Climb Bio (CLYM) outlines budoprutug CD19 data, 2026 trial readouts and cash runway
Rhea-AI Filing Summary
Climb Bio, Inc. filed a current report describing an R&D spotlight focused on budoprutug, its anti-CD19 monoclonal antibody for immune‑mediated diseases. The company highlights robust B‑cell depletion with a subcutaneous formulation in healthy volunteers and ongoing trials in primary membranous nephropathy (pMN), immune thrombocytopenia (ITP), and systemic lupus erythematosus (SLE).
Budoprutug has received FDA Orphan Drug and Fast Track designations for pMN and showed durable B‑cell depletion, anti‑PLA2R antibody negativity in evaluable patients, and clinical remissions in a small Phase 1b pMN study. Climb Bio also notes its second program, CLYM116, an anti‑APRIL antibody for IgA nephropathy, and states it is well‑resourced with cash runway anticipated into 2028, supporting multiple planned 2026 data readouts across budoprutug and CLYM116.
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8-K Event Classification
Key Figures
Key Terms
Fast Track Designation regulatory
Orphan Drug Designation regulatory
immune thrombocytopenia medical
primary membranous nephropathy medical
monoclonal antibody medical
Phase 1b financial
UNITED STATES
SECURITIES AND EXCHANGE COMMISSION
WASHINGTON, D.C. 20549
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CURRENT REPORT
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| Item 7.01 | Regulation FD Disclosure. |
On May 5, 2026, Climb Bio, Inc. (the “Company”) will hold its previously announced virtual investor event focused on budoprutug, its clinical-stage anti-CD19 monoclonal antibody, in development for primary membranous nephropathy, immune thrombocytopenia and systemic lupus erythematosus, beginning at 8:00 a.m. ET.
Copies of the press release and presentation relating to the investor event are attached hereto as Exhibits 99.1 and 99.2, respectively, and are incorporated herein by reference. A live webcast of the event, as well as a replay, will be available under the “News & Events” section of the Company’s website: climbbio.com. The information contained in, or that can be accessed through the Company’s website, is not a part of this filing.
The information in this Item 7.01, including Exhibits 99.1 and 99.2, shall not be deemed “filed” for purposes of Section 18 of the Securities Exchange Act of 1934, as amended (the “Exchange Act”), or otherwise subject to the liabilities of that section, nor shall it be deemed incorporated by reference in any filing under the Securities Act of 1933, as amended, or the Exchange Act, except as expressly set forth by specific reference in such a filing.
| Item 9.01. | Financial Statements and Exhibits. |
(d) Exhibits:
| Exhibit |
Description | |
| 99.1 | Press Release, dated May 5, 2026 | |
| 99.2 | Presentation, dated May 5, 2026 | |
| 104 | Cover Page Interactive Data File (embedded within the Inline XBRL document). | |
SIGNATURES
Pursuant to the requirements of the Securities Exchange Act of 1934, the registrant has duly caused this report to be signed on its behalf by the undersigned hereunto duly authorized.
| Climb Bio, Inc. | ||||||
| Date: May 5, 2026 | By: | /s/ Aoife Brennan | ||||
| Aoife Brennan, M.B., Ch.B. | ||||||
| President and Chief Executive Officer | ||||||
Exhibit 99.1
CONFIDENTIAL
Climb Bio Hosts Budoprutug R&D Spotlight Event Highlighting Topline Subcutaneous Formulation Data, Broad B-Cell Mediated Disease Opportunity, and Upcoming Data Readouts
Robust B-cell depletion observed with budoprutug subcutaneous formulation in healthy volunteers, supporting continued development
Budoprutug pMN, ITP, and SLE clinical trials enrolling to plan; Fast Track Designation received for pMN
Initial data from ITP trial anticipated in June; initial data from pMN and SLE trials anticipated Q4 2026
Company to host R&D Spotlight Webcast today, May 5, 2026
WELLESLEY HILLS, MASS., (GLOBE NEWSWIRE) – May 5, 2026 – Climb Bio, Inc. (Nasdaq: CLYM), a clinical-stage biotechnology company developing therapeutics for immune-mediated diseases, today announced progress updates for budoprutug, the Company’s anti-CD19 monoclonal antibody. The Company is hosting a virtual investor event focused on budoprutug today, Tuesday, May 5, at 8:00 a.m. ET. Climb Bio’s management team will be joined by David Jayne, M.D., Professor of Clinical Autoimmunity at the University of Cambridge and Director of the Vasculitis and Lupus Service at Addenbrooke’s Hospital.
“Budoprutug represents a differentiated and potentially expansive opportunity within the immune-mediated disease landscape,” said Aoife Brennan, M.B., Ch.B., President and Chief Executive Officer of Climb Bio. “We believe targeting CD19 with a monoclonal antibody approach offers a well-understood and scalable path to modulate B-cell biology, with the potential to drive durable clinical benefit for patients. We are advancing budoprutug across high unmet need indications with clear, B-cell driven pathology, including pMN, ITP, and SLE, with both intravenous and subcutaneous formulations in development. At today’s R&D Spotlight, we will be sharing positive topline data for our subcutaneous formulation and providing further perspective on CD19 as a therapeutic target, our development strategy, and upcoming anticipated clinical data. We believe there is substantial potential for budoprutug across a range of immune-mediated diseases and we look forward to the additional milestones anticipated this year.”
Budoprutug Data & Event Highlights
Budoprutug offers a differentiated CD19 monoclonal antibody (mAb) approach
| • | Fc enhanced design and high affinity support robust B-cell depletion |
| • | Early clinical data in primary membranous nephropathy (pMN) supports potential for long-term disease control |
| • | Combines breadth of CD19-targeting with simplicity and scalability of a mAb, with development of both intravenous and subcutaneous formulations to support potential for broad clinical adoption |
CD19 is emerging as a preferred pan-B-cell target for multiple immune-mediated diseases
| • | CD19 is broadly expressed across the B cell lineage, including early B cells and antibody-producing cells which are not fully addressed by an anti-CD20 approach |
| • | Targeting CD19 has the potential to achieve profound peripheral and tissue-level B-cell depletion, which may lead to a reduction of pathogenic, autoantibody-producing cells and long-term disease control |
| • | CD19 is a clinically proven approach as demonstrated by recent approvals in rare neurological autoimmune diseases |
Advancing budoprutug in pMN, ITP, and SLE, high unmet need indications where B cells are central drivers of disease
| • | Primary membranous nephropathy (pMN), immune thrombocytopenia (ITP), and systemic lupus erythematosus (SLE) studies enrolling to plan, on track for initial readouts across all studies in 2026 |
| • | Ongoing clinical studies evaluating budoprutug across the projected therapeutic dose range: pMN (200-1000 mg), ITP (250-1000 mg), SLE (100-600 mg) |
| • | Biomarker-driven designs expected to enable early assessment of mechanism and inform efficient optimization of dosing strategies and future trial design |
| • | Parallel development across renal and non-renal diseases has the potential to maximizes learning and expands long-term potential value |
Topline Data from Phase 1 trial of subcutaneous (SC) formulation in healthy volunteers supports advancement to patients
| • | Robust B-cell depletion observed; depletion was similar between SC and intravenous (IV) administration at matched doses |
| • | Budoprutug SC was generally safe and well-tolerated |
| • | Results support the advancement to a study in autoimmune disease patients to evaluate full B-cell depleting doses and optimal dosing regimen |
CONFIDENTIAL
Budoprutug anticipated 2026 milestones
| • | ITP Phase 1b/2a study – Initial B-cell and platelet data from low dose cohort (250 mg at 24 weeks) expected in June; additional data from higher dose cohorts by year-end |
| • | pMN Phase 2 study – Initial B-cell and anti-PLA2R data from the low dose cohort (200 mg at 12-24 weeks) expected in Q4 |
| • | SLE Phase 1b global study – Initial B-cell data expected in Q4 |
Webcast Information
The live webcast is accessible via the “News & Events” section of the Climb Bio website: https://ir.climbbio.com/. A webcast replay will be available on the Climb Bio website beginning approximately two hours after the webcast event and will be archived for at least 30 days.
