Great. Hi, everyone. I'm Matthew Vanden Bosch. I'm on the healthcare investment banking team at Goldman Sachs. I'm joined here today by Marino Garcia, the CEO of Dianthus Therapeutics. Marino, thank you for making the time. Oh, thank you for the opportunity to update everyone on what's going on at Dianthus. I appreciate it. Excellent. I guess for those a little less familiar, can you just provide a brief background on Dianthus? Sure. Dianthus Therapeutics, we are building a really exciting autoimmune company focused on rare diseases. Our first program is a very potent classical pathway inhibitor, an active C1s inhibitor called claseprubart, where we are taking it into building a nice sort of neurology neuromuscular franchise with it. We've already had two very strong catalysts or proof of concept moments in myasthenia gravis, the first indication with our phase II data back in September of last year, where we raised $288 million. Earlier this year with an interim responder analysis, it was actually an early CIDP, the second indication, where we raised $719 million on that announcement. We have $1.2 billion in cash, which will take us as a runway into 2030. It'll allow us to read out multiple catalysts for claseprubart, including the phase III for our MG trial, which we're starting imminently. We'll provide further guidance on when we expect the phase III results in CIDP. The third indication we're going after with claseprubart is MMN, multifocal motor neuropathy, and for that, we have our phase II results, which we'll read out in the fourth quarter of this year. We're on track, and everything there from a blinded perspective is looking really good in terms of the safety and tolerability, very consistent with everything we've seen in the two other indications with claseprubart. The whole idea here with this pipeline of product, claseprubart, is that we are going to deliver really great efficacy in the three neuromuscular conditions, and as a complement inhibitor, do it in a safer manner where we can avoid a box warning for risk of infections from meningococcal infection from encapsulated bacteria like meningitis, and do it with an autoinjector, a 2 ml autoinjector, actually the exact same one DUPIXENT uses, where patients could self-administer it every two or four weeks. In a very convenient form for patients to be able to live their lives independently of infusions or having to go through very long sort of self-administered subcutaneous injections, like, for example, with efgartigimod. That's our first program. Our second program we licensed in from Leads Biolabs in China. It's a bifunctional fusion protein. Again, pipeline of product potential best-in-class or best-in-disease potential there, that is targeting both BDCA2 or looking to reduce type I interferon on one side, on the other, BAFF/APRIL. The idea here is to bring about two mechanisms that we know work in certain conditions, like the first three indications we've announced, like SLE, Sjögren's, and dermatomyositis, where there's very strong evidence for both mechanisms, put that into one therapeutic, and hopefully to bring about better efficacy than any one mechanism can provide. We are in the clinic. We're in a phase I trial with healthy volunteer patients, healthy volunteers, and we're looking to read that out in the second half of this year. We're very excited about that as our next program at Dianthus. Excellent. You touched on this a bit. You had two very positive data readouts for claseprubart over the last year. Can you just go a little deeper, summarize the success that you saw in myasthenia gravis and in CIDP? Sure. Myasthenia gravis in September was a very important moment because it was the first time we had actual patient data. It was a small phase II, but despite only having just over 20 patients in each arm, we tested 300 mg, our target dose, and then a high dose, 600 mg. We didn't see any efficacy difference. We knew there wouldn't be. The 600 mg dose was really just there to reassure that we weren't going to leave any efficacy on the table and so on. Despite the fact that there was just over only 20 patients and it was primarily a safety study, all the efficacy endpoints were secondary endpoints, it was really strong, robust, statistically significant data, whether you looked at the MG-ADL or the QMG or multiple other efficacy measures. We had efficacy within the first week and all the way through the 13 weeks, and very robust despite the fact that placebo patients had an outsized response. The placebo response was actually higher than we would've liked to have seen. The lesson learned there is we had an MG-ADL as a screening criteria. MG-ADL is a very simply questioned, self-administered patient questionnaire. We didn't have a QMG. The QMG is, let's say, maybe a little more objective. It's physician-administered, and it takes up to two hours. We didn't want to have that as a screening criteria because we were a young company. It was our first trial. We wanted to encourage people to put patients in our