Good morning, welcome to the Climb Bio investors event focused on budoprutug and the CD19 opportunity. At this time, all participants are in a listen-only mode. A question and answer session will follow the prepared remarks. Please note this call is being recorded. I will now turn the conference over to Dr. Carlo Tanzi of Kendall Investor Relations. Please go ahead. Thank you and good morning. Prior to today's webcast, the company posted the presentation to its website, which can be found under the Investors and News section. Please note that various remarks that may be made during today's presentation about future expectations, plans and prospects for Climb Bio, expectations regarding the therapeutic benefits, clinical potential and clinical development of budoprutug and CLYM116, the anticipated timelines for reporting initial data from Climb Bio's ongoing and planned clinical trials of budoprutug and CLYM116, the anticipated timeline for initiating Climb Bio's parallel phase 1b clinical trial of budoprutug in patients with SLE in China, the potential commercial opportunity and limited competitive landscape for budoprutug, the expected patient populations in pMN, ITP, and SLE, the expected benefits of budoprutug's Fast Track Designation and Orphan Drug Designation in pMN, the sufficiency of Climb Bio's cash resources for the period anticipated, and other statements which are not historical facts. Actual results may differ materially from those contained in these forward-looking statements as a result of various important factors, including those discussed in the Risk Factors section of our most recent annual report on Form 10-K, which is on file with the SEC. In addition, any forward-looking statements made on today's call represent Climb Bio's views as of today only and should not be relied upon as representing its views as of any subsequent date. While we may elect to update these statements at some point in the future, we specifically disclaim any obligation to do so unless required by law. Any forward-looking statements should not be relied upon as representing Climb Bio's estimates or views as of any date subsequent to today. Today, I am joined by Climb Bio's President and CEO, Dr. Aoife Brennan, Dr. Edgar Charles, Climb Bio's Chief Medical Officer. In addition, we are pleased to include Dr. David Jayne, a practicing physician and professor of clinical autoimmunity at the University of Cambridge, and Director of the Vasculitis and Lupus Service at Addenbrooke's Hospital. Following the presentation, we will open the call to a Q&A session, which will also include additional members of the Climb Bio management team, Dr. Perrin Wilson, Chief Business Officer, and Dr. Susan Altschuller, Chief Financial Officer. With that, I'll pass the call on to Aoife. Thank you, Carlo, and thank you all for joining us for this R&D spotlight event focused on CD19 and our lead asset, budoprutug, and its potential in immune-mediated diseases. At Climb, our strategy is focused and deliberate. We're delivering differentiated monoclonal antibodies against validated B-cell targets with clear development paths in indications, including those impacting kidney health, that offer potentially meaningful therapeutic and commercial opportunity. We set a high bar for success, and we're making strong progress across our portfolio. Following a foundational year of execution in 2025, we're entering a data-rich period with anticipated readouts across all of our ongoing studies this year. Before turning to budoprutug, I will briefly touch on our other asset, CLYM116, which is also progressing well. CLYM116 is a next-generation anti-APRIL monoclonal antibody with the potential to deliver a best-in-class clinical profile in IgAN and other B-cell mediated diseases. It is the only sweeper monoclonal currently in development targeting APRIL. We in-licensed this asset in January 25 and rapidly generated head-to-head preclinical data versus a first-generation anti-APRIL antibody, suggesting the potential for greater potency and longer dosing intervals with low immunogenicity. CLYM116 is currently being evaluated in two parallel phase I studies, one conducted by the Climb team and one by our partner in China, MabWorks, which together will provide a comprehensive data set from healthy volunteers. We will present data at the upcoming European Renal Association meeting in June. This presentation will include modeling data from non-human primates that supported the design of both first-in-human studies, as well as initial safety data from our ongoing phase I study in healthy volunteers. Further data from the Climb-led healthy volunteer study, including biomarker data, will be presented at a dedicated CLYM116 spotlight event mid-year. Today, we're shining our spotlight on budo, our CD19 monoclonal antibody currently in clinical studies across pMN, ITP, and SLE, with recently completed healthy volunteer study of our subcutaneous formulation. Budo is designed to deliver B-cell depletion that is broad, deep, and sustained through a scalable and well-understood monoclonal antibody approach. While CD19 is often described as a crowded space, the reality is quite different. There are very few monoclonal antibodies in development targeting CD19 for B-cell depletion in immune-mediated diseases. In contrast, there are numerous complex modalities targeting CD19, which require administration in specialist referral centers given the need for specially trained staff and the ability to monitor patients for potential acute safety risks. As a result, mAb targeting of CD19 represents a clear and attractive white space. The opportunity for CD19 targeting monoclonal antibody is substantial. This has been validated by inebilizumab or UPLIZNA, which has demonstrated commercial success in rare neurological indications with increasing consensus projections since launch. We believe the advantages of the monoclonal antibody modality, including scalability, established safety, and the potential to deliver durable long-term disease control, support expanding this approach into additional indications. This is the path we are pursuing with budo. Our goal is to develop budo for patients who remain underserved by available therapies, delivering not only robust clinical outcomes, but also a therapy that can be safely and conveniently administered in real-world care settings. With that in mind, we're delighted to be sharing data from our recently completed trial of the subcutaneous formulation of budo on today's call, demonstrating encouraging activity and supporting further development. We are currently advancing budo across thee target indications, pMN, ITP, and SLE. These are indications where B cells are central drivers of disease, spanning renal, hematologic, and rheumatologic conditions with significant unmet need. Importantly, budo was recently granted Fast Track Designation by the FDA for the treatment of primary membranous nephropathy, underscoring both the urgency of need and its potential to deliver meaningful benefits. Budo's differentiated profile supports broad potential applicability across multiple indications, representing an expansive market opportunity. We expect to share initial data from our ongoing studies in pMN, ITP, and SLE later this year. Edgar will walk through each of these indications, the study design, and upcoming milestones in more detail in a few moments. First, to help ground today's discussion, I'm pleased to introduce Dr. David Jayne, our renowned physician scientist at the University of Cambridge in Addenbrooke's Hospital, with deep expertise in B-cell depletion and immune-mediated diseases. He will share his perspective on two key questions. How does CD19 compare to CD20 as a target for B-cell depletion? Can a monoclonal antibody deplete tissue-resident pathogenic B cells? Dr. Jayne, thank you for joining us. I'll hand it over to you. Thank you for inviting me to say a few words about targeting