Good morning and welcome to the Dianthus Therapeutics conference call. My name is Michelle, and I'll be the operator for today's call. A slide presentation to accompany this call is available on the investor section of the Dianthus Therapeutics website. Following the company's prepared remarks, we will move to Q&A session. Please note that today's call is being recorded. I would now like to turn the call over to Marino Garcia, CEO of Dianthus Therapeutics. You may begin. Thank you, Michelle. Good morning, everyone, and thank you for joining us today. Earlier this morning, we issued a press release with positive top-line results from our phase II MaGic Trial evaluating claseprubart and generalized myasthenia gravis, and we're very excited to share more details about these results with you today on this call. The impressive results we're presenting today are a reflection of the Dianthus team's commitment and passion, and I'd like to just take a moment to thank the team for their hard work in delivering a very well-executed and timely clinical trial. I'm very proud and grateful to be part of this team. Next slide, please. Just a note before I begin the presentation, we will be making forward-looking statements, so I would refer you please to our SEC filings for more information. Next slide, please. I'm joined today by Dr. Sim Randhawa, our Chief Medical Officer, Ryan Savitz, our Chief Financial Officer and Chief Business Officer, and John King, our Chief Commercial Officer. I will begin with a few introductory remarks about the best-in-class potential we see for claseprubart in myasthenia gravis, the first of our three neuromuscular indications we're pursuing. Next, Sim will review our phase II data in detail, and finally, I'll summarize and discuss next steps and upcoming milestones. Then we will open up the line for questions. Next slide. At Dianthus, we're building an exciting autoimmune company by rapidly advancing claseprubart, a next-generation complement inhibitor with a best-in-class potential to treat multiple classical pathway-driven diseases. Claseprubart is a very potent investigational monoclonal antibody with a long half-life that is designed to selectively inhibit the active C1s protein and therefore only inhibit the classical pathway of the complement system, leaving the lectin and alternative pathways intact to maintain the complement system's immune function. This unique combination of benefits means we could potentially have a very effective low-volume antibody with a lower risk of infections that can be delivered in a convenient, infrequent, self-administered autoinjector for patients suffering from various classical pathway diseases. Claseprubart is a pipeline and a product with the potential to be a first-line biologic across different neuromuscular conditions such as MG, CIDP, and MMN. And the results of our first trial in MG bolsters our confidence in claseprubart as a potential game changer for patients in the MG market and in the successful execution of our ongoing CIDP and MMN clinical programs. Next slide. Why did we choose MG as our first indication? The U.S. MG market is the largest of the three neuromuscular indications we're pursuing, with more than 100,000 patients that are AChR-positive patients that can benefit from effective biologics. The U.S. is a $3.5 billion market and growing, with only two classes of biologics competing for first-line use. The potential for significant growth is obvious, as the C5 inhibitors and FcRn have only penetrated approximately 10% of these patients despite having been available for patients for many years, and why is that? The reason we believe the market is so underdeveloped is that the current treatments have significant drawbacks, and the market still has significant unmet medical needs, and this is where we see the substantial opportunity for claseprubart to address these patient unmet needs as a potent, less burdensome, and easier-to-use biologic. This best-in-class potential should be able to grow the market by reaching more MG patients that would otherwise delay the use of more burdensome biologics. Next slide, please. In the MaGic Trial, our goal was simple: to evaluate three ways that claseprubart could potentially address the unmet needs of these patients. First, on efficacy, to be at least comparable to approved C5 complement inhibitors with a continuous effective symptom control and a 1.6-2.1-point improvement on MG- ADL versus placebo. Secondly, to have a clean safety profile comparable to the FDA-approved first-generation C1s inhibitor, Enjaymo, with a lower risk of infections and therefore no FDA Box warning or REMS. And finally, a patient-friendly convenience comparable to Dupixent, a $14 billion blockbuster, with the potential to have one-click delivery by a self-administered subcutaneous autoinjector just once every two weeks. We believe that achieving this TPP, this target product profile, would be a significant advance for patients suffering from MG and would position claseprubart as a potential first-line best-in-class biologic treatment. How did we do with our first trial, the MaGic Trial, against this target product profile? Next slide, please. Today, I'm beyond pleased to say that the phase II data supports our differentiated best-in-class target product profile for each of the three goals we set for the MaGic Trial and more. First, claseprubart demonstrated impressive results with rapid, sustained, and