Good afternoon. I'm Sam Semenkow, one of the senior biotech analysts here at Citi, and it is my pleasure to be hosting Dianthus at Citi's 2026 Biopharma Back to School Summit. I'm joined by Marino Garcia, CEO of Dianthus. Marino, welcome, and thank you so much for being here. Thank you, Sam, and thank you to Citi for allowing us to be here today and for hosting this webinar. Absolutely. So, why don't we just start maybe a little bit high level? You made a ton of progress across your pipeline this year, so lots of great updates have come from you guys. There's still a few catalysts outstanding before the end of the year. Could you just maybe recap and level set where the company stands today, and what can we expect through the end of the year and maybe over the next six-ish months? Sure. Thank you for that. Again, thanks for the opportunity to update everyone today. Over the last 12 months, with claseprubart, we have had two big moments in our development of claseprubart neuromuscular conditions. We had the very positive phase ll MaGic results in myasthenia gravis from September or exactly about a year ago this week. Then the CIDP update, the early interim responder analysis we announced in March, and then the fulsome update on our first 40 patients and as part of the interim responder analysis in June. From our perspective, claseprubart is now pretty much de-risked as a very potent neuromuscular therapy and antibody. The next update is on the third indication. It's our phase II results, with MMN, which we are expecting to announce our top-line results in December of this year. That is a phase II study. Originally, it was slated to have 12 patients per arm. We've over-enrolled, which is great. It shows a lot of enthusiasm for the program in the MMN community. So we'll have about 15 patients per arm. So relatively small phase II, mostly a safety study. That's the primary endpoint. Secondary endpoints are efficacy measures, mostly exploratory. The expectations there is, again, we'll report out if we see anything new on safety. I can tell you on a blinded basis to date, it looks very similar to MG, very similar to CIDP, so no new surprises. Of course, we're looking for just numerical trends. We're just looking for the numbers on the efficacy measure, the secondary efficacy endpoints to be moving in the right direction. Really, our goal is to get to a phase III start as fast as possible. Back in 2024, when we met with the FDA to discuss the MMN program, we would've liked to have been able to go straight into a phase III the way we did with CIDP because it is an sBLA. But at that point, the FDA really did not know what our phase III should look like. They didn't have any direction to give us in terms of what the primary endpoint should be, so it made sense to do a phase II. Obviously, like CIDP, would've loved to have had a precedent and been able to go straight into phase III. So, we'll move as quickly as possible into phase III with MMN. In terms of DNTH212, our next program, our bifunctional fusion protein, that is in a phase I SAD study in healthy volunteers. We'll provide an update on that by the end of the year and provide some visibility on when we'll start the MAD portion of the phase I and what our plans are over the next 12 months. We'll do that by the end of this year. Recently we announced DNTH312, that we are moving that into getting it phase I ready by the end of next year. Those are some of the big moments. On claseprubart, we will provide another update on CIDP. That'll be before the end of the year. Just provide guidance on when to expect top-line results for the phase III CAPTIVATE study. We'll also provide an update on what we truly think the end will look like in Part A. Remember, the goal of the study is to recruit 128 patients into Part B, and those are patients who will have responded on Part A. Right now, we're saying we need up to 256 patients in Part A to get to that 128 in Part B. But if our responder rates look consistent with what we updated earlier this year, and to date they do look consistent, they're staying fairly consistent. If those responder rates continue to remain consistent throughout the end of the year, then we won't need anywhere close to 200 patients even in Part A. So I'll provide a bit of an update on that, and that should be an important catalyst. On MG, we've just initiated the EMERGE study where we're studying two different doses, once every two weeks and once every four weeks. We are screening patients, and that is all on track, and we expect results from MG, top-line results from that phase III study in the second half of 2028. Thank you for that. It is a lot to dive into. I think I am going to choose to start in MG because that is where you ended. The phase II data that you presented is competitive. You have clean safety, convenient dosing presentation, and regimen. It is, I think, easy to see how you are a best-in-class complement inhibitor. But also more broadly, just across the gMG landscape, where do you see it fitting in? What segments of the market does claseprubart