Pleasure to introduce Dianthus Therapeutics. With us today, Marino Garcia, CEO; I see Ryan Savitz, the CFO, in the audience; and Jen Davis, as well, from IR. Ladies and gentlemen, thanks so much for joining us. It's great to see you. We're going to do about a 20-minute or so presentation, and the rest is going to be Q&A. Thanks so much. Appreciate it. Thank you for. My microphone on? Yeah. T hank you to you and the TD Cowen team for this opportunity to present today. Really appreciate it. I'll be making some forward-looking statements, so I just want to let you know, please go to our website and read our SEC filings for more information on the company. It's a really exciting time to be at Dianthus. Today, especially, for two reasons. One is we're still on track to put out our myasthenia gravis data, our phase II data, first data in actual patients suffering from neuromuscular disease. Later this year, the data looks like it's right on the cusp of Q3, Q4, end of Q3, beginning of Q4. Also because this morning we announced we have a new Chief Commercial Officer, John King, who's joined the company. John is a great addition to our team. John has very relevant experience that will clearly add value for Dianthus, for patients we're trying to serve, as well as our investors. He was the Vice President of Neurology Business Unit that launched the very first approved biologic into the myasthenia gravis market, Soliris, back during his time at Alexion. That obviously established a foundation for a $6.5 billion franchise over now at AstraZeneca that's still growing from first-line use in conditions like myasthenia gravis in the US market. He also established a foundation for a market nobody really knew much about back then, myasthenia gravis, which now obviously supports multi-billion dollar blockbusters and continues to grow. He then leveraged that experience to become Chief Commercial Officer at Ra Pharma. Ra Pharma was developing the very first C5 inhibitor that was a self-administered subcutaneous injection. He was putting this marketing strategy behind that, the commercial strategy behind that, when, as part of the executive team, they had a very nice exit and sold Ra Pharma for $2.5 billion to UCB. Again, a very nice outcome for investors there as well. With that combined experience, I'm very excited to have him on board. It's a huge confidence builder. I mean, he knows what he's looking for in terms of opportunities in the complement in myasthenia gravis space. He looked at our program, 103, which is our lead program. It's our highly potent classical pathway inhibitor that only inhibits the activated form of C1s. He looked at that, and he looked at our trial design, and he said, "This is going to be a winner." He's put his career into Dianthus, and we're very grateful for that. A s I mentioned, we are on track for data in myasthenia gravis, our first indication later this year. The whole point of 103, as I mentioned, it's a classical pathway inhibitor, and it only binds to the activated form of C1s. The idea here is to deliver efficacy that you expect from complement inhibition, that continuous, robust symptom control from C5 inhibitors. Do it with a low-volume antibody that you can put into an autoinjector so that patients can self-administer. Do it with a safer profile. I'll talk a little bit about that later and how we'll differentiate 103 and how it will be the best-in-class complement inhibitor in this market, as well as in MMN and CIDP, the two other indications I'll also get into in a few moments. We have phase one data that confirms that we have a highly potent classical pathway inhibitor with a differentiated safety profile, with a nice, robust 60-day half-life that allows for that infrequent dosing and accumulation to get to levels that we know shuts down the classical pathway. There is a pipeline and a product potential. I'll get into that in a few moments. We have a really strong balance sheet. The good news is we have cash to take us to the second half of 2027, removing any kind of upfinancing overhang once we get to the gMG data later this year. I mentioned the pipeline and a product potential. That's true for most complement inhibitors, and it's absolutely true for 103 as a potent classical pathway inhibitor. We have chosen to build a neuromuscular franchise around 103, and for various reasons, including the fact that there are very clear synergies from a clinical development standpoint as we go to the same investigators, the same site, but also from a commercial standpoint. The footprint would be the same going after the three different indications in markets like the US. These three diseases, rare diseases and autoimmune diseases, combine to over at least 100,000 patients in the US in terms of potential. The largest of the three, generalized myasthenia gravis on the left, that's obviously, many of you know, a blockbuster market. There is a huge opportunity here for a biologic that can deliver robust continuous symptom control like the C5s, but do it in a safer way without a box warning around the risk of infections like meningitis or for any safety issue and no REMS program, and also make it self-administered, infrequent autoinjector like the way we're going with 103. As I mentioned, we'll have data in this indication later this year, right at the end of Q3, beginning of Q4, it looks like right now. CIDP is the next emerging growth market. If you can imagine what myasthenia gravis was 5 to 10 years ago, that's where CIDP is. It's really creating a lot of excitement. We have an FcRn now approved there. IVIG is the gold standard. Very efficacious, but very much of a burden on patients. Anything that can take that