It's a great pleasure that I'd like to welcome Ryan Savitz, the CFO of Dianthus. Thanks so much for joining us today, Ryan. Yeah. Thanks, Maury, and thanks to the Jefferies team for hosting us. We're going to do Fireside Chat format. Maybe for those who are new to the story, if you can give a brief intro to Dianthus. Sure. The last nine months have been quite transformative for us at Dianthus Therapeutics, starting with our lead asset claseprubart. It's a highly potent active C1s inhibitor that's being developed across three neuromuscular indications, myasthenia gravis, CIDP, as well as MMN. I think where we sit now, we feel very good that we've de-risked the profile around these three neuromuscular conditions. It's really all about now execution with high quality to get to approval as quick as possible. Coming up, we're going to be initiating our phase III myasthenia gravis trial imminently, there we'll be testing two different doses, one shot every two weeks, as well as one shot once a month. In there, we're looking for a nice improvement on MG-ADL, as we saw in our phase II trial. What we've also added into this trial is a QMG cutoff criteria, which we didn't have in the phase II, and we think that will help better control for placebo. We're excited to kick off that trial imminently, 17-week trial, 65 patients per arm, and that will read out in the second half of 2028. Most recently, we had very positive interim responder analysis in CIDP. This is a two-part pivotal trial to support a BLA. What we announced in March was an early go decision on what was planned for less than 40 patients, we achieved 20 confirmed responders. That benchmark that we set to have that at least 50% response ratio was set by another active C1s inhibitor. Given this data that we saw to announce it early in March with less than 40 planned participants completing part A, we've made some trial amendments and adjustments to our pivotal trial to speed up the execution of that. We've removed the 600 mg dose arm from part B, and we've changed the ratio from part A to part B from 40% to 50%. Our goal here is to really cut down on any time advantage that riliprubart may have, which I'm sure we'll get into. Lastly, our third indication for claseprubart is multifocal motor neuropathy. It's a multibillion-dollar market just in the U.S. with very limited competition and a really high unmet need for well-tolerated and well-effective therapies. We'll have our phase II MMN data readout in the fourth quarter of this year. The primary endpoint there is safety, and we're looking for consistency of efficacy trends across the multiple measures there, and again, reading out in the fourth quarter of this year. Got it. It's a great overview, we can dig into each of the programs, maybe starting off with the phase III in CIDP. You mentioned the update in March. One of the things with the study is that you guys have full transparency into the patients and the data, you could only disclose a few. Sure Key takeaways from the ongoing study. As you've had conversations with investors and KOLs since the CIDP top line, are the key takeaways still the same, or how are you thinking about strategy from this point relative to Sanofi? Yeah. It's a good question. Given it is an ongoing trial, we couldn't disclose our actual response rate because we didn't want to compromise the integrity of the trial. Going into the interim responder analysis, we told investors to look out for three potential announcements that we would make in our interim responder analysis. The first was, are we keeping the dose in part A the same, 300 mgs, two mls every two weeks? That would mean we're seeing at least riliprubart-like efficacy with every two-week dosing. The second point was, are we keeping the 600-mg dose arm in part B? We never thought we needed that dose arm in part B, frankly. What we've seen is we've removed that dose arm now, given the robustness of the data. That also helps us on execution and speed to get to part B top-line data. The third piece we told investors is what is the ratio we're having between part A and part B? Initially, the ratio was set up for around 40% response rate from part A to part B. We've now increased that ratio to 50%. For us to be able to do so, we need to be very comfortable that we're well exceeding that 50% cushion because we're fine to over-enroll part B. We don't want to under-enroll part B. For us to change the ratio from 40% to 50%, not only does it make the trial quicker and faster, but also I think what's shown is really the robustness of the efficacy we've seen in that part A interim responder analysis. Got it. All makes sense. Maybe talk about how investigator and patient interest in the CAPTIVATE