have the opportunity to take meaningful share? Yeah. I will just add one element that you did not mention. In the market research we are doing with neurologists, one thing that came back very early on with some of the first neurologists we spoke to when we presented data to them is, "You guys should emphasize how fast this works." The stat sig separation on QMG and MG-ADL within seven days is also really impressive and important for MG patients and neurologists, and a key differentiator. So, in terms of where we expect, if you can imagine the MG landscape when claseprubart is available. You will have FcRNs and different versions of FcRNs available. You will have UPLIZNA, and maybe you will have BAFF/APRIL. We will see what the data looks like from Vor BioPharma and Vertex, et cetera. And then you will have the complement class, which has been the class that is. It is a foundational class in MG. It has been there forever, and it is still being used first-line. Obviously, efgartigimod has done a really good job of getting first-line use. C5s are being moved more and more to second-line. But within the complement class, you will have all sorts of different C5 inhibitors and only one C1s inhibitor, only one pure classical pathway inhibitor that will not have any boxed warning or REMS program, and that will be potentially a once-a-month subq autoinjector, like DUPIXENT. If you can imagine a label for a product like claseprubart, where you just take the safety and tolerability from ENJAYMO, sutimlimab, which is approved in the U.S. for cold agglutinin disease, just cut and paste that safety label, put it on ours. And then go to the dosing administration for DUPIXENT, but make it once a month. The exact same autoinjector. That is what we are going to be launching with. Put that into our label. An efficacy that is at least as good as C5s, potentially better, and works within the first week. Literally, after your first dose, you see efficacy. You should respond if you do respond. I think if we price that intelligently and competitively, that should get a pretty nice share of first-line use. In terms of second line, if someone started on an FcRN, the claims database, if you look at it in the U.S. right now, at least 40% of patients are not on therapy 12 months later. Clearly, FcRNs do not work for everybody. Clearly, some patients are not going to be tolerating it or are not enjoying the dosing administration challenges with a high-volume therapy. I think the next logical step would be something like claseprubart. I see it as being a major blockbuster, getting a fair share of first-line use, certainly getting a good chunk of second-line use. That easily with a large market like MG in the United States, where less than 20% of patients right now are on biologics. If you think about a healthier, younger, more active patient with a busy lifestyle, traveling, who wants something super easy, they can just travel with it, keep it at room temperature in their bag and give it to themselves wherever they are around the world when it is time to take their shot. I think claseprubart will be a very, very successful product in MG. You have talked about this with me, and I have my own survey data to back this up, that neurologists do want to use new therapies that get approved here, and sometimes as first-line therapies ahead of FcRNs, sometimes after FcRNs. It is a bit of a mix. I do see claseprubart fitting into that as well, and maybe you could talk to some of your market research that you did. Yeah. Our market research shows that if you have something where you can say, "Look, it is an autoinjector, you keep it in the fridge. If you need to travel, and you are not going to be home when your next dose is up in the next month, take it out, probably be able to keep it at room temperature up to four weeks. You can literally give it to yourself anywhere." It is an autoinjector. Go to the DUPIXENT website. Watch the patient video. It is amazing how easy it is. You do not see the needle. It is a 27-gauge needle. It will be very easy to self-administer. Literally takes five to seven seconds for the dose to be given, and you are done. We will have the stability data to show that you can keep it at room temperature up to four weeks outside of the fridge and travel with it. Physicians tell us that if you have something like that, no boxed warning, no REMS program, works really fast, potentially better efficacy than C5. There is a potential here for an upstream inhibitor to show. If we can control placebo response well in our phase III, and we think we know how to do that, and keep it to a 2-point improvement on the MG-ADL for the placebo arm, there is a potential here we could show better efficacy because it is an upstream inhibitor versus C5s. Something like that, even if it is similar C5 efficacy, just the safety advantage, just the dosing administration. Look at UPLIZNA. Honestly, it is a bit of a dirty drug, CD19. It is not perfect. Takes quite a while, months to see the efficacy kick in, but it is doing so well. Why? Because it is a new