CD19 for autoimmune disease. My name is Dr. David Jayne, and I am from the University of Cambridge in the U.K. B cells have several important functions in autoimmunity. They can develop into plasmablasts and plasma cells that generate pathogenic antibodies. These are seen, for example, in primary membranous nephropathy, ITP, and in lupus or SLE. B cells also support T cell autoreactivity. This has been shown in a variety of autoimmune conditions, including rheumatoid arthritis and multiple sclerosis. B cells have typically been targeted therapeutically by anti-CD20 monoclonal antibodies, such as rituximab or ocrelizumab. However, over the last two decades, various limitations have been identified with targeting CD20. Firstly, CD20-directed treatment fails to completely remove circulating autoantibodies. The graph on the left shows changes in anti-double stranded DNA antibodies in SLE with rituximab. What you can see is although there are reductions in anti-double stranded DNA antibody levels with rituximab, in the majority of patients, levels remain well above baseline, so they continue to have positive antibodies despite rituximab. Another aspect is that there is incomplete removal of tissue-resident B cells with CD20 targeting, and we know tissue-resident B cells play important roles in pathogenesis. Tissue-resident B cells are important in several different scenarios. In the example at the bottom on the right are B-cell infiltrates in the kidneys of patients with lupus nephritis, and these infiltrates are important negative prognostic features in the long-term outcome of lupus nephritis patients that are not adequately targeted by CD20. The consequence of these limitations is that CD20 targeting only has partial efficacy, and when it wears off, there is a high relapse rate. Why target CD19? CD19 promotes the growth, activation, proliferation, and signaling of B lymphocytes. CD19- positive cells play an important role in the pathogenesis of autoimmune disorders. CD19 has a broader distribution than CD20 within the B-cell and plasma cell compartments. We have experimental examples from preclinical models and in humans that hyperexpression of CD19 is associated with autoimmunity. Further building on the rationale for use of CD19 strategies, this cartoon describes the development of B cells from pro-B cells in the bone marrow all the way through the periphery to mature B cells and then plasma cells back in the bone marrow. As you can see, the different cell surface markers are expressed at different stages of development, with CD19 appearing early on pro-B cells and continuing to be expressed, unlike CD20, on plasmablasts and many plasma cells. CD19 targets other pathogenic B-cell subsets. An example of this is the so-called double- negative B cells, which are precursors of autoantibody-secreting B cells and have shown to be expanded in autoimmune diseases such as SLE, they're defined by a particular set of surface antigens. Other key roles of CD19 in pathogenesis are autoantibody-secreting plasma cells. Plasma cells in rituximab-refractory autoimmune patients can be targeted by CD19, as they do not express CD20. Clinical remission of rituximab-refractory autoimmune disease can be induced by anti-CD19 chimeric antigen receptor T cells or CAR T cells. CD19 -positive plasma cells are not short-lived plasmablasts, they may have a much longer lifespan than plasmablasts. Autoantigen-binding B cells in CD19 -positive plasma cells serve a critical role in perpetuating T cell activation in autoimmune disease. Moving to some practical examples. This is a patient who's received CD19-targeted CAR T therapy for vasculitis. The upper panels show the UMAP transcription profile before CAR T from a bone marrow biopsy, and the lower panels show cells from a post-CAR T bone marrow biopsy. The highlighted area is the B-cell compartment, and you can see that the B-cell compartment has been completely depleted by CD19-directed CAR T therapy. Looking at this concept in more detail, in this study, anti-CD19 CAR T therapy was compared to anti-CD19 T cell engager therapy and anti-CD20 depletion with rituximab or ofatumumab with respect to the ability to deplete tissue-resident B cells. Consistent with what I showed you on the previous slide, you can see in the right-hand panel that after CD19-targeted CAR T therapy, there's complete removal of B cells from the lymph node. It was also observed that the follicular structures comprised of dendritic cells, T cells together with B cells, and which support germinal center formation and thus autoantibody formation, were disrupted by CD19-directed CAR T therapy. In the central column, you can see in the bottom panel that B cells are abundantly present in the lymph node after rituximab treatment. Rituximab is not depleting the B cells in the lymph node very well at all. With ofatumumab in the left-hand panel, there is substantial B-cell depletion, even better than what was observed with the T-cell engager. A reduction in follicular structures was also observed. Taken together, these results suggest that a large degree of tissue-level B-cell depletion can in fact occur with a conventional monoclonal antibody approach. It is reasonable to hypothesize that even deeper B-cell depletion can be achieved by a monoclonal antibody that targets CD19. To conclude, durable remissions are associated with deep B-cell depletion and with depletion of plasma cells and can potentially be achieved with conventional monoclonal antibodies. Targeting CD19 rather than CD20 offers the potential for more complete B-cell and plasma cell depletion. This is likely to be particularly important in removing pathogenic antibodies relevant for the treatment of many autoimmune diseases. Thank you. Thank you, Dr. Jayne, for those insights, particularly your perspective on the depth of B-cell depletion and the potential value of CD19 as a therapeutic target. What you've highlighted reinforces the scientific rationale for targeting CD19 instead of CD20 and the potential of a CD19 monoclonal antibody approach in treating autoimmune disease. With that foundation in place, I'll now walk through how we're translating this biology into clinical development across our key indications, including pMN, ITP, and SLE, and what we expect to learn from our ongoing studies. CD19 is emerging as a preferred pan-B-cell target for B-cell depletion. CD19 is expressed from early B-cell development, the pro-B-cell stage, through mature B cells and antibody-secreting plasmablasts and on a substantial proportion of plasma cells. CD19 has broader B-cell expression coverage than CD20, which is not present on pro-B cells, plasmablasts, or plasma cells. This broader expression profile allows for more comprehensive depletion of the B-cell lineage, including the cells most responsible for pathogenic antibody generation. Importantly, since CD19 is not expressed on long-lived plasma cells, targeting CD19 is not expected to impair the protective antibodies, such as those induced by vaccines, which are important for preventing infection. Budoprutug is an investigational CD19-targeting monoclonal antibody with low picomolar affinity for CD19. It has been specifically engineered with low fucosylation to enhance engagement of immune effector mechanisms, including antibody-dependent cellular cytotoxicity. In preclinical studies, budoprutug demonstrated high potency and achieved robust and consistent B-cell depletion across physiologic compartments. Importantly, this is realized within a conventional monoclonal antibody framework, combining potency with the predictability, scalability, and clinical familiarity of a well-established modality. The combination of CD19 biology and FC enhanced design provides budoprutug with the potential to achieve deep B-cell depletion, including effects on tissue-resident and antibody-producing cells that may not be fully addressed by therapies that target CD20. We have