CLYM
Published on 05/05/2026 at 08:17 am EDT
MAY 5, 2026
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
© 2026 Climb Bio 3
Delivering Clinical Results and Advancing Development
Corporate Highlights
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*
* 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
© 2026 Climb Bio 4
Pipeline of Highly Differentiated mAbs
Anticipating initial readouts from all ongoing trials in 2026
PRE- CLINICAL
IND- ENABLING
PHASE 1
PHASE 2
PHASE 3
data mid-year '26
STATUS & ANTICIPATED MILESTONES
INDICATION(S)
Primary Membranous
Initial Ph2 data Q4 '26
Nephropathy
Budoprutug IV
Immune
Initial Ph1b data June '26
Anti-CD19
Thrombocytopenia
Additional Ph1b data YE '26
Systemic Lupus
FPI China Ph1b Q2 '26
Erythematosus
Initial Global Ph1b data Q4 '26
Budoprutug SC
Anti-CD19
Autoimmune
Disease
Initiate multiple dose patient study
CLYM116*
Anti-APRIL
IgA Nephropathy
Modeling/Ph1 HV safety June '26
Initial PK/PD Ph1 HV
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.
CD19 mAb Targeting Remains a White Space
Low competitive intensity for an established modality translates into opportunity for budoprutug
CD19 Autoimmune Competitive Landscape1
B-Cell Depleting Approaches
Rationale for a mAb Approach
>13
3
>18
Monoclonal
Antibodies
T Cell
Engagers
Cell
Therapies
Targeted immunomodulation without lymphodepletion
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
mAb = monoclonal antibody; TCEs = T cell engagers
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
Inebilizumab Consensus Sales Estimates1
Significant potential opportunity for budoprutug in B-cell mediated diseases beyond inebilizumab's neuro focus
$2,303
$2,122
$1,801
$1,458
$1,046
$655
$379
$244
$61 $155
$2,500
Global Net Revenue ($USD)
$2,000
$1,500
$1,000
$500
$0
2021 2022 2023 2024 2025 2026E 2027E 2028E 2029E 2030E
NMOSD approval, Jun 2020; IgG4-RD approval, Apr 2025; gMG approval, Dec 2025
gMG = generalized myasthenia gravis, IgG4-RD = immunoglobulin G4-related disease, mAb = monoclonal antibody, NMOSD = neuromyelitis optica spectrum disorder
Budoprutug Target Indications Represent a Robust Opportunity Set
Pursuing development in diseases with large addressable populations and significant unmet need
EPIDEMIOLOGY (US)
UNMET NEED
BUDOPRUTUG OPPORTUNITY
Primary Membranous Nephropathy (pMN)
~75,000
patients1,2
Progressive renal disease characterized by proteinuria, nephrotic syndrome and progressive loss of renal function5
No approved therapies
Potential for long-term disease remission based on initial clinical data
Fast Track Designation granted
Immune Thrombocytopenia (ITP)
~85,000
patients2,3
Systemic Lupus Erythematosus (SLE)
~240,000
patients2,4
Chronic bleeding disorder characterized by
the destruction of platelets6
Poor QoL, with majority of previously treated patients failing to achieve durable platelet response6
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 to achieve durable response and disease remission in the previously treated population
Potential for broad B-cell targeting and disease suppression with the safety and convenience of a mAb
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,
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
9
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)
Kidney biopsy of a patient with pMN
IgG
Failure to remove circulating autoantibodies
Incomplete removal of tissue resident B cells
Only partial efficacy
and high relapse rate
SLE: anti-DNA antibodies after rituximab SLE: B cells in the kidney drive poor prognosis
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
Unlike CD20, CD19 is expressed on pro-B cells, plasmablasts and many plasma cells
"Double-Negative" (DN) B Cells
precursors of autoantibody-secreting cells
expanded in autoimmune diseases
like SLE
Defined by:
CD19+ IgD- CD27-CXCR5- CD24lo
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
Before CAR T
Combined CD19 CD20 CD138
After CAR T
B cell compartment
Lymph node B cells after:
Obinutuzumab
CD19+
HE
Post-OBI
Rituximab
Post-RTX
anti-CD19 CAR-T
Post-CAR
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
© 2026 Climb Bio 19
CD19 is Emerging as a Preferred Pan-B-Cell Target
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
Naked mAbs targeting CD20 have been shown to deplete B cells in tissue2
Deeper depletion may be achieved by targeting CD19
Bone marrow
Blood, lymphoid organs, tissues
Bone marrow
Naive
B cell
GC
B cell
Memory
B cell
CD19-
plasma cell
CD19+
plasma cell
CD19+
plasma cell
Short-lived
plasmablast
Immature
B cell
Pre-pro
B cell
CLP
Legend
CD19
CD38
CD20
CD19 depletion
CD38 depletion
CD20 depletion
CLP = common lymphoid progenitor, GC = germinal center, mAbs = monoclonal antibodies
1 Adapted from Suan J Immunol 2025, 2 Tur Annals Rheum Dis 2024
© 2026 Climb Bio 20
© 2026 Climb Bio
Disclaimer
Climb Bio Inc. published this content on May 05, 2026, and is solely responsible for the information contained herein. Distributed via Public Technologies (PUBT), unedited and unaltered, on May 05, 2026 at 12:16 UTC.