option, and the only advantage it has is that it is an IV every six months. This market is hungry. It should be 40%-50% penetration of biologics. It is not because there is no therapy that is ideal yet. I think claseprubart gets very close to the ideal to really push that penetration of biologics in the MG market. You did not mention this yet, but you have a Q4 weekly dosing regimen included in the phase III, which could really even extend that dosing to just quarterly, which to your point about UPLIZNA, it has advantages. No. Our dosing regimen in our phase III is once every two weeks and once every four weeks. It will be once every two weeks in CIDP and MMN. But in MG, I think it will be every four weeks. I do not think we will see a difference in efficacy between those two. The reason is there is more and more evidence showing that you do not have to shut down the classical pathway the way every two-week dosing does. That getting somewhere above 70%, 75% inhibition of the classical pathway is enough to maximize efficacy in MG. If that is the case, we have a once-a-month drug. There is no question. That data comes from Janssen data, where they showed 75% inhibition, got them a fairly good improvement on the MG-ADL versus placebo. We have our own data from our open-label extension that shows that PK levels that are half of what our dosing every two weeks would achieve. Still, you have patients responding on the drug significantly. Really, it doesn't look like you need to get above 90% in MG patients in terms of inhibiting the classical pathway to maximize efficacy. We'll see. But we're still testing every two weeks. Either way, honestly, in terms of dosing administration, the feedback from neurologists and patients says this is a winner. It's infrequent. It's easy. No boxed warning, no REMS program. Either way, it's a win. But of course, if we can do it once a month instead of every two weeks, why not? Sure. For sure. Then maybe if we switch gears to CIDP from a commercial standpoint, I'd argue that there's even more white space in CIDP. Maybe it's a little bit easier to penetrate the market for a new therapy to take share. But the market is smaller. I'm wondering just how we think about claseprubart fit into that treatment landscape, since there are other complement inhibitors that are in development from argenx and Sanofi. Sure. Sam, if it's okay, I might challenge a little bit on something you said, which is that maybe CIDP there's more white space. If you look at the CIDP market historically, IVIG is really well-entrenched. If you've listened to argenx over the years, they've tried to really moderate expectations because IVIG is so well-entrenched, and it works in CIDP. I think the issue is if you have a treatment that is even more efficacious than IVIG, better tolerated, no boxed warning, and self-administration sub-Q like we are going, then yes. Then this market will be wide open for a therapy like that. FcRNs are not as effective as IVIG. They're better tolerated. They're more patient-friendly. Definitely a nice innovation for the space. But in terms of efficacy, there's nothing that comes close to IVIG right now on the market. Our data suggests that inhibiting the classical pathway in a very potent way, like we do with claseprubart, may improve how patients are responding to standard of care, including IVIG even further. That's what we're seeing in our Part A open label. Because of that, the biggest opportunity in CIDP is converting patients from IVIG, is having them switch. Right now, if they switch FcRN, there's a significant risk of relapse. What we're seeing in our Part A, which is an immediate switch from standard care, including IVIG, three-quarters of patients are doing even better on claseprubart than they were doing on IVIG. That was information we didn't know before this year. That's clearly what we're seeing in Part A of our CAPTIVATE trial. In terms of what that means, well, CIDP, the value of CIDP for us is definitely increasing because of that. On top of that, when you look at what our competition for classical pathway inhibition is, first with Riliprubart, they now have terminated MOBILIZE for futility. They will have one negative placebo-controlled trial, and they have VITALIZE, which supposedly was a positive futility analysis. That is moving forward. As far as I can tell, they will have one negative placebo-controlled trial, one positive placebo-controlled trial, possibly. I am not sure if you can file a BLA with that. I am not sure what they are going to do. If they believe, like I do, that you need a second placebo positive control trial to file your first BLA, that may mean they have to start another trial, and that would definitely delay their introduction to the market, and they would come after us. There is a strong chance here that Riliprubart does not even make it to market. If they do, that is fine. They are four times more injections than us. Let us assume everything else is equal, although we will probably have good data in refractory patients, and they will not have that