evidence from a human CD19 transgenic mouse model showing budoprutug's ability to achieve depletion of tissue-resident B cells in peripheral lymph nodes and bone marrow. While this transgenic model likely underestimates the potential of budoprutug tissue B-cell depletion, as the mouse does not have all the components of a human immune system, it does demonstrate the ability of budoprutug to act not only in the periphery but at the tissue level. We have further studies underway to support the potential for tissue-level depletion with budoprutug. We believe that depth and breadth of B-cell depletion is important, not just for controlling disease activity, but potentially for restoring normal B-cell homeostasis. Ultimately, this provides a rationale for exploring disease-modifying approaches with the goal of achieving durable clinical benefit and potentially treatment-free remission. As we have previously presented in the pilot study in patients with pMN, budoprutug dosed at either 100 mg or 200 mg has demonstrated compelling proof of concept with the potential for long-term disease remission. In this study, budoprutug achieved complete peripheral B-cell depletion in five of five evaluable patients. This effect was observed at a low dose of budoprutug, with reduction sustained out to one year after just two dose cycles. This robust B-cell depletion was followed by compelling reductions in pathogenic autoantibody levels as well as reductions in proteinuria, leading to clinical remission in all five patients and complete remission in three out of five patients. Remission was maintained for up to three years in the four patients who received four doses of budoprutug and who were followed long term, with three out of the four patients not requiring any further immunosuppression. This was a small data set, the durability of the clinical response after just four doses of budoprutug is particularly encouraging and provides early validation that budoprutug's mechanism is translating clinically. Based on this compelling initial proof of concept data, we are advancing budoprutug across multiple immune-mediated diseases where B cells are central drivers of pathology and where an anti-CD19 monoclonal approach has the potential to address an unmet need. This parallel development approach allows us to generate insights across indications, informing the ability to achieve B-cell depletion, defining the optimal dose in renal and non-renal indications, and assessing the potential for long-term disease control. I'm going to highlight each indication in more detail, covering the unmet need, scientific and translational rationale, and clinical trial designs. I'll also share top-line data from our phase I study of the budoprutug subcutaneous formulation in healthy volunteers and our next steps for development. We'll start with pMN. pMN is a progressive antibody-driven renal disease that can lead to significant morbidity, including nephrotic syndrome, chronic kidney disease, and ultimately kidney failure. The goal of treatment is to reduce proteinuria and induce clinical remission, which has been associated with decreased progression of kidney disease and development of kidney failure. Despite substantial advances in understanding disease biology, outcomes remain suboptimal for many patients. Targeting CD19-positive B cells has the potential to address the core disease drivers in pMN, in which pathogenic IgG4 autoantibodies are produced by CD19-positive B cells. These pathogenic autoantibodies bind the PLA2R antigen on the podocytes, leading to local formation and growth of immune complexes on the outer surface of the glomerular basement membrane. Recruitment of complement to the immune complex leads to podocyte cell injury, loss of slit diaphragms between the podocytes, and consequent leakage of increasing amounts of protein into the urine. This direct cause-and-effect relationship between autoantibody-producing CD19 -positive B cells and pathogenic destruction of the glomerular filtration barrier provides a clear biological rationale for targeting CD19 -positive B cells in pMN. PLA2R autoantibodies are the primary pathogenic driver in approximately 75% of pMN patients and are reflective of ongoing immunologic disease. Importantly, disappearance of PLA2R antibodies precedes reduction in proteinuria and clinical remission, which are reflective of restoration of the kidney filtration barrier. PLA2R antibody levels provide prognostic insight into the disease course, as higher titers are associated with a greater risk of kidney disease progression. Since the presence of PLA2R antibodies is indicative of ongoing immunologic dysregulation, PLA2R antibodies serve as a clinically important early biomarker of therapeutic responses for agents such as budoprutug that target B cells, the root cause of pMN. Despite advances in understanding disease biology, there are no currently approved therapies for pMN. Treatment approaches remain variable, often relying on broad immunosuppression despite its associated safety risks and comorbidities. KDIGO guidelines recommend treatment with rituximab, cyclophosphamide, or calcineurin therapy based upon risk estimate, which incorporates PLA2R antibody levels. Rituximab, although not approved for pMN, has been shown in the MENTOR study to be superior to cyclosporine in maintaining proteinuria remission up to two years, providing proof of concept for B-cell depletion as a therapeutic option in pMN. However, complete remission rates in the MENTOR study were low, and at two years, only 35% of patients achieved complete remission, which is the treatment goal to prevent kidney decline. Given the lack of approved treatments, there remains clear unmet need for a therapy that more directly and completely addresses the pathogenic biology of pMN and delivers improved outcomes for patients. PM represents a well-defined patient population with significant unmet need for therapies that are both more effective and well-tolerated. Approximately 75,000 patients in the U.S. have pMN, and it is a leading cause of nephrotic syndrome in adults. While about 1/3 of patients may achieve spontaneous remission, the majority, particularly those with moderate to high-risk disease, do not achieve spontaneous remission, and they are at risk for progressive kidney disease. It is these patients who are predisposed to complications and progressive kidney failure and for whom KDIGO recommends use of immunotherapy. Data from the completed phase 1b study in pMN suggests a compelling competitive profile for budoprutug. Although there are several investigational agents in development for pMN, none are currently approved, although rituximab is frequently used off-label. By targeting CD19, budoprutug has the potential to achieve pathogenically relevant B-cell depletion and immunologic and clinical remission with the potential for a highly competitive clinical profile. We are currently conducting the PRISM trial, a global open-label dose escalation phase II study in 45 patients with moderate to severe pMN. Dosing in this study begins at 200 mg, picking up where our phase 1b trial left off, and it is evaluating doses up to 1,000 mg with the goal of maximizing B-cell depletion. The study is currently enrolling, and it has a global footprint of approximately 45 sites across eight countries. The PRISM study's biomarker endpoints, particularly B-cell depletion and PLA2R antibody levels, are designed to make robust predictions of ultimate clinical efficacy and enable rapid identification of an optimal Phase III dose, providing for an accelerated development timeline. Preliminary efficacy will also be evaluated through assessment of proteinuria and complete and partial remission rates. Safety and tolerability will also be evaluated through assessment of adverse events. The PRISM study is progressing well, and we look forward to sharing additional data to further define budoprutug's potential in this