Good morning, everybody. I'm Marino Garcia, CEO for Dianthus. I will be providing a brief update. Oh, here we go. More. How are you doing? And then we'll open it up for some Q&A. Before I begin, just again, thank you to Jefferies for this opportunity today. I will be making some forward-looking statements, so I urge everyone please to go to our website and where you can read all our SEC filings. This is a very exciting time for Dianthus. We are rapidly advancing DNTH103, our very potent active C1s inhibitor, as a pipeline and a product across three exciting market opportunities, building a market-leading neuromuscular franchise, starting with Myasthenia Gravis, which we recently announced we are done with enrollment with our phase II trial, and we'll be having our top-line results out in the month of September this year. Next, with Chronic Inflammatory Demyelinating Polyneuropathy, a very exciting market opportunity where there's now very clear proof of concept for active C1s inhibition potentially being best-in-class efficacy for this disease. Finally, Multifocal Motor Neuropathy MMN, where again, there's also proof of concept for classical pathway inhibition delivering excellent efficacy, where we have the potential across these three different indications to develop a best-in-class first-line therapy with 103. Let me jump into the Myasthenia Gravis opportunity first. This is a very large rare disease, over 100,000 patients in the United States alone, dominated really by only two mechanisms of action that will compete today and into the foreseeable future for first-line use as biologics. Of course, the complement franchise from AstraZeneca leading with over $6 billion and continuing to grow, where they themselves have said their growth is coming from biologic naive first-line use in MG patients in the United States. Of course, the tremendous success that Efgartigimod has had in the Myasthenia Gravis space, the FcRn class. With both of those, we're looking at something approaching potentially $5 billion in revenues. Despite this tremendous success with these two franchises, there's still a significant unmet need in this marketplace, something that ideally the Target Product Profile, should we achieve it with 103, could really address very effectively. Recent market research we've conducted this quarter shows this market is huge, and there's still an opportunity to increase diagnosis. More importantly, over 90% of Myasthenia Gravis patients in the U.S. are still not on either a complement or an FcRn biologic. This highlights the orders of magnitude larger that this market could be, despite the tremendous success we've seen already from the C5s and FcRns. When we asked neurologists, we conducted a survey of a representative sample, a very robust study of neurologists that practice in the U.S. treating MG patients. When we asked them, "What are you looking for? What would you like?" Over 80% are looking for better efficacy, more specifically robust, durable symptom control. Over 70% would love to see a low-volume autoinjector, something like what you see with DUPIXENT or the GLP-1, something that a patient can very easily self-administer at home or on the road in a matter of a handful of seconds. Two-thirds of neurologists highlight that they would love to have a safer profile, no box warning around the risk of deadly infections like meningitis. Why are they talking about durable efficacy? It is clear with C5s, you do get efficacy. When a patient responds, it is very nice, robust, consistent symptom control. With FCRNs, they do see improvement in patients, but unfortunately, they cycle because of the off-cycle treatment period. You have patients going through a roller coaster of symptoms, as you can see from this slide with their MG- ADLs rebounding after they finished their four-week treatment. The idea here is for us to deliver C5-like efficacy and consistent symptom control in a subcutaneous every two-week autoinjector. When they talk about no box warning, this is another huge opportunity for DNTH103. Because it targets active C1s, it only inhibits the classical pathway, which is what's really driving the dysfunction in Myasthenia Gravis. 103 leaves the lectin and alternative pathway completely intact, so it could do what it's supposed to, which is fight against the risk of infections from encapsulated bacteria. This is not just a theory we have for 103 versus C5, C3, C2s, et cetera. This is a precedent that the FDA has already set. There is ENJAYMO or sutimlimab. It's the first-generation C1s inhibitor approved for Cold Agglutinin Disease. It's on the market. If you look at the label for ENJAYMO and compare it to any other complement inhibitor, you will see that it is a much cleaner, much safer profile. It has no box warning against the risk of infections, no REMS program. When we look at the Target Product Profile that we're aiming for with 103, what we're trying to do essentially is bring together the best parts of three best-in-class labels already approved on the market in terms of efficacy, similar efficacy to C5s. Simple. Physicians will tell you when it works, it works really well. They love the consistent symptom control they get with the C5s. In terms of safety, we're looking to get the same label ENJAYMO has as a first-generation C1s inhibitor that also does not touch a lectin or alternative pathway. In other words, avoid the box warning, the REMS program that you see with complement inhibitors today. Finally, the convenience of a DUPIXENT. If you look at their label, we're going to develop 103 with the same autoinjector, the Molly autoinjector from SHL, and with the exact same loading dose and then the every two-week self-administration. That's a $14 billion franchise. Clearly, patients really love that product. We're trying to combine those three parts of three approved labels in the