study has changed since your MaGic data announcement last fall. Are there specific aspects of the CAPTIVATE trial design that make it attractive for. Yeah patient participation? Post-gMG data, we started to really see a hockey stick in terms of enrollment. I think largely people were just waiting for to see a RCT trial with an active C1s inhibitor show out to be safe and effective, and we had that with gMG. We saw a nice halo effect from investigators that started to put their patients onto claseprubart in our CIDP trial. Going back to your other point, when we were designing the trial, we knew CIDP would be quite competitive. There's a lot of ongoing trials in the field. What we saw was argenx get approval in all adult patients with their 2-part trial as well, called ADHERE. There's a couple of key differences we made to the trial that we thought would be helpful from an investigator and patient perspective. In their trial, they forced patients to relapse, and then that had to be confirmed that they needed IVIg in order to be randomized or put onto their stage A. Only patients that relapsed before part A were put into part A, and they were measuring what percent of patients got back to their pre-Ig washout. In that trial, about two-thirds got back to their pre-Ig washout, and 1/3 Still remained not getting back to their baseline. What's really interesting about our data set as well as riliprubart, the other active C1s inhibitor in Sanofi's pipeline, is our data was showing an improvement on top of standard of care. One point as measured by the INCAT score, above and beyond your baseline. The other difference versus ADHERE that we knew would be an advantage for us from a recruitment perspective is that we recruit all patient types, standard of care treated, standard of care refractory, and naive. In the argenx trial, for example, they didn't recruit refractory patients. As we look at the other landscape across the other trial designs, we're competing against Sanofi's phase IIIs, right? Sanofi's in two phase IIIs. One is a head-to-head versus IVIg, a non-inferiority trial, and the other trial is versus placebo in refractory patients. In both those trials, you have a high probability of getting on placebo from the start. What's unique about our trial, our two-part pivotal trial, is in part A, all patients are getting drugged. There's no washout. We're taking all comers into the trial. Everyone gets drugged. Only patients that respond will then be randomized into part B. Part B is up to 52 weeks. If you get put on placebo, and you do relapse, you get rescued with standard of care, then you get put back on claseprubart because we knew it worked for you in Part A. You can be on OLE for up to two years. There's a lot of advantage that we had from a recruitment perspective, given our clinical trial design that has allowed us to accelerate timelines, frankly, in CIDP. Yeah. It's a really appealing trial design, and I could see how patients would prefer going that route. Yeah just based on that alone. Yeah. Lastly, we're only requiring patients to come in every two weeks for one injection. Versus riliprubart, theirs is two injections per week. Less of a patient burden than what we've seen with other competitive trials. Got it. Makes sense. With Sanofi and argenx phase III readouts expected next year, how are you thinking about the read-through to claseprubart's CIDP development path? Yeah. We're excited to see the riliprubart data, particularly the head-to-head versus IVIg, and I think that will be a meaningful point in time for the potential shift in the treatment landscape in CIDP. Right now, from an efficacy standpoint, people view IVIg as being the most efficacious in what's approved out there and then FcRn. If active C1s inhibition can show to be as effective as IVIg, it's got its advantages as it relates to convenience and safety versus IVIg, which we know has tolerability issues, black box warnings, and everything else that comes with it. We're really excited about where the shift in terms of the landscape is going for CIDP, and we know from our in vitro experiments that we have a much more potent classical pathway inhibitor than riliprubart. Multiple times more potent. If getting higher levels of inhibition of the classical pathway can lead to better efficacy, we would expect to see that. At a minimum, we expect riliprubart to have at least non-inferiority. I think if they show superiority, that would be quite a game-changer for the landscape in CIDP. Got it. Okay. For your phase III CAPTIVATE study, do you think that design is sufficient for a broad label? Yeah Do you think you need a dedicated superiority study versus IVIg from a commercial perspective? Yeah. Good