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© 2026 Climb Bio 1 Corporate Presentation JANUARY 2026
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© 2026 Climb Bio 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 Phase 1b clinical trial of budoprutug in patients with systemic lupus erythematosus in China and the projected enrollment of patients with systemic lupus erythematosus that have lupus nephritis; the anticipated benefits of Climb Bio’stechnology transfer and exclusivelicense agreement with Beijing Mabworks Biotech Co., Ltd. (“Mabworks”); 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 theseforward-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 licenseagreement with Mabworks; 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 investigational 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, 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; andraising 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 datehereof 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 anyobligation to do so, except as required by law.
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© 2026 Climb Bio 3 © 2025 Climb Bio 3 Deliver high impact, disease-modifying medicines for individuals living with immune-mediated diseases Scaling New Heights in the Development of Transformative Immune Medicines © 2026 Climb Bio 3 O U R M I S S I O N
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© 2026 Climb Bio 4 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 • 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 pMN = primary membranous nephropathy; ITP = Immune Thrombocytopenia; SLE = Systemic Lupus Erythematosus; IgAN = IgA Nephropathy Corporate Highlights
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© 2026 Climb Bio 5© 2025 Climb Bio 5 Climb Bio is Poised for a Data-Rich 2026 Five clinical studies underway, with initial readouts anticipated from all ongoing trials Budoprutug SC Initial Ph1 HV data – H1 ‘26 PK, PD, bioavailability Budoprutug pMN Initial Ph2 data – H2 ‘26 Budoprutug ITP Initial Ph1b data – H2 ‘26 Preliminary efficacy Budoprutug SLE Initial global Ph1b data – H2 ‘26 Preliminary efficacy CLYM116 Initial Ph1 HV data – mid ‘26 PK, PD 2026Key 2025 Achievements CLYM116 in-licensing and Phase 1 initiation Budoprutug ITP , SLE, and pMN PrisMN trial initiations Budoprutug SC Phase 1 initiation Clearance of budoprutug SLE IND in China ITP = Immune Thrombocytopenia; SLE = Systemic Lupus Erythematosus; pMN = primary membranous nephropathy; SC = subcutaneous; IND = investigational new drug; HV = healthy volunteers; PK = pharmacokinetics, PD = pharmacodynamics
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© 2026 Climb Bio 6 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. *Greater China defined as mainland China, Hong Kong, Macau, and Taiwan; Partner: Beijing Mabworks Biotech Co., Ltd. APRIL = a proliferation-inducing ligand, IV = intravenous, mAbs = monoclonal antibodies, SC = subcutaneous Budoprutug IV Anti-CD19 INDICATION(S) Primary Membranous Nephropathy Systemic Lupus Erythematosus Immune Thrombocytopenia Autoimmune Disease CLYM116 Anti-APRIL IgA Nephropathy Budoprutug SC Anti-CD19 PRE -CLINICAL PHASE 1 PHASE 2 PHASE 3IND -ENABLING CLIMB RIGHTS Worldwide Worldwide Worldwide Outside Greater China* Initial data H2 ‘26 Initial data H1 ‘26 Initial data mid ‘26 ANTICIPATED MILESTON ES Initial data H2 ‘26 Initial Global Ph1b data H2 ‘26 FPI China Ph1b H1 ‘26
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© 2026 Climb Bio 7 Pursuing Expansive Market Opportunities Addressing the needs of patients living with B cell-mediated diseases ANCA-AAV = antineutrophil cytoplasmic antibody-associated vasculitis, CIDP = Chronic inflammatory demyelinating polyradiculoneuropathy, IgAN = IgA Nephropathy, ITP = Immune Thrombocytopenia, NMOSD = Neuromyelitis optica spectrum disorder, pMN = Primary Membranous Nephropathy, SLE = Systemic Lupus Erythematosus, mAb = monoclonal Ab. Prevalence sources: B cell-mediated disease (internal research), IgAN (Tarpeyo CDER Integrated Review 2021, Filspari CDER Integrated Review 2022), ITP (internal research), pMN (internal research), SLE (Izmirly Arthritis Rheumatol 2021). TODAY Opportunity: >500k PATIENTS TOMORROW Opportunity: ~2M PATIENTS ITP ~85k pMN ~70k SLE ~240k Budoprutug, Anti-CD19 mAb CLYM116, Anti-APRIL mAb IgAN ~170k ANCA-AAV Bullous pemphigoid Lupus nephritis Myasthenia gravis NMOSD Pemphigus vulgaris Rheumatoid arthritis Sjögren’s disease Systemic sclerosis CIDP Idiopathic inflammatory myopathies IgG4 related disease