indication. We anticipate initial B-cell depletion data and PLA2R antibody data from the low dose 200 mg cohort at 12 -2 4 weeks in the fourth quarter of 2026. While the proteinuria data will take time to mature, we expect this early look at biomarkers to corroborate the B-cell and immunologic response data from our phase 1b study. Immune thrombocytopenia is a rare autoantibody mediated disease characterized by platelet destruction and impaired platelet production. The resultant low platelet count not only confers a substantial bleeding risk but also impairs quality of life. Patients often experience easy bruising, fatigue, functional limitations, anxiety, and depression. Without disease-modifying treatments, the clinical burden of disease is high. This burden includes recurrent bleeding events, which can require hospitalization and frequent steroid dependency with its accompanying side effects. B cells are central to disease pathogenesis in ITP. B cells secrete autoantibodies directed against glycoproteins on the surface of platelets. The opsonized platelets are phagocytosed by monocytes and splenic macrophages. Autoantibodies also bind to megakaryocytes that express surface glycoproteins like those on platelets. The deficient production of platelets in ITP is due to the abnormal humoral and cytotoxic responses directed against megakaryocytes in the bone marrow. Targeting CD19 has the potential to address a root cause of ITP by eliminating the pathogenic autoantibody-producing B cells, offering a potentially disease-modifying approach for ITP. rituximab, a standard off-label treatment for ITP, has demonstrated the potential for B-cell depletion to alter the course of disease. However, rituximab has notable limitations, including incomplete B-cell depletion, underscoring the need for continued therapeutic innovation. Notably, given the broader expression of CD19 across the B-cell lineage, targeting CD19 may overcome key limitations in approaches targeting CD20 as CD19 is expressed on plasmablasts and many plasma cells which drive autoantibody production, while CD20 is not. Published studies and clinical observations suggest that roughly 80% of ITP patients have limited durability of response following treatment with rituximab. Expansions of CD19- positive, CD20 -negative plasma cells have been observed in the spleens of patients following rituximab treatment, indicating the emergence of rituximab-resistant autoantibody-secreting cells following rituximab treatment. Targeting CD19 -positive populations, including plasmablasts and plasma cells, may enable more sustained reduction or elimination of pathogenic autoantibodies produced by these cells. First-line treatments for ITP include corticosteroids as well as IVIG and anti-D immunoglobulin. Many patients fail first-line therapy and cycle through subsequent treatments, including thrombopoietin receptor agonists, which are efficacious but often require chronic administration and are also associated with side effects such as bone marrow reticular formation and thrombotic complications. Rituximab is often used as off-label therapy, but as discussed on the previous slide, has notable limitations. After second-line failure, Syk inhibitors and BTK inhibitors are typically used, but less than half of patients achieve overall response, and less than 20%-25% of patients achieve a durable response, leaving room for disease-modifying treatment options with a more compelling profile. We believe a substantial unmet need remains in ITP for safe, efficacious therapy with a dosing regimen that provides an opportunity for treatment-free disease control. Chronic ITP patients often cycle through multiple therapies in order to maintain their platelet counts. A substantial proportion of patients progress to more advanced disease, where treatment options are limited and durable responses are uncommon. Notably, investigational therapies in ITP have not yet been able to improve upon this low level of response, suggesting a high unmet need remains for a more efficacious therapy. Safety and convenient dosing are also critical considerations in ITP, given the decrease in quality of life that many patients are already experiencing as a result of the disease. Available therapies come with particular safety considerations and burdensome oral dosing, other emerging therapies may present a trade-off of frequent infusions. Previously treated patients with chronic ITP represent a high unmet need population and a high-value opportunity for improved therapies that address the underlying drivers of disease. We've included this underserved patient population in our ongoing ITP trial. We are conducting a multicenter, open-label dose escalation study in previously treated ITP patients, including heavily pretreated individuals. The study is assessing three doses of budoprutug, ranging from 250 mg-1,000 mg. This trial is important not only for our exploration of ITP, but also for its ability to evaluate the safety, preliminary efficacy, and dosing of budoprutug in a non-renal indication. Enrollment in the first two cohorts is complete, and enrollment in cohort three is expected to begin in the second quarter. The ITP study is designed to define dosing in a non-renal patient population and characterize B-cell depletion, as well as both the depth and durability of platelet response, key parameters for assessing potential for long-term disease control in a previously treated ITP population. We anticipate sharing initial B-cell depletion and platelet response data from the low-dose 250 mg cohort with follow-up out to 24 weeks at a medical meeting in June of 2026, with additional data from higher dose cohorts by year-end. We expect the data to define budoprutug's potential path forward in ITP and establish a dose in a non-renal patient population. As a reminder, patients in this study have been previously treated with at least one agent for ITP, and the majority have cycled through multiple agents. This is a refractory patient population with remaining need for more effective, durable therapies. SLE is a complex autoimmune disease driven by autoreactive B cells and B-cell-generated autoantibodies, making CD19 a highly relevant therapeutic target. While anti-CD20 therapies have demonstrated the promise of B-cell targeting, clinical outcomes remain variable and responses incomplete, highlighting the opportunity for improvement. CD19-targeting CAR T therapies have further validated CD19 as a therapeutic target with compelling efficacy, but they are limited by safety considerations, scalability challenges, and access challenges. A CD19 monoclonal antibody approach has the potential to provide patients with disease control in a more accessible administration format. We have two ongoing studies designed to generate translational insights, including the relationship between dose, B-cell depletion, and clinical biomarkers to inform future development in this indication. While our global study begins at subtherapeutic doses and investigates single doses of budoprutug, our parallel study in China will provide complementary data with higher repeated doses of budoprutug, and it will provide an accelerated path to decisional readout. We have set a rigorous bar for success, and we will want to see compelling evidence of therapeutic activity in order to advance development. Each of our clinical trials of budoprutug in pMN, ITP, and SLE utilizes an IV formulation. In parallel, we are developing a low-viscosity, high-concentration, 175 mg/mL subcutaneous formulation, which may offer a differentiated convenience profile for patients. We have recently completed a phase I placebo-controlled single ascending dose study to evaluate the safety, tolerability, and PK/PD of subcutaneous budoprutug in healthy volunteers. Participants received subcutaneous budoprutug at doses of either 3 mg or 6 mg, IV budoprutug at a dose of 6 mg or placebo. Since this was a study in healthy