For you, Ray Crofton, one of the biotech analysts at Jefferies. It's with great pleasure that I'd like to welcome Marino Garcia, the CEO of Dianthus Therapeutics. Marino is going to go through a couple of slides, and then we'll jump over to the fireside chat. Thanks for joining us today, Marino. Thank you, Mauri. Thank you to Jefferies for the opportunity to provide an update on some of the exciting developments going on at Dianthus. Just a quick caution, I'll be making some forward-looking statements. I please refer you to our investor webpage, where we have all our SEC filings around the risks and around investing in Dianthus. Just very quickly, we are advancing a leading autoimmune franchise with two potential best-in-class therapies in the autoimmune space, where we're targeting very friendly, convenient, infrequent subcutaneous self-administration. I'll talk a little bit about Claseprubart, the first of these two programs. It's a potent active C1s inhibitor. We disclosed very exciting myasthenia gravis phase II data in September, where for 300 milligrams, 2 milliliters, so one shot every two weeks, we saw clear, consistent, rapid efficacy across five different efficacy measures. Since then, we've presented some additional data at AANEM in San Francisco in October. This data provides the rationale for why we're taking not just Q2 weeks, 300 milligrams, 2 milliliters, one shot every two weeks into our phase III program for myasthenia gravis, but why we expect better efficacy than what's been seen with complement inhibitors in the past, as well as why we are taking a Q4 week dosing paradigm of 300 milligrams every two weeks into phase III. In terms of dosing, why are we adding every month dosing? First off, it is a very active, sorry, potent active C1s inhibitor that has a 60-day half-life. Rationally, every four weeks should also be possible. What's really interesting is some analysis data we presented at AANEM looking at patients who are on placebo that had a relatively robust response on the MG-ADL of a 2.8 reduction in their MG-ADL score. What we saw is once they entered into the open label portion without a loading dose, just dosing of Claseprubart every two weeks, we saw that after just two doses at PK levels that are half of what we achieve with 300 milligrams, 2 milliliters every two weeks, we saw another big drop on the MG-ADL as well as the QMG. At week four, after only two doses in open label, these patients achieving only half the PK levels we see with every two-week dosing are seeing a very robust response on the MG-ADL as well as the QMG. That tells us that we may be able to dose every four weeks, a lower dose, and still see the kind of efficacy we saw in our phase II with every two-week dosing. In terms of rationale for better efficacy than what has been traditionally seen with C5s, we presented an in vitro experiment where we showed the benefits of being an upstream inhibitor, in other words, shutting down the complement cascade up at C1s at the classical pathway versus downstream just before the formation of the MAC, like the C5s do. That is, by being an upstream inhibitor, we prevent the deposition of pro-inflammatory toxins or split products like C3a and C3b from being formed and causing potential damage at the neuromuscular junction. This experiment just highlights how effective we are at preventing C3a and C3b versus ravulizumab, the number one complement inhibitor in the world, the C5. We believe that because of this mechanism, this unique mechanism as a complement inhibitor, as an upstream complement inhibitor, that we may see better efficacy. One of the things we looked at in our phase II is, okay, we had a relatively high placebo response compared to historically C5 or complement inhibitors in the myasthenia gravis space. What could we do? We looked at zilucoplan, the last C5 approved, they had a QMG screening criteria. They had a 12 or above, as well as the MG-ADL 6 or above. We said, what if we had a QMG screening criteria, let's say of 10, somewhere lower than 12? What if we had applied that in our phase II? What kind of results would we have seen with our 300 milligrams, 2 milliliters every two-week dose? As you can see in this slide, we would have seen something closer to a 3-point difference on the MG-ADL. As you can see, the placebo around 2.2, very similar to the 2.3 that Zilucoplan saw. As we move forward into our phase III program, we're going to be discussing with the FDA and other regulatory agencies the design of this program. We're not just testing every two-week dosing, as I mentioned earlier, we're also testing every four-week dosing of a 300 milligrams, 2 milliliters single shot that we can put into an auto injector. Once we have alignment with the regulatory agencies, we'll provide further update on timing of the start of this study, as well as when to expect top-line results. Another bit of news since we revealed our MG data and we raised $288 million, which provides us with a nice cash balance of about $525 million and a runway into 2028. We also licensed a very exciting potential best-in-class potential