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© 2026 Climb Bio 8© 2025 Climb Bio 8 Climb Bio Team Poised to Deliver for Patients Douglas E. Williams, PhD Independent, Chairman Aoife Brennan, MB, ChB Bo Cumbo CEO, Solid Biosciences Kim Drapkin, CPA Independent Judith Dunn, PhD President, Head of R&D, Vima Therapeutics Andrew Levin, MD, PhD Managing Director, RA Capital Stephen Thomas, PhD CEO, Sera Medicines B O A R D O F D I R E C T O R S Aoife Brennan, MB, ChB President and CEO Perrin Wilson, PhD CBO Chandra Adams, JD VP, General Counsel Edgar Charles, MD CMO Susan Altschuller, PhD, MBA CFO Cindy J. Driscoll, MBA SVP, Finance Adam Villa, MBA, MS SVP, Tech Ops Ashley Jones SVP, People & Workforce Strategy
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© 2026 Climb Bio 9 Budoprutug Anti-CD19
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© 2026 Climb Bio 10 Budoprutug: A Differentiated Anti-CD19 Approach CRS = cytokine release syndrome, ICANS = immune effector cell associated neurotoxicity syndrome, IV = intravenous, mAb = monoclonal antibody, pM = picomolar, SC = subcutaneous Cortazar ASN 2024 Durable B cell depletion, long dosing interval, with potential for IV and SC formulations Clear Opportunity • Only one approved CD19 mAb – positioned for rare diseases • Substantial potential for budoprutug in broader disease areas where a larger patient subset can benefit • Strong IP protection extending to 2045+ Potential Differentiating Benefits Rapid, deep and durable B cell depletion and favorable tolerability demonstrated in a pilot clinical study mAb modality confers distinct advantages Long dosing interval, with potential to formulate for both IV and SC administration • Well-established manufacturing and supply chains, favorable cost-of-goods and scalability • Minimal off-target effects, with a low risk of CRS and ICANS; no lymphodepleting chemotherapy preconditioning requirement • Ability to dose in the community setting; no in- hospital or special unit administration required 2 31
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© 2026 Climb Bio 11 CD19: Attractive and Validated Target for B Cell-Mediated Disease Ab = antibody, BLA = biologics license application, CAR = chimeric antigen receptor, IgG4-RD = immunoglobulin G4-related disease, mAb = monoclonal antibody, MG = myasthenia gravis, NMOSD = neuromyelitis optica spectrum disorder, SLE = systemic lupus erythematosus. Zhang Front Immunol 2023, Müller NEJM 2024, Novak NEJM 2025, Osborne Front Neurol 2024, inebilizumab prescribing information, Amgen press release May 1 2025 CD19 CD20 CD38 CD22 BAFF-R BCMA TACI Pro-B Pre-B Immature B Naïve B GC B Memory B Plasma blast Plasma cell Ab-secreting B cells CD19 expressed across B lineage cells including Ab-secreting cells Clinically Proven Approach Broad CD19 expression profile enables comprehensive, rapid and durable depletion of pathogenic B cells, while preserving protective antibody responses mediated by long-lived plasma cells CD19 expression profile provides potential efficacy and safety advantages relative to other targets CD19 CAR T Therapies • Have demonstrated potential for remission in SLE patients CD19 mAb Therapy (inebilizumab) • Approved for NMOSD and IgG4-RD • BLA filed for MG • Demonstrated benefit in rituximab relapse and where rituximab has failed
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© 2026 Climb Bio 12 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, 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
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© 2026 Climb Bio 13 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) Initial data expected H2 2026 Phase 1b/2a ongoing Chronic, multi-organ autoimmune condition with early clinical validation for CD19 via other modalities; subset of patients have kidney involvement (lupus nephritis) Systemic Lupus Erythematosus (SLE) Initial data from global study expected H2 2026 Global Phase 1b ongoing China Phase 1b in start-up Initial data expected H2 2026
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© 2026 Climb Bio 14 • Autoantibody mediated disease characterized by proteinuria, nephrotic syndrome and progressive loss of renal function • Untreated, ~30% progress to end-stage renal disease within 10 years and another 30% develop chronic kidney disease • Rituximab used off-label and considered first-line; 20-40% patients are refractory • Clear unmet need for disease-modifying therapies that deliver complete remission of proteinuria • Early demonstration of efficacy and approval possible based on a validated biomarker indicative of kidney damage: proteinuria Progressive renal disease Primary Membranous Nephropathy (pMN) pMN = primary membranous nephropathy; US Prevalence: internal research; Couser CJASN 2017, Ronco J Clin Med 2021, Teisseyre Front Immunol 2022, KDIGO 2021 guidelines No approved therapies Clear path to approval T H E C L I M B S O L U T I O N Budoprutug demonstrated compelling proof-of- concept in a pilot Phase 1b clinical study in pMN S I G N I F I C A N T O P P O R T U N I T Y ~70,000 patients in the US alone