trial, and we thought this would make it too burdensome. What we saw is that our placebo response was a little bit higher than we had hoped, and I think it was because some patients self-reported as being moderate to severe when maybe they weren't. Of course, when they got placebo, they had an outsized response. We did a post hoc analysis, and we said, "Well, what if we had had a QMG screening criteria like other complement inhibitors had?" We saw that placebo response would have been closer to a two. The separation from placebo would have been much more dramatic. We had very strong statistically significant data. The safety looked really great. It confirmed that 300 mg every two weeks was absolutely the target dose. What really excited us, though, after when we did some of the post hoc analysis and looked at some of the open label data, is it seems to indicate when we took patients who are on placebo and put them into the open label portion of the trial, we didn't give them a loading dose. We started injecting them only every two weeks, and as their PK levels crept up to the target PK level of 300 mg, what we achieved with 300 mg every two weeks, we saw that patients were having a really robust response on top of the already robust response they had in the blinded portion. What that told us is that at PK levels, half of what we achieve at steady state with every two-week dosing, we see a very strong response. That's the PK level we achieve at every four weeks. Like I told you before, we always thought we were overdosing, and our open label data seems to indicate that we don't need to achieve the high levels, the PK levels that we achieve with dosing every two weeks. What we could achieve with every four-week dosing will be enough. There was this independent data from Regeneron. They have a C3 inhibitor, cemdisiran, they read out in August, and they had a pretty nice robust response versus placebo. What's interesting, we don't know a lot about the drug, but what they did reveal at that point is that they only achieved 75% inhibition of the classical pathway. We get above 90% inhibition with every two weeks. Every four weeks, we get above 75% inhibition. What they proved is that as a complement inhibitor, if you're just somewhere in the high double digits above 75%, you're maxing out efficacy. Our every-four-week dosing should have a pretty good shot at being the same as every two-week dosing. We're taking both those doses into phase III versus placebo. That was a big moment, obviously, and it reassured folks that, yes, active C1s inhibition works and is very well tolerated. We had the CIDP data in March. I think most people expected it would work in CIDP. We had this interim responder analysis. We set off to 40 patients, complete part A, just to reassure people and let them know it's working. The reason people felt it should work is because riliprubart, which is an active C1s inhibitor in Sanofi's pipeline, I think they're only pursuing CIDP. There's some other indications they might be doing some earlier studies in, but CIDP looks like to be the only indication. They had a really strong proof of concept phase II study that showed somewhere around 50% of patients, when switched off standard of care for CIDP, had additional benefit on riliprubart. I think most people, like we, expected we would have similar data despite the fact that we're about seven times more potent. What's interesting, though, is what we started seeing in our open label CIDP data is that we were seeing significantly better response rates than what riliprubart had demonstrated, meaning that our difference in potency in a CH50 hemolytic assay, we weren't sure would that mean better efficacy. It definitely seemed to result in better efficacy, at least in CIDP. What that meant is that we got to our target of number of responders in the open label part A much sooner than expected. We were able to make the announcement sooner than expected. That, of course, really turned into that's how we were able to raise that $719 million in the follow-on. At least from my perspective, where I stand now with clase prubart is this antibody, in my mind, is de-risked. It works in neuromuscular conditions. We know in MMN it's going to work. empasiprubart, the C2 inhibitor from argenx, has shown proof of concept. They'll have phase III data later this year. We are seven times more potent than riliprubart, and we showed better efficacy in CIDP. In the assay that argenx used to demonstrate potency as a classical pathway inhibitor for their C2 inhibitor, when we replicate their assay in 10 days, we are 38 times more potent than them. Whatever efficacy data they show, we will at least be able to show that. Will we be better in MMN? We do not know. In CIDP, the answer seemed to be yes, potency matters. We are not sure in MMN. We will have to see the data. From my perspective, from an efficacy standpoint, safety tolerability, again, we are not done with all the trials, but it is looking really, really good. My focus with the team now is