product in a, sorry, pipeline in a product just like Claseprubart, DNTH212. It is a bifunctional fusion protein that targets both the innate and adaptive immune system and also has a YT half-life, so half-life extended so we can target self-administration, subcutaneous, infrequent dosing. What are we trying to achieve with DNTH212? It targets both BDCA2, in other words, reduction in type one interferon, and therefore addresses the innate adaptive, sorry, the innate immune system, part of the immune system, but it also targets BAFF/APRIL. It looks like it has superior Ig reduction to POVI, POVI TASEP, and a longer potential reduction or half-life. What we're trying to achieve with DNTH212 in this bifunctional fusion protein is to address the unmet need in conditions where both the innate and the adaptive immune system are at play in the disease. We wouldn't look to take this into a disease where only one of the two parts of the immune system is causing damage or causing the pathogenesis. This is where we see the potential for superior efficacy in conditions where both of the innate and adaptive immune systems are at play. The idea here is bring, deliver, or bring to the patient superior efficacy than any sort of monotherapy monoclonal antibody could without any new safety signals, so a clean, relatively safe, and clean and well-tolerated profile, and then put it into a Q4 week or less often, potentially Q8 week, subcutaneous self-administration and potential auto injector in the future. This is IND cleared in the U.S. and imminently cleared in China, and we'll start our phase I single-dose study in healthy volunteers in the very near term. In terms of key catalysts coming in the near term, as I mentioned, we'll start our phase III in 2026 in MG for Claseprubart, and once we have alignment with the FDA, we'll reveal the details of that study and the timing. CIDP, good news. We have our phase III interim responder analysis. Previously, we had guided to a second half of 2026 for top-line or announcement on how the study is doing with our first 40 patients in part A. That has now been moved up to the second quarter of 2026. With MMN, our phase II study, that is still on track for top-line results in the second half of 2026. Finally, with DNTH212, as I mentioned, we'll be starting our phase I healthy volunteer single-dose study imminently, and we'll have results for that in the second half of next year, as well as an announcement around the indications we're going to prioritize for this new program. With that, why don't we go into Q&A? Yeah, thanks for going over here. All right. Covered a lot in the intro there, but maybe a clarification question for the GMG pivotal study. Are you planning on meeting with FDA by the end of this year? Is it going to be early 2026? And then would you provide a status update after that meeting? Yeah, we haven't guided exactly when, but the meeting is imminent, as you can imagine. We've been preparing diligently for that. As soon as we're done with that meeting, we'll announce exactly when in the year in 2026 we'll start the phase III and when to expect top-line results. Got it. Recognizing that it's TBD at this point, I guess what's the range of possibilities for a number of patients that you might need for the pivotal, and how long do you think it could take to fully enroll the study? Yeah, I think that's part of the discussion we'll have with the FDA, but something similar to what's been done in the past, so high double digits, each arm will probably be the size of the study. What we've seen is typically from study initiation to completion of enrollment is about two years. I think that would be a fair assumption. Got it. Okay. For getting alignment on a 12-week study, there's some precedent from Zilucoplan, from their pivotal study. Do you anticipate pushback from FDA on this, given that most of the GMG studies tend to be 22+ weeks? No. I mean, we have good alignment with them on our 13-week study for our phase II. I fully expect that may be the length of our phase III study. Because we're testing once a month, maybe we'll add another four weeks so we can get one more dose of the once-a-month dose in there. Maybe it'll be 17 weeks, but that's part of the conversation we'll have with the FDA. Got it. So pretty confident it'll be something faster. Yeah, it'll be three months at shortest, and certainly, I don't think it'll be much longer than that. Okay. And then based on the MG-ADL and QMG kinetics you're seeing so far, do you believe that longer follow-up out to 22+ weeks could lead to deeper improvements, or are you nearing a plateau early on? I mean, if you look at the line graphs from our phase II study, we see clear separation both in the MG-ADL and QMG at week one. The sort of peak of efficacy we see relatively early in the study. It seems to stay relatively consistent out to the later weeks, up to 13 weeks. I do not really think we need longer-term data to see the peak efficacy. As I just showed you, I think the issue is when we saw our placebo response, it looks closer to three than two. Typically, historically, you see