statistically significant symptom improvement across multiple efficacy measures, including the MG- ADL, the QMG, and the MSE. These results support the potential for claseprubart to be a best-in-class complement inhibitor, especially when you compare the results to the number one blockbuster complement inhibitor, Ultomiris. Secondly, on safety, claseprubart was generally well tolerated with a clinical profile similar to placebo. We saw no related serious infections and no symptoms of autoimmune activation. These results support the goal of not having a Box warning or REMS program due to serious infections. Finally, the 300-milligram every two-week dose, the results were consistently robust, statistically significant, and clinically meaningful across all the measures we will share with you today. Both doses of 300 and 600 milligrams showed comparable safety and efficacy data with no statistical difference between them. Because we saw similar results across all efficacy measures between the two doses, we plan to advance the 300-milligram every two-week dose into phase III. Our low volume, two milliliters, supports our plan to deliver this in an SHL Molly autoinjector for self-administration, the same autoinjector Dupixent uses. Now, I know you're all eager to get to the details of the results, so let me now hand the presentation over to our Chief Medical Officer, Dr. Randhawa. Please turn to the next slide. Thank you, Marino. It is my pleasure to present this data, which shows for the first time positive efficacy results for an active C1s inhibitor in a randomized controlled trial in a neuromuscular disorder, and I would like to thank the investigators and site staff who brought this data to us. The data story is quite simple. Across all commonly assessed efficacy metrics in MG clinical trials, both treatment arms had impressive treatment effects versus placebo, with the low-dose 300-milligram Q2-week arm hitting statistical significance across the board. We ran a typical MG study enrolling patients with an MG- ADL of six or greater on at least one small molecule immunosuppressant and randomized them into placebo or two treatment arms where we added claseprubart 300 or 600 milligrams subcutaneous Q2 weeks. The randomized control period was 13 weeks, followed by a 52-week extension. As a reminder, our pre-specified threshold for significance was one-sided P equals 0.1. For the most common assessments we have provided, two-sided P equals 0.05 significance as well. Next slide. Baseline characteristics are well-matched for a phase II study. Stratification factors were U.S., ex-U.S., and one versus more than one immunosuppressant. Note, the MG-ADL and QMG are fairly balanced. Disease duration was shortest in the 300-milligram arm, which in this study was surprisingly a disadvantage as patients with longer disease duration had steeper declines in MG-ADL. Next slide. Let's start with the Myasthenia Gravis Activities of Daily Living, or MG-ADL, which is a patient-reported outcomes measure. As you can see on this graph, impressive results with the 300-milligram arm achieving a 4.6-point decline versus baseline and a 1.8-point decline versus placebo, and the 600-milligram arm achieving a 5.4-point decline versus baseline and a 2.6-point decline versus placebo. All of these results were statistically significant. However, the result was not statistically significant between the two treatment arms. Next slide. Moving forward, here we have the Quantitative Myasthenia Gravis scale, or QMG, which is a physician-administered quantitative scale across five functions. Again, impressive and consistent results in both treatment arms versus placebo, with the 300-milligram arm achieving a 4.4-point decline versus baseline and a 2.4-point treatment effect versus placebo. The 600-milligram arm achieved a 4.5-point decline versus baseline and a 2.5-point decline treatment effect versus placebo. And again, all of these results are statistically significant versus placebo for treatment effect, but not different between the two treatment arms. Next slide. Here we see rapid and statistically significant declines in the MG-ADL as soon as the earliest evaluation at week one and at every time point in CORE. Next slide. Now we see a rapid and statistically significant decline in QMG as soon as week one and at week 13 in both treatment arms. Next slide. The MG-ADL Christmas tree plot shows a robust effect versus placebo at all cutoffs in both treatment arms, with greater than 60% of patients improving by at least five points in both arms. Next slide. The QMG Christmas tree plot, similar to the MG-ADL plot, shows a robust effect in both arms, with more than 60% of patients in the 300 arm improving by five points or more. We also see some deeper declines in the 300 versus the 600 arm. Next slide. MSE in MG is generally defined as an MG-ADL of zero or one. Again, we see a very robust response versus placebo, with more than a third of 300-milligram patients achieving this important milestone and the 300-milligram arm achieving significance on this metric versus placebo. Next slide. Next, we have the Myasthenia Gravis Composite score composed of four metrics imported from the MG- ADL, three imported from the QMG, and three unique to MGC, and are composed of specific muscle strength assessments. As expected, on the left-hand side, given the MG- ADL and QMG results, MGC overall results are robust, with a 5.6 treatment effect versus placebo for