burden off and deliver efficacy is going to do very well in this market. The nice thing here is there is already proof of concept for active C1s inhibition. Sanofi, riliprubart, an active C1s inhibitor, excuse me, has shown really amazing efficacy in patients who are on IVIG stable and switched to active C1s inhibition, patients who are naive to IVIG, the gold standard therapy, and also something that FcRns will not have and do not have. That is data in patients who are refractory to IVIG. If they are refractory to IVIG, they do not get into FcRn trials. FcRns would not be expected to work. They have data showing 50% of patients, 50% response rate for patients who are refractory to IVIG, the gold standard efficacy, and switch to active C1s inhibition. We will talk a little bit about how we compare to riliprubart in a few slides. We have started a phase three program there. We will have interim responder analysis announcement in the second half of 2026, once we have our first 40 patients enrolled into the open label part A of our trial. Finally, multifocal motor neuropathy, MMN. This is a market that is earlier in its development. This is a market where FcRns will not work, so the competition is very limited. It is a complement-only market. It is a classical pathway complement market only. There, again, we have proof of concept from a direct competitor, empasiprubart, a C2 inhibitor from Argenx that shows really robust efficacy, and where we have very clear advantages versus their inhibitor, their complement inhibitor, which I will get into in a few moments. We have a phase two trial in that program as well, and we will also have data on that in the second half of 2026. Let me focus a moment for gMG, the biggest market opportunity and the first indication we're pursuing. This is a market that currently has only two mechanisms of action competing for first-line biologic use. It's complement and FcRn. There's nothing out there that competes first-line with these two mechanisms, and there's nothing really in the next 10 years that's going to compete first-line versus the two mechanisms, to be honest. Anything else that's developed that might be approved is very likely to be used more like second or third-line. This is the way the market's going to stay. For an autoimmune market, that's a very attractive situation where there's only two mechanisms competing for first-line biologic use. The opportunity here for 103 is to be the best in one of the categories, and that's in the complement class. If you look at what's approved, they're all C5 inhibitors. If you look at what's in development, they're all one form or another of a C5 inhibitor. There's no classical pathway inhibitor being developed into the myasthenia gravis market. We will be unique. The advantage is that we will be able to deliver robust efficacy, assuming the data shows that we have at least similar efficacy to what the C5s have been able to achieve. We will be able to do it with a lower risk of infections versus the C5 inhibitors, and I'll explain in a moment why, plus the fact that we will be able to put this into a low-volume autoinjector that patients can self-administer, giving back their freedom and their ability to live their lives without having to be tied to infusion centers certain times or to have to see a healthcare professional to have their therapy administered. We will compete against whatever the best FcRn is at the point we get approved in gMG. Is it going to be Vyvgart? Is it going to be another FcRn that maybe has continuous dosing and continuous symptom control instead of putting patients through the cycle that Vyvgart does, which is really not ideal for a chronic disease? Whatever the best FcRn is, we'll compete against the best complement inhibitor, which we believe will be 103, and that's it. If we don't get used first-line for certain patients, we'll be the first switch. That's how it's going to work for this market for a very long time into the near future, assuming, of course, we have great data and we are approved. I keep mentioning efficacy, and I keep mentioning our safety advantage. It's important to know when you look at the complement system, there's really multiple ways that, or a couple of ways that it can be triggered. The classical pathway is what's triggered in AChR-positive patients in the myasthenia gravis patient group. The idea here is stop the complement cascade as early as possible by targeting C1s, and therefore you'll prevent the formation of MAC. The issue with C5s is that they work really well, but they shut down the entire complement system. That means not only if it was triggered by the presence of, excuse me, an antibody-antigen complex like it is for AChR-positive patients, it also shuts it down if the system was triggered by the presence of encapsulated bacteria, and it was the lectin pathway that was triggered. If you are past the classical pathway in terms of inhibitors, if you're C2, C3, C5, you are going to end up having a box warning around the risk of infections. You're going to have a higher risk of infections. That means the box warning and the REMS program, which is quite a burden and kind of scary for patients. If you look at C1s inhibition, there is a product out there already that inhibits C1s. It's called Enjaymo, sutimlimab. It's the first-generation C1s inhibitor. It gives 6.5 to 7.5g of antibody every two weeks. It's 25 times more of our target dose, 300 milligrams every two weeks. It is approved for CAD, not an intramuscular indication. If you look at their label, it is the safest, it is the cleanest complement label. It has no box warning, no REMS program for any safety issue. It is the only complement