About Climb Bio, Inc.
Climb Bio, Inc. is a clinical-stage biotechnology company with a mission to deliver high impact, disease-modifying medicines for individuals living with immune-mediated diseases, including those affecting kidney health. The Company’s pipeline includes, budoprutug, an anti-CD19 monoclonal antibody that has potential to treat a broad range of B-cell mediated diseases, and CLYM116, an anti-APRIL monoclonal antibody being developed for IgA nephropathy. For more information, please visit climbbio.com.
About Budoprutug
Budoprutug is a clinical-stage, anti-CD19 monoclonal antibody with the potential to address a broad range of B-cell mediated, immune-driven diseases. Designed with enhanced effector function and low picomolar affinity, budoprutug targets and depletes CD19-expressing B cells, including plasmablasts and certain plasma cells, key sources of pathogenic autoantibodies. Early clinical data suggest budoprutug may offer durable B-cell depletion, rapid reductions in autoantibodies, and clinical remission in primary membranous nephropathy (pMN). Budoprutug is being evaluated in clinical trials for pMN, immune thrombocytopenia (ITP), and systemic lupus erythematosus (SLE). A subcutaneous formulation is also in development to enable broader patient access. Budoprutug has been granted Orphan Drug Designation and Fast Track Designation by the FDA for the treatment of pMN.
Forward-Looking Statements
This press release contains “forward-looking statements” within the meaning of the Private Securities Litigation Reform Act of 1995, including without limitation statements regarding: 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 systemic lupus erythematosus in China; the potential commercial opportunity and limited competitive landscape for budoprutug; the expected patient populations in primary membranous nephropathy, immune thrombocytopenia and systemic lupus erythematosus; the expected benefits of budoprutug’s Fast Track Designation and Orphan Drug Designation in primary membranous nephropathy; the sufficiency of Climb Bio’s cash resources for the period anticipated; and other statements containing the words “anticipate,” “believe,” “continue,” “could,” “estimate,” “expect,” “intend,” “may,” “plan,” “potential,” “predict,” “project,” “should,” “target,” “would,” “will,” “working” and similar expressions. Forward-looking statements are based on management’s current expectations of future events and are subject to a number of risks and uncertainties that could cause actual results to differ materially and adversely from those set forth in, or implied by, such forward-looking statements. Climb Bio may not actually achieve the plans, intentions or expectations disclosed in these forward-looking statements, and you should not place undue reliance on these forward-looking statements. These risks and uncertainties include, but are not limited to, important risks and uncertainties associated with: the ability of Climb Bio to timely and successfully achieve or recognize the anticipated benefits of its technology transfer and exclusive license agreement with Beijing Mabworks Biotech Co., Ltd.; changes in applicable laws or regulation; the possibility that Climb Bio may be adversely affected by other economic, business and/or competitive factors; Climb Bio’s ability to advance budoprutug and CLYM116 on the timelines expected or at all and to obtain and maintain necessary approvals from the U.S. Food and Drug Administration and other regulatory authorities; obtaining and maintaining the necessary approvals from institutional review boards at clinical trial sites and independent data safety monitoring boards; replicating in clinical trials positive results found in early-stage clinical trials or nonclinical trials; competing successfully with other companies that are seeking to develop treatments for primary membranous nephropathy, immune thrombocytopenia, systemic lupus erythematosus, IgA nephropathy and other immune-mediated diseases; maintaining or protecting intellectual property rights related to budoprutug, CLYM116 and/or its other product candidates; the outcome of any legal proceedings or other disputes; managing expenses; and raising the substantial additional capital needed, on the timeline necessary, to continue development of budoprutug, CLYM116 and any other product candidates Climb Bio may develop. For a discussion of other risks and uncertainties, and other important factors, any of which could cause Climb Bio’s actual results to differ materially from those contained in the forward-looking statements, see the “Risk Factors” section, as well as discussions of potential risks, uncertainties and other important factors, in Climb Bio’s most recent filings with the U.S. Securities and Exchange Commission. In addition, the forward-looking statements included in this press release represent Climb Bio’s views as of the date hereof and should not be relied upon as
CONFIDENTIAL
representing Climb Bio’s views as of any date subsequent to the date hereof. Climb Bio anticipates that subsequent events and developments will cause Climb Bio’s views to change. However, while Climb Bio may elect to update these forward-looking statements at some point in the future, Climb Bio specifically disclaims any obligation to do so, except as required by law.
Investors and Media
Carlo Tanzi, Ph.D.
