Welcome to the Jade Biosciences ERA 2025 Conference Call. Please note that this call is being recorded and will be available for replay on jadebiosciences.com. At this time, all participants are in 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. Thank you, and good morning, everyone. It is a very exciting time for patients living with IgA nephropathy. We have seen groundbreaking data from multiple programs emerge over the last few days, which we believe will redefine the IgAN treatment landscape. We appreciate you joining us today as we review key takeaways from our preclinical data presentation during the 62nd Annual European Renal Association Congress, which highlights JADE1 01's best-in-disease potential and shares how this work informs our clinical strategy for JADE 101, our lead candidate for IgA nephropathy. Before we begin, I'd like to note that today's discussion will include forward-looking statements. These include statements about JADE 101's development plans, potential benefits for patients, and our cash runway. Because such statements deal with future events that are subject to the many risks and uncertainties, actual results may differ materially from those in the forward-looking statements. For a full discussion of these 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. At Jade, we are developing potentially best-in-class therapies for a variety of systemic and organ-specific autoimmune diseases. 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 antibody therapeutics, enabling the development of potentially efficacious therapies that require less frequent dosing. Our initial pipeline includes one program licensed from Paragon and two programs with an exclusive option to license from Paragon, all with the potential to be best-in-class medicines across a number of autoimmune diseases. Our lead candidate, JADE 101, is a selective anti-APRIL inhibitor that is rapidly moving towards the clinic and will initially be developed for patients with IgAN a serious chronic autoimmune kidney disease. JADE 101 is an ultra-potent, half-life-extended monoclonal antibody that has the potential for best-in-class efficacy with convenient patient dosing and is expected to be dosed subcutaneously, no more frequently than once every eight weeks or six injections a year. In addition to JADE 101, we recently nominated our second development candidate, JADE201, and have a third undisclosed antibody discovery program, JADE-003. Both JADE201 and 03 are currently in the preclinical development phase. These programs broaden our pipeline and position Jade to address unmet needs across multiple important autoimmune indications. We plan to initiate a phase one trial evaluating JADE 101 in the second half of 2025 and anticipate interim results in the first half of 2026. This biomarker-rich data set in healthy volunteers is meaningful for Jade, as it will define our dose and dose interval to position JADE 101 to rapidly move into later-stage patient trials. We recently completed a reverse merger with Aerovate Therapeutics, with a concurrent close of a significant private financing totaling approximately $300 million in gross proceeds to date. We are well-capitalized, with current funding expected to support operations through 2027. IgAN affects approximately 169,000 people in the U.S., several hundred thousand in Europe, and more than a million people in Asia. The disease is most commonly diagnosed in young adults who have relatively few comorbidities beyond their chronic kidney disease. Because IgAN often requires lifelong treatment to preserve kidney function and prevent progression to kidney failure requiring dialysis or transplant, there is an urgent need for therapeutics that are both effective and provide convenient dosing. IgAN represents a multi-billion dollar opportunity. The U.S. branded market alone is projected to exceed $10 billion, with significant additional potential in Europe and Asia. Despite this disease burden, the IgA nephropathy therapeutic landscape remains severely limited. No currently approved treatment is reliably disease-modifying, and most options rely on nonspecific immunosuppression or 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, producing large and sustained reductions in pathogenic Gd-IgA1 and reduce proteinuria, stabilizing kidney function without any unnecessary immune suppression. Groundbreaking data presented last week at the ERA Congress provided compelling evidence supporting the clinical benefit of selective anti-APRIL agents. A planned interim analysis of the visionary phase three trial of sibeprenlimab demonstrated highly statistically significant and clinically meaningful proteinuria reductions, numerically the largest proteinuria reductions reported in a pivotal IgA nephropathy trial to date. Long-term follow-up from a phase II study with zigakibart, another selective anti-APRIL inhibitor, in patients at high risk of progressive kidney function loss demonstrated that a majority of patients achieved new strict and low proteinuria target goals in the proposed treatment guideline updates and also achieved hematuria resolution. Remarkably, across this high-risk cohort, eGFR stabilization was observed through 100 weeks of treatment, confirming the disease-modifying impact of the APRIL mechanism