inhibitor on the market that has that kind of a safety and tolerability profile. I'd be very happy to have that, and that's part of our profile, what we're aiming for with 103, even though it's 25 times more drug. This is what's going to also differentiate 103. It's not just the great efficacy and the dose and convenience. It's the fact that we're going to be able to avoid that box warning and that higher risk of deadly infections like meningitis compared to every other C5 inhibitor in the gMG market. CIDP, there's been a lot of excitement, and I thank my peers over at Sanofi for this, mainly because it's the first time we see an active C1s inhibitor working in any neuromuscular condition. It's the first time that a complement inhibitor has been shown to work in CIDP. The data that Sanofi has shown in their phase two is really quite impressive. They looked at three different patient groups, starting from the right here, patients who were naive to IVIG, the gold standard efficacy biologic in CIDP, 75% response rate. They looked at patients that were on the left here on IVIG and doing fine and switched right away to active C1s inhibition, taken off IVIG. Over 50% of them, although they were already doing well, improved on active C1s inhibition. That is a very interesting additional efficacy signal. Here's what's really impressive and differentiates this, especially versus FcRns. They also allow refractory patients. Argenx did not allow refractory patients in their trial. No FcRn will allow refractory patients into their trial. Why? Because if IVIG, which is the gold standard efficacy, doesn't work, FcRns have a similar mechanism of action and probably less efficacious. There's no way they're going to work. Sanofi allowed these patients into their trial, 50% of patients where IVIG did not work responded on active C1s inhibition. The combination of these two efficacy signals tells us that there's something about classical pathway inhibition that might be, if not equal to IVIG, maybe potentially even better than IVIG, which would be huge for patients suffering from CIDP. The thing to note about this, and now I'll get into how we're different from riliprubart, which is ahead of us in CIDP, they're in two phase three trials right now. They're dosing 600 mg, 4mL every week. If that was to be put into an autoinjector, which can take 2 mL in terms of volume, that's two autoinjectors a day, eight a month, 96 every year injections. We are targeting 300 milligrams, 2 mL every two weeks, like a Dupixent profile. That's two shots a month. That's 24 shots versus 96 at the end of the year. Much, much easier for patients. What gives us the confidence that dosing a quarter of the dose and less frequently than riliprubart is going to give us at least similar efficacy? We've conducted multiple head-to-head in vitro experiments looking at potency, whether two affinity assays and enzymatic assay and three different functional assays. We put them all on this slide so you can decide which assay you prefer, which one you want to focus on. The one we believe is the most relevant is the CH50 hemolytic assay, this one right here, which we bold out. This is the assay that we believe we use to talk to the FDA and EU regulators to justify our dosing. This is the assay that we believe is best to determine what levels, PK levels, do you need to get to, and therefore what dose should you administer to get above IC90 or 90% inhibition of the classical pathway, which is very robust efficacy or inhibition of the classical pathway. You can see here that we achieve IC90 at seven times lower amount of drug or seven times lower levels. In other words, you have to give seven times more drug of riliprubart to get the same level of inhibition, IC90. We are somewhere multiple orders of magnitude much more potent than riliprubart. That is what gives us the confidence that dosing at a quarter of the dose and less frequently because of our 60-day half-life, we will be able to get at least similar efficacy to what riliprubart has seen in CIDP. Finally, of the three indications, stop moving forward. There we go, MMN. Again, another area where we have proof of concept from a competitor, that classical pathway inhibition may be the ideal way to treat these patients. They have a C2 inhibitor, empasiprubart. They showed really impressive efficacy in terms of preventing relapse with patients who have MMN. They published this in the last couple of years, and they make it very clear that although a C2 inhibitor blocks both lectin and the classical pathway, that their efficacy is coming purely from their classical pathway inhibition, that the lectin pathway is adding no efficacy or no benefit. It does potentially add an infection risk because the lectin pathway, I think I mentioned earlier, is the pathway that's triggered by the presence of encapsulated bacteria. That's the pathway that you need to stay intact to be able to fight against deadly infections. We know MMN is an IgM-driven disease. We know we have a very potent classical pathway inhibitor. We're not sure that empasiprubart is not published, how powerful a classical pathway inhibitor it is. We know FCRNs won't work. They don't affect IgM. The lectin pathway is critical to fighting infections. We know we don't touch that. They block it with a C2 inhibitor. They're also an IV to give it on a weekly or every two-week schedule. Again, 300 milligrams, 2 milliliters, subcu autoinjector every two weeks, much more convenient for patients. This is a market a little smaller than three we couldn't own if 103 shows good efficacy data and is approved. There's nothing else that compares to 103 for this market opportunity. Let me get