Kendall Investor Relations
ctanzi@kendallir.com
R&D Spotlight: Budoprutug and the CD19 Opportunity MAY 5, 2026 Exhibit 99.2
Forward Looking Statements This presentation contains “forward-looking statements” within the meaning of the Private Securities Litigation Reform Act of 1995, including without limitation statements regarding: 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 clinical trial of budoprutug in patients with systemic lupus erythematosus (SLE) in China; the potential commercial opportunity and limited competitive landscape for budoprutug; the expected patient populations in primary membranous nephropathy (pMN), immune thrombocytopenia (ITP), and systemic lupus erythematosus (SLE); the expected benefits of budoprutug’s Fast Track Designation and Orphan Drug Designation in primary membranous nephropathy (pMN); the sufficiency of Climb Bio’s cash resources for the period anticipated; and other statements containing the words “anticipate,” “believe,” “continue,” “could,” “estimate,” “expect,” “intend,” “may,” “plan,” “potential,” “predict,” “project,” “should,” “target,” “would,” “will,” “working” and similar expressions. Forward-looking statements are based on management’s current expectations of future events and are subject to a number of risks and uncertainties that could cause actual results to differ materially and adversely from those set forth in, or implied by, such forward-looking statements. Climb Bio may not actually achieve the plans, intentions or expectations disclosed in these forward-looking statements, and you should not place undue reliance on these forward-looking statements. These risks and uncertainties include, but are not limited to, important risks and uncertainties associated with: the ability of Climb Bio to timely and successfully achieve or recognize the anticipated benefits of its technology transfer and exclusive license agreement with Beijing Mabworks Biotech Co., Ltd.; changes in applicable laws or regulation; the possibility that Climb Bio may be adversely affected by other economic, business and/or competitive factors; Climb Bio’s ability to advance budoprutug and CLYM116 on the timelines expected or at all and to obtain and maintain necessary approvals from the U.S. Food and Drug Administration and other regulatory authorities; obtaining and maintaining the necessary approvals from institutional review boards at clinical trial sites and independent data safety monitoring boards; replicating in clinical trials positive results found in early-stage clinical trials or nonclinical studies; competing successfully with other companies that are seeking to develop treatments for primary membranous nephropathy (pMN), immune thrombocytopenia (ITP), systemic lupus erythematosus (SLE), IgA nephropathy (IgAN) and other immune-mediated diseases; maintaining or protecting intellectual property rights related to budoprutug, CLYM116 and/or its other product candidates; the outcome of any legal proceedings or other disputes; managing expenses; and raising the substantial additional capital needed, on the timeline necessary, to continue development of budoprutug, CLYM116 and any other product candidates Climb Bio may develop. For a discussion of other risks and uncertainties, and other important factors, any of which could cause Climb Bio’s actual results to differ materially from those contained in the forward-looking statements, see the “Risk Factors” section, as well as discussions of potential risks, uncertainties and other important factors, in Climb Bio’s most recent filings with the U.S. Securities and Exchange Commission. In addition, the forward-looking statements included in this presentation represent Climb Bio’s views as of the date hereof and should not be relied upon as representing Climb Bio’s views as of any date subsequent to the date hereof. Climb Bio anticipates that subsequent events and developments will cause Climb Bio’s views to change. However, while Climb Bio may elect to update these forward-looking statements at some point in the future, Climb Bio specifically disclaims any obligation to do so, except as required by law.
Webcast Agenda Corporate Strategy & Budoprutug Opportunity Aoife Brennan, M.B., Ch.B. President and CEO, Climb Bio CD19: A Key Driver of B-Cell Mediated Autoimmune Disease David Jayne, M.D. Professor of Clinical Autoimmunity at the University of Cambridge Director of the Vasculitis and Lupus Service at Addenbrooke’s Hospital Budoprutug: A Differentiated CD19 mAb with Broad Autoimmune Potential Edgar Charles, M.D. Chief Medical Officer, Climb Bio Q&A session including Dr. Jayne and management
Developing differentiated, monoclonal antibody (mAb) therapeutics for immune-mediated diseases, including those affecting kidney health, with expansive commercial opportunities Leveraging clinically validated B cell targets, proven mAb modality, and indications with well-defined endpoints and established regulatory pathways Anticipating a data-rich 2026 with multiple clinical readouts across both clinical-stage programs Budoprutug - anti-CD19 mAb in development for pMN, ITP, and SLE; Fast Track and Orphan Drug Designations granted for pMN CLYM116 - anti-APRIL mAb in development for IgAN Well-resourced to advance clinical programs through meaningful value-driving milestones, with runway anticipated into 2028* Delivering Clinical Results and Advancing Development * Does not include the impact of proceeds from the April PIPE financing pMN = primary membranous nephropathy, ITP = immune thrombocytopenia, SLE = systemic lupus erythematosus, IgAN = IgA nephropathy Corporate Highlights
Initial Global Ph1b data Q4 ‘26 FPI China Ph1b Q2 ‘26 Pipeline of Highly Differentiated mAbs Anticipating initial readouts from all ongoing trials in 2026 Budoprutug SC and CLYM116 Phase 1 trials conducted in healthy volunteers (HV). *Climb Bio has worldwide rights outside Greater China (defined as mainland China, Hong Kong, Macau, and Taiwan); Partner: Beijing Mabworks Biotech Co., Ltd. APRIL = a proliferation-inducing ligand, IV = intravenous, FPI = first patient in, mAbs = monoclonal antibodies, PD = pharmacodynamic, PK = pharmacokinetic, SC = subcutaneous Budoprutug IV Anti-CD19 INDICATION(S) Systemic Lupus Erythematosus Immune Thrombocytopenia Autoimmune Disease CLYM116* Anti-APRIL IgA Nephropathy Budoprutug SC Anti-CD19 PRE-CLINICAL PHASE 1 PHASE 2 PHASE 3 IND-ENABLING Primary Membranous Nephropathy Initial Ph2 data Q4 ‘26 Initiate multiple dose patient study Initial PK/PD Ph1 HV data mid-year ‘26 STATUS & ANTICIPATED MILESTONES Initial Ph1b data June ‘26 Additional Ph1b data YE ‘26 Modeling/Ph1 HV safety June ‘26