question. From a label perspective or from an approval perspective, excuse me, this will be adequate according to our regulatory discussions. This would act almost as an sBLA, and come behind kind of MG or at a very similar point in time. Remember, VYVGART got approval in all adult patients with CIDP, and they didn't even enroll refractory patients. We're taking all patients, standard of care treated, standard of care refractory, as well as naive in our package. That would support, we believe, the BLA. Then, maybe for commercial reasons, there's a need to do a head-to-head. Again, remember, if riliprubart does beat us to the market, they'll have data out there showing active C1s inhibition. Right. We'll have a much more patient-friendly, convenient option by being one shot every two weeks, versus their option is two shots every week. Right. Yeah. Basically informs the space. Exactly Doctors can kind of make their own decision. That's right. Okay. Let's pivot to your phase II program in MMN. You mentioned the top-line data expected fourth quarter. The perception is that this is a smaller patient population relative to CIDP and MG. How are we thinking about this market opportunity? Yeah Why are you excited about it? We believe it's a multibillion-dollar market just in the U.S. Right now, prevalence numbers are showing that about 10,000 patients in the U.S. with MMN. From our physician surveys, about 81% of physicians believe MMN is underdiagnosed, and often it gets misdiagnosed as ALS. What we've learned from the MG market, the CIDP market, and other rare disease markets, is once you have more disease awareness, more biologics, and development, those prevalence numbers start to tick up. Already in and of itself, we think the MMN market is a large untapped space. The only approved therapy right now in MMN is IVIg. From our physician survey as well, about three-fourths of physicians say there's more room for better improvement in terms of more effective therapies for the treatment of MMN. With a space with very limited competition, it's just us and the C2 inhibitor from argenx and empasiprubart in development for MMN. This is really an opportunity to command a meaningful market share in this space. Remember, we're studying all allied neuromuscular conditions, gMG, CIDP, and MMN. This is just additive to CIDP and MG, and already a commercial infrastructure that's going to be built to tackle all three. There's a lot of commercial synergies that would come of this as well. Got it. $multi-billion just for MMN alone. Yeah. Right now, it's estimated that IVIg is selling around $800 million just in MMN. Right. As I've said, there's a lot of physician pushback on how effective that therapy is. I think with the growth and the prevalence figures that will come with more disease awareness and just better treatment options for patients, that market can be multiple billion dollars, and that's what argenx has already stated. They say this is a blockbuster market right now as well. Got it. You mentioned 10,000 patients in the U.S., but it could be underdiagnosed. Have you guys put out a range for what the upper limit is? We've said 10,000 for now. We'll continue to monitor claims and other data sets to better inform that. We certainly will be behind empasiprubart, but they've done a great job in the past, argenx has, in paving commercial stories and narratives. Right. Yeah. You're behind Empa. That could potentially work in your favor as you guys launch afterwards. Yeah. Makes sense. Yeah. Can you remind what you're going to report in the top-line data in fourth quarter, and what are the key differences between MoMeNtum and ARDA that investors should keep in mind? Sure. Our study is looking at 300 mgs every two weeks and 600 mgs every two weeks. 12 patients per arm, a total of 36 patients. 17-week RCT portion. The primary endpoint here is safety. The secondary endpoints are exploratory, we'll look for consistency of trends across those efficacy measures. At the end of the day, Maury, we really just want to get started in a phase III as quick as possible. We know classical pathway is the driver of disease here in MMN, we're just motivated to move as quickly as possible. If we were to go back in time, we'd have loved to move directly into a phase III, just like we did with CIDP, that road hasn't been paved yet in this market, Empasiprubart helped pave that way. You asked about some of the comparisons versus us and Empa. I'll talk about some broader comparisons and then trial comparisons specifically. We know that Empasiprubart inhibits the classical and the lectin pathway. They, in their own publications, as well as the literature that we've discovered, is that the classical pathway