Good morning and welcome to the Dianthus Therapeutics conference call. My name is Michelle, and I'll be the operator for today's call. A slide presentation to accompany this call is available on the investor section of the Dianthus Therapeutics website. Following the company's prepared remarks, we will move to a Q&A session. Please note that today's call is being recorded. I will now turn the call over to Marino Garcia, CEO of Dianthus Therapeutics. You may now begin. Thank you, operator, and thank you everyone for joining us today. Just a note before I begin the presentation, we will be making forward-looking statements, and I would refer you to our SEC filings for more information. Earlier today, we issued a press release announcing an exclusive license agreement with Nanjing Leads Biolabs for DNTH212, a first and potentially best-in-class phase I-ready bifunctional BDCA2 and BAFF/APRIL inhibitor. I would like to thank Leads for selecting Dianthus to globally develop DNTH212. This announcement builds on the momentum from September when we announced our positive data with Claseprubart in MG and expands our leadership position in the development of next-generation best-in-class therapeutics as we execute on our vision of building a leading autoimmune-focused biotech company. Please turn to slide three. I'm joined today by Dr. Simrat Randhawa, our Executive Vice President and Head of Research and Development, and Ryan Savitz, our Chief Financial Officer and Chief Business Officer. I'll begin with a few introductory remarks, and Simrat will then provide a detailed overview of DNTH212, our new exciting bifunctional fusion protein. Ryan will then review the transaction terms, and I will speak to how DNTH212 strategically bolsters our pipeline and advances our vision of becoming a leading biotech company in the autoimmune space. After our prepared remarks, we will open the line for questions. Please turn to slide four. Today's announcement expands Dianthus' leadership position in next-generation autoimmune therapeutics with a best-in-class potential. This exclusive license agreement grants Dianthus global rights outside of Greater China for DNTH212, a first and potentially best-in-class phase I-ready bifunctional BDCA2 and BAFF/APRIL inhibitor. Targeting BDCA2 and BAFF/APRIL fits our strategy of pursuing best-in-class therapeutics with validated mechanisms of action, pipeline, and a product potential with a differentiated and patient-friendly therapeutic. Favorable clinical data from litifilimab and povetacicept provide proof of concept for DNTH212. The combination of these complementary mechanisms targeting both the innate and adaptive immune systems offers the opportunity for enhanced efficacy and clinical outcomes for patients suffering from various autoimmune diseases. In addition, DNTH212 has demonstrated the potential for improved clinical benefit compared to litifilimab with superior in vitro inhibition of PDCs and versus povetacicept with superior Ig reductions in NHPs. Simrat will speak more about these data shortly. We're also excited about the potential for DNTH212 to be a convenient patient-friendly therapeutic with a subcutaneous self-administered once every four weeks or less frequent dosing regimen. DNTH212 has an FDA-cleared IND, and a phase I trial is expected to begin in the fourth quarter of this year with results in healthy volunteers expected in the second half of 2026. Importantly, following this transaction, we estimate pro forma cash of approximately $525 million to fund multiple catalysts and provide cash runway into 2028. Guidance that remains unchanged from our previous disclosure post our financing in September. Now, I'll hand it to Simrat to tell you more about this exciting potential therapeutic. Next slide, please. Thank you, Marino. Now on slide six, let's get into the details of this exciting molecule that targets key components of the innate and adaptive immune systems. The innate immune system is inhibited by targeting plasmacytoid dendritic cells or pDCs through modulation of p DC BDCA2, inhibiting type I interferon production, and via pDC enhanced antibody-directed cell-mediated cytotoxicity or ADCC, leading to PDC depletion. The adaptive immune system is inhibited via TACI with a single high-affinity CRD2 domain, leading to BAFF/APRIL inhibition and subsequent B-cell modulation. Finally, DNTH212 has an extended half-life due to FcYTE mutation. Next slide. Let's move on to our two cellular targets. PDCs are rare but are still the major producer of type I interferon, which is considered a master regulator of the immune system. Type I interferon should be produced in response to viral infection, but it is known to exacerbate a host of autoimmune diseases. B cells, obviously, are the central player in adaptive immunity, generating autoantibodies that drive disease pathology in a host of autoimmune conditions. BAFF/APRIL inhibition has been shown to be effective at