Good afternoon, everybody. This is Dan Lundquist, the healthcare specialist at BofA, and welcome to this year's 2024 Healthcare Conference in Las Vegas. Very pleased today to have Dianthus Therapeutics with us. We have Marino Garcia, the CEO of the company, who is going to run through a number of slides. And if there's any time at the end, we could have a question or two, but over to you, Marino. Thank you, Dan, and a big thank you to the Bank of America team for this opportunity to update folks on the exciting developments going on at Dianthus. Before I start, just letting you know, I'll be making some forward-looking statements, so I refer everybody, please, to our website and our SEC filings for more information. So, quick overview. Dianthus Therapeutics was founded in 2019 to develop what we're calling next-generation complement therapies to treat severe autoimmune diseases. Our lead program, DNTH103, exemplifies what we mean by next-generation complement therapies. It's a potent monoclonal antibody that targets the classical complement pathway by selectively inhibiting only the active form of C1s. The intention here is to be the first subcutaneous, self-administered, auto-injector dosed as infrequently as every two weeks, a Dupixent-like dosing administration profile to treat conditions like generalized myasthenia gravis. The exciting developments of the last year include the fact that we reported out our top-line phase I data that confirms that through the YTE half-life extension technology that we engineered into the antibody, we have a nice, healthy, long half-life of 60 days. We have a very potent classical pathway inhibitor, and that potentially could have a differentiated safety profile, specifically versus other terminal complement inhibitors, like the C5s in myasthenia gravis. Another exciting development is that there's now clinical proof of concept for classical pathway inhibition, demonstrated in the first three indications that we're targeting, the three neuromuscular indications of myasthenia gravis, CIDP, and MMN. I'll get into that in a few minutes, validating the potential of the pipeline within a product potential of 103. We have now initiated in the first quarter our first phase II program, and that's in generalized myasthenia gravis. We anticipate to have results for that in the second half of 2025, and we're on track to start two other phase II programs this year, starting with MMN next and then CIDP later in the year. We also executed on a successful PIPE earlier this year for $230 million, so we have enough cash on our balance sheet to fund operations well into the second half of 2027. We're very excited about the potential of 103 as a pipeline and a product with its best-in-class profile. And we've decided to start by developing it in three autoimmune or neuromuscular indications where there are clear synergies from a clinical development standpoint, as well as from a commercial standpoint. The first is generalized myasthenia gravis I mentioned earlier. That's a multi-billion-dollar market opportunity, where there's a real opportunity for a highly differentiated, potent inhibitor, classical pathway inhibitor like 103, to further penetrate and expand first-line use of biologics in gMG. CIDP, there's been some very exciting data presented as recently as the AAN by Sanofi with their active C1s inhibitor, which demonstrated very impressive efficacy in CIDP. It's the first time that an active C1s inhibitor has been shown to work in any autoimmune disease. It's the first time a complement inhibitor has been shown to work in CIDP. And they showed very clear efficacy signals in three patient cohorts in CIDP. One is treatment-naive patients, the other was in patients who were responsive to IVIG standard of care and were switched and still saw a significant portion of patients improve on the active C1s inhibitor. And finally, on patients who were refractory to standard of care or IVIG, also about 15% of those saw improvement on the active C1s inhibitor. So that's become a very exciting opportunity for 103. And then finally, MMN, a classical pathway-driven disease where FcRns won't work. It's a ripe field for complement inhibition, and there's only one other complement inhibitor being developed there, and that's empasiprubart, which is an IV C2 inhibitor from argenx, which has shown clear efficacy in their phase II trial. So we're very excited about the potential for 103, and we're starting with these first three indications. 2024 is a year of execution. We, as I mentioned, have already started with MG in the first quarter of this year. We plan to initiate MMN in the second quarter of this year, so before the end of this quarter, we expect to have an IND clearance and be able to begin our program in MMN. Then in the second half of this year with CIDP. The first data readout we've guided to is with MG, where we expect to see results from that phase II program in the second half of 2025. So drilling down a little bit into MG and the exciting commercial opportunity we have with a best-in-class drug like 103. MG is a very exciting rare disease, autoimmune disease market, and in the terms of the fact that it's a multi-billion-dollar market that's clearly supporting two growing franchises, and that's the complement inhibitors, the C5s from AstraZeneca and FcRNs, both being used first line as targeted biologics in MG. Within the complement class, Soliris, Ultomiris, you're seeing that that's over $6 billion franchise, and their growth is coming from the MG portion, which is about a third of their revenues, and as first-line use in treatment-naive patients in MG. And all those sales are from high volume IV infusions. And then, of course, the tremendous success we've seen from Vyvgart or argenx's FcRn inhibitor, again, also a high volume, most of those revenues coming from the IV form. So again, a blockbuster market where there's still a significant unmet need and opportunity for something like a 103 with DNTH103. And this slide I like to show because it gives you an sense of the kind of differentiation 103 can deliver just on dosing and administration. On the bottom, you see the IVs. That's what's driving the vast majority of the sales I just showed in the previous slide. That's Soliris, Ultomiris, and of course, Vyvgart as IV infusion, high volume IV infusions. There are now three subQ's that are approved in MG. Two FcRns that have to be delivered by healthcare professionals, and Zilbrysq, zilucoplan from UCB. It's the first self-administered therapy in the MG, biologic and MG market. But it's a C5 inhibitor, which carries a bit of a safety risk with its box