is the main driver of disease. A few months ago, they put out some in vitro potency data looking at classical pathway inhibition using the Quidel MicroVue CH50 assay. We replicated that assay, and what we're able to discover is that we are multiple times more potent at inhibiting the classical pathway than they are. At the end of the day, we'd expect to have at least equal efficacy to what they would have in a larger scale trial. If not, maybe superior efficacy. We'll see if higher inhibitions of classical pathway means better efficacy. We'll see how that plays out at the end of the day. As it relates to safety, like I said, they inhibit the lectin pathway. That is not a driver of disease in MMN. By inhibiting the lectin pathway, they have a higher risk from infections from encapsulated bacteria because there's no way for the complement system to act, and therefore prevent that from happening. We would anticipate they would have an FDA box warning and REMS. Lastly, they are testing IV. We don't know what dose they're using in the phase III. We are sub-Q with the ideal of every one shot every two weeks. As it relates to the trial design comparison, I know there's a lot of historical conversations around the IVIg rescue figure, because that's a number they initially published, I think when they initially had their data back in 2024. Since then, they've switched the primary endpoint in their phase III trial from IVIg rescue to now grip strength. IVIg rescue has kind of been pushed to the side a bit. I will caution any comparisons that could be made from our phase II MoMeNtum trial to their ADHERE trial on the IVIg rescue side. In their trial protocol, to have IVIg rescue in their protocol, you can have a MRC deterioration of 2 points or more, a 30% deterioration or reduction in grip strength, or a patient request to get IVIg. In our phase II trial, we do not allow patients to request IVIg at their will. It's up to you need to see one of those clinical deterioration markers. It's really an apples to oranges comparison to try to compare their IVIg rescue figures to ours at the end of the day. Again, we're looking for more consistency of trends across all efficacy measures and just get to phase III as quick as possible because we know classical pathway is the driver of disease here, and we're just excited to get into phase III as quick as possible. Got it. Makes sense. It sounds like the MRC and then the grip strength, those could be two measures where you could make some apples to apples comparisons or cross comparisons. Yeah. Again, it's a small study. Small study. Yeah, that is more than IVIg rescue, for sure. Got it. Okay. You didn't see a difference between the 300 mg and 600 mg biweekly doses in MG, and you're advancing the 300 mg dose in CIDP. Do you expect to see a dose effect in MMN? Good question. We do not. We do not expect to see any difference between 300 and 600 in the phase II MMN and fully expect to move forward with 300 every two weeks in the phase III. What we've learned, in MG, we don't think you need to be above IC90. In CIDP, from our data comparison in phase II versus the phase II riliprubart data, maybe in CIDP and MMN, higher levels of an inhibition of the classical pathway can lead to better efficacy. We know our relative potency versus Empasiprubart is quite large, and so we'll see what happens at the end of the day, but maybe higher levels of inhibition in diseases like CIDP and MMN can translate to better efficacy. Got it. Okay, makes sense. With argenx, they're going to have their MMN data fourth quarter. If they hit stat sig on non-inferiority for grip strength versus IVIg or even show superiority, what's the read-through to claseprubart and MMN, and what specifically are you watching for in the data set to inform? Yeah. We fully hope they at least hit non-inferiority on grip strength from a primary endpoint. Like I said, this is a market where there's really a need for more effective therapies, and IVIg just does not work very well in this patient population. I think given the relative potency comparison of us being at, say, IC50 six times more potent in our experiment, and at IC90 almost 40 times more potent, people can interpret that at least we should see comparable efficacy, if not superior efficacy to what they see. Again, you can't make that cross-trial comparison to a phase II to a phase III, and that's why I said we're so excited just to get directly into a phase III to further our development program there. Yeah, we know classical pathway is a driver there. We expect them to be successful. I think that should have good read-through to us. If for some reason they don't hit maybe non-inferiority even or stat sig, I think also we can interpret we're a much more potent classical pathway inhibitor. Maybe they're not achieving enough classical pathway inhibition. We'll see. Got it. Okay, makes sense. You're starting the pivotal study for claseprubart and myasthenia gravis in the middle of this year with top-line data expected second half of 2028. What's the status of the phase III study, and what are the key gating factors to starting the study now that you have FDA alignment? Yeah. No gating factors. That study will be kicked off imminently. Like I said, it's a 17-week trial evaluating two dose arms, 300 mg 2 mL every two weeks, and then 300 mg 2 mL once a month. One shot every two weeks and one shot once a month. 