CD19 mAb Targeting Remains a White Space Low competitive intensity for an established modality translates into opportunity for budoprutug mAb = monoclonal antibody; TCEs = T cell engagers 1 ClinicalTrials.gov, April 2026; includes clinical stage programs and approved programs (inebilizumab) Budoprutug Opportunity Limited competition in CD19 mAb space relative to TCEs and cell therapies | Administration profile intended to support outpatient and community use | Potential to address multiple B‑cell mediated autoimmune diseases CD19 Autoimmune Competitive Landscape1 B-Cell Depleting Approaches T Cell Engagers Monoclonal Antibodies >13 3 Cell Therapies >18 Rationale for a mAb Approach Established therapeutic class with understood safety profile and scalability Straightforward manufacturing and broad community access Targeted immunomodulation without lymphodepletion
Opportunity for a CD19 B-Cell Depleting mAb is Significant Inebilizumab's commercial success in rare neurological diseases supports the viability of a CD19 mAb approach gMG = generalized myasthenia gravis, IgG4-RD = immunoglobulin G4-related disease, mAb = monoclonal antibody, NMOSD = neuromyelitis optica spectrum disorder 1 Wall Street estimates, April 2026 Significant potential opportunity for budoprutug in B-cell mediated diseases beyond inebilizumab’s neuro focus Inebilizumab Consensus Sales Estimates1 NMOSD approval, Jun 2020; IgG4-RD approval, Apr 2025; gMG approval, Dec 2025 CAGR: ~50%
EPIDEMIOLOGY (US) Progressive renal disease characterized by proteinuria, nephrotic syndrome and progressive loss of renal function5 No approved therapies Primary Membranous Nephropathy (pMN) ~75,000 patients1,2 Potential for long-term disease remission based on initial clinical data Fast Track Designation granted Immune Thrombocytopenia (ITP) Systemic Lupus Erythematosus (SLE) Chronic bleeding disorder characterized by the destruction of platelets6 Poor QoL, with majority of previously treated patients failing to achieve durable platelet response6 Potential to achieve durable response and disease remission in the previously treated population Chronic autoimmune condition with severe disease manifestations that can affect virtually any organ system7 Majority of patients fail to achieve disease control with existing treatments7 Potential for broad B-cell targeting and disease suppression with the safety and convenience of a mAb ~85,000 patients2,3 ~240,000 patients2,4 UNMET NEED BUDOPRUTUG OPPORTUNITY Budoprutug Target Indications Represent a Robust Opportunity Set Pursuing development in diseases with large addressable populations and significant unmet need mAb = monoclonal antibody, QoL = quality of life 1 McGrogan Nephrol Dial Transplant 2011, 2 U.S. Census Estimates 2020-2025, 3 Feudjo-Tepie 2008, 4 Izmirly Arthritis Rheumatol 2021, 5 Ronco JCM 2021, 6 Gafter-Gvili Eur J Int Med 2023, 7 Marinho Front Immunol 2023
Targeting CD19 in autoimmunity David Jayne, M.D. University of Cambridge, UK Disclosures: Consultancy or lecture fees from Abbvie, Alentis, Amgen, Astra-Zeneca, Climb Bio, CSL Vifor, Fate, GSK, Novartis and Otsuka, and grants from CSL Vifor, GSK, Roche/Genentech and UCB
Functions of B cells in autoimmunity Develop into plasmablasts and plasma cells that generate pathogenic antibodies (e.g. pMN, ITP, SLE) Support T cell autoreactivity (e.g. RA, MS) Typically targeted by anti-CD20 monoclonal antibodies (e.g. rituximab, ocrelizumab) pMN = primary membranous nephropathy, ITP = immune thrombocytopenia, SLE = systemic lupus erythematosus, RA = rheumatoid arthritis, MS = multiple sclerosis Kidney biopsy of a patient with pMN IgG
Failure to remove circulating autoantibodies Incomplete removal of tissue resident B cells SLE: anti-DNA antibodies after rituximab SLE: B cells in the kidney drive poor prognosis Catapano F et al, Nephrol Dial Transpl 2010. Chang et al, J Immunol 2011 Only partial efficacy and high relapse rate Limitations with targeting CD20
Why target CD19 ? CD19 promotes the growth, activation, proliferation, and signaling of B lymphocytes CD19+ cells play an important role in the pathogenesis of autoimmune disorders CD19 has a broad distribution within B cell and plasma cell development
Zhang Z et al, Frontiers in Immunology (14) 2023 Rationale for Use of CD19 Strategies Unlike CD20, CD19 is expressed on pro-B cells, plasmablasts and many plasma cells
CD19 targets other pathogenic B cell subsets “Double-Negative” (DN) B Cells precursors of autoantibody-secreting cells expanded in autoimmune diseases like SLE Defined by: CD19+ IgD- CD27-CXCR5- CD24lo Yuzi L et al, Clin Exp Immunol 2023
Suan D et al, J Immunol 2025 Other key roles of CD19 in pathogenesis Autoantibody-secreting surface Ig+ CD20− CD19+ CD38+ plasma cells in rituximab-refractory autoimmune patients Clinical remission of rituximab-refractory autoimmune disease induced by anti-CD19 chimeric antigen receptor T cells CD19+ plasma cells are not short-lived plasmablasts Autoantigen-binding B cells and CD19+ plasma cells serve a critical role in perpetuating T cell activation in autoimmune disease
Ioanna Minopoulou et al, Ann Rheum Dis 2024 CD19 CAR-T in vasculitis: B and plasma cell depletion Combined CD19 CD20 CD138 Before CAR T After CAR T B cell compartment
Tissue depletion with anti-CD20 monoclonals Lymph node B cells after: Tur C et al, Ann Rheum Dis 2025 anti-CD19 CAR-T Post-CAR Rituximab Post-RTX Obinutuzumab Post-OBI HE CD19+
Conclusions Durable remissions are associated with a B cell reset and deep depletion of B cells and plasma cells Targeting CD19 rather than CD20 offers potential for more complete B cell depletion, which can potentially be achieved with a monoclonal antibody approach This is likely to be particularly important in removing pathogenic autoantibodies, which is relevant for the treatment of many autoimmune diseases
Budoprutug: A Differentiated CD19 mAb with Broad Autoimmune Potential