of action. With selective APRILs being studied in larger patient populations and with extended treatment duration, they continue to demonstrate an encouraging and favorable safety profile. Selective anti-APRIL inhibitors have the potential to rapidly emerge as the foundational therapy for IgA nephropathy. While selective APRIL inhibition has shown disease-modifying clinical benefit, not all B-cell targeting approaches impact plasma cells, the pathogenic cell type in IgAN. Clinical trials of broad B-cell depletion with rituximab or selective BAFF inhibition with agents like zigakibart have shown no meaningful reductions in pathogenic IgA, no improvements in proteinuria, and are unable to stabilize kidney function. These approaches spare plasma cells, limiting their therapeutic effect in IgAN. While no head-to-head trials have been conducted, and keeping in mind the limitations of cross-trial comparisons, available phase two and now phase three data suggest that selective anti-APRIL monoclonal antibodies can at least match the efficacy of dual APRIL-BAFF-TACI-Fc fusion proteins. The 51% placebo-adjusted reduction in proteinuria reported with the selective anti-APRIL sibeprenlimab in a phase three study numerically exceeded the 42% placebo-adjusted proteinuria decrease observed with the TACI-Fc fusion protein, atacicept. The disease-modifying benefit reported with the selective anti-APRILs can be achieved in the absence of the broader B-cell depletion observed with the long-term BAFF inhibition. This could be an important consideration, favoring the use of selective anti-APRIL agents over dual APRIL-BAFF inhibitors for long-term use, potentially patients needing decades of treatment in the young and otherwise healthy IgA nephropathy population. Furthermore, the selective anti-APRILs are monoclonal antibodies that provide superior pharmacokinetic properties, which are conducive to be further enhanced through half-life-extending protein engineering strategies to achieve extended and convenient dosing intervals that are especially valuable for potentially lifelong therapy. These convenient, infrequent dosing profiles are likely out of reach for the TACI-Fc fusion proteins that are intrinsically rapidly cleared in humans, resulting in short half-lives that are not readily extended through half-life-extending strategies. Therefore, we believe that selective anti-APRILs combine the potential to provide the full disease-modifying benefit of the mechanism in the most targeted way to avoid unnecessary immunosuppression and provide the most convenient dosing schedule desired for chronic long-term treatment. Based on the clinical validation of the anti-APRIL mechanism and the need for disease-modifying therapies that target pathogenic IgA depletion, we believe that selective APRIL inhibitors are well-positioned to become foundational treatment in IgAN. The profile of JADE 101, which Andrew will further describe, has the potential to be best in class. Sibeprenlimab is the most advanced anti-APRIL monoclonal antibody, and we believe the interim results of the Visionary study make it the current benchmark for the anti-APRIL class. The sibeprenlimab data to date suggests there is still room to improve the profile of selective anti-APRIL therapies. The sibeprenlimab phase three study administered 400 mg subcutaneously every four weeks, a dose which is estimated to be roughly equivalent to the middle dose of the sibeprenlimab phase II study. Based on these results, which use intravenous body weight-adjusted dosing, the phase three sibeprenlimab dose is not predicted to fully suppress APRIL in all patients throughout the dosing period. The largest reductions in proteinuria and the highest rates of clinical remission have been associated with maximal suppression of APRIL, suggesting sibeprenlimab's subcutaneous dosing is not fully optimized and leaves some efficacy on the table. Furthermore, while the every four-week dosing interval for sibeprenlimab will provide the least frequent dosing potentially available in IgAN patients in the near term, it still requires 12 injections per year, providing further opportunity for a differentiated treatment that provides more convenient and less frequent dosing to minimize the burden of a lifelong disease. JADE 101 was designed as a best-in-class selective anti-APRIL inhibitor by addressing key limitations in potency, target coverage, and frequency of administration. It binds APRIL with femtomolar affinity, many orders of magnitude higher than sibeprenlimab, and was engineered with half-life extension designed to maintain full suppression of APRIL throughout an extended dosing interval. Our goal with JADE 101 is to completely inhibit APRIL throughout the dosing interval, which we believe will translate into superior clinical activity as measured by greater decreases in proteinuria and more patients getting to ambitious treatment goals, including less than 0.3 g of protein per day, which is considered clinical remission. We believe this level of efficacy may be achieved with a more convenient, less frequent dosing schedule of no more than every eight weeks or six subcutaneous injections per year, a potentially more convenient approach for patients who may need decades of treatment to manage their condition. As more