Good morning and welcome to Jade Biosciences' JADE201 Conference Call and Webcast. Please note that this call is being recorded and will be available for replay on jadebiosciences.com. At this time, all participants are on a listen-only mode. Following the formal remarks, we will open the call for questions. Now, I'd like to turn it over to Tom Frohlich, Chief Executive Officer of Jade Biosciences. Please go ahead, sir. Thank you and good morning, everyone. We're excited to share the progress Jade Biosciences is making as we work toward building a pipeline of novel therapies that we believe can meaningfully change the standard of care in autoimmune disease. Earlier today, we announced private financing for gross proceeds of approximately $135 million. This investment strengthens our balance sheet and provides the capital we need to advance our pipeline meaningfully through the next stages of development. On today's call, we'll focus on our second development candidate, JADE201, a half-life-extended afucosylated monoclonal antibody targeting the B-cell activating factor receptor, or BAFF-R. We'll walk you through the opportunity, its best-in-class potential, and how our preclinical work informs our development strategy for the candidate. Moving to slide two. Before we begin, I'd like to note that today's discussion will include forward-looking statements. These include statements about Jade's development plans, product candidates, and our cash runway. Because such statements deal with future events and are subject to many risks and uncertainties, actual results may differ materially from those in the forward-looking statements. For a full discussion of those risks and uncertainties, please review our filings with the U.S. Securities and Exchange Commission. Please also refer to our corporate website, jadebiosciences.com, for additional information and disclaimers. I'm joined today by Dr. Andrew King, Jade's Chief Scientific Officer and Head of R&D. We also have our Chief Financial Officer, Brad Toms, available for Q&A. Onto slide three. At Jade, we are developing potentially best-in-class therapies for numerous systemic and organ-specific autoimmune diseases. As a reminder, Jade is the fourth company founded on assets licensed from Paragon Therapeutics, a leader in antibody discovery and protein engineering. Paragon has a strong track record of discovering and optimizing highly potent and half-life-extended monoclonal antibody therapeutics, enabling the development of potentially efficacious therapies that require less frequent dosing. Our initial pipeline includes two programs licensed from Paragon and one additional program with an exclusive option to license from Paragon, all with the potential to be best-in-class medicines across multiple autoimmune diseases. Our lead candidate, JADE101, is a selective APRIL inhibitor that is currently in phase I and will initially be developed for the treatment of IgA nephropathy, a chronic autoimmune disease that leads to end-stage kidney disease for most patients. JADE101 is an ultra-high affinity half-life-extended monoclonal antibody that has the potential for best-in-class efficacy with convenient patient dosing and is expected to be administered subcutaneously, no more frequently than once every eight weeks. IgAN affects approximately 169,000 patients in the U.S., several hundred thousand in Europe, and more than one million in Asia. It is a large unmet need and represents a multi-billion dollar opportunity. The U.S. branded market alone is expected to surpass $10 billion, with significant additional potential in Europe and Asia. Despite this disease burden, the IgAN therapeutic landscape remains severely limited. No currently approved treatment is reliably disease-modifying, and most options rely on nonspecific immunosuppression for supportive care. We believe selective anti-APRIL therapies will become the foundational treatment in IgAN, moving to frontline therapy because they have the potential to be disease-modifying. They produce large and sustained reductions in pathogenic IgA and proteinuria and stabilize kidney function without unnecessary immune suppression. JADE101 has the potential to be best in disease therapy for IgAN as it addresses key limitations in potency, target coverage, and frequency of administration. We believe that full APRIL suppression throughout the dosing interval will maximize the clinical benefit available to this mechanism of action, and none of the existing anti-APRIL or dual-APRIL BAFF inhibitors have demonstrated full APRIL suppression throughout their respective dosing intervals as the dose is taken forward for late-stage development. In September, we announced that we had dosed the first cohort of participants in our first-in-human healthy volunteer study of JADE101 and remain on track to read out interim biomarker-rich data in the first half of 2026. We are confident that these data will give us the information required to decide on our dose and dose interval to move forward into later-stage clinical trials. Our goal is to differentiate by demonstrating full APRIL suppression throughout at least an eight-week dosing interval, which we believe would enable JADE101 to demonstrate best-in-class clinical activity and convenience for IgAN patients. These characteristics are especially important for IgAN patients who are often diagnosed young and have few comorbidities outside of their asymptomatic kidney disease. In addition to JADE101, our second