placebo responses closer to two. We asked ourselves what is going on there. If you look at the baseline characteristics for the QMG, the physician-administered scale that takes up to two hours, the placebo, I think, was relatively similar to what we've seen historically, but the QMG for the 300 and the 600 arms were a little lower than what we've seen in the past. We said, what if we had a QMG screening criteria like Zilucoplan? Would that help sort of keep placebo control more in line with what has been seen historically in MG trials with complement inhibitors? That is what I just showed here, and we showed at the AANEM, is that, yeah, just having a relatively moderate QMG score of 10 or above, as well as the MG-ADL screening criteria, helps to control the placebo response a little bit. We had a three. A three change on the MG-ADL by 13 weeks. I mean, there's nothing on the market that's shown those kinds of scores. That's why I think 13 weeks should be plenty of time. We just need to make sure we control a little bit for some of these high placebo responders that sometimes you get in MG trials recently. Then we can really shine a light on the benefits of being an upstream inhibitor versus downstream inhibitor and potentially extract even more efficacy for these patients. Got it. You showed the open label extension, some of the open label extension data as well, where you see some deepening of effect there. What are the chances of having some bias there, and how could you mitigate that, or how could you potentially parse out what that impact is? Keep in mind that efficacy in open label is for placebo patients only, right? These are patients who had a response supposedly on placebo, but when they get actual drug, that deepening of efficacy is even more dramatic on top of what they already responded from the placebo. We're not seeing that with the patients who went from active to open label. We're not seeing a further deepening of that response. Got it. Okay. Does that answer your question? Is that what you were getting at? Yeah, yeah, I think so. Yeah. I guess for the placebo group doing so well, though, is there any type of bias in there? Oh, I see. You're getting at bias. I mean, these patients thought they were on drug for 13 weeks. That 2.5 improvement on the MG-ADL we saw just after two doses in open label is on top of the 2.8 improvement they had in the first 13 weeks. I think that is a real response. It's at PK levels at half of what we expect or see at 300 milligrams every two weeks. Remember, we have a very potent active C1s inhibitor that has a 60-day half-life. We always knew there was a potential here for a once-a-month dose. We said very clearly for the last couple of years, we do not expect a dose response between 300 and 600. If we don't see a dose response, I think it's our responsibility with a 60-day half-life to at least test the once-a-month dose, right? That means we haven't found our minimally effective dose. I think the regulators will be very happy to see that in addition to our every two-week dosing. We'll see. We'll see what kind of efficacy we can get. I fully expect we will not see a dose response between our 300 every two weeks and our 300 every four weeks. I think we'll see that every four weeks is the dose we take forward into MG. Got it. Okay. Let's talk about CIDP. Sure. You've got the phase III up and running. You're going to have the data update second quarter of next year. You bumped up the timelines there. You said the bar is approximately 40%-50% for improvement of at least one point on NCAD, but Sanofi's phase II showed about 50%-52%, and your drug's more potent. I'm guessing the lower end is just because you're being conservative there and assuming that you're going to get some variability, but maybe just walk through the assumptions. Yeah. I mean, look, depending on which poster you look at from Sanofi at what time point, they had anywhere from 40%-50%. That tells us that that range tells us that we would be about similar. Remember also, their study was 24 weeks, their phase II. We're doing it after only 13 weeks. So we're saying if in the first 13 weeks, we see a one-point improvement on NCAD score that's anywhere in the 40%-50% range, that's telling us we're relatively the same to Riliprubart, but with much better dosing and administration. We do have a more potent antibody. The question is, by being a more potent active C1s inhibitor, is there more efficacy you can extract in CIDP? That's the question. We expect at least similar efficacy, if not better, but in either case with much improved dosing and administration. Got it. For that study, just talk about differences in inclusion and exclusion criteria or anything else on baseline characteristics relative to Sanofi's phase II. It's very similar to the Sanofi phase II. We take patients who are on standard of care, for example, IVIG or refractory to IVIG standard of care or naive. I expect a very small percentage of these patients are going to be naive to standard of care. We switch them immediately. That's a big difference in our phase III trial versus, let's