patients face this difficult diagnosis and have a need to remain on long-term therapy, we believe the demand for safer, more effective, and more convenient durable treatments will only grow. The importance of innovative disease-modifying therapies in IgA nephropathy is further underscored by the proposed updates to the KDIGO treatment guidelines for the management of the disease. These updates are anticipated to be adopted in the fall of 2025. The draft guidelines recommend that kidney biopsies be performed in all adults with the presence of proteinuria of 0.5 g per day or higher when IgAN is suspected. We believe this change will increase the rate of diagnosis and allow for earlier intervention, which is critical given the progressive nature of the disease. The guidelines also redefine the criteria for treatment initiation and intensification, establishing that all patients with proteinuria greater than 0.5 g a day are considered at risk for progressive kidney function decline, whether or not they're currently receiving therapy. When proteinuria remains above this target, the guidelines recommend that additional treatments should be initiated. Importantly, proteinuria remains the only validated early biomarker for assessing disease activity and guiding clinical treatment decisions in IgA nephropathy. The updated KDIGO guidelines now recommend that treatment goals that maintain proteinuria below 0.5 g a day and preferably under 0.3 g a day, reinforcing the need for therapies capable of delivering deeper and more durable responses. As more treatments are approved for IgAN, the treatment goals are becoming more ambitious, highlighting the need for effective proteinuria-lowering therapies. Perhaps the most notable, the guidelines for the first time direct that management of IgAN should incorporate treatments that reduce pathogenic forms of IgA, the central driver of IgAN. This represents a shift in the therapeutic framework from nonspecific immunosuppression and supportive care to targeted disease-modifying approaches. The anti-APRIL class is well aligned with this direction. APRIL is a key survival factor for plasma cells and drives the production of pathogenic IgA. Therapies that selectively block APRIL have demonstrated significant and sustained reductions in IgA proteinuria, stabilization of kidney function in clinical trials, accompanied by favorable safety profiles. JADE 101 can potentially fill the treatment needs highlighted by the proposed updates to the KDIGO guidelines. JADE 101's profile demonstrates potential best-in-disease properties designed to capture the full efficacy available to the selective anti-APRIL class to maximize proteinuria lowering and get more patients to ambitious treatment goals. The extended half-life and PK profile provides the potential to minimize treatment burden with no more than one convenient subcutaneous injection every eight weeks or six injections per year, all while avoiding unnecessary immune suppression. I'll now pass it over to Andrew King, our Chief Scientific Officer and Head of R&D, to take us through the design of JADE 101, the preclinical data presented at ERA, and our initial clinical development plans. Thanks, Tom, and good morning, everyone. JADE 01 is a novel, fully human, neutralizing monoclonal IgG1 antibody with ultra-high binding affinity and novel CDRs supporting provisional composition of vanopatin filings. The antibody is built on an effector null IgG1 backbone such that it acts as a neutralizing antibody devoid of effector function and incorporates the clinically validated YTE Fc mutation to promote antibody recycling and half-life extension. This molecular design enables prolonged target engagement and systemic exposure, supporting dosing intervals of eight weeks or potentially longer. JADE 101 was also specifically engineered to reduce target-mediated drug disposition, or TMDD, and avoid high molecular weight immune complex formation. These are factors that have historically limited early anti-APRIL programs. By selectively inhibiting APRIL but not BAFF, JADE 101 is designed to target disease-driving plasma cells while preserving broader B-cell development, maturation, and function. I'm excited to provide an overview of our presentation at the European Renal Association 2025 Congress, where we shared for the first time a detailed preclinical characterization of JADE 101 that supports its potential to be a best-in-class anti-APRIL monoclonal antibody for the treatment of IgAN. Our findings demonstrate a differentiated profile for JADE 101, with several potentially significant advantages compared to sibeprenlimab. We consider sibeprenlimab to be the benchmark to beat, as it is the most potent anti-APRIL monoclonal antibody currently in clinical development, has the least frequent dosing schedule at every four weeks, and is the furthest advanced, with positive interim analysis from a phase three trial and a BLA accepted with priority review by FDA. JADE 101 is a novel, fully human monoclonal antibody selected from a de novo antibody discovery campaign with ultra-high APRIL binding affinity and engineered to extend pharmacokinetic half-life. JADE 101 binds to APRIL with affinity in the femtomolar range, approximately 50 femtomolar, which is around 750 times higher APRIL binding