development candidate is JADE201 and the primary focus of today's call. We also have a third undisclosed antibody discovery program, JADE-003. Both JADE201 and JADE-003 are anticipated to enter first-in-human studies in the first half of 2026 and the first half of 2027, respectively. These programs broaden our pipeline and position Jade to address unmet needs across numerous autoimmune indications. Jade's pipeline is supported by a strong financial foundation. As mentioned this morning, we announced a private placement of approximately $135 million in gross proceeds. We are grateful for the support of such a strong syndicate of new and existing healthcare-focused investors. These proceeds are expected to fund operations into the first half of 2028. Specifically, we expect the proceeds will support the clinical development of JADE101, which is now being evaluated in a phase I healthy volunteer study. The proceeds are also expected to enable progression into late-stage IgAN patient trials and to support exploration of JADE101 in additional autoimmune indications, such as those mediated by IgM. In addition, the funds will support research and development activities for JADE201 in multiple autoimmune diseases and JADE-003, along with general corporate expenses and working capital. Let me now turn to JADE201. JADE201 is a half-life-extended afucosylated monoclonal antibody that targets the B-cell activating factor receptor. It is engineered with a dual mechanism of action: first, by enhancing effector functions to directly kill B-cells through antibody-dependent mechanisms, and second, by blocking BAFF signaling to remove critical activation and survival pathways for B-cells. Importantly, JADE201 incorporates half-life extension technology, which has the potential to significantly prolong its duration of action while fully maintaining pharmacological potency. We believe this profile positions JADE201 to deliver deeper and more durable B-cell depletion than existing approaches, while also enabling less frequent subcutaneous dosing. That combination of dual mechanisms, half-life extension, and dosing convenience could represent a major advance, one that not only improves efficacy but also reduces the treatment burden and improves quality of life and compliance for patients. We plan to initiate a first-in-human study evaluating JADE201 in patients with rheumatoid arthritis in the first half of 2026. Given its mechanism, we believe JADE201 has broad potential across a number of autoimmune diseases, representing a total addressable market of more than $80 billion. We are encouraged by the recent success of Novartis' ianalumab, another afucosylated anti-BAFF-R. That program has now delivered positive results, meeting its primary endpoint in phase III trials of Sjögren's syndrome and immune thrombocytopenia, and is currently being evaluated in multiple additional registrational studies across autoimmune diseases like SLE and lupus nephritis, which validates BAFF-R as a next-generation B-cell target. With that, I'll hand it over to Andrew to take you through JADE201 's mechanism of action and the preclinical data that supports its best-in-class potential. Thank you, Tom, and good morning, everyone. We're on slide five now. I'm excited to walk you through the science behind JADE201, a half-life-extended afucosylated anti-BAFF-R monoclonal antibody and its potential across multiple autoimmune diseases. B-cell depletion is a validated approach to autoimmune disease, but first-generation therapies have important limitations. They often achieve incomplete depletion, sparing pathogenic autoreactive B-cells in circulation and in lymphoid and target organ tissues, and risk resistance and relapse as a result of elevated BAFF signaling that drives B-cell repopulation and autoreactivity. Ianalumab, an afucosylated anti-BAFF-R monoclonal antibody, has demonstrated clinical proof of concept of addressing these challenges with promising activity across multiple autoimmune indications, including multiple phase III studies. JADE201 builds on this clinical proof of concept for BAFF-R targeting, adding half-life extension technology to provide extended receptor occupancy, with the goal of delivering deeper, more durable B-cell depletion with less frequent subcutaneous dosing. This is particularly relevant in systemic autoimmune diseases, where tissue B-cells are key drivers of autoimmunity and tissue injury. What excites us about JADE201 is that, like ianalumab, it uses a dual mechanism of action with the goal of more effectively targeting the pathogenic tissue B-cell populations and directly blocking the BAFF-R upregulation that occurs as a compensatory response to B-cell depletion, a process that contributes to the persistence of autoreactivity. With that context, I will describe JADE201 's mechanism of action and the preclinical data supporting its potential to be a best-in-class therapy. On slide six, JADE201 is designed to work through a dual mechanism of action that directly addresses the key limitations of earlier B-cell depletion strategies. First, it enhances cytotoxicity through glycoengineering. Afucosylation increases affinity for Fc receptors, driving stronger antibody-dependent cellular cytotoxicity, or ADCC activity, which is expected to enable potent, deep, and sustained depletion of BAFF-R-expressing B-cells. Second, it pharmacologically blocks BAFF signaling through the BAFF receptor, cutting off the compensatory response to