inhibiting antibody production and B cell activation in these autoimmune indications. Next slide. In vitro data of DNTH212 versus litifilimab, currently a phase III BDCA2 inhibitor, shows on the left comparable interferon suppression and on the right superior pDC depletion. Next slide. In an NHP single-dose study, DNTH212 showed superior immunoglobulin reduction versus both telitacicept and povetacicept. This data drives potential for superior efficacy in at least Q4 week dosing. Next slide. It is comforting to have clinical trial data supporting both BDCA2 and BAFF/APRIL inhibition. On the left, we highlighted litifilimab positive phase II data in SLE. That compound is now in CLE phase III. On the right, we provide a few examples of successful BAFF/APRIL inhibition, such as in IgA nephropathy and Sjögren's. Next slide. We have a wealth of targets appropriate for our dual interferon B cell inhibitor. On the left, our indications with clinical evidence for one mechanistic DNTH212 target and biologic rationale for the other. On the right, our indications where current science supports the benefit of DNTH212 dual targeting. We will provide our prioritized list of targets in 2026. Next slide. This is a clinic-ready asset with a standard healthy volunteer SAD planned to initiate later this year, followed by a more targeted SAD in SLE patients. Next slide. Finally, the 212 TPP targets first-line use in multiple indications due to dual mechanism-driven superior efficacy, a well-characterized and very manageable safety profile based on individual mechanistic clinical trial data, and finally, attractive infrequent subcu dosing. Next slide. Thank you, and now I'll turn it over to Ryan. Thank you, Sim. As you can see, this is an extremely exciting opportunity for us to continue to grow our pipeline with a differentiated, potentially best-in-class therapeutic. Importantly, the terms of this transaction provide us this favorable upfront and near-term economics for a phase I-ready program. Next slide, please. As depicted here on slide 15, under the agreement, we will pay Leads up to $38 million, comprised of $30 million in upfront and near-term milestone payments, plus an additional $8 million milestone upon the initiation of a Dianthus-led phase I study. Additionally, Leads will be eligible to receive up to $962 million in success-based development and regulatory approval milestones and sales-based milestones across multiple indications, along with tiered royalties from the mid-single digits up to a low double-digit royalty on ex-China net sales. Importantly, our Q3 2025 estimated cash balance pro forma from the impact of this transaction is approximately $525 million, and we are reaffirming our previously disclosed cash runway guidance into 2028, enabling us to fund multiple near-term catalysts from both claseprubart and DNTH212 over the next several years. With that, I'll turn it back over to Marino to provide some additional strategic perspectives on how this transaction extends our leadership in severe autoimmune diseases. Thank you, Ryan. Next slide, please. The addition of DNTH212 expands our leadership position in developing next-generation therapeutics with best-in-class potential. As you can see here, DNTH212 is quite consistent with our strategy of ensuring our programs demonstrate benefits across four key value drivers, similar to what we have demonstrated with claseprubart. First, DNTH212 has a validated mechanism of action across multiple conditions, as established by other BDCA2 and BAFF/APRIL targeted therapies. As Sim described, we believe DNTH212 has best-in-class efficacy potential with patient-friendly, convenient dosing and administration. Finally, DNTH212 has a clear pipeline and a product opportunity in multiple autoimmune disorders where type I interferon and B cells have been implicated. We look forward to announcing our priority indications in 2026. Next slide, please. DNTH212 was designed to target known drivers of autoimmune disease with the potential to deliver superior efficacy, a favorable safety and tolerability profile combined with patient-friendly convenience, very similar to claseprubart's potential benefits. We believe DNTH212 has the potential as a differentiated first-line therapy across multiple autoimmune diseases and with robust IP protection, with composition of matter expected to expire no earlier than 2044. Next slide. I would conclude by once again reiterating how excited I am about the opportunity ahead for Dianthus. 