affinity than sibeprenlimab. This higher binding affinity has the potential to enable complete suppression of APRIL at low plasma concentrations of JADE 101 to deliver the full efficacy available to the anti-APRIL mechanism and further support an extended dosing interval. JADE 101 binds to a unique epitope on the trimeric APRIL protein, and we believe this novel epitope contributes to the differentiated properties of JADE 101 that I will describe. In competition ELISA assays, JADE 101 potently and completely blocks the binding of APRIL to its two receptors, BCMA and TACI, that are responsible for plasma cell survival and IgA secretion, respectively. As a result, JADE 101 is able to potently and fully block APRIL-mediated signaling through both BCMA and TACI measured in cellular reporter assays. In a translational model system, B-cells from healthy human donors were cultured under conditions to support plasma cell differentiation. Stimulation with APRIL resulted in significant plasma cell proliferation and IgA secretion, which could be completely blocked by JADE 101 at low concentrations. This effect to block APRIL-mediated plasma cell proliferation and IgA production is a key mechanism by which anti-APRIL therapies deliver potentially disease-modifying impact in IgAN patients by preventing the formation of pathogenic immune complexes. We have also observed a differentiated PK/PD profile for JADE 101 in non-human primates, which has historically been a highly translationally relevant model for both the PK of YTE half-life extended monoclonal antibodies as well as the biomarker-rich response to the anti-APRIL mAb. The PK/PD profile is characterized by an effectively extended half-life, deep and sustained IgA reductions, and successful mitigation of the impact of TMDD. TMDD has been a challenge for other anti-APRIL monoclonal antibodies, significantly limiting the dosing interval of those agents by requiring them to target high C trough values to avoid the loss of pharmacological activity that accompanies the rapid clearance associated with TMDD. Following a single 30 mg per kg IV dose in non-human primates, sibeprenlimab had a short linear clearance phase with a half-life of approximately seven days before demonstrating rapid non-linear clearance at concentrations below 40 micrograms per ml, which resulted in a loss of pharmacologic activity and corresponded to serum IgA reductions returning back toward baseline. Engineering YTE half-life extension on the IgG1 framework into sibeprenlimab incrementally extended linear half-life by approximately twofold but had no impact on the entry into the rapid non-linear clearance phase at the TMDD threshold around 40 micrograms per ml, resulting in only modestly extended IgA reduction. In contrast, a single 30 mg per kg IV dose of JADE 101 in non-human primates demonstrated an extended and slow linear clearance phase with a half-life of approximately 27 days, nearly fourfold longer than sibeprenlimab, and continued to linear clearance down to about 2 micrograms per ml, well below the sibeprenlimab TMDD threshold of 40 micrograms per ml. The long half-life of JADE 101, along with its ability to mitigate TMDD, resulted in deep and sustained reduction in IgA for greater than 100 days following a single 30 mg per kg dose in non-human primates before initiating IgA recovery towards baseline. Furthermore, a seven and a half-fold lower dose of JADE 101 at 4 mgs per kg outperformed the IgA reductions of both sibeprenlimab and YTE half-life extended sibeprenlimab dosed at 30 mg per kg. These non-human primate profiles provide us confidence that we can deliver our target product profile of deep APRIL and IgA suppression with a dosing interval of no more frequently than every eight weeks in IgA nephropathy patients. Subcutaneous administration of JADE 101 in non-human primates showed high bioavailability and reproduced the long, slow linear clearance phase and sustained IgA reductions observed following IV administration at saturating doses. Following a single 100 mg per kg subcutaneous dose in non-human primates, the apparent linear half-life exceeds 30 days. These data support our plan to initiate the JADE 101 first-in-human healthy volunteer study with subcutaneous dosing. JADE 101 was designed to avoid the formation of high molecular weight complexes that can be generated when monoclonal antibodies bind trimeric proteins like APRIL through a daisy-chain-like phenomenon. These high molecular weight complexes have the potential to be rapidly cleared, contributing to a TMDD effect. They can be immunogenic, triggering an anti-drug antibody response, and can also deposit in tissues, potentially producing tissue injury. JADE 101 was specifically selected with a novel binding epitope that does not induce large molecular weight complex formation and therefore mitigates the potential risk associated with these large complexes. It is likely that the combination of the higher binding affinity of JADE 101, saturating target binding at lower concentrations, and the avoidance of large molecular weight complex formation contribute to Jade 101's ability to significantly limit the impact of TMDD, and along with YTE half-life extension, deliver prolonged and predictable exposure that support extended dosing intervals. In