upregulation of BAFF that typically follows B-cell depletion. This additional mechanism is anticipated to be impactful where ADCC cannot be effectively engaged due to low receptor expression or in settings with sparse availability of effector cells, including NK cells. Blockade of BAFF will act to reduce B-cell activation, proliferation, and inflammatory responses, and can ultimately drive B-cell death through starvation from this important pro-survival signal. We believe this dual mechanism may enable JADE201 to be particularly well-suited for targeting tissue-resident B-cells in lymphoid tissues and ectopic germinal centers, where autoreactivity is established and drives disease. We've seen clinical validation of this dual mechanism in Novartis' ianalumab program, including salivary gland biopsy data in Sjögren's disease showing profound tissue B-cell depletion. Moving to slide seven, the goal with the design of JADE201 was to possess the desirable properties of ianalumab, such as its high BAFF-R receptor affinity and enhanced ADCC activity, to deplete BAFF-R-expressing B-cell subpopulations. However, ianalumab has a relatively short human half-life, so we designed JADE201 to incorporate half-life extension to mitigate this limitation. These attributes we believe will provide for extended receptor occupancy, with the goal of delivering deeper, more durable B-cell depletion with less frequent subcutaneous dosing. JADE201 contains novel CDRs supporting composition of matter patent filings and incorporates glycoengineering to generate an afucosylated monoclonal antibody with high affinity to Fc receptors, enabling enhanced ADCC-mediated B-cell depletion. It also contains the LS modification in the Fc to increased affinity to FcRn, promoting antibody recycling and an extended pharmacokinetic exposure. Combined, these features suggest the potential for JADE201 to represent a best-in-class anti-BAFF-R therapy. As you can see on slide eight, based on our preclinical work, JADE201 successfully retained the desirable attributes of ianalumab, including its high affinity BAFF receptor binding and blockade, with EC50 values in line with ianalumab across multiple assays, confirming that the addition of half-life extension did not compromise target engagement or potency. JADE201 also maintained full effector function-mediated B-cell depletion. We observed robust ADCC in both primary human B-cells and the Raji B-cell line. Importantly, binding to Fc receptors and C1q was preserved, ensuring effector function was retained despite the LS Fc modification. Taken together, these data validate JADE201 as a high affinity anti-BAFF-R monoclonal antibody with enhanced ADCC activity that preserves ianalumab's proven biology while successfully incorporating half-life extension into the antibody design. We believe this results in an optimized next-generation molecule designed to maintain potency and activity while improving durability and patient convenience. On slide nine now, we are encouraged by early pharmacokinetic and pharmacodynamic results from non-human primates demonstrating preclinical proof of concept. In the left panel, pharmacokinetics were roughly dose proportional across a wide range of doses from 0.001 to 10 milligrams per kilogram intravenously. In the middle panel, measures of BAFF--R receptor occupancy were assessed, showing dose-dependent BAFF-R occupancy both in terms of magnitude and duration of receptor coverages. Doses of one milligram per kilogram and higher approach complete BAFF-R occupancy, and most importantly, on the right, the single subcutaneous dose of JADE201 achieved dose-dependent, deep, and sustained B-cell depletion. The apparently accelerated recovery at 10 milligrams per kilogram versus one milligram per kilogram is potentially related to NHP ADAs or a hook effect that can be observed with higher saturating doses of B-cell depleters. We are currently measuring ADAs to distinguish these possibilities. Deep B-cell depletion appears to require very high levels of BAFF receptor occupancy, suggesting the half-life extension incorporated into JADE201 has the potential to provide deeper and more durable B-cell depletion through extended BAFF-R coverage. On slide 10, we also saw differentiated pharmacokinetics. In head-to-head non-human primate studies, JADE201 demonstrated an approximately twofold increase in half-life relative to ianalumab. Ianalumab has a relatively short half-life in humans of approximately 10 days, and therefore the twofold half-life increase in JADE201 extends the duration of BAFF-R coverage with less frequent dosing. Moving to slide 11, we're highly encouraged by the promising preclinical profile of JADE201 and look forward to moving it into the clinic in the first half of 2026. Because JADE201 delivers enhanced B-cell depletion, it isn't appropriate to begin in healthy volunteers. Instead, we identified an autoimmune patient population where the benefit-risk is justified and feasibility and efficiency of enrollment is higher. Similar to Novartis' approach with ianalumab, we will conduct a first-in-human for JADE201 in patients with rheumatoid arthritis. We view this as a way to efficiently generate a meaningful data set for this first-in-human study, but it does not necessarily reflect indication prioritization for future development. The trial will be a randomized placebo-controlled single-ascending dose design. This study aims to establish safety, tolerability, and pharmacokinetics while