CD19 is Emerging as a Preferred Pan-B-Cell Target CLP = common lymphoid progenitor, GC = germinal center, mAbs = monoclonal antibodies 1 Adapted from Suan J Immunol 2025, 2 Tur Annals Rheum Dis 2024 Broad B-cell expression profile with potential for achieving deeper and more durable B-cell depletion CD19 plays a mechanistic role across all stages of B-cell development, providing potential for profound and durable depletion of B cells and pathogenic autoantibodies1 Bone marrow Blood, lymphoid organs, tissues Bone marrow Pre-pro B cell Immature B cell Naive B cell GC B cell Memory B cell Short-lived plasmablast CD19+ plasma cell CD19+ plasma cell CD19- plasma cell CLP CD20 depletion CD38 depletion CD19 depletion CD20 CD38 CD19 Legend Naked mAbs targeting CD20 have been shown to deplete B cells in tissue2 Deeper depletion may be achieved by targeting CD19
Budoprutug is a Highly Potent, Fc-Enhanced Anti-CD19 mAb Designed for optimal biological activity, with potential for both IV and subcutaneous administration ADCC = antibody-dependent cellular cytotoxicity, IV = intravenous, mAb = monoclonal antibody, pM = picomolar 18 pM precisely-tuned, low-fucosylated Fc region increases potency vs wild-type Fc STRONG TARGET BINDING ENHANCED B CELL DEPLETION KEY FEATURES binding affinity to CD19 counters low antigen density 100x ADCC ≥175 mg/mL SUBCUTANEOUS DOSING POTENTIAL High concentration formulation with low viscosity
Budoprutug Has the Potential to Deliver Deep B-Cell Depletion Budoprutug demonstrated depletion of tissue-resident B cells in a human CD19 transgenic mouse model Company data on file. huCD19 transgenic C57BL/6J mice treated with budoprutug IV or Vehicle IV QW x 4. B-cell measurements taken at sacrifice 7-8 days post-last dose of budoprutug Lymph Node Bone Marrow Data expressed as % of CD45+ live cells, mean (SEM) Vehicle 0.1 mg/kg 1 mg/kg 10 mg/kg 100 mg/kg Vehicle 0.1 mg/kg 1 mg/kg 10 mg/kg 100 mg/kg 20 15 10 5 0 %B220+CD20+ 6 0 2 4 %B220+CD20+
AEs = adverse events, DLTs = dose limiting toxicities, LLOD = lower limit of detection, PLA2R = phospholipase A2 receptor, pMN = primary membranous nephropathy, SAEs = serious adverse events, UPCR = urine protein creatinine ratio 1 Cortazar ASN 2024, 2 Cortazar ASN 2025; Phase 1b pMN: budoprutug (100-200 mg) administered in two IV infusions, 14 days apart, at Wk 0 and Wk 24 Rapid and complete circulating B cell depletion observed in 100% (5/5) patients at doses of 100-200 mg Sustained reductions out to 1 year + after two dose cycles Anti-PLA2R antibody negativity achieved in 100% (3/3) evaluable patients All patients achieved complete (3/5) or partial (2/5) clinical remission by Week 48 Long-term control up to 3 years after initial dosing observed in 4 patients who received up to 4 doses2 No deaths, no drug-related SAEs, no discontinuations due to AEs, no DLTs Clinical Proof-of-Concept Demonstrated in Pilot Study in pMN Budoprutug administration resulted in durable B-cell depletion, serologic remission, and clinical remission (as measured by proteinuria) Anti-PLA2R Autoantibodies (RU/mL) 14 19.6 5.9 UPCR (g/g) 0.3 0.98 0.14 0.325 0.09 0.11 CD20+ cell count (cells/µL) NEGATIVE COMPLETE REMISSION LLOD 5.02 Week Week Week anti-PLA2R1 Proteinuria1 B Cells1
Developing Budoprutug Across Multiple Diseases Pursuing development in lead indications with high unmet need and clear B-cell driven pathology Primary Membranous Nephropathy (pMN) Progressive IgG4-mediated renal disease with clear pathophysiology support targeting of CD19-expressing B cells, with demonstrated clinical proof of concept Phase 1b completed Phase 2 ongoing Chronic disorder, affecting a single organ (blood cells), for which B-cell depletion has demonstrated clinical proof of concept Immune Thrombocytopenia (ITP) Phase 1b/2a ongoing Chronic, multi-organ autoimmune condition with early clinical validation for CD19 via other modalities Systemic Lupus Erythematosus (SLE) Global Phase 1b ongoing China Phase 1b in start-up Ongoing Studies Designed to Answer Key Clinical Questions Ability to achieve deep B-cell depletion ● Optimal dose in renal and non-renal indications ● Potential for long-term disease control
Seferiana Living with primary membranous nephropathy
pMN is a Progressive Renal Disease With Poor Outcomes Patients with uncontrolled pMN suffer from kidney failure and other comorbidities pMN = primary membranous nephropathy 1 Adapted from Nazareth J Mang Care Spec Pharm 2019, 2 Adapted from Troyanov Kid Intl 2004 Goal is to induce complete remission to prevent declining kidney function and eventual kidney failure2 Patients with uncontrolled disease suffer from major comorbidities1 (% patients experiencing complication over 1 year period, n=2,689) NR PR CR 1.0 0.9 0.8 0.7 0.6 0.5 0.4 0.3 0.2 0.1 0 Survival free from renal failure P<0.001 NR<PR<CR Years 0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 No Remission (NR) Partial Remission (PR) Complete Remission (CR)
Clear Pathophysiology Supporting Targeting of CD19 in pMN Pathogenic antibodies are IgG4 isotype and are secreted by CD19+ B cells GBM = glomerular basement membrane, PLA2R = phospholipase A2 receptor, pMN = primary membranous nephropathy Adapted from Ronco Nature Rev Disease Primers 2021, MENTOR: Fervenza NEJM 2019 B cells secrete anti-PLA2R antibodies that bind PLA2R on podocytes, forming subepithelial immune complexes. This leads to complement-mediated podocyte injury, disruption of the glomerular filtration barrier, proteinuria, and the development of nephrotic syndrome Plasmablasts and plasma cells are the source of the pathogenic autoantibodies Disappearance of pathogenic antibodies precedes clinical remission Rituximab MENTOR trial established B-cell depletion as a therapeutic option in pMN Podocyte Cytoskeleton GBM Endothelium Capillary Lumen PLA2R Slit Diaphragm Disruption and degradation of cytoskeleton Loss of Slit Diaphragm Proteinuria Protein Anti-PLA2R Antibody Vesicle Immune Deposit Thickened GBM Complement activation Loss of Slit Diaphragm Formation of new matrix
Anti-PLA2R is a Predictive and Prognostic Biomarker in pMN Immunologic recovery precedes proteinuria resolution; titer has been associated with long-term risk of disease progression Abs = antibodies, PLA2R = phospholipase A2 receptor, pMN = primary membranous nephropathy 1 Adapted from Lener KI 2021, 2 Adapted from Kanigcherla KI 2013 Anti-PLA2R titer associated with risk of kidney disease progression2 Anti-PLA2R reflects active autoimmune disease; immunologic recovery precedes resolution of proteinuria1 Severity Time (months-years) Podocyte damage Proteinuria resulting from podocyte injury Slowly resolving proteinuria in absence of autoimmune activity (clinical recovery and clinical remission) Onset of autoimmune disease activity Appearance of serum anti-PLA2R Abs ‘Kidney as sink’ 3 2 4 5 1 Doubling of serum creatinine - free Time from sample (years) P<0.001 Low Mid High 0 1 2 3 4 5 0.5 0.6 0.7 0.8 0.9 1.0