because of ending the MOBILIZE trial. Then there is empasiprubart. We will get further updates, I am assuming, on their progress later this year. Empasiprubart is of the three, Riliprubart, us, and empasiprubart. Of the three, it is the weakest of the classical pathway inhibitors. Does that matter? I am not sure. I know for sure they block the lectin pathway as well as the classical pathway. That means they are going to have a boxed warning. There is no other way for your complement system to respond to the presence of encapsulated bacteria. If you block both lectin and alternative, in your classical pathway, there is no way for them to initiate the cascade, trigger the alternative pathway to rev up and create more MAC to go and lyse the bacterial infection. They will have a boxed warning, and they are an IV. In the end, if they do get approved for CIDP, there will be another option, obviously. But that one will have a safety disadvantage and certainly a dosing administration disadvantage. That is assuming efficacy is equal. Again, if potency matters in CIDP, we should have better efficacy as well. That is it. There is really nothing else right now that I see coming into the CIDP market. For us, we are very, very focused on getting to the best label possible there, of course, and a positive outcome with CAPTIVATE, our phase III trial. The strategy will be very focused on going after the IVIG patient population. If you talk to patients who have CIDP on IVIG who are stable and doing well, they will tell you they thank God for IVIG. It saved their life. But boy, would they love to be able to get on something else. Even if it is just similar in efficacy, if you come to the market with something that looks like it might be even better and better tolerated, no boxed warning, and self-administration, sub-Q self-administration, that is a game-changer. One last point. The largest patient population we are recruiting into CAPTIVATE are patients who are stable on standard care, including IVIG. Think about that. These are patients who are supposedly doing fine, and they are on IVIG. Why would they risk going into a trial and changing their therapy? It is because they are looking for something that is equal or better on efficacy, but just much better tolerability and much easier to take. That is really the huge unmet need in CIDP. When you talk to physicians sometimes, though, to your point, IVIG is very entrenched. I guess, what do you think physicians want to see in order to change that treatment paradigm? Also, particularly, IVIG is still used as a diagnostic for CIDP. Is there a first-line opportunity down the road once physicians have more experience? Or is it just in the beginning that you are really focused on that switching market? Yeah. When I say switching focus, I am just saying that is the largest opportunity because there is a huge amount of patients who have been diagnosed and on IVIG. Of course, positioning it as a good first-line therapy will be the ideal position to take. In naive patients in our trial, we are seeing near 100% response rates on the early patients that we have seen in Part A. Look, when we have the results from CAPTIVATE, I think what physicians are going to be very interested in seeing is what happened when you just switch patients within seven days. There is no washout, there is no making patients relapse like you saw in that ADHERE trial. In CAPTIVATE, we literally take a patient who is on standard care or IVIG, within seven days, just switch them. What happens? If you see very little relapse rates, if you see maybe another chunk of patients who stay stable, but they are now on a much better tolerate, easier to take drug. If you are seeing what we saw in our first 40 patients, close to three-quarters of patients doing better, improving. That is how we would define a responder in Part A. These are patients who are being switched immediately and doing better. If you look at our slide deck and our corporate deck, it is not just one point improvement on the INCAT. It is every measure consistent across very robust response rates. Physicians are going to be very comforted by that. And then if on top of that, you are able to not have a boxed warning, no REMS program, and it's an autoinjector the patient can give themselves anywhere they are around the world every two weeks like a DUPIXENT. I think that as long as we don't do anything crazy on pricing, and if we are going to be more expensive than IVIG. Do I expect some payers to maybe say you have to try IVIG first? Sure. But can you imagine what do you know what neurologists and patients are going to do? "Okay. We're going to try IVIG. Payers tell us we have to do this. If you can't tolerate it, though, then we can try something else." No patient's going to come back and say, "I love this. This is great. I tolerate it really well. I love the dosing administration." That's not going to happen with IVIG. There's just a huge opportunity. For us, CIDP, I think it's very fair to say it's become an even bigger opportunity now than MG was. And MG was always