on response rates by background therapy. Since the majority of patients represented in the go analysis were receiving background standard of care, I'm curious if there were any discernible patterns or differences in response rates observed based on prior background therapy, whether that be steroids or IVIG. Can you also comment on the median time to response? I know it's a small end, but curious if you were seeing responses concentrated around a certain timeframe or if they were dispersed across the 13-week evaluation period. Thank you. Yeah. I'll be very open. I know the answers to all of your questions, you know, since obviously we have patient-level data. There are several of which it's just not the right time to speak about publicly. The reason for that, frankly, is just to maintain the integrity of our study, right. In other words, this is a registrational study. We are at the beginnings or the beginning phase of recruitment. The last thing we wanna do is to influence physicians or patients in terms of their expectations in Part A, because what we wanna do is make sure that our Part A response rate is as rigorous as possible, that these are true responders, so that the ones on placebo, you know, will deteriorate, and we have a successful Part B, right. That's part of the reason why we've released limited information. What I feel is fair to say is that number 1 is that our response rates were not clustered, and you wouldn't expect them to be in a disease like this because CIDP patients are each one's kind of their own individual story. Fast-forward 20, 30 years, we may find out that CIDP, the way we look at it today, is 3 or 4 different diseases that have similar external physical symptoms. This is why patients have very different courses and very different responses to therapy. In that type of situation, you wanna see exactly what we see, which is people have very different periods in terms of when they respond to something. Some respond very well and some don't, right? That's exactly what we've seen in our study. In terms of different subgroups, all I will say is no surprises. The only surprise is what Marino mentioned earlier, what I've mentioned with caveats as well, which is that it seems like overall, the response rates are higher than what we anticipated, but the pattern of them is pretty much what we expected. Does that answer your question, Danielle? It does. Thank you so much. Thank you. Next question. Thank you. Our next question comes from Ryan Deschner with Raymond James. Your line is open. Congratulations on the results today. real quick, given the substantial reduction in enrollment for CAPTIVATE, how much time do you think you could realistically shave off your timeline to potential approval in CIDP? What needs to happen logistically with regulators to remove that 600 milligram dose arm in CAPTIVATE? Thanks. Look, in terms of speed, clearly, we've been doing really well, and now the changes we're making to the trial will accelerate our ability to get to top-line results. We'll provide guidance on what that looks like later this year. I'll tell you what's on my mind is, just a couple of years ago, riliprubart was probably about 3 years ahead of us to market. Based on their delays, based on our acceleration to date, that difference is now in the 1-2 year frame. What I'm looking for is further updates from them, then you'll get further updates from us later this year, then we'll see if we've been able to, you know, minimize or nullify that first-to-market advantage they had at one point. That's what I'd like to see, and that's what I'm really focused on right now. On the second part of your question, I'll hand it to Simrat. Yeah, we have pretty rapid mechanisms in most countries that we're gonna leverage to cut the 600 arm off. I don't feel like we're gonna waste any patients recruiting to 600 right now. Yeah. It's gonna happen. This is something that we suspected early on when we first started seeing patients coming to Part A. Team's ready to execute really quickly on this. Thank you. Let's go to the next question. Thank you. Our next question comes from Colleen Kusy with Baird. Your line is open. Great, good morning. Thanks so much for taking our questions. Given the strength of data that you're seeing so far, is there any reason you'd want head-to-head data versus IVIG, either for regulators or for commercial, or would that be something you'd entertain, maybe in a post-marketing setting? Look, I'm eager to see the head-to-head data from especially from riliprubart. Of course, that'll inform us because at this point, we believe anything that riliprubart could do, we probably could do or match for sure or do better. Once we see that data, then we can decide how we go about creating our own head-to-head data versus IVIG. It may not be in the same form that they've done it because we don't need it for registration. It'll be a purely, as you said, commercial requirement or nice to have. Yeah, it's something we definitely have in our mind, and I think, you know, with the data we see from our competitors will inform that. Great. Thank you. Thank you. Next question. Thank you. Our next question comes from Bill Maughan with Clear Street. Your line is open. Good morning and congratulations. To ask a little bit more on the timing of responses. If we assume that you are more potent than riliprubart, would