the 300 arm and a 5.5 treatment effect for the 600 arm versus the placebo arm. Looking at unique to MGC muscle strength scores on the right-hand side also reveals robust results in both arms versus placebo. Next slide. Wrapping up individual efficacy results, we have the MG Quality of Life 15, a patient-reported outcome measure that scores 15 items across physical, psychological, and social domains. Again, robust results versus placebo, and in this case, the 300 arm achieving significance versus placebo. Next slide. Finally, the efficacy summary takes us back to how I started this data presentation: impressive and consistent treatment effect versus placebo, with statistically significant treatment effect across all metrics in the 300 arm. Next slide. Now let's move to safety results: fairly comparable AE profile in the treatment arms versus placebo. Some highlights are balanced infections overall. There are no related serious infections in either arm, and certainly no infections suspicious in any way as driven by complement inhibition. Injection site reaction experience is pleasing, with few patients having generally mild and singular events. There were more patients with an ANA of 1: 320 or greater at any time point in RCT as listed in this chart. None of these patients exceeded a titer of 1 over 320. We used the 1 over 320 bar in this chart as our screening criteria allowed patients with an ANA under 1 and 320 to be randomized. The number of treated patients with an ANA of 1 over 320 declined at week 13, and there was no indication of autoimmune activation as witnessed by the fairly benign rash and arthralgia experience. Next slide. This data set gives us and will give our PIs great confidence in proceeding with a phase III study. Clearly, we're taking the 300 Q2-week dose forward. We're also considering adding a 300-milligram Q4-week arm based on encouraging initial PK efficacy seen in OLE. With that, Marino, I hand it back to you. Thank you, Sam. Next slide, please. I mentioned at the beginning how our efficacy data supports our goal of developing a best-in-class inhibitor for myasthenia gravis. As you can see here clearly, claseprubart did extremely well when compared to currently approved C5 inhibitors on the MG- ADL, what will likely be the primary endpoint in our phase III trial. Whether you look at the absolute reduction in scores or the placebo-adjusted improvements, claseprubart performed as we had hoped, this despite having a relatively high placebo response when compared to previous complement inhibitor studies. Next slide, please. Looking at secondary efficacy measures such as the QMG and MSE, which Sam talked about, and comparing claseprubart versus Ultomiris, the number one blockbuster C5 inhibitor that's still growing and still being used as a first-line treatment in myasthenia gravis, I think you will agree these results are very impressive and build our confidence that we may have a clearly differentiated and best-in-class complement inhibitor. Next slide, please. I also mentioned earlier that the MG market is the largest of the three neuromuscular markets that we are pursuing with claseprubart to maximize its pipeline and product potential. MG is just the first step as we build an exciting neuromuscular franchise with claseprubart, leveraging its potential as a pipeline and a product and a best-in-class profile in the large and growing U.S. Neuromuscular market, starting with MG with its large population as the foundation and then building on that with CIDP and MMN. These three indications represent over 150,000 patients in the U.S. alone as of today and will likely continue to grow over time. CIDP is our next exciting opportunity for a highly potent and differentiated active C1s inhibitor like claseprubart. Sanofi presented exciting phase II data with its active C1s inhibitor, riliprubart, demonstrating meaningful efficacy in CIDP in standard of care treated, refractory, as well as IVIG and IV patients. These results were the first proof of concept for an active C1s inhibitor in any autoimmune condition and for any complement inhibitor in CIDP. Today's data in myasthenia gravis significantly increases our confidence that we have the right dose in CIDP and then the overall successful execution of the CIDP program. Finally, MMN is a disease where the classical pathway plays a critical role in the underlying pathology as proven by our genetics in 2024 with the Argenx C2 inhibitor and claseprubart, which provided proof of concept for the potential of classical pathway inhibition in this indication. This is our only competition in this third indication as FcRns won't work in MMN. We see claseprubart as a very well-positioned versus the Argenx C2 in MMN with its convenient sub-Q self-administered autoinjector target profile and high selectivity for the classical pathway supporting a more convenient option with a potentially reduced likelihood of infections. Next slide, please. Looking ahead, the next year will be a catalyst-rich year for Dianthus. First, as Sam mentioned, we plan to initiate a phase III trial in Myasthenia Gravis in 2026, evaluating, of course, our every two-week 300-milligram dose, but also a monthly 300-milligram dose. Next, we continue to expect top-line phase II results in MMN and an interim responder analysis from part A of our phase III pivotal CIDP trial in the second half of 2026. We also look forward to three other external catalysts, including Sanofi's