65 patients per arm. In terms of the changes that we've made from the phase II, we have added a QMG exclusion criteria into the trial that we did not have in the phase II. When we did some post hoc analysis from our phase II, we noticed that if we added a QMG cutoff of 10, which is kind of in line with what other competitor programs have done, our placebo moves from a 2.8 down to a 2.2. That's more in line with competitive trials in MG. We think by adding in this more strenuous kind of QMG criteria into our phase III, we can potentially better control for placebo there. What we're hoping to see in the phase III is at least C5-like efficacy, if not better. There's a reason for us to believe that by being an upstream inhibitor, we could potentially have better efficacy. Because C5s are very good at shutting down MAC, which is the main driver of disease in MG, but we also prevent C3a and C3b from forming. Those are two additional pro-inflammatory split products that C5s cannot prevent. We think that's additional damage being done in these MG patients, and by us preventing those two pro-inflammatory split products, that could lead to better efficacy over the long term. Got it. For the QMG cutoff of 10, how does that impact enrollment? It seems like you guys are still sticking with the same timelines. Yeah. It shouldn't impact at all enrollment. I think we have a lot of excitement from the investigator community to get started on MG as quick as possible. That's kind of shown as the robustness of the efficacy that was seen in our phase II MaGic data. A very patient-friendly, convenient profile with sub-Q shot every two weeks or once a month and a very clean safety profile. It's kind of got a unique value proposition that investigators are really excited to get going on in the phase III. Got it. Also one of the reasons for screen failure rates in our phase II MG trial was elevated ANAs, which we knew had no impact in terms of any clinical effect. That ANAs have now been removed. Right From the phase III, that should help with enrollment as well, given how high the screen failure rate was because of that. Yeah. Makes sense. You've previously mentioned the potential to replace the IV loading dose with sub-Q loading injections. Do you plan to run a PK bridging study to demonstrate comparability to the IV loading strategy? Is this necessary from commercial? Yeah. Good question. We are using the SHL Molly in terms of what we want on day one from a commercial point of view. The SHL Molly is a well-adopted, easy-to-use auto-injector. It's what DUPIXENT uses across their portfolio. We've got alignment with the FDA to ensure that at day one, we have that auto-injector available for use in patients. We've kind of gone a pathway ahead of us to get that approved in the label on day one. Got it. Okay. There were two reports of waning efficacy with AstraZeneca's ULTOMIRIS, which is dosed every eight weeks. For your monthly 300 mg dosing arm, how confident are you that PK and exposure will be sufficient to maintain MG-ADL improvements across the majority of patients? Sure. In our phase II MaGic MG study, we did a little mini experiment in our open label extension. In the RCT portion, patients got a loading dose because we want them to get to steady state as quick as possible. In the OLE, patients did not get a loading dose at all. What we want to do is see PK accumulation and any impact on PD. Placebo patients that then transitioned to the OLE, given no loading dose, and after two doses of claseprubart, they had a meaningful reduction on the MG-ADL of 2.5 points that has been sustained. That was only at a PK level about 65 micrograms per mL. That's about half the steady state of 300 mg every two weeks. With a 60-day half-life, that gives us a lot of confidence that we can also see the same impact with once-a-month dosing. That 65 micrograms per mL translates into 300 mg, 2 mL once a month, half the dose of what you can get with claseprubart every two weeks. There's a lot of growing evidence externally that