say, like what the FcRNs have done or like Argenx did with that here. They take patients that are on standard of care. They didn't allow refractory patients into their programs. I just don't think an FcRN would work in a patient that is refractory to IVIG. They took patients who are on standard of care stable. They took the IVIG away, made them relapse, and then put them in their open label part A. When you see that 67% response with efgartigimod in ADHERE, you have to remember that's after patients relapse. That means a third of those patients never got back to baseline. The difference with the phase II riliprubart study from Sanofi is they didn't make patients relapse. They switched them within a week to the active C1s inhibitor. If you look at those patients who were on standard of care and stable, they still were able to get additional efficacy in 50% of those patients who were stable and fine on IVIG before. That's a really impressive number. Those patients were not made to relapse. The refractory data, about 50% as well, improvement, patients who are refractory to standard of care. Again, you're not going to see FcRn data in refractory patients because it's not going to be studied in those patients. It wouldn't potentially work there. They had really impressive data in naive patients, which is not a surprise. Again, I think as we go forward in CIDP trials, it's going to be harder and harder as more treatments are available to find naive patients. I expect the vast majority of the patients we'll see, certainly in the first 40 that we are looking at in our part A for our interim responder analysis, will be either in the refractory or stable standard of care grouping. Got it. In terms of screening and so on, like I said, it's very similar to what Riliprubart had in their phase II. We're essentially replicating what they've done in part A. When you do this data update, I guess what exactly are you going to show? Yeah. The FDA would like you to just say go or no go. That's it. They're very concerned about you revealing any data that affects the integrity of the trial. We're going to have to be very careful around that. At a minimum, what I think people will be able to see, and this is information we would have to enter into clinical trials anyway, is an update on what N do we expect into part A in order to feed whatever N we have in our part B. All you need to do is make a simple division, and you see if that number is anywhere around 40%-50%. If we expect 40%-50% of the patients in part A to respond in order to feed our part B target recruitment, then you would be able to conclude that we're seeing at least similar efficacy to Riliprubart. That is at a minimum what we'll be able to say. Go and then update this trial size. That is something I know investors would like to hear more about. We're looking to see what we could do that would not in any way upset the FDA or any regulatory authority. Got it. For the 40%-50%, it sounds like that's kind of the bar, but you think your antibody is more potent than Riliprubart, and you've got some data to support that preclinical and clinical. Do you think you could do better than 50%? I guess what are your thoughts? The question we do not know in CIDP is if you are a more potent classical pathway inhibitor, do you get more efficacy? In MG, we always thought we were overdosing. That likely we could get away with once-a-month dosing. We do not know with CIDP. There have not been dose-ranging studies. Sanofi has only ever tested 600 milligram, 4 milliliter every week. We are testing one 300 milligram, 2 milliliter shot every two weeks, a quarter of the dose and less frequent as well. We will see what kind of efficacy we can get if there is a potential for superior efficacy because we are more potent, but we expect at least similar efficacy with the dosing administration advantage. Got it. Kind of jumping ahead a bit, but how do you think about pricing across the three different settings where you're developing? Yeah. I mean, that's an interesting question. The advantage in a way we have is that we're going to know what the pricing for MG is at the point we get the approval in MG, if we do. Riliprubart should be on the market, so we'll know where they priced for CIDP. Argenx's efgartigimod is somewhere in the $350,000 a year in MG, and it's double that with CIDP because of its continuous dosing in CIDP versus the cyclic dosing in MG. We'll see where Riliprubart prices itself. With MMN, it's likely that empasiprubart, the C2 inhibitor from Argenx, will also be the first approved complement inhibitor in that market. We'll have a pretty good understanding of the pricing landscape, and then we'll pick the pricing that makes the most sense where we can maximize the value across the entire portfolio for Claseprubart. Look, if we have MG dosing every four weeks and then CIDP and MMN every two weeks with the same auto injector, same dose, then that'll give us an even greater opportunity to be flexible in terms of how we price for CIDP and MMN being smaller markets than MG. Right. Got it. Let's talk about MMN. You're going to