U.S. into one package for patients. We went to the neurologists, this representative sample of neurologists in the United States, and we asked them, "How do you respond to this Target Product Profile?" You can see nearly 80% said, "If you can deliver C5-like efficacy, that will get first-line use. That will perform really well in this market." When we showed them the safety target and the fact that we would avoid the label, again, over two-thirds of physicians said, "Yeah, that will be very, very well received on the market." Of course, with the convenience of a DUPIXENT and the autoinjector, where you can self-administer, you do not see the needle, and it can be done in anywhere from five to seven seconds. Again, over three-quarters of neurologists said, "Yeah, that would do really, really well." We believe if we can achieve this Target Product Profile in the Myasthenia Gravis market, we will have a best-in-class complement inhibitor, and then we will compete against whatever the best FcRn is for first-line use, and we will get a very, very successful product on the market for these patients. Moving to CIDP, I mentioned that there's already proof of concept with another active C1s inhibitor. That's Rilepabart in Sanofi's pipeline. Over the last couple of years, they have been presenting their open-label phase II data, which is really quite impressive. What I'll highlight is these are patients who were refractory to IVIG or already doing well on IVIG or naive to IVIG, IVIG being the gold standard treatment for CIDP patients. You can see north of 50% response rates when these patients were switched immediately to Rilepabart, the active C1s inhibitor. That includes patients, and this is, I think, a very, very important data point, patients who were not responding to IVIG, patients who were refractory to IVIG. This is a patient group that FcRns will never be able to show efficacy in because FcRns, I think most neurologists will tell you they're seeing it's less efficacious than IVIG, but it's a better tolerated, more patient-friendly version of IVIG. With active C1s inhibition, what we see now with Rilepabart's data is you take patients who are refractory and don't tolerate IVIG or where IVIG is not working for them, you switch and over 50% improved on active C1s inhibition. When you pair that with the fact that patients who were on IVIG and doing fine and they also were switched to active C1s inhibition, these are patients who already were responding and doing relatively well, over 50% got even better on active C1s inhibition. This is really, really exciting data and suggests that classical complement pathway inhibition or active C1s inhibition may be at least equal to IVIG on efficacy and potentially even better. That confidence is shown by Sanofi is conducting two phase III trials. They'll have results from those trials very likely early in 2026. One of them is a head-to-head trial versus IVIG, a non-inferiority trial. If that trial is successful, that will set a new precedent in terms of efficacy for the CIDP market. The question then becomes, of course, how do we compare to Rilepabart since they're ahead of us in CIDP, they're also an active C1s inhibitor? We conducted six different head-to-head in vitro experiments comparing potency between Rilepabart and DNTH103: two affinity assays, one enzymatic assay, and then three functional assays. The assay we really believe is the most important is the CH50, which is bolded or highlighted in the middle of the three functional assays. It is just clear that we have a much more potent active C1s inhibitor, meaning you can give significantly less antibody and shut down the classical pathway. That is a major advantage for 103 that translates into being able to give much less injections to patients. The dosing for Rilepabart is 600 milligrams, 4 milliliters every week. If it was delivered in an autoinjector, that can take up to 2 milliliters. We are talking about two shots every week or eight shots a month. 103 is aiming for one shot, 300 milligrams, 2 milliliters every two weeks. At the end of the month, it would be two shots. Literally four times less injections with 103 because of its superior potency in shutting down the classical pathway over Rilepabart. We're very excited. We're in a phase III trial for CIDP, and we will have interim responder analysis from Part A, which is an open-label 300 milligram every two-week dose in 2026. The third indication, MMN, is smaller than the other two, but still a significant opportunity. This is a disease we know is IgM-driven, we know is classical pathway-driven, and we know FcRns don't work here. This is a complement-only market. The only other competitor is Argenx's empasiprubart, which is a C2 inhibitor that inhibits the lectin pathway, not just the classical pathway, and has to be delivered by IV. We only inhibit the classical pathway, which is the only pathway you need to inhibit in MMN to get efficacy. We do not touch a lectin pathway, so very likely we will have an advantage in terms of risk of serious infections. Very likely they will end up with a box warning like every complement inhibitor that is not just a pure classical pathway inhibitor. Of course, we are looking for subcutaneous self-administration versus an IV for empasiprubart. Let me just move ahead so we can have some time for questions. Oh, I went a little too far. Let me go back. Apologies. I am trying to get to the slides. In the end, what we are trying to do is just deliver a unique combination of benefits as we pursue the power of consistent control with one click. In terms of the confidence that this drug can deliver, it's about the fact that it can deliver potentially best-in-class efficacy and very consistent symptom control across all the three different neuromuscular conditions, and doing so by inhibiting only the classical pathway and therefore