2026 will be a very exciting year with multiple near-term catalysts across our portfolio and two clinical stage next-generation therapies focused on severe autoimmune diseases. We continue to expect an interim responder analysis from part A of our pivotal phase III CIDP trial and top-line data from our phase II MMN trial in the second half of 2026. We also expect top-line phase I results from DNTH212 in healthy volunteers in the second half of 2026, and we plan to announce our prioritized indications for DNTH212 during 2026. We're excited about the potential for Dianthus with both of these next-generation therapies, and we look forward to keeping you updated on our progress. With that, we will open the call for questions. Thank you. Thank you. To ask a question, please press star one on your telephone. To withdraw your question, please press star one one again. Our first question will come from Alex Thompson with Stifel. Your line is now open. Good morning, congrats on the deal, and thanks for taking our questions. I guess the first one, what work can you do preclinically to get confidence that blocking both of these pathways isn't going to drive an increased infection risk versus both targets alone? For next steps here, what do you need to see coming out of China and the phase I data, either in healthy or SLE patients, to move forward and start your own work in the U.S.? Thanks. Yeah, so I don't think there's going to be any relevant preclinical information that we're going to develop to address what was asked. What I would say is that we looked at a lot of assets, and I don't think we got into that here in terms of different opportunities that are on the market. Frankly, a lot of them these days are bifunctional. One of the critical things that went into the decision-making around this asset is what exactly are you inhibiting across your two arms? What is the potential for increased efficacy based on the type of data that's available clinically or biologically, but also rationally based on what you're targeting? You know, are you really going to face this massive increased synergistic risk in key areas such as what you've just mentioned around infection? From that standpoint, I would say we chose two targets in which the safety profile is particularly well-characterized and relatively benign. Right? If you take a look at the interferon experience, it relegates itself to the reactivation of some viral infections such as herpes. That is easily managed with vaccination. If you take a look at the BAFF/APRIL axis, at least the recent trial experience in the course of the last six or seven years, again, gives you a relatively benign infection experience and one that doesn't necessarily overlap substantially with the core concerns that you have with interferon suppression. That's why we chose this asset in the first place. We're not going to know until we do the experiment. The work that we've done when we looked at this asset and we've considered the profiles of each individual mechanism, we don't really expect any increase in synergistic risk. We expect to inherit the profiles of both of these products. In terms of the second question, what data can you repeat the second question? I think it was largely around the healthy volunteer study in China. Yeah, I guess what do you need to see coming out of those studies to start your own work in the U.S.? Will you have to wait for total completion, or what are you looking for? I think that in order for us to proceed and understand what else we would need to do from a safety standpoint, remember what we've shown you is a SAD study, right? We've shown you a SAD study. Clearly, we have two options to move past the SAD study. One is a classic MAD in healthy volunteers leveraging sort of the target doses we expect to use in disease. The second one is to incorporate a MAD somehow in a sort of phase II study. We haven't come to a decision on which of those two we're going to do. In order to get to that point, yes, we need to see the totality of the data, I would say from the healthy volunteer SAD data. The SLE component is a nice additional bonus of data we may receive, but at least in my opinion right now, it's not essential for us to move forward. One more thing that came to my mind that's sort of triggered by the fact that you asked us about the healthy volunteer study and then you had that first question around infection risk. The FDA saw this plan. They're fully aware that there's this bifunctional antibody and a company has come to them to do a healthy volunteer study. I can tell you that the FDA response was incredibly reassuring as somebody who just sort of went through them before with another asset, at least, you know, our consultants before I showed up did. Looking at the responses that we received, for example, from DNTH103 and comparing them to this bifunctional asset, extremely reassuring. FDA did not encumber this study with any additional testing, any additional vaccination requirements, really any additional way that you would look at dosing or stopping dosing to evaluate. It was a very sort of green light forward from FDA. I think even from their standpoint right now, they're not seeing sort of adding these two things together as adding substantially to overall risk. Our next question will come from Maury Raycroft with Jefferies. Your line is open. Hi, congrats on the update and thanks for taking