summary, JADE 01 is a novel monoclonal antibody that binds a unique epitope on APRIL with ultra-high affinity, blocking APRIL from binding and signaling through its receptors BCMA and TACI to reduce human plasma cell proliferation and IgA secretion in vitro. JADE 101 exhibits an extended pharmacokinetic half-life, significantly attenuates the influence of TMDD observed with other anti-APRIL monoclonal antibodies, and mediates deep, sustained IgA reductions in non-human primates. The unique binding mechanism of JADE 101 does not induce large molecular weight complex formation and thereby avoids the risk associated with immune complexes. Overall, we believe the profile supports the potential of JADE 101 to be a best-in-class disease-modifying treatment for IgAN, with the goal of providing a convenient, infrequent dosing schedule to reduce patient burden. We are very encouraged by this promising preclinical profile of JADE 101 and are excited to advance JADE 101 into a phase one healthy volunteer study, which is on track to initiate in the second half of this year. This study will characterize the safety, tolerability, pharmacokinetics, and pharmacodynamics of single ascending doses of JADE 101 administered by subcutaneous injection. In addition to evaluating safety and the extended pharmacokinetic half-life of JADE 101, the biomarker-rich response to the anti-APRIL mAb is highly consistent in healthy volunteers and IgAN patients and is expected to be predictive of clinical efficacy. We anticipate disclosing interim PK/PD data from this study in the first half of 2026, which will enable us to select the dose and dose interval that is designed to provide complete and sustained APRIL suppression accompanied by deep reductions in IgA that we believe maximizes clinical responses in IgA nephropathy. The extremely informative nature of the JADE 101 first-in-human healthy volunteer data helps support an efficient and potentially accelerated development plan in IgA N. With that, I'll hand it back to Tom. Thanks, Andrew. IgAN represents a large commercial opportunity with a total addressable market of more than $10 billion in the U.S. alone. We believe that selective anti-APRIL therapies will become the most commonly used class of agents in IgAN, moving to front line and becoming foundational therapy because they have the potential to be disease-modifying, reduce pathogenic IgA, and stabilize kidney function while avoiding unneeded immune suppression. The properties of JADE 101 described in the ERA poster demonstrate it has the opportunity to become the best-in-disease IgAN therapy. The femtomolar potency, binding profile to attenuate TMDD, and YTE half-life extension provide the opportunity to completely inhibit APRIL throughout the dosing period, which we believe will translate into better clinical activity. As a result, it is our view that JADE 101 will have greater reductions in proteinuria, allowing more patients to achieve low proteinuria targets recommended in clinical guidelines, including clinical remission. This activity can potentially be achieved with best-in-class convenience with one injection, no more frequently than every eight weeks. We've built a high-caliber team of accomplished drug developers and company builders with deep expertise advancing programs from discovery through late-stage development, approval, and commercialization. With the completion of our recent reverse merger and the closing of a significant private financing totaling approximately $300 million in gross proceeds to date, we are well capitalized, with current funding expected to support operations through 2027. This includes funding JADE 101 through the healthy volunteer data readout in the first half of 2026, which, as Andrew mentioned, will guide dose and dose interval selection for patient trials. Because IgAN is a biomarker-rich indication, changes in IgA and APRIL observed in the healthy volunteers are expected to translate directly to patients, making this data set especially informative. We look forward to sharing more information on JADE201 later in the year, including disclosing the mechanism of action, lead indication, and initial clinical development plan. This program remains on track to enter the clinic in the first half of 2026. Our exclusive focus as Jade on autoimmune diseases enables us to build not only deep domain expertise but also strong partnerships with clinicians in the patients' communities we serve. We have had a very productive first year since Jade's founding in June 2024. We have accessed three high-quality autoimmune programs, built a highly talented clinical development team, and secured funding that we expect to last through 2027. We are extremely excited about our plans for the upcoming 12 months, including generating clinical data for JADE 101 and advancing 201 into the clinic, and for the potential impact our pipeline can have for patients living with autoimmune disease. With that, I'll hand it back to the operator to open it up for questions. Thank you. We will now begin the question-and-answer session. To ask a question, you must be dialed in by phone and press star one one on your telephone keypad. We ask that you please limit yourself to one question and one follow-up to allow time for everyone. Our first question comes