being able to deliver a safer profile than other complement inhibitors and avoiding the box warning and REMS program in a super convenient manner. That DUPIXENT-like less than 10-second autoinjector that patients can give themselves anywhere they are around the world and without ever having to see the needle. As I mentioned, we have our Myasthenia Gravis data coming in September of this year in just a matter of about three months. That's the first of a series of very exciting catalysts. We'll have MMN data in the second half of last year. We will have our interim responder analysis from our phase III Part A open-label study in CIDP in the second half of next year as well. What I would highlight is there are two very important external catalysts in between all these catalysts for us, and that is Sanofi's two phase III trials in CIDP. One is in refractory patients versus placebo, again, data that you will never see from FcRns, and the other being that very exciting head-to-head versus IVIG non-inferiority trial. We are really eager to see that data because that could set a whole new precedent in terms of efficacy and a new gold standard for CIDP patients. That data should come, we are thinking by probably early 2026. As Sanofi has said, they would file the BLA by the end of 2026. We do have $332 million in cash. The good news here is we have a nice healthy runway. We're fortunate to have a nice healthy runway beyond these catalysts into the second half of 2027. With that, I'll open it up to questions. Thanks, Marino. Maybe I'll start off with a question. Just congrats on the market research data that you have in there. Wondering if in that survey for the neuromuscular specialists in the general. Thank you. For the neuromuscular specialists and the general neurologists, if you kind of gave them a wish list of what other indications they would want 103 to be used in, and if that was one of the questions and what some of the answer was. Yeah, no, we didn't ask that question. It's an interesting question. Maybe we'll add it to future market research. No, in this research, we really focused and really tried to understand what are they looking for in Myasthenia Gravis specifically. Part of the criteria was, as we went to over 80 neurologists, that we wanted a representative sample of neurologists in the United States that treat Myasthenia Gravis and that had enough patients and where they spent the majority of their time in practice treating these patients so that we could get really robust responses. For this market research, we really just focused on MG. Got it. Makes sense. For the MG readout in September, I wanted to ask a couple of quick questions on that. Sure. I guess just what's the latest you're seeing on higher-setting expectations for that update? I'm going to go back to the Target Product Profile slide. Excuse me. Essentially, in terms of efficacy, we're looking to get C5-like efficacy. And if you look at the labels for Soliris, Ultomiris, Zilucoplan, the last C5 inhibitor approved for MG, you see that the MG- ADL placebo-adjusted scores are anywhere from 1.6-2.1 improvement on the MG- ADL. So we believe if we're in that range, we can confidently say, "Okay, this looks like it's similar." Again, they're not head-to-head trials, but it looks like it's similar in efficacy to C5s. No infections from encapsulated bacteria due to drug. That will help reinforce the improved safety profile versus other complement inhibitors. And of course, the 300 milligram every two-week dose being efficacious. I think if we deliver that package of data in September, then we can confidently say that this is well on its way to being the best-in-class first-line option in the Myasthenia Gravis market for the complement category. Like I said, we'll compete against whatever the best-in-class FcRn might be when the drug gets to market. Got it. Makes sense. What are your expectations for the placebo response? Are you doing anything unique there to help manage placebo response? Yeah, I think what you're alluding to is the fact that recent trials, specifically with FcRns, we've seen placebo rates creep up. I think that's a general problem across the whole industry, not just in Myasthenia Gravis. Look, we're doing everything we can control. We're going to good quality sites. We're working with investigators directly. We're not depending on any CRO to help manage any of these sites. We have our own people going to the sites, making sure that they're really well-trained and looking for basically just delivering quality data. Of course, making sure that the patients are stable, quality patients. I mean, in the end, that's the best we can do. I would expect our placebo rates to be comparable to historical trials, whether it's a few years ago or more recent. We'll have to see when we deliver the data in September. Got it. Okay. For the data update, anything more on specifics that you're saying that you're going to report as far as potentially kinetics of response over time? Is that something you're going to share? Yeah, we're looking to be as transparent as possible. This is a very important pivotal moment for the company. My goal will be for investors to leave that disclosure feeling very confident in 103. We'll look to be as very direct and transparent as possible with the efficacy measures people expect, the QMG, the MG- ADL, the minimal symptom expression numbers, and of course, the safety table, et cetera. I think people will, I mean, that's our objective for the release in September. Got it. And it'll be probably press release and then company conference? Yeah, very likely. Yeah, your typical press release early morning and then call before market. Got it. Okay. If the data is positive in September, when do you expect that you could have an end-of-phase II meeting to discuss a pivotal with FDA? Yeah, the team's doing a great