my questions. I'm wondering if you could talk more about PK and PD endpoints in part A that you're going to be looking for, and what constitutes a go/no-go for progression into part B and beyond. Based on the preclinical data, maybe talk about the relative impact on BAFF versus APRIL versus what we see with povetacicept and other biologics. Mori, I would say that I think the PD data for me is very uninteresting because I kind of already know it's going to, you know, if you just take rational expectations, you know the construct of the molecule. These are two targets that should not be a mystery to anybody at this point, right? There's clinical data, there's PD data around them. We understand the affinities of our receptors and what they're already doing from a PD standpoint in NHPs. I would say the only thing that I would kind of want to check box on in humans would be suppression of interferon levels. I fully expect it to be very consistent with the lilifilimab data. I would be very surprised if it didn't achieve the same results. On the BAFF/APRIL front, not much except if you ask a question that we just can't answer because we don't actually have detailed data on BAFF/APRIL. What we have right now is immunoglobulin data. It would be good to get the breakdown of relative suppression. I don't know exactly what we would do with it, but I think for a complete story, it would be good to understand which of the two we're inhibiting more. I would say that again, the CRD2 domain is well accepted as the high affinity domain for both. I can shoot you around a publication exactly on that from the NIH. We expect it to be high affinity for both, frankly. Got it. That's helpful. Yeah, if you want to send the publication, that'd be great. Thank you. Our next question will come from Myles Minter with William Blair. Your line is open. Hey team, this is John on for Miles. Congrats on a very interesting deal and thanks for taking our questions, two from us. Maybe first a bit of a follow-up to the prior question. Do you think you could talk a little bit more about what factors in DNTH212 you think contribute to that superior APRIL/ BAFF profile compared to povetacicept and lilifilimab on immunoglobulin reductions? Is it a best-in-class TASI CRD2 or is it something else, like maybe some potentially some additional efficacy from B cell depletion with the ADCC? Any color there will be helpful. Second, do you think you have the ability to concentrate this down to a prefilled syringe or into an autoinjector? What kind of viscosity would you expect there? Thanks. Okay. Related to, first of all, the data that we showed you is single dose and NHPs. In that data, what I would say you see at least similar data to povetacicept. That makes sense because the TASI construct is very similar to povetacicept. It uses that CRD2 high affinity domain. The other differences can be chalked up to maybe two things. Number one, maybe a different experiment, or number two, there are real differences because the rest of the molecule is different. Until you do the experiment, it's not just about the CRD2 domain, but it's about so many other things that are just related to what that domain is stuck on top of that happens to work better. Right? For now, this is the data we have. My hope and expectation is that at a minimum in humans we're equivalent to PO. It could be better based on the NHP data. That's how I look at it. In terms of the effector functions on B cells, that's not really how this molecule is constructed. The effector function is designed to really exhibit itself when it's bound to PDCs. You're right, we don't know. There could be mild depletion of B cells. Again, we're going to have to wait and take a look at healthy volunteer patients to see if that's what we're seeing in terms of overall count. For now, I would say the expectation should be set as immunoglobulin profile similar to povetacicept, very potent interferon suppression in a molecule that can be dosed every four weeks. What we're doing that's unique is targeting the innate and the adaptive immune system with the best current technology available. On the question around the CMC and the ultimate goal in terms of how we would deliver this for patients, our plan from a CMC perspective is to put this into potentially a prefilled syringe, but ideally into an autoinjector that patients can self-administer. Our goal is at a minimum every four weeks and potentially less frequent than that. That's the goal we have set for our team and the goal I fully expect we'll achieve. Very helpful. Thank you. The next question will come from Yaron Werber with TD Cowen. Your line's open. Great. Congrats on the deal. It looks very synergistic. I got a couple of questions. Maybe just the first one. povetacicept, as you mentioned, hits CRD2. A TASI hits CRD1 and 2. TELI also CRD1 and 2 and the N-terminus. TASI, you know, similar, and it's got even another intracellular domain that it's binding