a huge blockbuster opportunity for us. In my defense, that's what I meant by more white space. Possibly for that. If you can show that you are switching patients off of standard care and they're getting better in a very robust manner very quickly, I think that's a game-changer in CIDP. For sure. I look forward to that update that you're going to share Yeah at the end of the year for timing on that. I look forward to that too. Yeah. Well, I'll try to be patient. I do want to spend a little bit of time on MMN since it is your next data catalyst. You gave us a little bit of a preview on what to expect there. It's a safety trial. You're looking for trends. Is there a threshold? If everything moves in the same direction, is that enough to convince you to move to phase III? Maybe complicating or helping, we'll see, you're also getting argenx's MMN data around the same time. How should we in the investment community really think about positioning as we move into that? How should we frame our expectations, I think, is a better way to say it. Sure. Look, I do not want to sound overly confident or flippant here. There is almost nothing that we can see in phase II that will convince us not to go into phase III. We know MMN is IgM-driven. That is triggering the classical pathway. We know MMN is a classical pathway-driven disease. We know dosing every two weeks with 300 mg, we are getting very potent inhibition of the classical pathway. There is almost nothing that we are going to see that is going to prevent us from going into phase III. Literally, again, this phase II trial was a safety trial study, primarily. We are not seeing anything new, no surprise. We expect to see some numerical changes on the secondary endpoints, the efficacy endpoints. We do not expect any statistically significant. The numbers are too small. Just like with empaciparab, their study was a little bit larger, actually, their phase II with empaciparab, and they did not see any statistically significant. That is it. We are just going to move to phase III as fast as possible. The key is, what can we learn from argenx's phase III? My hope is that they show non-inferiority to IVIG, and that their study was a success, and that the primary endpoint should be grip strength. Then we will just replicate what they have done, go to the FDA, get agreement, and start the study as fast as possible. If they show non-inferiority but not superiority, that leaves the door open. If in MMN, you can get better efficacy by being a more potent classical pathway inhibitor, then it leaves the door open for us to potentially show superiority. If they show superiority versus IVIG, that is fantastic. That shows that even not being a very potent classical pathway inhibitor is enough to show that you are better than IVIG and MMN. IVIG is not great in MMN, but it is approved, so that would be a really great development for patients and certainly should give investors comfort that we will show the same because we are a more potent classical pathway inhibitor. Now, there is a scenario where somehow they do not show that they are even non-inferior if they have a failed study. If that is the case, I would just remind investors we had the same situation with Riliprubart and Sanofi in June with MOBILIZE. After a couple of days of intensive discussions with investors, I think people were reassured that they have to remember we have a very potent classical pathway inhibitor, more potent than Riliprubart and even more potent than empaciparab. We are 7 x more potent than Riliprubart at the IC90. On the CH50 Wieslab assay, we are 38 x more potent than empaciparab in a head-to-head comparison we have in our slide deck using the same assay that argenx used to demonstrate their potency in their publication. If they somehow just did not shut down the classical pathway enough, I remind people, at 300 mg every two weeks, we get over 90% inhibition. That is really shutting down the classical pathway. We will see efficacy. I cannot really imagine right now why we would not go into phase III, even if empaciparab's study is a fail, because we do have a different classical pathway inhibitor, a much more potent classical pathway inhibitor. I hope they are successful. That will be reassuring for everybody. Patients will benefit from that, and then we can come in with a better profile once we get approved. Yeah. Assuming we get approved, of course. Looking forward to seeing the data from your trial as well argenx's one. Yeah. Something to look forward to. I do want to leave a little bit of time to talk about your early-stage pipeline, DNTH212 and DNTH312. They are both very interesting assets. For DNTH212, you have prioritized SLE, Sjögren's, and dermatomyositis. Once we get the data later this year for the healthy volunteer study, how should we think about how you are going to prioritize and go about the path of developing DNTH212? Right. To be clear, what we were going to provide by the end of this year is just an update on how the SAD portion, the single-dose portion of our healthy volunteer phase I study