data from two phase III trials of riliprubart in CIDP and Argenx's phase III results from claseprubart in MMN. I expect their results should have positive read-throughs to claseprubart and Dianthus as they have in the past. As a reminder, we have a strong balance sheet with a cash balance of approximately $309 million as of June 30th to fund operations into the second half of 2027. Next slide. I will wrap up now with this slide that I believe highlights the vision we have for claseprubart as we pursue the power of consistent control with just one click. This target profile, which is supported by our impressive phase II results today, would position claseprubart as a clear, best-in-class, first-line biologic treatment across all our neuromuscular franchise. With that, could we please open the call for questions? Thank you. Thank you. To ask a question, please press star one one on your telephone and wait for your name to be announced. And to withdraw your question, please press star one one again. And our first question will come from Alex Thompson with Stifel. Your line is open. Hey, great. Congrats on the data, and Marino and team. I'm sure you're feeling great about it. I guess maybe two from us. On the decision to potentially pursue Q2-week and Q4-week in phase III, maybe can you talk about, again, the totality of the data that gives you confidence in Q2-week and then the preliminary OLE data around supporting Q4-week? And then maybe can you touch on what you're seeing from complement pathway inhibition across both arms in the study and if that is consistent with what your expectations were? Thanks. Thank you, Alex. And I really appreciate those questions. I think I'll hand it over to Sim. Sure. So yeah, we have a lot of confidence in the Q2-week 300 dose. It starts with the fact that before we even started any of our programs, when we looked at our performance on various complement inhibition assays and the information that was publicly available and what was needed, we felt that the 300 dose was the right dose and the 600 dose was really just a piece of safety, if anything else. And so we went into this trial pretty much assuming, based on everything we knew, that the 300 dose was going to be the right dose. Then what we saw in the study. So upfront, you look at the MG-ADL, and I'm sure a lot of people are going, "Well, why aren't you going with 600?" Well, that's just one piece of data. And it's one piece of data in a relatively small study. When you look at the totality of the data, including the QMG, including the MGC, including the MGC muscle scores, right? So when you look at all of that information and you tie it in with the MSE, which of course has become an extremely popular endpoint and way to look at patients with autoimmune disease, not just in MG, but across the board, you see the results don't point you anywhere to 600. So we look at it as more a vagary of a single endpoint in a small study rather than something that's showing a treatment effect of 600 over 300. So that's one. Two, I think you asked me about what we were seeing in terms of PD and PK. Generally, very consistent with what we saw in our Healthy Volunteer study. I think the other question was, yeah, what are we seeing in the OLE that gives us confidence? Got it. Q4-week is a good dose. Yep. So I'm going to caveat all OLE conversations, right? We did a data cleanup on the core. And as you know how these things go, we received our data a handful of days ago, right, on core, and then we looked into the extension to see where interesting questions might come to us based on our data. So we anticipated this one, and so we did a little bit of work here. And the reason we have a lot of confidence also comes from early signals in our OLE, specifically looking at the placebo arm. So in our extension, nobody received an IV load. And we always knew, and I think we talked to several of you as we launched this adventure, that the placebo arm was going to be interesting to us exactly because we don't have an IV load, and therefore we're going to be able to see how patients perform going from zero gradually up on the PK ladder. And what I can tell you is that the early signals in placebo are very encouraging. So in other words, at PK levels well south of what we are achieving in the 300-milligram sub-Q Q2-week arm, we are seeing signs of what looks like at least robust efficacy on MG-ADL in the placebo arm. So that's another piece of information that's guiding us to Q4-weeks. If I could also add, Alex, we've been very consistent on our messaging that if we'd saw these two arms perform equally, then it would confirm what we suspected is that both doses are already at the top end of the efficacy curve. And the question has always been in neuromuscular conditions like MG, what level of inhibition of the classical pathway do you really need to achieve, or the complement system do you really need to achieve to have the kind of improvements we've seen historically with complement inhibitors? And so the message has always been if these two doses perform well, Q4-week is on the table. I will say that some Phase III data from Regeneron at the end of August, their siRNA-based C5 inhibitor, was eye-opening. The fact that they had a significant improvement on the MG-ADL, we don't have a lot of data, but it sounds like it was a positive trial using the MG-ADL, and they disclosed that they only achieved 75% inhibition of the complement system. That's, in