warning around the risk of infections from encapsulated bacteria. And unfortunately, it's also a prefilled syringe injection that you have to give yourself on a daily basis. So when you look at something like 103, where we're aiming for an auto-injector, Dupixent-like profile, without the risk of... With a lower risk of infection from encapsulated bacteria, where you could put it into an auto-injector, patients can self-administer wherever they are. You can see the opportunity we have to differentiate 103 with and change the standard of care within MG. Now, we know complement inhibitors are well-established and work because of their ability to block the formation of the MAC by inhibiting the classical pathway. But one thing that people need to understand is the difference between targeting C1s and being a terminal inhibitor is that we are leaving the lectin and alternative pathways intact. So the idea here is to deliver the efficacy that complement inhibitors can deliver in conditions like MG, and but leaving the lectin alternative pathway intact allows the complement system to still be able to fight against the risk of infections from encapsulated bacteria and avoid deadly infections like meningitis. So if you were to look at the label of Enjaymo's label, sutimlimab, which is a C1s inhibitor approved for cold agglutinin disease and out in the market, you can see it's the only complement inhibitor approved on the market without a box warning around the risk of infections. And that's the safety profile we're aiming for and could differentiate us from other terminal inhibitors like Zilbrysq, Ultomiris, and Soliris. So again, the efficacy without the burden of the additional safety risk. So where are we with DNTH103 in our clinical development? Well, as I mentioned, we reported out phase I data in September of last year. That was the results of eight different cohorts, IV SAD cohorts, subcutaneous SAD cohorts, as well as subcutaneous MAD cohorts, for a total of 60 healthy volunteers. This is a summary of the data we saw. On the left here, you can see very nice linear PK. This is from the IV cohorts we tested and pretty much confirms that we have about a 60-day half-life. The middle graph shows the nice accumulation we see by dosing subcutaneously every 2 weeks with DNTH103. On the right side is we graphed every single data point from every single healthy volunteer of every cohort, and it pretty much confirms that the IC90 or the level of inhibition, or sorry, the PK levels we need to achieve to achieve at least 90% inhibition of the classical pathway is about 87 mcg per ml. This data is what allows us then to model out what would happen if after a short loading dose, what, what, what is the steady state of 103 dosed subcutaneously, 300 mg, 2 ml shot every two weeks? As you can see from this graph, the peak troughs is somewhere around 125-115 mcg per ml. On average, about 120 mcg per ml. That is a significant margin above the 87 mcg per ml target we define as the IC90 for DNTH103. So again, with dosing every 2 weeks, we expect to see tremendous efficacy with DNTH103 in conditions like myasthenia gravis, MMN, and CIDP. So I mentioned we started our MG program in the first quarter of this year. This is the design of the program. We, after a short loading dose to get patients up to closer to steady state, it is a short 12-week study, so we want to get them there as quickly as possible. Then we randomize patients into three arms: placebo, 300 mg every 2 weeks, which gets us above the IC90, as I just showed you in the previous slide, and then another higher dose that we're testing, which is 600 mg every 2 weeks, to get us significantly above the IC95, just to see if there's any additional efficacy we can get with DNTH103 by inhibiting the classical pathway even more so than three hundred mg could every two weeks. We expect the top-line results from this in the second half of next year. Just to make clear, the phase III program was essentially, would essentially be the same design, potentially only one active arm and just larger numbers, but it would be pretty much the same length of time, 12-week study. This study is looking at safety, with secondary endpoints being MG-ADL and QMG and other efficacy endpoints. Obviously in phase III, those would become the primary endpoint. I mentioned that there was exciting data from CIDP. This is just to highlight that it is a very attractive market for DNTH103, where there's still a significant unmet need, and now there's clinical proof of concept that's been delivered by riliprubart, the active C1s inhibitor in Sanofi's pipeline. As I mentioned, they've shown very clear efficacy in three patient cohorts: treatment-naive, treatment refractory, as well as patients who are stable on IVIG or standard of care. The main difference between our active C1s inhibitor and Sanofi's active C1s inhibitor is they're dosing about 600 mg every week, which would be translated into two shots, two subcutaneous shots every week. Our target profile or our target dose is one shot every two weeks. So at the end of the month, it could be potentially two injections versus eight injections. And that's a result of, we just believe we have a more potent antibody that inhibit, or active C1s inhibitor, I should say. And then with MMN is also a very attractive opportunity, where there's clinical proof of concept demonstrated by classical pathway inhibition, specifically by the C2 inhibitor being developed by argenx, which showed additional efficacy data at J.P. Morgan earlier this year. What's interesting about the MMN market is, although it's a smaller market than the other two, it's one where FcRNs won't work. It's IgM driven, so it's really just complement inhibition. And, the C2 inhibitor from argenx is an IV that has to be delivered every week or every two weeks. And because it's a C2 inhibitor, it not only blocks the classical pathway, which is where it's getting its efficacy from, but it also blocks the lectin pathway, which adds a safety risk around the risk of infections from, encapsulated bacteria, things like meningitis. So we're very excited again about DNTH103 being a best-in-class option for patients with MMN. So, in the last few seconds I have here, just to reiterate, this is a year of execution. We've already begun our MG program. Up next is our MMN program, and then later this year, our CIDP program. For DNTH103, we will have top-line data for MG in the second half of next year, and we just reported out our Q1 results, which confirm we have $377 million in our balance sheet, which would take us to the second half of 2027. Thank you very much for your attention.