is going. Right. Then provide visibility into 2027, when are we going to start the MAD portion, and then our thinking around the three indications, and when those studies will start. That is going to be the update later this year. I still believe, and we still are planning for SLE to be the first indication we go after, because that is where the highest probability of success is. We will have another de-risking moment from our competitors will be Biogen's phase III data in SLE with litifilimab, which is their BDCA2 therapy. We look like we are more potent in terms of PDC depletion. We are hoping they will have statistically significant and be a positive outcome, and show separation from placebo. Then again, that should reassure folks that DNTH212 should have at least similar efficacy, probably better because it has the BAFF/APRIL side. Later this year, we will provide an update on how the single-dose portion of the phase I healthy volunteer study in China is going, and provide more of an update on when we will start the MAD studies and when to expect, or the MAD cohorts, I should say, and then when to expect data from that as well. The MAD cohorts are going to be also in healthy volunteers or those being- Yes. If we are looking to do any part of the phase I in patients, we will also provide an update on that. Got it. Understood. You also mentioned you recently unveiled DNTH312, which is I guess next generation claseprubart, if I may. Yeah. The C1s and the BAFF/APRIL dual inhibitor. Very interesting life cycle management for claseprubart. Also allows you to expand beyond claseprubart. Can you just talk about your vision for how you are thinking about developing this molecule as well? Yeah. I am really excited about that one, because obviously it builds on our experience now we have with claseprubart. We know claseprubart inside out. The idea here is if you can imagine by the time our clinical development, clinical operations, regulatory, everybody is done with developing claseprubart and handing it off to the commercial organization to go launch, we have all this expertise, all these relationships, all these insights we have learned from developing claseprubart in MG, CIDP, and MMN. All of a sudden we give that same organization DNTH312, which is essentially a more powerful version, a potentially more effective version than claseprubart or any BAFF/APRIL in certainly the three neuromuscular conditions. So the idea here is to take all that expertise, all those lessons learned, all those relationships, KOLs, investigators, all that knowledge, and then apply it and move as quickly as possible with DNTH312. There is definitely more indications we can go into with DNTH312 because of the BAFF/APRIL side as well as the active C1s inhibition side. Those indications we will determine at some point in the near future, but definitely starting with CIDP, MMN, and like I said, MG. It has a longer patent life, and you can just imagine the kind of franchise we could build in the neuromuscular field, and that expertise that we are building with claseprubart, and then we will have built with commercial by the time DNTH312 also launches. It is really exciting. With the extended IP and the extensions we will probably get to that IP, we could be in this neuromuscular field into the 2050s with this franchise. It is really, really exciting. Yeah. Looking forward to seeing that one progress over time. We are at time, but I wanted to give you maybe an opportunity to share any closing remarks that you had, maybe recap the runway, cash runway for us. I think you have done a great job at outlining the catalyst, but if you want to emphasize that as well. Sure. Look, for claseprubart, it is our phase II MMN data in December, as well as argenx's phase III MMN data with efgartigimod in the fourth quarter. With DNTH212, it is our healthy volunteer update, and Biogen's litifilimab update on their SLE phase III study with their BDCA2. On CIDP, I think that will be an important catalyst. We will provide an update on claseprubart and when to expect that phase III study to read out, and how we are seeing the N that we need in Part A in order to get to 128 patients in Part B, how we see that evolving. Like I said, if the current trends continue, then we are not even going to need 200 patients in Part A to get to that 128 patients in Part B. We have $1.2 billion in the bank, that takes us into 2030. We have plenty of cash to execute on all three programs and all the different indications, and read out all the important catalysts in the next few years. That gives us just a lot of optionality. The team is doing a great job, and I am feeling really, really pumped, really excited. I cannot wait. I could see DNTH212 and DNTH312 adding even more value to the company and for shareholders over the next few years than claseprubart has to date. I feel like we are just getting started. Yeah. Lots to look forward to. Well, thank you so much for the time. This has been wonderful, and I really appreciate you being here, Marino. Thank you, Sam. I really appreciate it.