a way, a groundbreaking bit of information that tells us that getting above IC90 was always really an artificial, if you like, goal. And so if achieving something like 75% or 80% inhibition of the classical pathway is enough to give you similar results, we're very confident that's what Q4-week would be doing. And remember, we have a 60-day half-life. So every four weeks or every 30 days is very much well within our half-life timeline. Great. Thank you. And the next question is going to come from Yatin Suneja with Guggenheim. Your line is open. Hey, guys. Let me add my congratulations as well. Two questions for me. First is on the baseline characteristics. I mean, you did have a little bit of lower disease duration at baseline. How that might have impacted the result on the 300-milligram dose? So that's one. And second, if you can comment on the ANA positivity that we saw, seems like dose-dependent, any dsDNA conversion there. Thank you. Yeah. So in terms of baseline characteristics, intuitively, you would expect that lower disease duration favors response. That's not what we saw in this dataset. When we looked at our dataset, actually, there was a relatively strong correlation between those patients who had longer disease duration and steeper declines in MG-ADL. That was surprising to us. We don't know why, but that's what we saw. It was not an advantage for the 300 arm in any way. Then the second question was around ANA. ANA, yes, it does look like there were more cases in the higher dose arm than the lower dose arm. What I would say, though, is let's remember, ANA without the context of specific symptoms, so without the suspicion of SLE driven by symptoms, it's pretty much a useless test, right? The specificity or the sensitivity of the test is incredibly low. There are quite a few healthy people who walk around with positive ANAs and never have an issue in their life. So we're not entirely sure what to do with this piece of information in the context of our molecule. What's important to remember and the specific reason why we put adverse events of rash and arthralgia in our safety table is because we did not see any patients who had a hint or a suspicious hint of developing any lupus-like syndrome, and you would pick that up to these types of specific AEs, and I can say that we haven't seen that in OLE as of now either. The next question was, I think, around double-stranded DNA. In terms of the data we have presented, the one patient in the 300 arm was double-stranded DNA positive. Reminder, that patient also exhibited no symptoms consistent with any connective tissue disorder. I will just add that the track record now for all three C1s inhibitors is really comforting. Neither Enjaymo or riliprubart and now with our phase II trial claseprubart have ever reported any patient having any autoimmune activation or any drug-induced lupus-like symptoms. So this theoretical risk remains just that, theoretical. We have not seen anything that would hint at that happening in our trial. Okay. Thank you. And the next question will come from Gavin Clark-Gartner with Evercore. Your line is open. Hey, guys. Congrats on the really great data. I just wanted to follow up on the last point you mentioned, Marino, on the Enjaymo experience on the different titers. Because I think in the FDA review docs, they outlined that up to 25%-30% of patients had at least one SLE autoantibody on the panel turned positive, but without any clinical symptoms, there did not seem to be any issue in the FDA review. And in fact, they didn't really know what to make of this. I'm curious if you could elaborate on that any further. Yeah. I mean, I'll take that piece. I think this speaks to the fact that the idea of looking at ANA and double-stranded DNA came from the very useful place of taking people who show up with a set of symptoms over time that can be fatigue, joint pain, a rash, I don't know, etc, and within that differential, you have lupus or SLE. Within that framework, checking an ANA at a certain titer and a double-stranded DNA is useful because it might guide you to a diagnosis of SLE. These molecules by themselves are not pathogenic. They don't cause any harm on their own, so in that context, it's useful. I think what you're seeing from the Enjaymo data, what you're seeing if you go out and screen a bunch of healthy volunteers, what you're seeing if you just go to a hospital and you take a bunch of sick people for different reasons, whatever it may be, heart problems, cancer, whatever, and you just go check ANAs and double-stranded DNAs, you'll find very high levels because for whatever reason, those disorders or just being healthy can sometimes lead to the presence of these molecules, but they're not pathogenic. I think that's what you're seeing in the Enjaymo data. For whatever reason, when you have a C1s inhibitor, you can get an increase in these molecules, but they don't seem to translate into a clinical issue. So I think that's what they've seen. I think that's probably what's being experienced by riliprubart, and that's what we're seeing as well. Can I add also, Gavin? What's interesting is when we saw at the end of the trial, what was the number one reason for screen failures? I fully expected that it would be that patients were not AChR positive, which is the only patients we were randomizing. It was actually patients who were at 320 or higher titers on ANA. That was amazing. And it just says that the general