volunteers in whom it's not appropriate to completely deplete B cells, budoprutug doses were selected to produce measurable but submaximal B-cell depletion. Safety profiles were comparable between the budoprutug subcutaneous and IV groups. PK interpretation for subq doses was limited, as most of the concentrations were below the limit of quantification. Robust PD effects were observed. All active groups demonstrated rapid B-cell depletion, reaching approximately 80% reduction from baseline. B-cell depletion was similar between subcutaneous and IV administration arms, suggesting adequate systemic exposure to achieve robust PD activity. To summarize, subcutaneous budoprutug showed robust effects on B-cell depletion in healthy volunteers, with similar tolerability to max dose IV budoprutug, despite being studied at doses predicted to produce only modest impacts on B cells. The totality of the data to date in non-human primates and healthy volunteers supports continued development of the subq formulation. In NHPs, budoprutug exhibited high bioavailability as well as a favorable safety and tolerability profile. In healthy volunteers, there was comparable PD safety and tolerability between the subq and IV administration routes. These data support the feasibility of subq administration and provide the rationale for continued development in immune-mediated diseases. Our next step will be to advance the subq formulation at full B-cell depleting doses in patients with autoimmune diseases and to identify the appropriate regimen for further development. Our ongoing clinical development program is building the foundation for budoprutug's potential long-term value across multiple B-cell-mediated diseases. By evaluating a broad dose range across renal and non-renal indications, we are generating the data needed to demonstrate deep and durable B-cell depletion, confirm safety and tolerability, and inform optimal dose selection for future pivotal trials. Upcoming data readouts throughout 2026 are expected to provide important validation of biological activity, including effects on B cells, autoantibodies, and disease-relevant biomarkers. Together, these data and their milestones position the potential of budoprutug to support differentiated durable disease control and a scalable development path across multiple indications. With that, I'll turn it back to you, Aoife. Thanks, Edgar and Dr. Jayne. As you heard, there are multiple immune-mediated diseases where patients have inadequate disease control with existing therapies. We are excited to be evaluating the potential of budo to address these needs by targeting the pathogenic B cells that are the drivers of the disease pathology. As we look ahead, the data readouts expected throughout this year will be important in defining budo's clinical profile. We believe budo is well-positioned to become a foundational therapy across a range of immune-mediated diseases, and we look forward to sharing our progress with you as the year unfolds. Thank you again for joining us today. We'll now move into the Q&A portion of the webcast. To ask a question you will need to press star one one on your telephone and wait for your name to be announced. To withdraw your question please press star one one again. Please standby while we compile Q&A roster. One moment for our first question. Our first question will come from the line of Yasmeen Rahimi from Piper Sandler. Your line is open. Good morning, team. Thank you so much for a very thoughtful presentation and discussion. Maybe the first question is, and thank you for more a granular timing of the three data readouts. Given that the ITP B -cell and platelet data is expected here for the low dose in June, maybe help us understand whether there is any translation from the B -cell response in ITP to pMN or SLE, which are expected later in the quarter. Also maybe help us think about now with really the subq data on hand that continues to show, you know, a similar product profile to IV. How do you think about sort of what work is needed to advance the subq into phase III? Maybe I'll have a last follow-up. Thanks, Yas. This is Aoife Brennan here. I'll take the first one around kind of the read-through and pull, then hand it over to Edgar Charles to talk about how we think about the subq and dovetailing it into some of our development programs. Yes, you're right, we have an upcoming presentation of the early data from the ITP study. I think the real You know, there's probably two questions in each indication. Number one is, can we deplete B cells deeply and durably at a well-tolerated dose? I think that's something that we're going to learn from some of the initial readouts. The second part to that is how does that B -cell depletion translate to the clinical endpoints may be different across indications. I think, you know, the initial data we see will be instructive on the first part. But, you know, there'll be some disease-specific issues and questions that we'll need to address within each of the indications we pursue. I do think the relationship between B-cell depletion and the clinical endpoints may be different in the various indications. You know, we're building the story here. We're de-risking step by step, and I think that will continue as we go through the year and you start to see some of the data readouts that we have coming up. For the second part, maybe on subq, I'll hand it off to Edgar, who's been leading the charge on the development side. We're already seeing some good, you know, signs with subcutaneous and in healthy volunteers. What we're really looking for is seeing a good, robust B-cell depletion at doses that we can take into patients with autoimmune disease. We're going to be going next to look at higher doses in patients, looking at safety tolerability as well as B-cell reductions. Ideally, to get to a place where we could have similar levels of B-cell reductions with subq compared to the IV formulation. I think that opened up a lot of options for going into the indications in which we're already studying IV, potentially, as well as going into different indications. You can envision a variety of spaces where subcutaneous administration would be preferred to IV. I have questions, so maybe we'll move on, and then I queue to the queue at the end, if that's okay with you, just so that we can get through some of the other people we have in line. Thanks so much. Thank you. Our next question will come from the line of Chris Raymond from Raymond James. Your line is open. Hey, thanks, and thanks for doing this call. Very helpful. Just two questions. On the subq formulation, I know this is early in your testing it at lower doses here, but any sort of sense of what a dosing frequency might be in subq? Maybe a part B to that question is, you know, with a subq formulation, again, this is preliminary data, but if it continues to go well, why not advance this drug into gMG, which obviously is a de-risked indication? The second question I guess I have is on pMN. The initial data you guys have at 100 mg - 200 mg look pretty promising, but I think you're taking it all the way up to 1,000 mg. Maybe just what additional efficacy are you looking to see if you go that much higher? Thanks. Yeah. For the frequency question, I think that remains to be determined. We have some really nice data in healthy volunteers that we've shared today. I think continuing to study the full B-cell depleting dose in patients with autoimmune diseases will help inform and illuminate steps forward. I think broadly there are kind of two approaches. Number one is give the equivalent of the IV regimen with a subq route of administration. The other path that I think is also viable is to give lower doses more frequently. Subq, you know, it enables that. I think we will make that decision based on data. You know, we're gathering data now to really build and inform that model in how we might pursue subq going forward. Your