gives us the confidence that you don't need to be about at IC90 to have an effect in MG. Our 300 mg every 2 mL was always targeting 90% inhibition of the classical pathway. From our data as well as other external sources, we don't believe you need to be at that IC90 level. Right before we reported our MaGic data in September, Regeneron with cemdisiran, the C5 inhibitor, came out with data both for the monotherapy as well as the combo, where in the monotherapy, they had quite a robust improvement on the MG-ADL, greater than two points. What was great in that press release was that they said they only achieved about 75% inhibition of the complement system. In their combo, they had almost complete shutdown, but their data was better in the monotherapy arm. Again, growing evidence that you don't need to be above IC90 or even at 90% inhibition in MG specifically, further gives us the confidence that we don't expect to see a dose response in our phase III between once every two weeks and once a month. Got it. Okay, that makes sense. For the MG market, there's a perception that it's crowded. We're tracking these new programs that keep- Sure coming out of the woodworks. How do you see the space evolving? Yeah over time? Currently, there's really two foundational classes, FcRns as well as complement. What's interesting about the market dynamics within MG is less than 20% of patients are on a biologic today. If you look at other analogs in other spaces, take the MS market, for example, how do you grow that biologics penetration? You grow that through more patient-friendly, safer alternatives. We'll compete very well against the C5s and displace the C5s by having no FDA box warning or REMS and a much more patient-friendly administration option. Maybe by being upstream, there may be potential efficacy advantage. We'll see at the end of the phase III. I think the still problem with the FcRns is the cyclic dosing. Again, they have very nice impact through week four, but then when patients are off drug for those kind of drug holidays, their MG-ADL is rebounding. What we're hearing from physicians is they want that durability of symptom relief. While you said MG seems to be crowded, there's a lot of competitors in there, it's largely two foundational classes, complement and FcRns. We are the only complement inhibitor in development that has that safety advantage of being upstream and no potential for FDA box warning. Again, less than 20% of patients are on a biologic today, there's a lot of space for allow that market to grow. It's not just us saying that. You look at AstraZeneca and their earnings last year. They said they expect the biologics market to grow to about 50% of MG patients in three years. That would put us at 2028, 2029. That is a meaningful expansion in the market where there's already about $4 billion of MG sales today across FcRn and C5s. Yeah. That's really helpful. We are really interested in the DNTH212 program. Sure Have a bunch of questions there, but we don't have much time left. Maybe talk about the program. You're going to have healthy volunteer data update second half of this year. How are we setting expectations for that update? Yeah. This relates to DNTH212, which we in-licensed last year from Leads Biolabs. It's a bifunctional fusion protein targeting BDCA2 on one side as well as BAFF/APRIL on the other side. We're looking at diseases where both the innate and adaptive immune systems are at play. We're looking for superior or enhanced efficacy by targeting both sides of the innate and adaptive side. We just announced in our Q1 earnings that we have prioritized our top three indications being Sjögren's, SLE, and DM. Just like claseprubart, where we have a nice neuromuscular franchise, with DNTH212, we're building a nice synergistic rheumatology franchise. We'll have phase I healthy volunteer data out of China, like you said, in the back half of this year. We're looking there for PK/PD signals to help inform future dosing as it relates to our clinical development plan beyond the phase I trial. Got it. We're out of time. Maybe in closing, if you just want to talk about key catalysts ahead investors should be focused on in cash runway. Sure. The next catalyst for us is our phase II MMN data in Q4 of this year. We'll also have our DNTH212 phase I healthy volunteer data the back half of this year. Some competitor readouts that we've discussed in terms of Empasiprubart as well as riliprubart over the next 12 months, which will have potential read-through to us as well. At the last quarter, we ended with about $1.2 billion of cash, which takes us into 2030, well through a lot of these key catalysts. Got it. Thanks so much for joining us today, Ryan. Thank you.