execution. Just execute as fast as possible, get to market as fast as possible. Why? Because in MG, the market is evolving. Still less than 20% of U.S. patients that are eligible for biologics, AChR-positive patients who are on biologics, less than 20%. That market is evolving. The sooner we can get out there, the more we can do with this asset with patients. In CIDP, at one point, riliprubart had a three-year advantage. Now it is looking like it is less than two years. They will have another update later this year. Every time they have an update, they delay when to expect their phase III data. We will see what they say later this year. We will have an update later this year on how our CIDP trial is going, too. I would like to get that advantage down to as small an advantage as possible, because every quarter, every few months that we can cut into their advantage just means more market share for us. That is why it is so important. With MMN, of course, it is really just us and empasiprubart. The sooner we can get to market for claseprubart and Dianthus. With DNTH212, it is about making sure we understand what is the optimal dose in terms of risk benefit or in terms of tolerability and the PDs, who are looking to maximize the impact on type I interferon as well as on the B-cell side with the BAFF/APRIL side of DNTH212. Now our focus is on making sure we get that right and kick off the clinical programs in SLE, Sjögren's, and dermatomyositis as quickly as possible as well. Makes sense. For MMN in particular, you have touched on this a couple times. You have the data coming- Yeah. Phase II data coming later this year. Yeah. Can you just talk a little bit more about what we should look for in the data? Yeah. Why investors should be excited about that as a commercial opportunity? Yeah, look, MMN has been always a little bit underappreciated and living in the shadow of MG and CIDP. Now that we have those two big pivotal moments behind us, more attention is being paid to MMN, which I'm happy about. It really helps that argenx is also talking about MMN a lot more now. We really, like argenx, believe this is a blockbuster opportunity. 70%-80% of physicians, if you talk to them, neurologists that treat MMN in the U.S. will tell you nothing really works that well. IVIG is not that effective, certainly not as effective as it is in CIDP, for example. Partly because of that, it's severely underdiagnosed. They agree, 80%, I think, of the physicians we talked to said it is definitely underdiagnosed. Yes, it's smaller than the other two, but nothing really works, and there's only one other competitor. It's really only two biologics, two classical pathway inhibitors, claseprubart with Dianthus and empasiprubart from argenx. I think this market is a multi-billion dollar opportunity. I think in our slides we have at least a $5 billion market in the U.S. in biologics by 2035. It's us versus empasiprubart. What are the difference between us and empasiprubart? First off, we know we have a much more potent classical pathway inhibitor. They're a C2 inhibitor. They block both the lectin and classical pathway. They finally published, using the Quidel MicroVue CH50, what their potency looks like at the IC50. They didn't give the IC90. We said, okay, that's their assay of choice. That's where they talk about their potency, so we use the exact same assay. We did a head-to-head, our antibody versus theirs. At the IC50, we got very similar numbers for them, we know we're doing this right. It's very consistent results. At the IC50, we're about six times more potent. I think what you want to do is maximize your inhibition of the classical pathway to really make sure you're maximizing efficacy in any disease, especially one like MMN, where we know classical pathway inhibition works. At the IC90, we're 38 times more potent. That's really dramatic. I remind you, versus riliprubart, we're seven times more potent at the IC90, and we saw better efficacy in CIDP. In MMN versus empasiprubart, we're 38 times more potent at the IC90. I can't say yet whether that means better efficacy in MMN. We'll have to see what the data looks like. We have a much more potent antibody. We don't touch lectin alternative pathway. The precedent for this mechanism, C1s inhibitor, ENJAYMO, sutimlimab, is out there and approved for Cold Agglutinin Disease, and it has no box warning, no REMS. I believe if you block the lectin pathway, you're going to inhibit the complement system's ability to fight against the risk of infection. It's very likely going to end up with a box warning, just like alternative pathways inhibitors have it, C3 inhibitors, C5 inhibitors, et cetera. Very likely they'll have a box warning, and we won't. Finally, they're an IV. I don't know what dose every month, but it's a dose they did not, I don't think, test in phase III. They had 10 and 30 mg per kg once a week or once every two weeks in phase II, but they're testing a once-a-month IV, and I don't think they've disclosed what dose in their phase III for MMN. We'll obviously have a