No Approved Therapies for pMN, Unmet Need Remains High KDIGO Guideline recommends off-label use of rituximab or CNIs, but remission rates are low, highlighting the need for disease-modifying therapies that deliver complete remission of proteinuria Ab = antibody, eGFR = estimated glomerular filtration rate, KDIGO = Kidney Disease Improving Global Outcomes, CNI = calcineurin inhibitor, PLA2R = phospholipase A2 receptor, pMN = primary membranous nephropathy 1 Adapted from KDIGO 2021 Guideline for the Management of Glomerular Diseases, 2 Fervenza NEJM 2019 KDIGO Guideline recommends treatment with rituximab, cyclophosphamide or CNI-based therapy based on risk estimate1 PRESENTATION TREATMENT MENTOR demonstrated benefit of rituximab vs. CNI, but only 35% patients achieved CR at 2 years2 Complete Remission (CR) Rate 1 year 2 years Rituximab 14% 35% CNI 1.5% 0% Low Risk Normal eGFR Asymptomatic proteinuria or improvement seen in last 6-12 months Wait and see with supportive care Wait and see or Rituximab or CNI Normal eGFR Symptomatic proteinuria with no improvement in last 6-12 months Not fulfilling high risk criteria Moderate Risk Elevated serum creatinine for >6 months Proteinuria decrease <50% in 6 months AND at least one of the following: Significant proteinuria >6 months, reduced eGFR, moderate PLA2R Ab or urine protein excretion High Risk Rituximab or CNI + rituximab or Cyclophosphamide + prednisolone Very High Risk Life threatening nephrotic syndrome High PLA2R antibody levels Low rate of response to rituximab Cyclophosphamide + prednisolone
Large Addressable Patient Population in pMN Majority of patients who do not achieve spontaneous remission will require treatment to prevent risk of progressive loss of kidney function PLA2R = phospholipase A2 receptor, pMN = primary membranous nephropathy 1 McGrogan Nephrol Dial Transplant 2011; ~1 per 100,000, 2 U.S. Census Estimates 2020-2025; assumes 28-year duration of pMN, 3 Crouser CJASN 2017, 4 KIDGO 2021 Guideline for the Management of Glomerular Diseases KDIGO Recommendation4 Immunosuppressive therapy should be considered in patients: with elevated anti-PLA2R and proteinuria >3.5 g/d at diagnosis for those who fail to reduce proteinuria <3.5 g after 6 months of supportive care Patients At Risk for Progressive Loss of Kidney Function (Moderate, High, Very High Risk) ~50,000 Spontaneous Remission (Low, Moderate Risk) ~25,000 pMN Adult Diagnosed Prevalence: ~75,000 ~66%3 ~33%3 1,2
Budoprutug Has a Highly Competitive Profile in pMN High serologic remission (anti-PLA2R negativity) and complete clinical remission rates support a potentially strong and differentiated clinical profile IV = intravenous, PLA2R = phospholipase A2 receptor, pMN = primary membranous nephropathy, q6m = every 6 months, SC = subcutaneous. Serologic remission defined as <14 RU/mL, complete remission defined as UPCR ≤0.3 g/g for budoprutug, rituximab, obinutuzimab and UPCR <0.5 g/g for povetacicept and felzartamab, partial remission defined as UPCR between <3.5 g/g and ≥50% reduction from baseline. 1 Cortazar ASN 2024, 2 Fervenza NEJM 2019 - immunological remission not reported, 3 Fervenza Kid Int 2008, 4 Fervenza CJASN 2010, 5 Roccatello Autoimmun Rev 2016, 6 Hu CJASN 2024, 7 Su KI Reports 2024, 8 Lin Kid Med 2024, 9 Madan KI Reports 2025, 10 Rovin KI Reports 2024 Budoprutug (based on completed pMN Ph1b) Rituximab Obinutuzimab Povetacicept Felzartamab Target CD19 CD20 CD20 BAFF/APRIL CD38 Serologic remission (anti-PLA2R negativity) 100% (3/3)1 64–95%2 (titer decrease) 90-92%6-7 100% (4/4)9 23% (6/26)10 Complete or partial clinical remission 100% (5/5)1 60% (39/65)2 85% (50/59) to 95% (20/21)6-7 100% (5/5)9 35% (9/26)10 Complete remission 60% (3/5)1 UPCR ≤0.3 g/g 14-41%2-5 UPCR ≤0.3 g/g 29-38%6-8 UPCR ≤0.3 g/g 40% (2/5)9 UPCR <0.5 g/g 0% (0/26)10 UPCR <0.5 g/g Dosing 2 IV doses administered 14 days apart, then q6m 2 x 1000 mg IV doses administered 7 days apart, then q6m 2 x 1000 mg IV doses administered 14 days apart, then q6m 80 mg SC every 4 weeks 9 IV doses over 6 months Note: To date, there are no FDA-approved therapies for pMN Table above reflects cross-trial comparisons and not data from head-to-head studies; differences exist between trial designs and participant characteristics and caution should be exercised when comparing data across trials.
PrisMN: Budoprutug Phase 2 pMN Study Global, open-label, dose escalation study enrolling patients with moderate to severe pMN NCT07096843 ACEi = angiotensin converting enzyme inhibitor, ARB = angiotensin receptor blocker, eGFR = estimated glomerular filtration rate, MN = membranous nephropathy, PLA2R = phospholipase A2 receptor, pMN = primary membranous nephropathy, UPCR = urine protein creatinine ratio Dose escalation starts at previous Phase 1b dose and escalates to 1000 mg 600 mg 1000 mg 200 mg OPEN-LABEL, DOSE ESCALATION STUDY N = 45 15 patients per cohort, enrolled sequentially Global footprint - ~45 sites across 8 countries Population 18-70 years of age Confirmed diagnosis of pMN, no secondary causes of MN UPCR ≥ 2.0 g/g PLA2R antibody positive Adequate trial of ACEi/ARB, with stable dose for ≥ 4 weeks eGFR ≥ 35 mL/min/1.73m2 ≥ 6 months since any prior B cell depleting agent USA Argentina Brazil Chile China Georgia Taiwan Ukraine
PrisMN: Budoprutug Phase 2 pMN Study Biomarker endpoints provide potential to rapidly identify a Phase 3 dose NCT07096843 eGFR = estimated glomerular filtration rate, Ig = immunoglobulin, IV = intravenous, LTFU = long term follow-up, PD = pharmacodynamic, PK = pharmacokinetic, PLA2R = phospholipase A2 receptor, pMN = primary membranous nephropathy, UPCR = urine protein creatinine ratio TREATMENT PERIOD LTFU Week 0 Week 48 Week 24 Week 36 = Budoprutug IV (2 doses, 14 days apart at Week 0 and Week 24) Primary Objective Safety and tolerability Secondary Objectives Preliminary PK and PK/PD PD markers (B cells, anti-PLA2R, total Ig) Preliminary efficacy: complete and partial remission at week 48 (UPCR and eGFR) Biomarker data will drive Phase 3 dose identification, while long-term follow-up will evaluate potential for disease remission Initial B-cell depletion and anti-PLA2R data from the low dose cohort (200mg at 12-24 weeks) anticipated Q4 2026