MG population, a very high percentage, have that, but yet they are completely symptomless when it comes to anything that looks like lupus and without a history of lupus. So it's just one of those things that just is, frankly, clinically relevant in this situation. All right. Great. That's super helpful. And I just wanted to quickly follow up on Alex's first question on Q4-week dosing potential. So I don't see evidence of a dose response here, which I guess is the first step to figuring out if four weeks could be a viable regimen. But can you just lay out what your plans are for looking at the additional exposure response, PD response analyses from the blinded portion to support the four-week dosing potential? Thank you. Yeah. I think that part now is pretty straightforward. Once this rush of making sure we've wrapped up the core data and have communicated it properly is over, our attention is really going to focus on what's going on in the extension. As most of these studies go, a lot of your recruiting is somewhat back-ended. So what that means is you have a lot of people who kind of come into the study in the second half of your recruiting period, and they're kind of going through the meat of the extension right now. So what I would anticipate is really over the next month or two, having enough information to have a much more definitive position, looking at the extension data, looking specifically at the placebo arm and how they're performing, not just on MG-ADL, but of course on all the other metrics, which we haven't done yet, QMG, etc., and also making sure there isn't any additional effect in the 600 arm, which to my eyeballs tells me there isn't. We just want to make sure over time that there isn't, right? And so I would anticipate in the next couple of months with a more deep dive in OLE that we'll have a better answer on that. Gavin, it's Marino. Let me also add. So that's looking internally, of course, at the data. My background as commercial, having spent many of my years of my career in commercial, I'm looking outside as well at the competition. I'm looking at it. We have a very potent antibody with a 60-day half-life. I'm looking at the fact that 300 milligrams gets over 90% inhibition of the classical pathway, knowing that every four weeks it's probably around 80%, let's say, and that's part of the calculations we'll have to make. And then I look at the pozelimab data from Regeneron. Again, that was groundbreaking, not because of the efficacy they saw. It's the efficacy they saw at a very low level of inhibition compared to our 300 milligram every two weeks. That's 75% inhibition delivered for them. It delivered for them even better than the combination treatment, which of two C5s, which got close to 99% inhibition of the classical pathway. When I look at all this evidence together, and again, the fact that 300 and 600 milligrams pretty much performed equally in this trial, I don't see what there is to lose to go for and add an arm of Q4-week. I mean, if for whatever reason that didn't work and it was Q2-week, okay, we're back. We hit our target profile. I do pick something like dosing and administration. But why not go further? Why not push that differentiation? I don't see any much of a downside, to be honest. All right. Great. Thanks so much, guys. Congrats again. Thank you. And the next question will come from Rami Katkhuda with LifeSci Capital. Your line is open. Hey, guys. Congrats on the update, and thanks for taking my questions as well. I guess it's great to see validation of 300 mg claseprubart as kind of the appropriate go-forward dose in neuromuscular disease. Based on the results, are you expecting to include a Q4-week dosing arm in Captivate for CIDP or in MMN in the future as well? And then secondly, do you expect a higher proportion of previously FcRn-treated patients in the pivotal phase III trial for MG, and could that influence the efficacy results at the end of the day? Yeah. Yeah. Great. Thank you, Rami, and great questions. Let me hand over to Sim to take the second question, and I can come back to thoughts on dosing and administration for our other indications. Yeah, so we would welcome having more FcRn patients in our phase III study as long as they're appropriately washed out from drug, and given the half-life is not all that long, it's not that hard to do. One of the things that we're running into is in many of the geographies that we operated in in our phase II study, it seems like quite a few countries in Western Europe have a lot more liberal policies in terms of prescribing FcRns and complement inhibitors in general because they tend to see the value of biologics in MG, so they're surprisingly well reimbursed and covered. And what that means is that your usual source of patients from somewhere in Western Europe in particular, right, where you have people who entered a study, an FcRn study, they did well, they're off the study, they go through the extension, now they're off drug, and they're looking for something else to get, by and large, is hard to find in Western Europe because those people are still getting drug because they showed in the clinical trial that it worked for them. So they continue to receive drug. In other parts of the world, which we'll be expanding to for sure, we're going to be looking for those patients. I don't think it's going to influence the efficacy because ultimately they're going to have to meet the same criteria everybody