from the line of Tyler Van Buren with TD Cowen. Your line is now open. Hey, guys. Good morning. Thanks for the presentation. The preclinical data are striking. It was a great weekend for you all at ERA. Forgive me, but I'm going to ask two questions. The first one is just, can you let us into the discovery process and tell us how this novel APRIL epitope was unveiled? Related to the second question, just given these data, what do you believe is the maximum IgA or proteinuria reduction that can be achieved in patients, and how might that translate to long-term improvements in eGFR relative to the incumbents? Thanks, Tyler. Yeah, really good questions. Maybe I'll start with addressing the second question and then hand it over to Andrew to elaborate more on connection with reductions of proteinuria and how we can expect that to impact long-term eGFR and kidney stabilization. He can also walk through a little bit about the discovery process around the epitopes. Yeah, as mentioned, we believe that JADE 101 with the profile described has the possibility to be the best-in-class selective anti-APRIL, which we believe is the best class for IgA nephropathy. In terms of expectations, it's really quite difficult to kind of pin down a precise number, but we were highly encouraged by sibeprenlimab's 51% placebo-adjusted reduction in proteinuria. They did that, as described, without optimized dosing. They presented in their ERA presentation that the 400 mg subQ is equivalent to around the 4 mg per kg IV they used in their phase II trial. We did see in that trial that they were not maximizing anti-APRIL reductions throughout the dosing interval, and we believe that we can achieve more suppression throughout the dosing interval to actually get greater reductions in proteinuria and more patients down into the clinical remission range. Mimicking more what they saw at their high dose, that 8 mg per kg. We have seen that these reductions in proteinuria—it's very well established that reductions in proteinuria and getting patients back into the normal range—are associated with long-term preservation of kidney function. We do anticipate that we can get more patients into that goal and do it with more convenient dosing. Andrew, do you want to elaborate on that and then also talk about the discovery process? Yeah, thanks for the question, Tyler. In terms of the discovery of JADE 101, it was from a de novo antibody discovery campaign executed by the exceptional antibody discovery experts and protein engineers at Paragon Therapeutics. The campaign involved immunization of humanized mice, and the team had identified two really important limitations of the currently available anti-APRIL monoclonal antibodies. One was relatively low affinity, and the other, as we highlighted, was TMDD beginning at relatively high concentrations, which really limited the pharmacodynamic runway and requires high and frequent dosing to be avoided. The team hypothesized that a potential reason for TMDD at these high thresholds was the production of high molecular weight immune complexes that has been reported with trimeric proteins. APRIL, as a trimeric protein, has three separate binding sites for an antibody, which can potentially result in the formation of large immune complexes. With this recognition and hypothesis, the team incorporated a screening paradigm that not only selected antibodies for ultra-high binding affinity but also screened for in vitro antibodies that avoided large immune complexes through that daisy chain phenomenon. As you saw today, the result of that campaign is an exceptional antibody with ultra-high binding affinity in the femtomolar range and effective mitigation of TMDD as a result of avoiding large immune complex formation based on the unique epitope which JADE 101 bound to. Thank you. Our next question comes from the line of Laura Chico with Wedbush. Your line is now open. Good morning. Thank you very much for taking the question. Just one for me. I know most of the focus this weekend has been on the sibeprenlimab data. Tom, you mentioned this, but wondering if you could expand a little further on the implications of the zigakibart eGFR data, more specifically on the JADE 101 programs. The follow-up would be on the phase one data that we're anticipating in the first half of 2026. What would you need to see to explore longer dosing intervals beyond the Q8 week estimate? Thank you. Thanks, Laura. I really appreciate the question. Maybe I'll take the zigakibart implications and then pass it over to Andrew for what we expect to see or what we'd like to see in the phase one trial. Yeah, we thought the zigakibart data was extraordinarily meaningful for the selective anti-APRIL class. It showed eGFR stabilization out to 100 weeks. This is now the longest interval or the longest period of time studied by any of these agents. We had previously seen 96-week data from the dual APRIL BAFF inhibitor, atacicept, which did show promising stability. There were questions about what is the role of BAFF in terms of increasing that kidney function stability over time. But seeing zigakibart really establish that stabilization of kidney function over that two-year time period really gives us confidence that it is APRIL that is driving efficacy within IgA. We know that that is