into the I mentioned we have phase one data. Let me just quickly summarize how we looked at multiple SAD cohorts as well as MAD cohorts, IV as well as subcu. This is just summarizing that this is the data that tells us that we have a 60-day half-life. We get nice accumulation dosing every two weeks, which we want. We want to get to certain levels so we know we're shutting down the classical pathway. We measured the PK/PD relationship for every single healthy volunteer at every single data point for every single cohort. That is what allowed us to calculate that we just need to get above 87 micrograms per mL in people, so high double digits to know that we're shutting down the classical pathway and getting very strong inhibition. We modeled what happens after a short loading dose if we dose 300 milligrams every two weeks. You can see that our peak trough is somewhere between 125 and 115 micrograms per mL, so about an average of about 120. That is a good 40% level above our target to get 90% inhibition of this classical pathway. This data is what gives us confidence that we have a potency and a dosing schedule that will allow to maximize efficacy at this dose. Our safety table, there are no serious adverse events, no infections related to the complement system. Basically telling us that we have a very well-tolerated, very safe antibody. I mentioned the gMG data is coming later this year. This is the trial. It is the largest phase two trial conducted in gMG. We are testing two doses. Our target dose of 300 milligrams every two weeks. We're also throwing a higher dose. Just to answer the question, well, what happens if you get above IC95? Like, what if you really get up there in the levels of inhibition? I don't believe we're going to see a difference in efficacy. To test the theory and to see what happens and ensure for investors that we are not leaving any efficacy on the table and that we have more than one shot on goal, we added a higher dose of 600 milligrams every two weeks. As I mentioned, we'll have data for this in the September, October or end of Q3, beginning of Q4 timeframe. CIDP, exciting here is that we are going straight into a phase three. For those of you who are familiar with the ADHERE study from Argenx, it's very similar. Couple of differences. We're not making patients fail before we get to the we put them into the open label portion. There's no way a trial today will be able to recruit if you make people do that. We're just having the local investigators confirm diagnosis, CIDP, and we have an independent review panel or board of KOLs who are also going to review every patient and confirm. Only after they're both confirming the patient on CIDP, then we put them into our trial. We give them 300 milligrams every two weeks in the open label, part A. Only patients that respond are then randomized to the placebo-controlled. Again, we're doing two doses here. Very high probability of success if you believe the riliprubart data, if you believe we're a more potent drug, that we're actually giving more drug than riliprubart is, and that we can at least achieve similar efficacy. This is about the highest probability of success you could imagine for a phase three program for CIDP. We will have an interim responder analysis announcement like Argenx did. We're doing it with 40 patients. They did it with 30. We'll have that by the second half of next year. Another big difference I should point out versus the ADHERE program is, as I mentioned earlier, we are allowing patients who are refractory to IVIG into this trial because of that robust efficacy we've seen with riliprubart. There's no reason for us to screen those patients out like the FcRn programs do. Finally, MMN, very similar, just 17 weeks to the gMG trial, testing two doses, same thing versus placebo. We will have results in this program in the second half of next year. To wrap it up, we list all the different benefits of 103. I just want to leave you with this. What are we trying to do? We're trying to take the best parts of three best-in-class labels and put them together into one package for patients. It's take the efficacy of the C5s, the only biologics approved today for gMG that have continuous and very robust symptom control. Take the efficacy from Soliris, put that into our label. Go and get the label from the C1s inhibitor that's approved on the market, sutimlimab. Take the safety and tolerability, which you'll see is if you compare it head-to-head to every other complement inhibitor on the market, including the C5s, it is the cleanest, it is the safest. There's no box warning for any issue, no REMS program. Even though it's 25 times more drug than us, cut and paste, put that in our label. Finally, go to Dupixent. We're using the same autoinjector, the SHL Molly, $14 billion drug. That autoinjector is obviously very well adopted and liked by patients. Take the dosing administration profile of Dupixent, cut and paste, put that in our label. The combination of those three best parts of the three best-in-class labels out there into one package for gMG patients as well as CIDP and MMN, we believe we have what will be a real game changer and a very highly differentiated first-line biologic for patients with gMG, CIDP, and MMN. As I mentioned, we'll have data in gMG later this year. We'll have our MMN data next year as well as our interim responder analysis for CIDP. In between those, we're expecting to see the data from riliprubart from their two phase three trials that they're conducting in CIDP. There will be some nice internal as well as external catalysts between the second half of this year and the second half of 2026. With that, you're on. I'll take some