else does. And also, physicians are intelligent, right? So they tend not to look at a patient, even if they meet your criteria that you set down. If they think there's something about them and this is not the right drug for them that you're offering, they're not going to put them in the study. So if a patient had a particularly bad experience, for example, on an FcRn inhibitor, most physicians are not going to take that patient and pluck them into a trial like ours. On the first question, for Captivate, our CIDP trial, remember the part A is an open label 300 milligram every two-week dose. We'll have an opportunity over the coming months to see how patients are responding to that dose in CIDP and further evaluate whether we even need the 600 in the randomized portion and also whether there's a Q4-week open. Potentially in the future, we could do another trial for CIDP and test that Q4-week. For MMN, again, next year, we will have the results of our phase II trial looking at 300 and 600. Again, there, if we don't see a difference in efficacy, that'll open up the door. If we see good robust results, of course, that'll open the door for phase III testing at Q4-week. We still need to see more data. Those are different neuromuscular conditions. But what I can say is from this trial, it gives us confidence that that 300 milligram target dose we've always had for all three indications is very potent and will work. That's what we expect. Got it. Thank you very much. The next question will come from Yaron Werber with TD Cowen. Your line is open. All right. Thanks so much and congrats on a very nice data across all endpoints. Maybe just a couple of questions as relating to the loading dose and then your open-label extension, Marino. Can you just remind us the two loading doses? Are you seeing any differentiation between them, and which one would you advance in the phase III? And then, as you said, in the OLE, the patients at that point who crossed over did not get a loading dose at the 600. What did you learn from that in terms of PK? I'm just trying to get a sense kind of how this would roll into future studies. Thank you. Sure. Let me hand that to Sim to talk a little bit about the loading doses and what we're seeing in the OLE. Right. So the loading dose for the 600 was 15 milligrams per kg, and the loading dose for the 300 was 10 milligrams per kg. Those loading doses were chosen in order to get us to steady state in an efficient manner. In other words, the steady state that would be achieved by these two regimens of Q, Q2 weeks over long periods of time, right? It's just to get us there quickly. And so that's the rationale behind the loading doses. That's how it was explained to regulators, and that's how it kind of moved forward. So what did we learn from our OLE? The reason I had mentioned earlier that the placebo arm in the OLE would be interesting is because you don't have a loading dose. The loading dose basically takes you to a higher PK immediately, and then you come down very rapidly to your steady state, whereas not giving a loading dose allows you to go from no drug exposure whatsoever and gradually go through the various levels of PK. That's why when we look at, for example, OLE week four, right, they've only received two doses of 600 sub Q. We know at that time point what their PK is. It's a lot lower than the steady state of 300 every two weeks, and yet we're seeing substantial additional MG-ADL effect on top of the placebo effect these patients already exhibited during the course of the core study. Yeah. Let me just correct those. It's 15 and 20 milligrams per kg loading dose. Just remember, if you look at the Dupixent target product profile, which we've said is always our target for dosing administration, they have loading doses with multiple sub Q shots day one, and then day seven start self-administering Dupixent every two weeks. Essentially, that's what we're aiming for in our label. We're just using an IV in clinical trials because it's just simpler, but we're working with the FDA on how we translate that into sub Q self-administered autoinjector shots that the patient could give themselves over the first one or two days. And then at day seven, they can start self-administering every two weeks. So I just wanted to clarify that point. Time for your question. We're good? And our next question comes from Myles Minter with William Blair. Your line is open. Hey. Thanks, everyone. Congrats on the data. I think investors are just debating why you're taking 600 mg off the table for the phase III at the current time. Can you just talk a little bit about how you balance the data that you saw that shows equivalent efficacy with 300 milligrams versus the safety in particular, the ANAs that popped up in 600 milligrams versus 300 versus maybe trying to maintain differentiation versus real approval? I just think that there's debate over those sort of three factors as to why you're moving with 300 mg in a phase III. So any clarity there would be great. And then secondly, just on the safety profile, the infections that you did see in the trial, it looks like less incidence in the claseprubart arms. So just wondering whether we should make anything of that. That seemed interesting to me. Thanks very much. Go ahead, Sim. Yeah. So I'll start with the infections. Yeah. I mean, again, if you look at the numbers, you would say 10% versus 5%, etc., higher incidence of infections in the placebo arm. Of