what's inhibiting plasma cells and decreasing Gd-IgA. And so seeing that data really gave us renewed confidence that we can achieve high levels of clinical activity and stabilize eGFR function without the unnecessary immunosuppression across broader B cells with BAFF. Very impactful, and we believe this really just helps establish the dominance of the selective anti-APRILs for the treatment of IgA. Andrew, would you like to talk about what we expect to see in the phase one data and how that impacts our choice of dose interval? Yeah, thanks, Tom, and thanks, Laura. As Tom mentioned earlier, what we learned from the sibeprenlimab phase two study was the best clinical response to the anti-APRIL mAb, that's quantitatively the largest reductions in proteinuria, as well as the highest rates of clinical remission, were associated with complete APRIL suppression. Our goal is to define a dose and dose interval of JADE 101 that can completely suppress APRIL throughout that dosing interval. That will be accompanied by large and significant sustained reductions in IgA. We do believe focusing on the APRIL biomarker itself is the most critical in terms of defining that dose and dose schedule to ensure we not only deliver a convenient therapy for IgAN patients, but the maximum efficacy available to the mAb. Also, what we've seen by exploring the publicly available data on anti-APRIL monoclonal antibodies historically is that the PK, free APRIL suppression, and IgA reductions observed in healthy volunteers is highly predictive of and consistent with what we'll ultimately see in IgAN patients. Therefore, we have strong conviction we can use this healthy volunteer data and, in particular, the dose and duration by which APRIL is completely suppressed to be able to define the dose and dose schedule to move forward with into later-stage clinical development. That sets up for a potentially very efficient and potentially accelerated development program. It is really the dose and dose interval that suppresses APRIL fully before it begins to rebound. We'll define that dose moving forward. Thanks very much, guys. Thank you. Our next question comes from the line of Alex Thompson with Stifel. Your line is now open. Hey, great. Thanks for taking our question. I guess maybe as a follow-up, if you could talk a little bit about specifically kind of what the half-life benchmarks would be to support potentially dosing much less frequently than every eight weeks in humans. Also, to expand on this question around IgA and APRIL suppression, clarifying an accelerated path forward in IgAN. Could you expand on that a little bit? Are we talking about potentially an adaptive phase two, three that might eventually be a pivotal trial? How are you thinking about accelerating IgAN development? Thanks. Thanks, Alex. Great question. Andrew, actually, you've been looking into both of these questions in quite a bit of detail. Do you want to take the lead on it? Sure. Happy to, Tom. In terms of our future clinical development, we haven't provided any guidance on that so far as we haven't interacted with regulatory authorities, including the FDA, although we're planning that strategy at this time. We can see historically in IgAN, there have been accelerated development programs looking at the Alpine, Vertex development program, a very small lean open-label phase two before initiating a registration phase three. There remains a number of options on the table that we need to discuss and get alignment with regulators. We do think being able to define the dose and dose schedule for a mechanism that's disease-modifying, has shown large treatment effects, and overall has a safe and well-tolerated safety profile really does provide some flexibility. We will be looking for partnering with health authorities to define what that clinical development plan is once we have the phase one healthy volunteer data in hand. In terms of the translation of non-human primate YTE half-life extended antibodies into humans, the typical translation is a two- to four-fold increase in half-life from non-human primates to humans, with on average a three-fold increase in half-life. If we look at the lower range of that translation, approximately two-fold, it puts us in the 50-60 day human half-life range, which we think comfortably allows us to be able to deliver a Q8 week dosing schedule based on the high affinity of JADE 101 and the mitigation of TMDD, potentially allowing pharmacological activity at lower C trough exposures than the other anti-APRIL monoclonal antibodies. That is the rationale behind our confidence in guiding on delivering at least a Q8 week dosing schedule in humans. There is potential upside for that if the translation is more favorable on the higher end to extend dosing intervals beyond that. As we mentioned, the great part about this MLA is we will see that soon in the healthy volunteer data by being able to track the depth and duration of APRIL inhibition. We look forward to disclosing those data in the first half of 2026. Thank you. That concludes the question and answer period. I will now turn it back to CEO Tom Frohlich. Thank you, Operator. On behalf of the entire 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. This concludes today's conference call. All parties may now disconnect.