questions. Go ahead, Marino. I'll say it out loud and you can. I can repeat the question for you. Yeah. For gMG, the MaGic study, there's going to be data in the second half of the year. How validated is the C1s biology relative to C5? Then secondly, what do you want to see? Maybe give us a little bit of a sense. The primary endpoint of 12 weeks, sort of what do you want to see and how is it powered on efficacy? I showed you earlier the complement system. We know with AChR-positive patients and gMG that, I mean, gMG is referred to as a classical pathway-driven disease, a classical pathway disease. The literature, I mean, the reason we g MG as our first indication is because it was the most de-risked, not just from a clinical development pathway that's been well-trodden by others, but the fact that it was where the biology and the science was the most clear that a classical pathway inhibitor will see efficacy in patients who are AChR-positive and gMG. I mean, we believe the C5s have proven that out because there's really no reason to block the lectin alternative pathway. Those pathways are not creating the dysfunction in myasthenia gravis patients. Ironically, back when we were deciding which indications to go after, we picked gMG because it was the surest bet and it gave investors the most comfort. Lo and behold, our competitors decided to go and put that all upside down and come out with really great MMN data showing that classical pathway inhibition works and then CIDP data that shows that classical pathway inhibition works. All of a sudden, from an investor standpoint, those are the markets that have the clearest proof of concept for classical pathway inhibition. The science is really clear. If you shut down the classical pathway, you should see efficacy in gMG. I want to point out that zilucoplan, when they were trying to decide which dose to study to take forward in their phase two, they used the CH50 hemolytic assay to measure levels of inhibition. What are they measuring? They're measuring inhibition of the classical pathway. That's what that assay measures. It doesn't measure how much you're shutting down lectin or alternative. It's purely classical pathway. If you get above IC90, you know you've got a powerful inhibitor that should work in gMG. That was the assay that C5 zilucoplan used. The logic is very clear. We should have efficacy if you believe that the classical pathway is the main culprit in the gMG pathology. Was there another posterior question? I'm sorry. The second question is, just remind us how the MaGic study is powered. Sixty patients, primary influence of 12 weeks. Yes. [crosstalk] What do you want to see in 12 weeks? [crosstalk] Thirteen weeks. It's a phase II. It's powered for safety. That's the main primary endpoint. Of course, we're looking at MG-ADL, QMG, and every other efficacy measure as a secondary endpoint. It is the largest phase II. Zilucoplan also had a similar design, smaller numbers. I think it was 16 patients, correct me if I'm wrong, in each arm. They still had P value. We expect if we get anywhere near the C5 level of inhibition and efficacy, we should have a positive P value as well on efficacy. With gMG, I'm just going to stay there. Any thoughts on maybe even including another arm or looking into AChR negative patients? No. We don't expect that we would work in patients who are AChR negative. It's because you need autoantibody positive to deposit complement. [crosstalk] Exactly. That's what triggers the classical pathway, and that's what we're targeting. Like a laser, we're trying to just shut down the pathway that's triggered by an AChR-positive patient. I can repeat the question. Go ahead. In my observation, just my own observation from somebody who's minimally informed, a lot of these pathways have alternative bypass mechanisms where you skip one of the cascades and still get where you get one of the Factor B or Factor D is that sort of substitute in. To what degree, both for C1 inhibiting at the C1 level or curious for the competitive landscape inhibiting at C2, do you see that potential, if any, to see bypass versus truly 100% shut down that cascade if you effectively block your target enzyme? In AChR-positive patients, we're very, very confident that all you need to do is just shut down the classical pathway. We'll see what the data later this year shows, obviously. I wasn't asking clinically so much. I was asking on the science itself. If you shut down your target C1s, do you completely shut down the complement pathway, or are there bypass mechanisms, factors, or just that you can skip C1? We haven't seen that in any of our experiments, in vitro experiments. We don't touch lectin. We don't touch alternative. When we test our antibody in in vitro experiments, we do it with a serum from gMG patients. We've done it with CIDP serum from patients. We're not seeing anything that tells us that there's something going on that it might be skipping where we stop the cascade. There's no MAC being skipped. If you use the mechanism of blocking C2, is there any way to bypass? We don't have a C2, so we haven't done that. I was just curious if you knew from the complement cascade. No. There's been nothing to tell us that. I mean, C2 is further down from C1, and it's also shutting down the lectin pathway. The only pathway it doesn't touch is the alternative pathway. There's been no evidence to show that. It's only been studied in MMN, but they have really great efficacy there. I haven't seen anything that tells me that there's some other mechanism that could be bypassing where we block. Thank you. I know we're over time. I'll ask one last question. Sure. What about going into ocular gMG?