John Living with immune thrombocytopenia
ITP is a Chronic Bleeding Disorder with Multiple Comorbidities Autoantibody-mediated disease characterized by low platelet counts, leading to bruising, bleeding episodes, hemorrhage, and fatigue ITP = immune thrombocytopenia , QoL = quality of life 1 Adapted from Cooper ‘Perceptions’ AJH 2020, 2 Michel Eur J Haematol 2009, 3 Lawrie Br J Haematol 2023, 4 Kuter ASH 2024, 5 Cooper ‘HRQoL’ AJH 2020 Patient report of ITP symptoms at diagnosis1 (I-WISh Survey, n=1,507) Patients reporting sign/symptom as severe (%) 20 70 60 50 40 30 20 10 0 Patients reporting sign/symptom (%) 40 60 80 100 Petechiae Bruising Fatigue Epistaxis Hematoma Dizziness Blood in urine/stool Extra bleeding during surgery Thrombosis Headaches Depression Menorrhagia Anxiety Bleeding gums Bleeding cuts Typically diagnosed ~55 yrs, increased incidence with age2,3 High clinical burden, driven by steroid dependence and bleeding‑related hospitalizations4 Patients experience easy bruising, fatigue, functional limitations, and emotional impact5 Physicians prioritize bleeding prevention, QoL improvement, and normalization of platelet counts1
Anti-CD19 is a Potentially Disease Modifying Approach in ITP Targeting CD19 has potential to eliminate pathogenic, autoantibody-producing B cells, which are a critical disease driver in ITP ITP = immune thrombocytopenia Adapted from Lopez Blood Reviews 2025 B cells secrete anti-platelet autoantibodies which bind to platelets and mark them for destruction by macrophages Autoantibodies also bind megakaryocytes, impairing platelet production Rituximab established B-cell depletion as a therapeutic option in ITP
Potential for Sustained Elimination of Pathogenic B Cells with CD19 Broader expression of CD19 across B cell lineage may overcome limitations of anti-CD20 therapies ITP = immune thrombocytopenia, mAbs = monoclonal antibodies 1 Adapted from Mahevas J Clin Invest 2013, 2 Crickx Kidney Intl 2020, 3 Lucchini Haematologica 2019 B cell targeting via CD20 (rituximab) has demonstrated benefit in ITP, however up to 80% fail rituximab, likely due to the presence of CD19+/CD20- B cells1-3 Anti-CD20 mAbs do not eliminate plasmablasts or plasma cells, which continue to drive anti-platelet antibody production, while CD19 is expressed on plasmablasts and certain plasma cells2 Normal pre-rituximab post-rituximab CD19+/CD20- plasma cells expand within B cell niches post anti-CD20 treatment1 74.9% 2.4% 1.2%
ITP Remains Poorly Controlled After Steroid Failure Limited effective options, with a need for therapies that deliver durable platelet responses with improved safety and lower treatment burden ASH = American Society of Hematology, BID = twice daily, BTK = Bruton’s tyrosine kinase, ITP = immune thrombocytopenia, MOA = mechanism of action, RW = real world, SYK = spleen tyrosine kinase, TPO-RAs = thrombopoietin receptor agonists 1 ASH 2019 Guidelines for ITP (Neunert Blood Advances 2019), 2 Climb Market Research 2026, 3 fostamatinib prescribing information, 4 rilzabrutinib prescribing information Corticosteroids remain first line, followed by TPO-RAs or off-label rituximab1; SYK/BTK typically used after second line failure2 Fostamatinib3 Approved in 2018 Rilzabrutinib4 Approved in 2025 MOA SYK inhibitor BTK inhibitor Platelet Response 37-48% 64% Durable Response 16-18% 23% Warnings Hypertension Hepatotoxicity Diarrhea Neutropenia Hepatoxicity Dosing Oral, BID Oral, BID Study duration: 24 weeks; Definitions of platelet response and durable response varied across studies Fostamatinib prior therapy: 94% corticosteroids, 53% immunoglobulins, 48% TPO-RAs Rilzabrutinib prior therapy: 96% corticosteroids, 55% immunoglobulins, 69% TPO-RAs, 35% rituximab Durable responses remain low (~20%), with meaningful gaps in safety and treatment burden ASH 2019 Guidelines1 RW Treatment Practice2 Newly Diagnosed ITP Initial therapy: Corticosteroids TPO-RA, rituximab, or splenectomy fostamatinib, rilzabrutinib, or rituximab (if not already used) Treatment Required Watch & Wait Steroid-dependent or unresponsive Treatment failure
Significant Opportunity for a Disease Modifying Approach in ITP Chronic ITP patients often cycle through multiple therapies to maintain platelet control ~80-85% Require Initial Therapy3,4 3L = third line, ITP = immune thrombocytopenia 1 Feudjo-Tepie 2008, 2 U.S. Census Estimates 2020-2025,3 Moulis Haematol 2025, 4 Climb Market Research 2026 ~50-55% Become Dependent/Resistant3,4 ~45% Experience Treatment Failure3,4 40-50% of patients require chronic therapy ~20% progress to 3L+ disease, representing the highest unmet need Later-line ITP represents a high-value opportunity for disease-modifying therapies Patients in 3L+ Chronic ITP ~17,000 Diagnosed Adults with Primary ITP 1,2 (23.6 per 100 K) ~85,000 Require Initial Therapy (corticosteroids) ~70,000 Escalate to Second Line Therapy ~35,000
Budoprutug Phase 1b/2a ITP Trial Multi-center, open-label, dose escalation study enrolling previously treated patients with ITP NCT07043946 ITP = immune thrombocytopenia Evaluation of 3 doses, ranging from 250-1000 mg 500 mg, n=9 1000 mg, n=9 250 mg, n=6 OPEN-LABEL, DOSE ESCALATION STUDY Up to 9 patients per cohort, enrolled sequentially Recruitment ongoing in 20 sites across 5 countries Bulgaria Greece Serbia Spain Ukraine Population ≥ 18 years of age Insufficient response to 1 or more prior therapies Platelet count < 30,000/µL; confirmed on 2 occasions ≥ 24 weeks since any prior B-cell depleting agent
Budoprutug Phase 1b/2a ITP Trial Designed to define dose and establish depth and duration of B-cell depletion and platelet response NCT07043946 ITP = immune thrombocytopenia, IV = intravenous, LTFU = long term follow-up Primary Objective Safety and tolerability Secondary Objectives Pharmacokinetic profile Effects on B-cell depletion (pharmacodynamic response) Effects on platelet counts (ITP clinical response) Platelet response will be assessed during the treatment period, and long-term follow-up will evaluate potential for disease remission TREATMENT PERIOD Week 0 Week 36 Week 12 Week 48 Week 24 LTFU = Budoprutug IV (2 doses, 14 days apart at Week 0 and Week 24) Initial B-cell depletion and platelet data from the low dose cohort (250mg at 24 weeks) anticipated June 2026 Additional data expected by year end
Marisa Living with systemic lupus erythematosus