more convenient option because we're testing 300 mg, 2 mL every two weeks, self-administered autoinjector. That's it. That's going to be the competition. Will we have similar efficacy? We'll see. Safety, I think we'll have an advantage on box warning, and then certainly on convenience, we will have a better option for patients with MMN. I think this is definitely a multi-billion dollar market opportunity that we will layer on top of CIDP and on top of MG, all with one target, neuromuscular specialists and neurologists in the market. I'm really excited about it. We have this data coming later this year. In terms of what to expect from our data, we have to remember, this is a very small study. There is only 12 patients per arm. We are testing 300, 600, and placebo. It is primarily a safety trial. I can tell you from a blinded perspective, it is looking very consistent with what we saw with MG and CIDP, so very reassuring. Yes, we are looking at some efficacy endpoints, like grip strength, so on, and secondary endpoints. This study is far from being powered for stat sig. I know I said that for MG was almost twice the size of this trial per arm. Really trying to manage expectation. All we are looking is for signals and trends that look right in efficacy. We really want to move to phase III as fast as possible. empasiprubart has shown that classical pathway inhibition works, we hope that they will have really good data when they report out their phase III in the fourth quarter. There will be the inevitable temptation to compare our phase II to their phase II, their RAISE trial they read out a couple of years ago. I will caution again, there is a couple of reasons why you cannot do cross-trial comparisons for other than the obvious reasons. One is it is a smaller trial. We have a much smaller trial. Secondly, they really focused on how patients on empasiprubart did not need as much IVIG rescue as placebo patients. I think it was somewhere around 90% reduction in the need for IVIG rescue. We obviously are looking at that as well, that endpoint is now irrelevant. The primary endpoint in phase III is grip strength. The reason you cannot compare whatever we are going to show in terms of percentage of patients who required IVIG rescue is because empasiprubart, if you deteriorated by at least 2 points on the MRC 10 or 30% on grip strength, that meant they saw clinical deterioration, you would get IVIG. They also had another element. If a patient just asked for it. We do not have that. We have the MRC, we have the grip strength to define clinical deterioration, if a patient just asked for the IVIG, that was not enough to give it to them. Obviously they had some patients, not an insignificant number of patients on placebo that asked for IVIG even though they were not showing clinical deterioration, we will not have that. You are not going to be able to compare percentages. I just caution on that. Essentially, like I said, what we are looking for is does the safety tolerability look the same as what we have seen previously in MG, CIDP, what we are seeing currently in CIDP? Yes. Perfect. Are we seeing some trends, some signals on the efficacy that we expected? Really the job for the team is going to be to get to a phase III as fast as possible. Excellent. Let's talk a little bit about commercial dynamics then in CIDP. You touched on competitive landscape in MMN. Sure. Let's just talk for a second about competitive landscape for complement approaches in CIDP. Yeah. Look, I think a lot of investors are very excited about CIDP. It makes sense. There is a treatment paradigm change coming in CIDP that's pretty significant. Up until very recently, IVIG was seen as the gold standard in efficacy. Frankly, it still is. It's still seen as the most effective treatment for CIDP. efgartigimod is a very nice novel innovation for CIDP patients, but it's inferior to IVIG on efficacy. It's just a much better tolerated, much easier to use version of IVIG, but not as effective. I think that's why, for example, you didn't see, I think, any companies studying FcRn won't study refractory patients to IVIG. Because if IVIG didn't work, it's very unlikely an efgartigimod or any FcRn will work. It's clear that IVIG is still the most effective treatment, and now we have a nice option for patients who may be naive. Try efgartigimod first, because if they respond, fantastic. It's much better tolerated and easier to take than IVIG. That's great. Maybe if a patient couldn't tolerate IVIG at all, you try efgartigimod. If a patient doesn't respond to IVIG or they respond really well to it and can tolerate it, there's really no other option. What we saw with riliprubart in their phase II, and we're seeing in our open label phase III portion of our phase III trial, is that classical pathway inhibition seems to be more efficacious than IVIG. Patients who are on IVIG or standard care and stable or refractory to IVIG or standard care switched immediately to riliprubart, you saw about a 50% improvement. We did the same thing. We switched