also being biomarker-rich. We will measure BAFF-R occupancy, soluble BAFF levels, and immunophenotype B-cell subpopulations by flow cytometry to assess the depth and duration of depletion. Because RA patients respond rapidly to B-cell depletion, we will also incorporate exploratory efficacy measures such as DAS-28, which may provide additional insight into Jade's therapeutic profile even at this early stage. With that, I'll now hand the call back to Tom. Thanks, Andrew. Turning to slide 12. As you've heard today, JADE201 is designed to build directly on the clinical validation of ianalumab, but with meaningful enhancements, namely half-life extension technology that is designed to support deeper and more durable B-cell depletion with less frequent dosing. We believe this profile positions JADE201 with best-in-class potential across multiple autoimmune diseases, representing a total addressable market of more than $80 billion. It's important to note how JADE201 compares to existing B-cell depleting therapies like rituximab. While rituximab has demonstrated clinical benefit in many autoimmune diseases, it comes with limitations, namely slow, inconvenient IV infusions and incomplete tissue B-cell depletion that may lead to relapse. By contrast, JADE201 is designed to achieve deeper levels of B-cell depletion, reaching resident tissue B-cells where rituximab often fails, and to do so with the convenience of a subcutaneous injection. As shown on the slide, there are many indications across multiple therapeutic areas where B-cell dependence is well validated and rituximab has shortcomings. We will focus on executing our first-in-human study in patients with RA, and as data continues to emerge from our study and from ianalumab, we will prioritize indications where we believe we can demonstrate the most significant patient benefit, including potential first-in-class and potential best-in-class indications. Taken together with JADE101, these programs give us the opportunity to shape the next generation of treatments for autoimmune disease. On slide 13, with commitments for approximately $135 million in new financing, Jade is well capitalized, with funding expected to support operations into the first half of 2028. These proceeds will enable our plan to advance JADE101 through the phase I data readout and into patient trials, progress JADE201 into the clinic in the first half of 2026, and continue executing on our pipeline. Just as importantly, we continue to build a team of highly experienced drug developers and company builders with deep expertise spanning discovery, clinical development, regulatory strategy, and commercial execution. This combination of innovative science, strong financial backing, and seasoned talent gives us the foundation to move quickly and decisively. We are very excited about the year ahead, particularly the clinical data we expect for JADE101 and the transition of JADE201 into human trials. Above all, we are motivated by the potential impact our therapies may have for patients living with autoimmune disease. With that, I'll hand the call back to the operator to open the line for questions. Thank you. We will now begin the question and answer session. To ask a question, you must dial in by phone and press star 11 on your telephone keypad and wait for your name to be announced. To withdraw your question, simply press star 11 again. Please stand by while we compile the Q&A roster. Our first question coming from the line of Alex Thompson with Stifel. Hey, great. Thanks for taking our questions. And a couple here. I guess the first one on the PK/PD disconnect with the B-cell depletion, as evidenced also by the ianalumab dosing in the clinic and their short half-life, how are you thinking about the translation of your non-human primate PK to humans? What kind of dose do you think we could achieve? And then on the phase I proof of concept study, do you have plans to disclose any early cohorts, or do you expect to go through the whole six cohorts before disclosing any data? Thanks. Yeah, great question, Alex. And thanks for joining and asking the questions on the call. Maybe for the first question on the PK and NHP translation, maybe I'll ask Andrew to take that, and then we'll move on to the phase I timing and readout. Yeah, thanks for the question, Alex. Novartis is evaluating two different dosing schedules as part of their phase III program with ianalumab. Firstly, Q monthly dosing, which we think, based on our modeling simulation, roughly covers BAFF-R receptor occupancy throughout that dosing interval, and also Q 12-week dosing interval, which doesn't provide that sustained coverage of BAFF-R occupancy and is really more reliant on the sustained B-cell depletion and the delayed recovery you get with B-cell depleters in humans, similar to the six-monthly dosing schedule of rituximab, for example. So as they read out their phase III clinical data, that will be particularly important for us to guide the target with this dual mechanism of action. We believe that sustained BAFF-R receptor occupancy does add significant mechanistic value in the ability to block that compensatory upregulation to BAFF that occurs following B-cell depletion. And with a twofold longer non-human primate half-life, we believe we'll be able to at least double the interval for full receptor coverage relative to the first-generation molecule. Great, great. Thanks. And maybe I'll just take the second question, and Andrew can add on if I've