to. Any thoughts on the merits of hitting CRD2 exclusively versus also having CRD1 for stabilization? I have another question as well. Yeah, I think we should just send the paper around to everybody because it's going to come up a lot, and it's a very good question. CRD2 is a domain you want to concentrate on. CRD1 is a pretty low affinity domain for APRIL/ BAFF. CRD2 is where the money is. I think that's why folks are gravitating now to having molecules that are CRD2 specific. That's the answer. It's just higher affinity. You don't really lose anything. There are good publications around it, and now there's good data to back it up. If your goal is really potent suppression of the axis, which results in the deepest ability to reduce IgG using the BAFF/APRIL axis, you want to concentrate on CRD2. That's what we want to do, and that's why it's constructed that way. There were other questions that I'm kind of forgetting now. What else was there? Yeah, sorry. Go ahead, Yaron. Yeah. Within your indication set, the one that's missing is IgA nephropathy, which is fairly validated but seems fairly crowded. There's obviously proof of concept in Sjogren's and cutaneous and in lupus as well. You have a few other ones like DM, scleroderma, PV, and HS. Can you maybe just talk about some of the biological rationale for that? Thank you. Yeah, you know, you're on it. It's Marino. It's a good question. There are so many indications, and we could have added quite a few more to that list. We have a prioritized list of indications in our minds, but for competitive reasons, we just don't want to reveal them just now. You're right. There's multiple, multiple ways that we're going to, we could take this molecule forward. It's going to ultimately, the list and the prioritized list of indications is going to take into account probably a success, biological rationale, clarity, and efficiency of the clinical development program and the regulatory process, and of course, the ultimate commercial opportunity. We look forward to updating everybody on how we're going to maximize the potential of this pipeline and a product in the new year. I think the one thing I did want to address is a very good question, which is around, you guys checked off biological rationale. What is that? I think we owe some more details maybe in the future iteration of the corporate deck around that. When we say that there's biological rationale, what we mean is that it's a situation where maybe in one of the mechanisms, we don't have clinical data that just says, "Dot, it's going to work." Right? We don't have BAFF/APRIL or IL-1 or, sorry, type I interferon suppression data in a particular indication that says, "Yes, it works." We gravitate to biological rationale. What that essentially means is for the pDC access, it means that there's a strong type I interferon signature in the disease, which can be really one of two things, and usually, it's both. We'll document that in a future iteration. It means there's elevated interferon levels, and it just kind of makes sense. At the end of the day, it's been noticed in a particular disease that clinical course varies by interferon level and that there's interferon gene signature as well. In other words, there are genes that are being turned on when interferon is present that cause damage in autoimmune disease. That's what that means. We can provide more detail on that piece in the future. I think it's open. Our next question will come from Rami Katkhuda with LifeSci Capital. Your line is open. Hey guys, congrats on the deal and thanks for taking my questions as well. I guess, can you touch on the different expression levels of BDCA2 versus BAFF/APRIL and how that could influence 212's PK? Secondly, how much collaboration and data sharing is there with Leads? Will you be able to leverage their data in the future beyond phase I to kind of help select and expand indication selection for you as well? Yeah. There's, you know, I'm not going to go into magnitudes of numbers right now, but there's a lot more BAFF-APRIL than our BDCA2 targets. The dosing is largely going to be based around, if you can inhibit BAFF/APRIL sufficiently, you're going to get to BDCA2. That's the answer. It's a pretty simple answer. It's completely swamped by the BAFF/APRIL part. We feel pretty confident, and that's why we showed you sort of the chart specifically around DNTH212 and lilifilimab and povetacicept, saying, "Look, single dose experiment, apples to apples, NHPs, this is what you get with both molecules. This molecule is dosed Q4." Right? That's kind of what's driving our minimum of Q4 week dosing. We think that BAFF/APRIL is going to dominate that dosing paradigm, and we can deliver that in the administration schedule that Marino has mentioned. I'll leave it to you. Yeah, sure. Rami, thanks. Good question. This is going to be a very strong collaboration. We're going to have access to each other's data. We're going to be able to