immediately within seven days to claseprubart, and we're seeing materially better results. Again, I spoke to the potency differences earlier. It seems to be translating to better efficacy so far. We'll see at the end of the trial if those numbers hold up, but it's looking very promising. When I look at the CIDP market in the future, what I think we're going to see is that classical pathway inhibition is seen as the most potent, effective way to treat CIDP, then IVIG, and then FcRn. Now, which one will be used first, second? How will physicians tackle CIDP patients? We'll see. I think if you have a clearly more effective treatment that's much better tolerated and safer than IVIG and certainly a lot more convenient, I don't see how classical pathway inhibition won't be the first line. Like I said, up to this point, the efficacy we're seeing looks superior to riliprubart. It looks superior to the other active C1s inhibitor, and I think it's because of that potency difference. It may be that the most effective treatment will be claseprubart, then riliprubart, then IVIG. Then FcRn below that. Where does empasiprubart fit in there? I don't know. We have to see some data at some point in CIDP, but certainly in terms of its potency around classical pathway inhibition, it's the least potent of the three complement inhibitors, riliprubart, sutimlimab, and empasiprubart. It's the least potent. I don't know what that will mean in efficacy, but right now it looks like the more potent you are, the more efficacy you have. Excellent. Let's move, shift gears a little bit to myasthenia gravis. Sure. Can you talk a little bit more about the phase III design? Sure. Some of the enhancements that you made based on what you saw in the phase II. Yeah. I kind of hinted at it earlier. Yeah. The first thing is we are going to have a QMG screen criteria. We're going to try to keep that placebo response down to what we've seen historically, around a two-point improvement, so we can let the antibody really show what it can do. We're testing, of course, 300 mg every two weeks, one shot every two weeks, self-administered, like a DUPIXENT, exactly the same dosing administration as DUPIXENT. Then we're testing it once every four weeks. We are making the trial larger, but we think it's worth to test that every four-week dose because, again, as I mentioned, the open label data, the cemdisiran data, Regeneron, everything is telling us that just north of 75% inhibition, PK levels are half of our steady state at 300 mg every two weeks, seem to look like it could be just as efficacious. That trial, we said would start mid-year. Everything's on track to get that study started. The part that I'm most excited about is we had a regulatory update after our CIDP announcement where we agreed with the FDA that looking at ANAs, testing for ANAs, screening out for high ANAs or even double-stranded DNA is irrelevant, right? That was just something to look at in phase II, but we should not bother with it anymore. It doesn't mean anything. Our number one reason for screen failures in MG, and the reason we weren't able to report out our data even earlier than when we did, is because MG patients just have high ANAs. We had a huge amount of patients that basically couldn't come into our trial. Very frustrating for the investigators, for the patients, for us. We couldn't put them in our trial because of their very high levels of ANA. That's gone now. We agreed we don't need to track it. We don't need to screen for it. It's irrelevant. That should help between the enthusiasm we're feeling with our investigators, because they've seen the phase II results from MG. They're hearing about the CIDP results because it's open label, so everybody's talking to each other. It's a small community, the neuromuscular specialists. I think we have a really good chance of certainly meeting the timing expectations we have for data in the second half of 2028. That trial we're really excited about, everything's going really well. The team is just doing a phenomenal job on execution. How do you see the commercial market playing out in myasthenia gravis? Is that more crowded FcRns have a foothold? What's your perspective? Oh, for sure. It's the most crowded of the three indications we're going after. I want to point out a few things, argenx is saying this as well, which I'm really happy to hear. Less than 20% of patients who should be on biologics in the U.S. with MG are on biologics. This market could easily be two to three times larger. It's not just about competing for market share. It's about growing this market. What does the market need to grow? Well, if you look at autoimmune markets, historically, what got them to 40%-50% penetration biologics, you got to make it really easy. An autoinjector, no box warning, just really simple, good efficacy. That's what claseprubart offers. We'll see if anybody else can offer the same combination of those three things, efficacy, safety, and the convenience of an autoinjector, self-administered infrequently. The other