second question about myasthenia gravis I think is interesting. It's one that we get quite a lot, given how well-validated commercially that opportunity is. You know, it's a very, very crowded space. We'll continue to watch and see if there is an opportunity for us to do something for patients with a subq B-cell depleter. As of today, we're very much on the sidelines on myasthenia gravis and watching obviously the UPLIZNA launch, I think will be informative of our decision around going forward as well as some other kind of emerging products in that space. If we see there's an opportunity to deliver value for shareholders and something for patients that we lose the needle, we would absolutely reconsider that. Regarding dose and pMN, you know, you're absolutely right. We saw encouraging signs in our initial study in pMN with 100 mg and 200 mg. We are pushing dose in our next study to achieve an even deeper B-cell depletion and perhaps even a better immunologic suppression and overall remission rate. Thank you. Awesome. Thanks, Chris. Next question. Thank you. Our next question will come from the line of Joseph Catanzaro from Mizuho. Your line is open. Hey, everybody. Appreciate you taking my questions here. Maybe a quick one from me. I guess maybe sort of following up on Chris's last question. The PK/PD relationship that you guys are thinking about looking across this wide range of doses and maybe what the CD20 experience tells you. As you go to higher doses, should we expect deeper B-cell depletion, faster B-cell depletion, and/or more durable B-cell depletion? I guess somewhat relatedly, when you look at CD20 experience in renal versus non-renal, what does that tell you about where you could land with budoprutug in renal and non-renal indications? Thanks. Yeah. I think to follow on to Edgar's answer around the pMN study, what's really important here is that we, you know, make sure that we get the right dose for it before we initiate phase III. You've only one opportunity to do that, and that's in your phase II program. We've clearly pointed out that there may be a renal and a non-renal dose. The reason being that, you know, these pMN patients often have a lot of proteinuria at baseline when you're dosing them. You're only giving two IV infusions at baseline, and if you're losing 30%-40% of that protein in your urine because of the high baseline proteinuria in these patients, that's obviously gonna impact exposure, and it's therefore going to impact B-cell depletion. I think it's possible that, you know, we may need to dose a little higher in these very severe pMN patients like the patients that we're currently enrolling in PRISM. That's where the real unmet need is, and that's the group that we're focusing on for further development. I think that's just, you know, a super important concept. You know, I think when it comes to finding the right dose, there's what that you can measure and what you can't measure when it comes to B cells. You know, we've developed the most sensitive B-cell assay that we'll be sharing, you know, a little bit more detail on as we start to give some of the readouts this year. I think what's equally important is what happens to some of the important clinical endpoints, like the PLA2R antibody level. It's possible that you can get to a dose that looks great on B-cell depletion, but actually a subsequent dose may be preferable when it comes to some of the immune biomarkers. We're studying all of that in the ongoing studies, where, you know, we want to make sure that we choose the right dose to go forward. So far, safety and tolerability has not been a limitation. You know, we feel that it's important to do this kind of dose range finding in the diseases of interest. We believe that may be applicable to other diseases as well, as we kind of focus on really understanding the PK/PD, we think we may be able to apply that to other diseases outside of the diseases that we're currently evaluating. Anything you'd add there, Edgar? No. That was really complete, Aoife. Great. Yeah. Very, very helpful. Thanks for taking my question. Thanks. Thank you. Our next question will come from the line of Colleen Kusy from Baird. Your line is open. Hey, everyone, it's Nick on for Colleen. Thanks for taking the question, and congrats on the progress. First, just wanna start out if you could just lay out some expectations for on what we can see with these initial readouts. Secondly, just given the e-expansion of UPLIZNA development, such as in CIDP autoimmune hepatitis, does this give you an idea of where to possibly move next with budo? Thank you. Great. In terms of the upcoming readouts, I'll share that and then, you know, tag team with Edgar again here, becoming a pattern, to talk about UPLIZNA and some of those indications. For ITP, we previously guided to having data in the second half of 2026, we've now disclosed that we have a June presentation, which will predominantly focus on safety, B cells, and platelet response in the low dose cohort at the three to six-month follow-up time point. As I mentioned, we'll also be sharing details about our high sensitivity B-cell assay that we're using across all of our studies. Those patients will continue to be followed per protocol. They'll get a second dose around six months, we'll also have data from the higher dose cohorts as we go through the year and into the second half. I think you can see what you can expect is this upcoming presentation in June, followed by subsequent disclosures as the dataset matures and as we conclude enrollment in some of those higher dose cohorts. For pMN, we're super excited about the PRISM study, and we announced that we dosed our first patient in November. As we think about, you know, the second half of the year, we have almost completed enrollment in the first cohort. We're seeing enrollment accelerate as we get some of our sites up and running. And we anticipate that the first cohort will be at the three to six-month time point at the time that we share some of the initial data. Like everything else, we'll continue to look and allow the data to mature and look at the complete response endpoint as more patients start to get to that 12-month time point, which is really the import, you know, that's the start of when you can start to see the complete response rate. You can see proteinuria trends earlier, and we'll be sharing B cells, PLA2R, and proteinuria from that first cohort later this year. Really, I think a very exciting kind of calendar as we think about some of these upcoming readouts, and we're excited to progress. Anything else? Yeah. I think inebilizumab expansion into other autoimmune diseases is really a further testimony to the potential for CD19 targeting in autoimmune disease. You, you can envision that CD19 targeting would be efficacious in a variety of B-cell driven autoimmune diseases in CIDP and AIH makes sense. You know, in contrast to UPLIZNA, we have higher picomolar affinity for CD19, and we do have our subcutaneous formulation under development. I think what we'll do is we'll take all the data that are coming out of our current studies as well as our future plan study in patients in subcutaneous formulation to make a decision about next indications we wanna pursue. Thanks, Nick, for the question. Great. Thank you. Thank you. Our next question comes from the line of Julian Harrison from BTIG. Your line is open. Hi. Thank you for taking my questions, and appreciate you hosting this. Across the three declared indications so far for budo, pMN, ITP, and lupus, I'm wondering if you have a good sense for how much CD20 targeted therapies are currently utilized. Do you expect that use captures the total cancer budo most likely? Do you maybe expect budo to likely grow those market categories as well? Yeah. That's a great question, Julian. I'll pass that one over to Perrin, who's really following the commercial and competitive landscape here most