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© 2026 Climb Bio 15 Completed Phase 1b Study Established Proof of Concept in pMN Budoprutug evaluated in an open-label, dose escalation study in adult patients with pMN (NCT04652570) IV = intravenous, LTFU = long term follow-up, PLA2R = phospholipase A2 receptor, pMN = primary membranous nephropathy, UPCR = urine protein creatinine ratio Cortazar ASN 2024; Baseline characteristics for primary analysis set (N=5), PLA2R from patients with positive anti-PLA2R antibodies at baseline (N=3) Patients had moderate to severe disease at baseline • B cells: 145 ± 116 cells/µL • PLA2R: 71 ± 16 RU/mL • UPCR: 4.03 ± 1.66 g/g N=8 enrolled N=4 ≥1 dose N=4 ≥1 dose N=2 4 doses N=3 4 doses 200 mg 100 mg Primary analysis set LTFUDOSING REGIMEN Week 0 Week 72Week 48Week 24 (induction) (maintenance) = Budoprutug IV infusion (2 doses, 14 days apart)
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© 2026 Climb Bio 16 0 8 16 24 32 40 48 56 64 72 80 0 50 100 150 200 250 300 350 week CD20+ cell count (cells/µL) Budoprutug Administration Resulted in Durable B Cell Depletion Rapid and complete circulating B cell depletion observed in 100% of patients at doses of 100-200mg LLOD = lower limit of detection, pMN = primary membranous nephropathy Cortazar ASN 2024; Phase 1b pMN: budoprutug administered in two IV infusions, administered 14 days apart, at Week 0 and Week 24 LLOD: 5.02 Complete circulating B cell depletion (CD20+ count < 5 cells/μL) achieved in all 5/5 patients • Rapid depletion: LLOD reached as soon as 2 weeks after first dose • Sustained reductions out to 1 year + after two dose cycles Primary analysis set, N=5
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© 2026 Climb Bio 17 Budoprutug Administration Resulted in Serologic Remission Anti-PLA2R antibody negativity achieved in 100% (3/3) evaluable patients Ab = antibody, LLOD = lower limit of detection, PLA2R = phospholipase A2 receptor, pMN = primary membranous nephropathy Cortazar, ASN 2024 ; Phase 1b pMN: budoprutug administered in two IV infusions, administered 14 days apart, at Week 0 and Week 24. 1. Stefan 2022, 2. Ronco J Clin Med 2021 anti-PLA2R Ab assay positive >14 RU/mL1 Patients from primary analysis set with anti-PLA2R antibodies at baseline, N=3 PLA2R antibodies are the primary disease driver in pMN and a key biomarker of clinical response2 • ~80% of pMN is mediated by anti-PLA2R autoantibodies • Disappearance of anti- PLA2R antibodies precedes clinical remission
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© 2026 Climb Bio 18 Budoprutug Administration Led to Clinical Remission (Proteinuria) All patients achieved complete or partial clinical remission by Week 48, as measured by UPCR pMN = primary membranous nephropathy, UPCR = urine protein creatinine ratio Cortazar ASN 2024, Cortazar ASN 2025; Phase 1b pMN: budoprutug administered in two IV infusions, administered 14 days apart, at Week 0 and Week 24 Complete clinical remission UPCR < 0.3 g/g All patients achieved complete (3/5) or partial (2/5) clinical remission by Week 48 • 2 patients with partial clinical remission achieved serologic remission, suggesting further progress to full clinical remission may be possible Long-term control of proteinuria for up to 3 years after initial dosing was observed in 4 patients who received up to 4 doses of budoprutug • In 3 of these patients, no further immunosuppressive treatment was required Primary analysis set, N=5 Proteinuria (UPCR) is a key measure of kidney function and is the primary outcome measure in pMN
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© 2026 Climb Bio 19 There were no deaths on study There were 3 SAEs, none considered to be related to budoprutug by the investigator No discontinuations due to AE No dose limiting toxicities (DLTs) were observed 4 patients reported infections on study of which 3 were cases of COVID-19 and 1 was bacterial pneumonia Safety AE = adverse event, SAE = serious adverse event Cortazar ASN 2024 Budoprutug was generally well tolerated in the completed Phase 1b pMN trial at doses of up to 200mg, supporting exploration of higher doses in ongoing and future studies 8 Patients received at least one injection of budoprutug and were included in the safety analysis population in the completed Phase 1b pMN trial
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© 2026 Climb Bio 20 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; 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, 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%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%3-5 UPCR ≤0.3 g/g 29-38%6-8 UPCR ≤0.3 g/g 40% (2/5)9 UPCR <0.5 g/g n/a10 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.