have data second half of next year from your phase II program. Argenx is also going to be having data from their C2 sweeping antibody EMPA second half of next year as well. Maybe just talk about how you view these two different programs and if you're going to present data in a similar way as Argenx so we can compare and contrast. Yeah. For MMN, it's an underappreciated opportunity. I think we have to remember, yes, it looks like it's smaller than MG and CIDP, but FCRNs don't work there. It's IgM-driven. There's nothing really now approved or that works really well. IVIG doesn't work that well in MMN. Eventually, at the end of the road, if Argenx is successful with empasiprubart and we're successful with Claseprubart, there'll be two complement inhibitors, and that's it. The difference between us and the C2 inhibitor from Argenx is, A, we don't block the lectin pathway. There's no need in MMN to extract any efficacy there. That's just a safety overhang. Very likely will lead to a box warning around the risk of infections. It's an IV. We're taking a single auto injector, one dose, one shot, five to seven seconds every two weeks into MMN. We're looking to have similar efficacy to what they saw in their phase II. Our phase II is very similar to the phase II they conducted. Like with our MG data, we'll be as transparent as we can and show all the efficacy that we can from the top line results. Like you said, we are on track for data in the second half of next year. Got it. For the grip strength, just setting expectations on what you'd want to see there, I guess how do you think about that? Just very similar to what's been presented for Argenx and where you go to see their phase III results. That'll give us a little bit of what the bar is for a phase III study. We can take that advantage of safety and the dosing administration and compete effectively and have similar efficacy at least to their C2 inhibitor. We do believe we have a more potent classical pathway inhibitor. Just like CIDP, we're not sure is there a threshold that once you get above that in terms of inhibition of the classical pathway, you're not going to get any more efficacy. We're not sure what that is. We will see. We potentially could have better efficacy than a C2 inhibitor in the long run. Would you do your data update after Argenx, or does it not matter? We'll do it when we have our results. Hopefully, like I said, we'll see their results before, and it'll give us a little bit of perspective, but it may be at the same time or maybe before them. Got it. Okay. We're almost out of time, but for two and two, wanted to ask just how you think about Biogen's phase III data that they're going to have next year and just read through from that to your program. Yeah. I mean, look, SLE is one of those conditions that there's been quite a bit of frustration, obviously. This is for lupus. Yeah, for SLE. That's right. One of the things that was very exciting about the DNTH212, during the diligence process, we talked to KOLs and we showed them the data, the preclinical data. The clear feedback from them is, this is exactly what we need for this condition. We need something that tackles both the innate and adaptive immune system. There is some excitement for Biogen's program. We look like we have better PDC reduction and depletion, but we'll see if that translates into better reduction of type I interferon or efficacy there. On the BAFF/APRIL side, we look like our new year is deeper and longer than what you see with POVI. Again, we'll see if that provides any additional efficacy there. The real benefit here is being able to take both those mechanisms into one therapy forward for SLE. That's where at least the KOLs we spoke to, they do expect some complementary efficacy because of that. That could be more efficacious than any one approach, one monotherapy, monoclonal approach to SLE. That's the hope. Got it. This has been a great conversation. Maybe just to close out, if you can comment on just key catalysts ahead investors should be focused on. Yeah. I think I mentioned that during my opening remarks, but 2026 is going to be another pivotal year. This was a really important year for us. Now in 2026, we'll announce the exact details of our phase III program in myasthenia gravis and the timing for the start and for when to expect top line results. CIDP, we're very pleased to move that catalyst up from the second half to the second quarter. Team's doing a phenomenal job of recruiting and screening patients into our program there. We'll have that in the second quarter of 2026 and the top line results for MMN in the second half of 2026. Those are just internal for Claseprubart. For the DNTH212, we are imminently starting a phase I single dose trial in healthy volunteers, and we'll have results of that in the second half of this year. I think people will be looking for what kind of dosing are we looking at potentially taking forward into patients in phase II, but also are there any new safety signals which we don't expect. Got it. Thanks so much for joining us, Marino. All right. Thank you. All right. Thank you.