thing is, well, UPLIZNA just launched from Amgen. It takes months for that to kick in and really show any efficacy, if it does show efficacy. It's got its side effects and its issues. The big advantage is simple, is it's once every six months IV. That's really nice. It's very convenient. Patients don't get these drugs if you have MG for convenience. They're looking for efficacy. Despite its less than ideal profile, I think it's beating expectations, and I think it's because, again, it's being used second-line, by the way, mostly. Even with the FcRns out there, even with the under-penetration biologics, there are a lot of patients out there who are just looking for more options, and that just proves it. For me, the MG market, people feel like, "Oh my God, that's it. It's over. FcRns own it." Not really. There's a huge potential for growth, and there's still a lot of patients out there that are not satisfied with what's offered. Even in the worst case scenarios where you assume claseprubart is a second-line option to FcRns, which I do not believe is going to be the case at all, I think we're going to have a very nice first-line position in MG. It's still a multi-billion dollar blockbuster. Just add on top of that CIDP and MMN and, well, it doesn't take much to get to a multi-billion dollar peak. I think with MG, it's about continuing to grow the penetration of biologics, continue to educate physicians on why we should be treating those patients earlier, faster with biologics, just having more options that are very convenient, safe, and with good efficacy. Excellent. Switching gears just to the DNTH212 asset and the rheumatology franchise. You mentioned the in-licensing, how it came into Dianthus and the prioritized indications. Maybe just touch a little bit on clinical development plan and how you're thinking about pursuit of those indications in the months ahead. We're very excited. It looks at least similar or better in terms of PDC depletion and type I interferon reduction rituximab on one side, on the abatacept side, the IG reductions look like the DNTH212 is deeper and longer than povetacicept. Could have a nice infrequent biologic in our hands here with a best-in-class, both abatacept and BDCA2 inhibitor. Right now, the goal is to figure out what's the right dose. We're taking two mechanisms, putting them together into one bifunctional fusion protein. It's about figuring out how do we maximize the PK/PD curve while also making sure that we manage for any potential tolerability or safety signals. That work is ongoing with healthy volunteers. We plan to report out what we found and what doses we think we plan to take into the part B of our phase I trial, which is SLE patients, and potentially into MAD or phase II studies as quickly as possible. That's really the next step. We're very excited. We're working with Leads, our partner in China. The phase I study is being done in China. I'm very excited about the potential here for DNTH212. If we can get to that optimal PD profile and dosing profile without any significant new safety or tolerability signals that change the risk-benefit profile, then this drug could be really big. It'll be a nice way to build the company over the next few years on top of claseprubart as our foundation. Excellent. Last question here, just keeping an eye on time. You're very well funded. You talked about a $1.2 billion of cash and runway into 2030. You're in a great spot. Can you just talk about your focus areas for this year and just general aspirations for the company? Yeah, look, from the very beginning, this has been about building a very exciting, independent, self-sustaining biotech autoimmune company, focused on rare diseases for now, over the long term. Pipeline has always been a priority. I'm very pleased with where we are today. There's more to do and stay tuned for any future developments there. The immediate focus, like I said, claseprubart, it's about execution. Just speed and quality, not or, both. It's to be able to get this option to patients as quickly as possible in the market and therefore be able to be part of that solution to growing the penetration of biologics and MG and change the treatment paradigm in CIDP and potentially in MMN. With DNTH212, again, it's just making sure we zero in on a tight range around dosing to take into the MAD phase II portion and get moving as fast as possible. Now that we have the cash potentially, try to do as many of the pivotal trials in parallel as quickly as possible with the team and build a really nice rheumatology franchise there to complement our, no pun intended, our complement inhibitor in the neuromuscular space. That's our primary focus. The team is growing. We're doing really well. I'm just really eager to see how the company develops in the next couple of years. It's been a fantastic five years, and the way we've grown every year, and I expect that we're going to continue that trajectory in the next few years. Excellent. Thank you again for the time. Thank you, Matt. Really appreciate it.