build on each other's data and look to, you know, use whatever data is generated from each company to build our case from a regulatory standpoint, also from a clinical development standpoint. It is going to be very much a real partnership through our joint steering committee. Yeah, and one more thing there is that for 103, we have a development partner in China. The team right now is very experienced in terms of how to work with a Chinese development partner. We already have the system set up to have a joint steering committee with our partners in 103. The collaboration has been absolutely amazing, as a matter of fact. I think it's going to drive a couple of our studies. We've actually expanded it beyond what our original agreement was because it's been such a good collaboration for us. We're excited to work with Chinese partners at this point. Yeah, he's referring obviously to Nanjing, our partner for Claseprubart. Our CIDP program is in China, and we fully expect our phase III MG program will also be involved in China. Yeah, it's been an incredibly positive experience for us so far. Our next question will come from Yaten Sunija with Guggenheim. Your line is open. Hi, this is Selma for Yaten. Thanks for taking our question. You have shown a deeper IgG suppression and greater PDC inhibition in preclinical work. Do you attribute that mainly to higher potency of the compound, or does it reflect some level of functional synergy between the two pathways? Thank you. Not sure about the second one. Could be. Could be that there's some synergy between the two pathways that's leading to deeper depletion in pDCs. Remember, the molecule itself is optimized for ADCC on pDCs. We're getting automatically more depletion than lilifilimab was designed to deliver. The piece around pDC depletion is very deliberate. That's the mechanics of the molecule. I would say that the overall type I interferon or reduction is about similar to lilifilimab. That's the one in class and best in class, therefore, that we have to compare ourselves to. The question of synergy, I think this is where it's just going to be really interesting. If we step beyond clinical data, company dynamics, all that, and advancing science in immunology, we're going to find out a lot as we go through healthy volunteers and patients where those areas of mechanistic synergy are. Of course, the way we've presented it to keep it clean is largely true, but also, it's not so clean, right? There's not just an innate immune system and an adaptive immune system. There are some overlaps. I think we're going to find a few mechanistic overlaps along the way. They may not be particularly strong, but we have to do the experiment in humans to find out what they are. Not in test tubes. Thank you. The next question will come from Colleen Cousey with Baird. Your line is open. Great. Good morning. Congrats on the deal and thanks for taking our questions. Leads Biolabs is not a company we're super familiar with. If you could maybe kind of walk us through what stood out to you about them and why you think they're going to be a great development partner going forward. Sure. This is Ryan speaking. Leads is a publicly traded company out of China who has expertise in drug development across oncology and autoimmune. They've had recent success out-licensing to other parties in the autoimmune space within bi- and trispecifics historically. We did an extensive search and evaluation effort to expand our pipeline over the last couple of years. We wanted to have an asset that had similar characteristics, as Marino alluded to, to really the value proposition of Claseprubart. We wanted to validate mechanisms of action, potential best-in-class characteristics, and pipeline their product potential across severe autoimmune diseases. Ultimately, our search led us to this unique and differentiated asset from Leads. Throughout our partnership with them, getting to today's announcement, they've been a great partner and collaborator, and we're really impressed with the science and their kind of history of developing unique and differentiated assets. Understood. That's helpful. Thank you. I know we'll get more information on the indication selection next year, but I'm hopeful that you've laid out some initial target areas. Will some of these be more driven by interferon versus BAFF/APRIL? How would you expect to prioritize which indications based on the mechanism? Good question. This is Marino. As I kind of alluded to earlier, we're going to do it the same way. We have done it already, but we're going to do some more confirmation work. The same way we did it for Claseprubart originally. We're going to take all the indications, and then we're going to rank them based on various factors, such as probability of success in the clinic, probability of success in the commercial sphere, and probability of success there. The regulatory and development pathway, how clear it is, and so on, to minimize risk