missed anything. In terms of the six cohorts and how we plan to read those out, it's a little bit early for us to guide exactly on what and when we're going to read out the timing of that data or publicly disclose it. We're currently just in CRO startup phase, and we're finalizing country selection and looking at study startup times. And as we get more granularity on those parameters, then we will look to update our guidance on the disclosure of the timing at some point next year. Just to note, though, this is a biologically active molecule with B-cell depletion. So we do have to start at quite low doses, well below MABEL. So we do want to make sure that we are generating data that really is quite representative of the characteristics of the medication before we disclose. So we do want to ensure that we have a high-quality data set to release before we make any public disclosures around it. The good news, as Andrew pointed out, is that we are going into RA patients partly for the clinical feasibility of the recruitment, but also partly because we do believe that we will be able to get a good measure of B-cell counts and look at the phenotyping of those B-cells to really characterize the compound appropriately and then as well look at some glimmers of efficacy as measured by DAS-28 in RA. So it will be quite an interesting readout for the compound. And similarly, we are encouraged by RA, but as Andrew pointed out, it likely won't rise to the highest priority indication for further development into phase II initially as one of our lead indications. There are several other indications that will probably rise to a higher priority as we move the program forward. But yeah, thanks for the questions, Alex. Thanks so much. Thank you. Our next question coming from the line of Laura Chico with Wedbush. Your line is now open. Good morning. Thanks very much for taking the question. I have two. And Tom, just kind of carrying on from your remarks on the RA, what are the most important markers we should be looking at in terms of the phase I data? Is it a DAS-28 score? And I guess I'm just trying to triangulate on what you need to see in terms of a target product profile. In the IgM populations, obviously, we have the benefit of seeing IgA and APOL reductions translate very well. I guess what would be most impactful in this initial cohort? And then I have a follow-up. Yeah, great question, Laura. And it is a typical phase 1 study, so we will be looking at safety and PK first and foremost. But we do have that really privileged situation where we will be able to look at some signs of clinical activity. Andrew, do you want to get into a little bit more detail about exactly what we're going to be looking for there? Yeah. The primary endpoints, as Tom mentioned, would be around safety and tolerability. Secondary endpoints, including pharmacokinetics, will be more focused on the pharmacodynamics rather than the clinical efficacy. The pharmacodynamics include measures of BAFF receptor occupancy, BAFF ligand, and importantly, the depth and duration of B-cell depletion, including subpopulations of B-cells through immunophenotyping. We are in a very privileged position to look at exploratory measures of efficacy. However, the sample size is relatively small. There's five active, one placebo per cohort. And as Tom already mentioned, we need to start low in the dose level and titrate up cautiously because of the enhanced B-cell effector function. So the first several cohorts will be sub-therapeutic. That will be very helpful in developing PK/PD models at the population level, but won't be fully efficacious. So it will be a relatively small number of RA patients at the top couple of doses that will achieve the full therapeutic dose. So it's really an exploratory endpoint and opportunistic. And we don't really want to anchor specifically around that because of the small sample size. But you do see with rituximab rapid responses on DAS-28 within a 12-week time period where you see about a 30% reduction in DAS-28 from a baseline of six to four in the rituximab trials. So we do think it's opportunistic to be able to look at those exploratory efficacy endpoints. However, I don't really want to anchor around them as not the primary objective of the study. Understood. That makes sense, Andrew. And then maybe just one quick follow-up. Could you talk a little bit more about that ADA profile in the non-human primates at this point and just thoughts on implications for human subjects? Is this just more of an artifact of an antibody in an NHP model? Thank you. Yeah, exactly, Laura. JADE201 is a fully human monoclonal antibody, potentially immunogenic to a non-human primate's immune system. Not infrequent to see ADAs in non-human primate studies. So we are in the process of validating for ADAs across the study, really to support the appropriate PK/PD interpretation of that data set, but with no risk of translatability from ADAs in non-human primates to humans. Thanks very much. Thank you. Our next question coming from the line of Tyler Van Buren with TD Cowen, Yolandis Melvin. Hello, this is Sam Rollenhagen on for Tyler Van Buren. Congrats on the announcement and officially expanding the Jade pipeline beyond APRIL and IgM. So just thinking ahead, we know about the dual-targeting APRIL BAFF antibodies, and Jade is clearly taking a different approach. But is there potentially an opportunity to combine both JADE101 and JADE201 in the future? And if so, in what