course, that doesn't mean anything, right? I mean, complement inhibitors are almost certainly not protective against infections. I think the best you can take away from that is that, as we expected, complement inhibitors, if there's a risk of infection, it's a very specific subset of infections, so not a broad set like viral infections. So you don't tend to see this broad infection signal, and that's exactly what happened, right? These doses of claseprubart, the infection rate was essentially equivalent regardless of the numbers being higher in placebo. And what's more important to me on the infection side is the fact that there were no serious related infections, right? That's really where I think the data pops, that in the course of this study, there was nothing that could be tied back either by investigator or ourselves to the fact that a patient had a serious infection and that was due to a complement inhibitor. In fact, the only one that we saw was a UTI in a relatively debilitated patient that was related and serious because they were hospitalized, and it ended up being in the control arm. So I wouldn't make more of it than that. It doesn't seem like in this study, claseprubart was accountable for any infection risk above and beyond placebo. Then, in terms of, again, why 300? Well, I'll say a lot of what I said before. We have to look at the totality of the data. So just like with infections, if you took a look at just that one overall arm, you'd say, "Well, yeah, the numbers are a lot higher in placebo. What does it mean?" It doesn't mean anything. It just means there are 22 people in the study. That's all, right? And I think it's the same thing with the MG-ADL. It only takes two or three people who maybe weren't responders to anything in the control arm to drive a result. You have to look at everything else. And I think I put a lot of weight on the QMG. I also put a lot of weight on the muscle sum scores in MGC, which is on one of the slides on the right. The reason for that is that it's looking at the same types of metrics two different ways: shoulder strength by resistance and shoulder strength by endurance. So when you start to see these very consistent results, both on MGC and on MSE, on MGC muscle strength and on QMG, and then a higher rate of MSE in the 300 arm as well, that's kind of what's guiding us to 300. Now, of course, you always want to go to a lower dose, right? If you feel like there isn't an efficacy penalty or a substantial one to pay, you always want to use the lowest possible dose because I don't care what drug you give. If you're able to give less, you will deliver less problems to patients in the future for sure. So part of what we have to do is also try to find that minimum effective dose. And I think that's a piece of going to Q4 weeks. But the 300 Q2 weeks, in my mind, when you look at the entire strength of the FAS data, which is why we've shown you so much information, right, seems to be very, very equivalent to what we're seeing with the 600 arm. Yeah. If I can also just reiterate, maybe if we can pull up slide 26. Remember, our target product profile has always been to differentiate ourselves and be able to win in the MG market is to deliver the most convenient, the most patient-friendly dosing and administration. And Dupixent every two weeks auto injector has always been our goal. And that achieves very potent inhibition on the classical pathway. And if I can pull up slide 26, if possible, when I look at the MSE there on the right, that is the highest minimal symptom expression rate ever seen with a complement inhibitor, period. I mean, when you look at it, how it compares to Ultomiris, that is very, very impressive. Frankly, that's probably the goal when you're treating these patients, is to get them to a point where they are not thinking about their disease, where they're not feeling the symptoms. And 300 did better. And so this gives us a lot of confidence that 300 is absolutely the right dose. And again, there was no statistically significant difference on the MG-ADL between 300 and 600. So at one point, we were asked if we didn't hit stats, would we combine the two doses? We didn't need to do that here. But if you did, you'd see a nice north of two-point difference for claseprubart. And that's what we fully expect we'll see in a larger trial going into phase III with 300 milligrams every two weeks. Thank you. I would now like to turn the call back over to Marino Garcia for closing remarks. Thank you. And thank you, everyone, for your attention and joining us today. Really appreciate it. Look forward to engaging with some of you as we go forward from here. But again, I just want to thank Sim, the Dianthus team in general, for a very well-executed and timely study. I have to say we were hoping to see these types of results confirming the 300 milligram Q2 week as a classical pathway inhibitor would work in Myasthenia Gravis. It's a first proof of concept. We've already got proof of concept from other classical pathway inhibitors in CIDP and MMN. So overall, for this neuromuscular program, we feel like the level of risk has been significantly reduced, and it's really given or bolstered our confidence as we move forward in developing this very potent antibody in MG as well as CIDP and MMN. I look forward to providing further updates as we go forward. Thank you very much. This concludes today's conference call. Thank you for participating. You may now disconnect.