Strong Rationale for Anti-CD19 mAb in SLE CD19 mAb approach could provide optimal profile of disease control, safety, and broad patient accessibility BAFF = B-cell activating factor, CAR = chimeric antigen receptor, CRS = cytokine release syndrome; ICANS = immune effector cell associated neurotoxicity syndrome, LN = lupus nephritis, mAb = monoclonal antibody, SLE = systemic lupus erythematosus 1 belimumab prescribing information, 2 obinutuzumab prescribing information, 3 Scherlinger Annals Rheumatic Diseases 2019, 4 Müller NEJM 2024 mAb approach can overcome key CAR T-cell challenges Low risk of CRS and ICANS, no lymphodepletion required Long treatment interval with the ability to easily retreat as needed Administered in the community setting Likely reasons for anti-CD20 treatment failure are addressable with CD19 targeting Persistence of CD19+ self-reactive B-cell subsets Continued production of pathogenic autoantibodies by plasmablasts Rapid recovery of pathogenic B-cell subsets but up to 55% of patients still fail to achieve disease control Anti-BAFF mAb approved for SLE/LN1, anti-CD20 Ab approved for LN2, and rituximab used off-label3 CD19 CAR Ts demonstrate strong efficacy B-cell targeting has promise but have significant risks and access challenges 8/8 SLE patients treated with anti-CD19 CAR T-cells achieved disease remission by 6 months4
Parallel Global and China SLE Studies Designed to assess B-cell depletion and kinetics of re-repopulation of B-cell subsets Global study: NCT07011043 China study: NCT07564596 FPI = first patient in, IV = intravenous, LTFU = long term follow-up, SLE = systemic lupus erythematosus, SLEDAI = SLE disease activity index China Phase 1b/2a Study Global Phase 1b Study Enrolling adults with seropositive SLE; SLEDAI ≥ 8; refractory to adequate trials of at least 2 therapies Enrolling adults with seropositive SLE; SLEDAI ≥ 6; refractory to adequate trial of at least 1 therapy Initial data from low dose cohorts in the Global Study anticipated in Q4, with FPI in China Study on track for Q2 = Budoprutug IV Day 1 and Day 15 TREATMENT PERIOD Week 0 Week 28 LTFU DOSE ESCALATION, N ~18 Up to 6 patients per cohort enrolled sequentially DOSE EXPANSION, N ~12 Up to 12 patients at dose identified in escalation period 300 mg 600 mg 100 mg Dose selected; administered as 2 doses, 14 days apart = Budoprutug IV Day 1 SINGLE ASCENDING DOSE COHORTS, N ~30 30 mg 100 mg 10 mg 200 mg Up to 6 patients per cohort enrolled sequentially Subtherapeutic doses TREATMENT PERIOD Week 24 LTFU Week 0
Budoprutug – Subcutaneous (SC) Formulation
Budoprutug SC Formulation Phase 1 Trial Completed NCT07090655 HV = healthy volunteers, IV = intravenous, SC = subcutaneous Follow-up continued for subjects whose B cell count was not above 50% of baseline or above lower limit of normal by week 8 Day 1 = Budoprutug SC or IV, Day 1 INPATIENT Week 8 Day 4 FOLLOW-UP SINGLE ASCENDING DOSE COHORTS 8 subjects per SC cohort (6 budoprutug: 2 placebo) 14 subjects in the IV cohort (12 budoprutug: 2 placebo) Cohort 1: 3 mg SC Cohort 2: 6 mg SC Cohort 3: 6 mg IV (matched dose) Low doses of budoprutug were chosen to achieve non-complete (~50%) peripheral B cell depletion in HV Evaluation of pharmacodynamic effects of budoprutug SC and IV in healthy volunteers
AUC = area under the curve, HV = healthy volunteers, IV = intravenous, SC = subcutaneous Company data on file Budoprutug SC administration demonstrated ~80% B-cell depletion; similar magnitude and time course of depletion between SC and IV Robust B-cell Depletion Observed with Budoprutug SC in HV Budoprutug SC was well-tolerated; safety profile consistent between SC and IV 6 mg 6 mg 3 mg Placebo SC IV 6 mg 6 mg 3 mg Placebo SC IV
Budoprutug SC: Future Direction Data in NHPs and healthy volunteers support continued development of SC formulation, with plans to advance to a study in patients to confirm dose and regimen PD = pharmacodynamic, NHPs = nonhuman primates, SC = subcutaneous Healthy Volunteers (low dose) Next Steps Nonhuman Primates Data confirmed bioavailability and demonstrated favorable safety/ tolerability Evaluation of SC formulation at a full B-cell depleting dose regimen in patients with autoimmune diseases Robust PD effects support continued clinical development
Dose pMN ITP GL SLE CH SLE 10 mg 30 mg 100 mg 200 mg 250 mg 300 mg 500 mg 600 mg 1000 mg ◆ ◆ ◆ ◆ ◆ ◆ ◆ ◆ ◆ ◆ Laying the Foundation for Budoprutug’s Long-Term Potential Emerging data will further inform safety and the ability to achieve deep B-cell depletion, the optimal dose in renal and non-renal indications, and the potential for long-term disease control Range of budoprutug doses assessed across studies will inform dose selection for future trials SC data in healthy volunteers ITP, B cell & platelets, low dose – June pMN, B cell & PLA2R, low dose – Q4 Global SLE, B cell & Ab, low doses – Q4 ITP, additional data – YE Anticipated 2026 Data Readouts Anticipated Study Milestones & Next Steps China SLE – FPI Q2 ‘26 SC – Initiate multiple dose patient study Ab = antibody, CH = China, FPI = first patient in, GL = global, ITP = immune thrombocytopenia, PLA2R = phospholipase A2 receptor, pMN = primary membranous nephropathy, SC = subcutaneous, SLE = systemic lupus erythematosus ü ◆ ◆ ◆
ITP = immune thrombocytopenia; mAb = monoclonal antibody, pMN = primary membranous nephropathy, SLE = systemic lupus erythematosus Meaningful Near-Term Milestones Upcoming data expected to define dose, durability, and clinical profile for budoprutug Market White Space CD19 monoclonal antibodies remain underrepresented in immune-mediated diseases, creating a compelling opportunity for leadership Core Indications Informed by Biology and Market Opportunity Targeting pMN, ITP, and SLE, diseases united by B-cell pathology and high unmet medical needs Validated CD19 Target CD19 is broadly expressed across the B-cell lineage, including early B cells and antibody-producing cells—populations not fully addressed by an anti-CD20 approach Monoclonal Antibody Design Potential to combine potency with the scalability and clinical familiarity characteristic of monoclonal antibodies Budoprutug: A Differentiated CD19 mAb with Expansive Potential
Q&A Session Aoife Brennan, M.B., Ch.B. President and CEO, Climb Bio David Jayne, M.D. Professor, University of Cambridge Edgar Charles, M.D. Chief Medical Officer, Climb Bio Perrin Wilson, Ph.D. Chief Business Officer, Climb Bio Susan Altschuller, Ph.D., MBA Chief Financial Officer, Climb Bio