job preparing for that upside scenario where we're ready to go to the FDA as fast as possible and get the phase III started as fast as possible. We're not guiding to timing for that, but that's something the team's already been working on for months. Got it. Okay. You mentioned the Sanofi CIDP program where we could get a phase III readout beginning of next year. What are we going to be looking for? I think it's beginning of next year. I don't think they've guided, right, specifically. We're insinuating by early next year because they're looking to file the BLA, they said, by the end of 2026. So I'm assuming they need at least, say, nine months to put it together. Got it. Okay. Yeah. In that update, when we see the data, what are you going to be looking for? Could that potentially change your strategy for your CIDP program? It's a really good question. For the refractory patient group study, which is versus placebo, we expect to see that being successful. Based on the phase II data, I'm very confident that that will be well received. The IVIG head-to-head is what I'm really interested in. It's a non-inferiority trial. Interestingly, whenever I hear Sanofi present, they call it superiority, but it's a non-inferiority trial. I'm going to assume when they say superiority, it's just because that's what they hope to see or that maybe that's what they expect to see. Look, non-inferiority alone will be a huge hit because I think if you speak to neurologists who treat CIDP, they'll tell you they love IVIG has been lifesaving for patients. It's just a huge burn in terms of treatment, in terms of dose administration, in terms of side effects, the waning effect until the next dose, et cetera. These are things that patients really, really dislike. When it works, it works really well. If they show non-inferiority, it basically says, "If IVIG is the gold standard and it's more efficacious than FcRns and you show that active C1s inhibition is equal to IVIG, you've pretty much now shown that you can get similar efficacy, much better tolerated, easier to administer, and it's superior to FcRns." That dynamic in the CIDP market would be incredibly beneficial, obviously, for 103 because then we come out with a better active C1s inhibitor. I'm looking to really understand, especially the IVIG head-to-head trial. If they show a positive trial, then that's something we will consider doing as well in the future. Got it. Maybe one question on MMN too. I do not know if you can comment more on just how the status of that study is going. For your readout second half of this year, it could be at about the same time as Argenx's readout. What are you going to be looking for there to compare and contrast? Is it going to be primarily based on safety? You said this year, but I think you mean next year, right? Yeah. The trial is on track as we had planned. What am I looking? Again, we're looking for similar efficacy. The fact that we are dosing every two weeks sub-Q will be obviously a clear advantage versus an IV. In terms of infections, again, we're looking to not have any drug-related infections due to encapsulated bacteria, things like meningitis in our trial. Whether we'll see it in their trial or not, I'm not sure. I think just that the ability to say, "Look, you only need to shut down the classical pathway. You don't need to shut down the lectin pathway." That provides no benefit for these patients. If anything, it just adds risk. If you can do it in a much more convenient fashion, then if we have similar efficacy, it's clear which one will be the first choice. Right now, there's nothing else. FcRns won't work here. Yes, it's a smaller market, but let's remember that 10 years ago, people thought MG was a very small market. With time, diagnosis, better-informed physicians and market, you saw that market grow. CIDP, same thing is happening. I think MMN is similar to those two. It's just at an earlier stage in development. We'll see that market also grow. Why I'm excited about MMN is simply this. Whatever assumption you make about what share of market we're going to get in MG and CIDP, it's going to be bigger in MMN. It's going to be a much bigger slice of that pie that 103 can capture. I think we underestimate or I think some people underestimate the potential in the MMN market for 103. Got it. I am definitely looking forward to the GMG data in September. It is going to be de-risking for the drug. Going back to the question about just potential other indications you can go into and kind of create that DUPIXENT-like pipeline in the drug scenario, with Argenx's data updates coming with dermatomyositis and also with the delayed graft function, could that help inform your strategy there or how are you going to? Absolutely. Yeah. No, we have a lot of active work looking at life cycle potential opportunities and new indications. Our competitors have been incredibly helpful for us in the last few years. We will be looking at all that data and additional data from other competitors to see if there's an opportunity for us to go after. We have two very high bars for any new indication, right? One, we're looking for where there's already some proof of concept for the mechanism. That is why we picked these three indications. We're building a really nice neuromuscular franchise that has nice clinical development synergies, has really clear commercial synergies. It just makes sense. There will be a halo effect of efficacy in one, helping the other, et cetera. Any new indication, we want to see that similar kind of proof of concept and synergies with what we're already building. There has to be a very good commercial opportunity. For those indications that meet those two criteria, they'll be very likely added on to our future plans. Got it. Any other questions? Okay. Thanks, Marino. Thank you very much again, Mr. Jefferies, for the opportunity.