we also potentially assume that you may see responses faster and not only just more frequently? On the other side of the timeline, is there any thought that you may be leaving some responder rate points on the table by looking at a week 13 endpoint versus looking a little bit further? Thanks. I think in general, if a drug works and you're more potent, then you probably should see results a little bit quicker. Without knowing their dataset and their specific points at which they responded, I have no way to accurately answer that question yet. It's possible. I don't know. I just know that overall, we're really pleased with the responders that we're seeing. In terms of lengthening the study, it's a balance, right? Because there's cost involved. There was cost involved. There's the fear of dribble drabbles at the end who maybe aren't true responders. Again, you know, my focus and the team's focus, yes, we wanna see responders, but we also wanna make 100% sure that we're doing everything we can to get true responders who should relapse once they're off of our drug. The fear, of course, is the longer and longer you go and you get a dribble drabble at the end, was that a real responder or somebody who's just been in there long enough to feel better on their own? We cut it at 13 weeks. We saw the results that we saw and then so we didn't really feel a need to extend it any further. That's the best answer I have to give. Yeah, I think the... Here's the bottom line. as Simrat said earlier, extending Part A was an option if we weren't seeing pleasing results in the first 13 weeks. We didn't just see pleasing results that told us that, "Okay, we have a go." We saw results that materially were better than our expectations. I just wanna make that clear. It's, it's not results that we say, "Okay, this is great and met our objectives." This is clearly much better than we had hoped and expected based on precedent data with riliprubart. absolutely 13 weeks was the right decision. Got it. Thank you. Next, Thank you. Next question. Thank you. Our next question comes from Laura Chico with Wedbush. Your line is open. Hi, this is Dennis on for Laura Chico. Thanks for taking our question. How do the CAPTIVATE study modifications change your powering assumptions around Part B? Yeah, we basically have eliminated the 600 arm, and we increased the responder rate from 40% to 50%, so it resulted in a reduction in Part B. Sorry, I think we went from 192, 92 to 128 patients in Part B. We got rid of the 600 arm and now it's actually stronger power to show a separation because 300 and 600 split the alpha before, and now we're not splitting the alpha. Does that answer your question? Yep. Thank you. Okay, great. Next question. Thank you. We'll take our last question from Jake Batchelder with William Blair. Your line is open. Hi, this is Jake on for Myles Minter. Thanks for taking our question. I just wanted to confirm that you guys have regulatory alignment on a sufficiently sized exposure database now with this 128 patient downsizing. Thank you. Yeah, I mean, we didn't go back specifically to regulators to ask them if this number of patients in Part B is adequate, but we use our sort of common sense based on our conversations and other indications that we've just had, such as MG, where we have far fewer patients overall that are going to be dosed. We feel pretty comfortable that the overall exposure data, especially with sort of a 1-year Part B, 13 weeks ahead of that, to over a year in a registrational setting plus an extension beyond that. Let's not forget that regulators do look at, from a safety perspective, which is a question you're really asking, they do look at like doses and similar indications. We have 300 milligram data all the way from phase 2 with people with 1-year extension. It'll be tested again in phase 3, and we have the same doses and higher in MMN. We feel like we have plenty of safety data. Does that answer your question? Yeah. Thank you so much. Thank you. All right. Great. Thank you. If I could just close. Thank you, everybody, for attending the call today. I just wanna again highlight how proud I am, how overjoyed I am with the results we've seen so far and the Dianthus team's execution. Big thank you to them. You know, the fact that we're making this early call, and on top of that, raising the bar and changing our ratio from Part A to Part B because of the materially better, materially significantly better results we're seeing than expectations and the precedent set with this mechanism of action. You know, it's just better than everything we had hoped at this point. Especially because we're seeing consistency in terms of the baseline characteristics with patients. We don't have more naive patients, for example, than riliprubart had as a percentage. The fact that we're seeing very consistent results across different geographies, different healthcare systems, different ways of treating CIDP in different countries. It is really a great moment for Dianthus, and I'm especially excited for CIDP patients and what this drug could do for them. So with that, let me conclude again and thank you. If anybody would like to any investors would like some time with the Dianthus team today, please reach out, and we'll do our best to schedule some time with you. Thank you. Thank you for your participation. You may now disconnect. Good day.