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© 2026 Climb Bio 21 DOSING REGIMEN LTFU PrisMN: Budoprutug Phase 2 pMN Study Enrolling Biomarker endpoint provides potential to rapidly identify dose to carry forward into Phase 3 (NCT07096843); initial data anticipated in H2 2026 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 Population • 18-70 years of age • UPCR ≥ 2.0 g/g; designed to ensure adequate enrollment of patients with UPCR > 5.0 g/g • PLA2R antibody positive Primary Objective • Safety and tolerability Open-label, dose ranging study Week 0 Week 72Week 48Week 24 (induction) (maintenance) Week 36 = Budoprutug IV infusion (2 doses, 14 days apart) 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) Mid Dose High Dose Low Dose DOSE ESCALATION 15 patients per cohort, enrolled sequentially
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© 2026 Climb Bio 22 Immune Thrombocytopenia (ITP) • Autoantibody mediated disease characterized by the destruction of platelets • Results in bruising, bleeding episodes, hemorrhage and fatigue • ~80% fail first line glucocorticoids; ~40% progress on second line TPO-RAs • Rituximab has demonstrated the potential to achieve long-term disease remission, but only ~20% maintain remission • Surgical removal of the spleen may be considered for chronic cases or when therapeutic interventions fail • Platelet response can demonstrate early proof-of- concept and served as primary endpoint measure for approvals in ITP Chronic bleeding disorder Limited treatment options Defined endpoint T H E C L I M B S O L U T I O N Budoprutug has the potential to achieve disease remission in this high unmet need population S I G N I F I C A N T O P P O R T U N I T Y ~85,000 patients in the US alone BTK = Bruton’s tyrosine kinase, pMN = primary membranous nephropathy; US Prevalence: Internal Research; StatPearls Pietras 2024, Gafter-Gvili A Euro J Int Med 2023, Lucchini Haematologica 2019, Internal Research
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© 2026 Climb Bio 23 Strong Rationale for CD19 Approach in ITP Potent anti-CD19 approach offers the promise of sustained elimination of anti-platelet antibodies ITP = Immune Thrombocytopenia, mAb = monoclonal antibody, RTX = rituximab Mahevas J Clin Invest 2013, Crickx Kidney Intl 2020, 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 cells • 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 some plasma cells Broader expression of CD19 across B cell lineage may overcome limitations of anti-CD20 therapies Normal pre-RTX post-RTX 1 10 100% plasma cells in spleen HV CD19+/CD20- plasma cells expand within B cell niches post anti-CD20 treatment 74.9% 2.4% 1.2%
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© 2026 Climb Bio 24 Budoprutug Phase 1b/2a ITP Trial Enrolling Designed to define dose and regimen, and establish depth and duration of platelet response and B cell depletion (NCT07043946); initial data anticipated in H2 2026 ITP = Immune Thrombocytopenia, LTFU = long term follow-up, LLN = lower limit of normal = Budoprutug IV infusion Day 1, Day 15 DOSING REGIMEN Week 0 Week 52Week 36Week 12 Week 48Week 24 LTFU OPTIONAL SECOND CYCLE based on platelet response DOSE ESCALATION Up to 6 patients per cohort enrolled sequentially DOSE EXPANSION Up to 6 patients at dose identified during escalation period Cohort 2 Cohort 3 Cohort 1 FOLLOW -UP UNTIL B CELL RECOVERY (LLN or ≥ 80% OF BASELINE) Dose selected; administered as 2 doses, 14 days apart Population • N ~ 30 patients • Insufficient response to 1 or more prior therapies • Platelet count <30,000/µL Primary Objective • Safety and tolerability Secondary Objectives • Pharmacokinetic profile • Effects on B cell depletion (pharmacodynamic response) • Effects on platelet counts (ITP clinical response) Open label, dose escalation and expansion study