closely. Perrin? Yeah. Thanks, Julian. I think, you know, if we focus in on pMN and ITP, which we talked a bit about earlier. You know, rituximab is used in both of those indications off label. I think, you know, it meets some of the needs of patients. Some patients do achieve a response to remission, but ultimately are not served long term with these therapies. I think that's where we think budoprutug can come in. You know, looking at the breadth of expression with CD19, we think, you know, particularly as it relates to pMN, which is an IgG4 driven disease, we think, you know, hitting those early precursor cells and then also the plasmablasts and many of the plasma cells is really going to give us a distinct advantage over the CD20 approaches. You know, I think the same is true in ITP. Edgar took you through where, you know, taking the spleen of those ITP patients who are resistant or have failed rituximab, you see really the expansion, B-cell cohorts or that CD19 -positive population. We think, you know, budoprutug has the opportunity to really deliver great results for patients not only in the front line, but perhaps also in those, you know, CD20 failure patients. Thanks, Julian. Thank you. One moment for our next question. Our next question will come from the line of Laura Chico from Wedbush. Your line is open. Good morning. Thanks very much for taking the question. One for me on the pMN competitive landscape. With the PRISM data coming up, I guess I'm trying to understand what are you hoping to see from budo that might help it compare and contrast versus other mechanisms? We have APRIL/BAFF, CD38, a number of other mechanisms advancing in pMN. Maybe you could talk a little bit more about how you see the market evolving and the segmentation, but also how does budo kind of slot in versus some of these other mechanisms. Just lastly, I believe Amgen has a phase II UPLIZNA study in SLE with lupus nephritis as well. Anything else that you could articulate to clarify on kind of differentiation there? Thank you. Yeah. Another great question for Perrin. Yeah. As we discussed today, you know, particularly in pMN, no approved therapies, CNI, rituximab, commonly used off-label, I think this underscores the unmet need there. You know, looking ahead in pMN, we think the next key competitive inflection point is really the upcoming obinutuzumab MAJESTY readout at ERA. You know, we expect these data to be positive, but anticipate only an incremental improvement over what's been historically observed with rituximab. You know, this is really supported by the phase III data from a Chinese study of a next-generation CD20 agent, which was presented at ASN last year, which, you know, showed just that modestly higher complete renal remission rates compared to what had been seen with rituximab previously. Edgar, do you want to comment a little bit about the APRIL/BAFF mechanism there? Yeah. You know, we, yeah, again, we think CD19 is really the best target for pMN for all the reasons that we've mentioned in the IgG4 producing plasmablast, which are squarely expressive of CD19. Povetacicept is, you know, has released a little bit of data in pMN. As a BAFF/APRIL inhibitor, it really addresses more of a downstream pathophysiology rather than the root cause of disease, which would be targeted by a CD19 therapy. We think that budoprutug has the potential to have more deeper, more durable responses without the need for chronic regular dosing, such as monthly dosing to povetacicept study. Okay. Thanks, Laura. Thank you. Our next question will come from line of Danielle Brill from Truist. Your line is open. Hi. Good morning. Thank you so much for the questions. Maybe for Dr. Jayne, if I may. Can you comment on the role and prevalence of double -negative in CD20 -negative, CD19- positive B cells across ITP, SLE, and pMN? I'm wondering where you believe budo's activity against these populations creates the greatest differentiation versus other B-cell-directed approaches. Maybe as a follow-up to that, to what extent do you believe Roche's obinutuzumab and its greater potency observed as a CD agent overcomes the limitations that have historically been observed with rituximab? Also, where do the gaps remain? Thank you. Thank you for the question. The term double -negative B cells usually defines a subset of B cells that lack CD27 and CD5 surface markers. They retain CD19 and CD20. They've been identified because they seem to be particularly important in the pathogenesis of lupus, and there's been relatively less work done in the other indications that are under discussion. I mentioned them because they would be a suitable target for CD19 therapy. They're also clearly a target for CD20, and they are a measurable, circulating representation, if you like, of pathogenic B cells. Your second question related to obinutuzumab, I think this was touched on a little bit in my presentation. There's no doubt obinutuzumab is achieving better responses in the periphery and better responses in lymph nodes in terms of B-cell depletion. I think the real problem is that obinutuzumab remains restricted to CD20 and is not affecting the CD20 -negative plasmablasts or plasma cells. There's certainly data from rituximab, although less at the moment from obinutuzumab, that it's the CD20 -negative cells that persist and drive a relapse in these disorders. I think the advantage here of CD19 is really the broader cell coverage, including plasmablasts and plasma cells. The key question is whether this broad coverage to that state of follicular disruption that we referred to, which we think is consistent with long-term treatment-free remission, which is really, really the goal in autoimmunity. We know CD20 -negative cells are a component of what you have to do to get there. Very helpful. Thank you so much. Thanks, Danielle. Thanks, Dr. Jayne. Thank you. Our next question will come from the line of Thomas Smith from Leerink Partners. Your line is open. Hey, guys. Good morning. This is Brian on for Tom. Appreciate you guys hosting the event, and thanks for all the nice updates here. Just two questions from us, maybe first on the SLE study in China. Do you have a sense of how we should think about the similarities or differences of the patient population of lupus patients enrolled in China versus your ongoing global study? Second, for the phase II pMN study, we noticed some minor changes to eligibility on ClinicalTrials.gov related at maximum age and eGFR inclusion criteria. Would you be able to comment on these changes and just how enrollment is progressing to date? Thanks. Yeah, Brian, I can take the first, the nostril, and then let Edgar address the inclusion-exclusion criteria. For China, I think, you know, you can see today that we've shared the design for both the global study and the China study. Both are very, very complementary. In SLE, I think it's a particularly important in terms of the genetic background for these patients, particularly with regard to safety. We think the most important thing that we can achieve across both studies is really understanding the dose that can achieve B-cell depletion in a well-tolerated manner in these kind of fragile SLE patients. You can see from other modalities that often it's the SLE patient populations that are most prone to some of the short-term safety and tolerability issues. What was, you know, primary goal for us was to really make sure we were able to evaluate a number of doses from a safety and tolerability perspective, as well as understand the dose that can achieve deep B-cell depletion in this SLE patient population. I mean, obviously, we'd love to see some trends on efficacy as well, but that was a kind of a very much a secondary endpoint here. We think both studies are going to be super complementary in that, and will really address the question you're getting at, is whether there are ethnic differences in those patients when it comes to PK/ PD, and the safety and