and just increase probability of success. We'll take all those factors into account and then weigh each indication and then come up with that. That'll be part of what we'll communicate when we announce our list of indications. Gotcha. Thanks for taking our questions. The last question will come from Danielle Brill with Truist. Your line is now open. Hi, good morning. Thank you so much for the questions. I wanted to take a step back. I have a couple of bigger picture questions. First, I wanted to understand the rationale here a bit more. When did the asset come across your radar? Was there anything specific that you learned or in the data that made you feel like you needed to transact now ahead of the phase I data? Are there any other assets in development for autoimmune diseases that target both innate and adaptive immune signaling? Thank you. I'll just start with an opening comment, and then I'll ask Ryan to add a little more. The vision for the company has always been that we would be developing next-generation best-in-class therapies for severe autoimmune diseases and with a pipeline and a product potential. We've been very fortunate with Claseprubart and the amount of success we've had and all the ways that, you know, both our competitors and with our own data, we've been able to de-risk that asset. The time now was right with that success behind us, especially with the phase II MG data with Claseprubart, to continue to build out our pipeline beyond a single product. The team, I'm going to hand it to Ryan, but I can tell you it's been a long process. There's over, you know, I won't say how many, but triple-digit number of assets that have been looked at globally from a very extensive search and evaluation perspective and effort. This was the asset that we were most excited about, where we thought there was a real opportunity here to create a significant amount of value, not just for us, but for patients. Ryan, do you want to add anything? Yeah. On that front, we had very stringent kind of criteria of what we thought would demonstrate a best-in-class asset for us. Like I said, it had to have a very similar value proposition to Claseprubart in characteristics. Validated mechanisms of action, potential best-in-class characteristics, and pipeline that product potential across severe autoimmune diseases. We thought this program was very synergistic to where we are with Claseprubart today. To your question about other kind of competing molecules, we're not aware of any other BDCA2 BAFF/APRIL inhibitors currently in development at this time. I would be shocked if there aren't other innate and adaptive immune system molecules out there because it just absolutely makes sense. This is what the field's been waiting for for 10, 20 years, right? Within our company, we have a lot of experience in multiple functions with indications targeted by rheumatologists. What that means is we have very easy access to top KOLs in rheumatology, right? Speaking to them, this is exciting for them, right? This is what they wanted to see for a long time. Sometimes that question is generated in two different ways, right? One is, is there another competitor on the way? Two is, are you guys cowboys out there doing something no one else is doing? I don't know which way the question was posed. I'm just taking care of the second part, which is, no, this scientifically makes a tremendous amount of sense. It is going to be welcomed by the community of treaters. This is what they've been waiting to see somebody do. You can imagine the extensive diligence we went through. When you hear KOLs say, this is exactly what we need, it's just our ability to combine two therapies that target innate or adaptive immune system is just very expensive and difficult to prescribe. To put it together into one package for some of these patients from some of these diseases where both mechanisms may be implicated is very, very exciting to the KOL community. Thank you. That does conclude today's question and answer session. I would now like to turn the call back over to Marino for closing remarks. Thank you everybody for your interest and the really great questions. I can tell you I'm very, very excited. This has been quite an extensive effort over the last couple of years to continue to build out on our vision to become a leading autoimmune biotech company and to have an asset like this that we know from KOLs fills a significant unmet need out there and has all the similar key value drivers that our lead program, CLASSIPRIBART, has, which again, it's a proven mechanism of action, potential pipeline in a product, the convenience of subcutaneous self-administration and infrequent dosing. I think this is exactly the kind of asset that fits perfectly into the current organization. Thank you for your interest and look forward to updating you more in the future. This concludes today's conference call. Thank you for participating, and you may now disconnect.