indications may a dual APRIL BAFF approach be ideal over just a BAFF only or an APRIL only approach? Thank you. Thanks for the question, Sam. Yeah, we do think that there's quite an advantage over the dual APRIL BAFF. As you're aware, Sam, the TACI receptor programs are the receptor fused onto an Fc fragment, and the BAFF segment really is targeting the ligand. So you do not get that dual mechanism of action that we are getting with JADE201 with that afucosylated Fc region, which is enhancing the effector function. So we do believe that JADE201 will lead to really better B-cell depletion as well as the BAFF starvation and do that in a very robust way. So we do believe there's large advantages of targeting the BAFF-R versus what the TACI receptors are doing. Great question on potential combination of JADE101 and JADE201. We don't have anything in the plans yet, but we are keeping a very close eye on things because we don't see anywhere really where those TACI receptors are showing signs of clinical activity. We do think that there could be an opportunity for a best-in-class selective anti-APRIL like JADE101 that does have that full suppression of APRIL throughout the dosing interval and will have the longest dosing interval of any of those agents. Combined with BAFF-R, which has those characteristics that we just described, JADE201 could potentially be kind of a best of both of those targeting agents. If you combine those, they could have activity across a number of different disease areas. We're seeing some data emerge in Sjögren's with telitacicept. We know there's some data in MG. We do know that povetacicept is quite active in areas like pMN as well. So we do think possibly, as we go forward, we could think about a combination strategy between the two agents. But that said, we need to get through the monotherapy trials first and really characterize the programs and get them on their way in their lead indications. And then we can start thinking about a combination strategy later down the road. Got it. Very helpful. Thank you. Thank you. And as a reminder to ask a question, please press star 11. Next question in queue coming from the line of Vamil Divan with Guggenheim, Yolandis Melvin. Great. Thanks for taking the call and thanks for taking the question and hosting the call, and congrats on the progress here, so maybe just one more from me. Appreciate all the comments so far, but just as you think about, there's so much activity in the immunology space, so can you talk maybe how you see the positioning of BAFF-R relative to some of the other approaches like CD19, CD20, even CAR-T, obviously moving into some of these indications? How do you see those mechanisms playing in relative to what you're doing here? Thank you. Yeah, great question, Vamil. And thanks for asking because we do appreciate there are a lot of agents and a lot of players in the autoimmune space. That said, we do think it is an extraordinarily large unmet need, and there are opportunities for multiple winners across all of these indications. And then the other thing we also know is each autoimmune indication has its own specific biology. It has its own benefit-risk tolerance as well in terms of the severity of the disease. So we do think there's room for many, many different agents across these indications, just both from a market size, but also tailoring specific autoimmune therapies. But that said, we do think BAFF-R has some very specific advantages, some of the advantages that Andrew described, but specifically against the CD19s and the CAR-Ts. Andrew, do you want to talk a little bit about the differentiation of our mechanism versus CD19s and CAR-Ts? Yeah. The dual mechanism of action is particularly important, not just the B-cell depletion, but the ability to block that upregulation of BAFF that plays an important role in B-cell repopulation and really acts to maintain autoreactivity with the potential to drive resistance and relapse, particularly coming off drug. So that's one important distinction relative to the other strategies. Secondly, recent data from Novartis from Sjögren's disease patients with six months of treatment using repeat biopsies of the salivary gland demonstrated an 84% reduction in B-cell populations within the salivary gland of Sjögren's patients. So really getting at the source of pathogenic autoreactive B-cells that drive tissue injury, which has been challenging for other B-cell depleting strategies to be effective at because of the sparse presence of effector cells to engage ADCC. So the dual mechanism of action appears to be important there. And one final differentiation for the BAFF strategy is it avoids taking out early-stage B-cells, the pre and the pro B-cells within the bone marrow. They don't express BAFF-R. These are antigen-naive. They're non-autoreactive. They're non-pathogenic B-cells. So it really spares that immature non-pathogenic cell type, which is another distinction from some of these other strategies that have been highlighted. Okay, thank you. Thank you. And that concludes the question and answer period. I'll now turn it back to CEO Tom Frohlich. Great. Thank you, Operator. On behalf of the Jade Biosciences team, thank you for joining us today. A replay of this webcast will be available on our website. If you have any further questions, please feel free to reach out to our investor relations team at ir@jadebiosciences.com. Thank you. This concludes today's conference call. Thank you for participating.