tolerability piece. We'll be, I think, very excited to see the data and the totality of the data across both studies because I think both will be integrated and very, very important. In terms of eligibility, Edgar, do you want to speak to that? Regarding the pMN study, as Aoife mentioned, enrollment is on track. We're close to completing enrollment in the first dose cohort. We did broaden the inclusion criteria with a higher age exclusion, as well as lower the eGFR exclusion, really to capture a broader variety of patients that we may wanna study going into phase III. Thanks, Brian. Thanks so much. Thank you. One moment for our next question. Our next question will come from the line of Leland Gershell from Oppenheimer. Your line is open. Yeah, good morning. Thanks for hosting this event. A couple questions from us. First for the company. You know, given the potential for very deep B-cell depletion with budoprutug, I guess, you know, do you ultimately envision this as more of a sort of a finite reset regimen with retreatment guided by biomarkers or a true chronic maintenance therapy? Is there any I know your early clinical data is fairly limited, but any observations you can draw there about relapse kinetics and retreatment intervals? Then I have a question for Dr. Jayne. I think it's too early to tell from the data. We are certainly looking to have a one-or-two-and-done type approach where one or two cycles may be sufficient to have a long-lasting remission. We've already seen from our initial pMN study that one or two cycles of budoprutug led to durable remission at least up to three years in our pMN patients. We certainly hope to recapitulate that in our phase II study. I think that really goes to the heart of our exploration of dose regimen. It also may depend upon indications. Some indications may be more amenable to a reset that leads to a drug-free remission than others. We're certainly gonna be learning from all of our indications and dose regimens together to come up with an idea of a dose regimen for our registrational studies. I think to add to that is that even if a patient does require chronic administration of therapy, you know, that can be achieved with a monoclonal antibody. Depending on, you know, the benefit risk for that individual patient, that's something certainly that's in scope and not precluded, unlike some of the other kind of more complex modalities. I'll now open the floor to your next question for Dr. Jayne. Great. Thank you. Yes. Just wanted to ask your opinion. You know, obviously, the guidelines recommend RITUXAN and, you know, other CD20 antibodies for pMN, but those remission rates that are substantial, meaningful non-responders, and budoprutug looks lined up to be the first actual approval. Here we've seen phase III data. I guess, you know, what would you, Dr. Jayne, like to see out of budoprutug's development that could potentially put that candidate as a first-line therapy in pMN? Thank you. The common result with Rituximab, you get a response in terms of reduction of proteinuria to subnephrotic levels, but you much less commonly get what I would call a complete renal response, a response well below 0.5 g, mg per mg. I think the first thing that I'd be looking for with budoprutug would be the depth of the proteinuria response. Clearly, you're gonna look at impact on circulating autoantibodies, such as anti-PLA2R. These do not correlate perfectly with clinical response. Because this is a B-cell-targeted therapy, you're gonna get an earlier readout on autoantibody levels. I'll be looking within the first six months, a clearance of pathogenic antibodies. As I alluded to with Rituximab, we often don't see complete clearance of pathogenic antibodies. Great. Thanks so much, Dr. Jayne. Thank you. Our next question will come from the line of Matt Phipps from William Blair. Your line is open. Good morning. Thanks for all the additional disclosures this morning around the bit of development. You know, I was wondering, as you're looking at the subq development, do you think there will be a need or do you plan to explore any kind of a, sort of loading dose followed by, you know, maintenance? Maybe, you know, two doses up front and then one as a maintenance. Then for many of these ongoing studies, do you think you'll be able to get any lymph node biopsies to try to look at that deep, deeper level B-cell depletion? Thank you. Thanks, Matt. I think, you know, as I mentioned earlier, I think it's a little too early for us to identify the ideal regimen, but we do look to the CD20s. I mean, they're B-cell depleters. We can learn from their development. There you can see that, you know, particularly in the case of KESIMPTA, there is this kind of concept of a number of doses in quick succession to deplete the initial B-cell count and then the maintenance of the monthly subq at a low dose to kind of maintain B-cell suppression in the MS indication. Certainly that is one model that's likely viable. You know, I think really understanding some of the modeling, some of the CD19 and CD20 kinetics that we'll evaluate at the full B-cell depleting dose, as well as some of the indications that we plan to pursue, will help us identify what the ideal dosing regimen looks like. You know, more to come for sure on that. Yeah, regarding lymph node biopsies, we certainly aim to get tissue from some of our ongoing studies to look at deep B-cell depletion. In respect to the earlier question about double -negative B cells, our high sensitivity B-cell assay is also multidimensional from a flow cytometry standpoint. We'll be interrogating for disappearance or reemergence of those types of populations through the use of CD27 and CD11c. Thanks, Matt. Thank you. The next question comes from the line of Mayank Mamtani from B. Riley Securities. Your line is open. Yes, good morning, team. Thanks for taking our questions and appreciate the helpful detail here. Maybe just building on the prior question on landscape positioning, and as we look into the ERA data set for MAJESTY, you know, if you could talk to the clinical parameters that are relevant to follow, even for not just for CD20, but also BAFF/APRIL. We understand a bit more on the CD19 mediated impact on long lived plasma cells, you know, both from a safety and immune research standpoint. Relatedly would be helpful to hear, you know, level of PLA2R remission, you know, that makes sense for you to see here, you know, that could inform a potentially expedited path to a pivotal phase III program. I think what's most important in pMN is the approvable endpoint, which is a complete renal response, that we understand from the MAJESTY study is a 24-month endpoint. We know that that's positive. We haven't seen the proportion of patients that achieve that endpoint. And we also don't know at this point how much granularity we'll get with the upcoming presentation on some of the earlier time points that in the short term are going to be more meaningful for us as we can start to accrue and mature our data set. We'll be watching that presentation. We'll have a team on the ground at ERA. I think once we see some of those data, we'll be able to better answer your question around kind of some of the early time points of PLA2R and the proteinuria trends and how much data we have on each of those endpoints as we go through this year. An exciting time for pMN for sure, going from a space with nothing approved to now a number of products in the pipeline. Certainly good for patients. Thanks so much. Great. Wonderful. Q&A session. I know there's a lot happening this morning, so it's Cinco de Mayo. Thanks so much everyone for joining us, and we look forward to having future spotlight events as we go through the year and keep everyone updated on our two very exciting programs. Thank you, operator. Thank you for your participation in today's conference. This does conclude the program. You may now disconnect. Everyone, have a great day.