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© 2026 Climb Bio 25 • Steroids given first-line but are not a long-term solution • ~50% of patients on approved biologics relapse • Off-label rituximab is a mainstay of treatment, underscoring need for more effective therapies • Autoreactive lymphocytes and autoantibodies mistakenly attack tissues and organs throughout the body • Wide array of autoantibodies cause disease manifestations that can affect virtually any organ system; subset of patients have kidney involvement (lupus nephritis) • Relapses may lead to cumulative damage and organ failure • CD19 CAR T-cell therapies have demonstrated potential for remission; but modality limits broad utility and patient access Chronic autoimmune condition Systemic Lupus Erythematosus (SLE) Approved biologics includes anti-BAFF (B-cell activating factor) and anti-interferon therapies. CAR = chimeric antigen receptor, IFN = interferon, mAb = monoclonal antibody, PoC = proof-of-concept, SLE = systemic lupus erythematosus. US Prevalence: Izmirly Arthritis Rheumatol 2021, Wang BMC Research Notes2022, Marinho Front Immunol 2023, Wu J Manag Care Spec Pharm 2023. High unmet need Established PoC for CD19 T H E C L I M B S O L U T I O N Budoprutug offers potential for broad B-cell targeting with the safety and convenience of a mAb S I G N I F I C A N T O P P O R T U N I T Y ~240,000 patients in the US alone
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© 2026 Climb Bio 26 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, IFN = interferon, LN = lupus nephritis, mAb = monoclonal antibody, SLE = systemic lupus erythematosus Furie NEJM 2025, Scherlinger Annals Rheumatic Diseases 2019, belimumab prescribing information, Roche Press release March 5 2025, 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/LN, anti-CD20 mAb filed for LN, rituximab used off- label CD19 CAR Ts demonstrate strong efficacyB-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 months
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© 2026 Climb Bio 27 Budoprutug Global SLE Phase 1b Trial Enrolling Designed to define optimal dose and assess depth and duration of B cell depletion and autoantibody reduction (NCT07011043); initial data anticipated in H2 2026 IV = intravenous, LTFU = long term follow-up, PD = pharmacodynamic; PK = pharmacokinetic; SLE = Systemic Lupus Erythematosus Week 0 = Budoprutug dose Day 1, single IV infusion DOSING PERIOD Week 24Week 4 SINGLE ASCENDING DOSE COHORTS, N ~30 Cohort 2 Cohort 3 Cohort 1 Cohort 4 LTFU Up to 6 patients per cohort enrolled sequentially Population • N ~ 30 patients • Seropositive SLE with SLEDAI≥8 • Refractory to adequate trials of at least 2 therapies • Stable protocol-limited background therapy at entry Primary Objective • Safety and tolerability Key Secondary/Exploratory Objectives • Effects on B cell depletion (PD response), autoantibody levels, and protective antibody levels • PK and PK/PD profile • Preliminary signs of clinical activity • Kinetics of re-population of B cell subsets and antibodies after depletion Open-label, dose escalation study
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© 2026 Climb Bio 28 Budoprutug China SLE Phase 1b Trial in Start-up Companion to global study, with potential to evaluate lupus nephritis; Dosing of first patient anticipated H1 2026 IV = intravenous, LTFU = long term follow-up, PD = pharmacodynamic; PK = pharmacokinetic; SLE = Systemic Lupus Erythematosus, SLEDAI = Systemic Lupus Erythematosus Disease Activity Index Population • N ~ 30 patients • Seropositive SLE with SLEDAI≥6 • Refractory to adequate trials of at least 1 therapy • Stable protocol-limited background therapy at entry Primary Objective • Safety and tolerability Key Secondary/Exploratory Objectives • Effects on B cell depletion (PD response), autoantibody levels, and protective antibody levels • PK and PK/PD profile • Preliminary signs of clinical activity • Kinetics of re-population of B cell subsets and antibodies after depletion Open-label, dose escalation study = Budoprutug IV infusion Day 1, Day 15 DOSING REGIMEN Week 0 Week 28 LTFU DOSE ESCALATION Up to 6 patients per cohort enrolled sequentially DOSE EXPANSION Up to 12 patients at dose identified in escalation period Cohort 2 Cohort 3 Cohort 1 Dose selected; administered as 2 doses, 14 days apart
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© 2026 Climb Bio 29 Budoprutug – Subcutaneous (SC) Formulation Anti-CD19
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© 2026 Climb Bio 30 IV = intravenous, mAbs = monoclonal antibodies, SC = subcutaneous Source: FDA-approved labels. Concentration normalized to mg/mL; where multiple indications or dosing regimens are approved, the highest volume single dose was used Ability to formulate as both IV and SC provides optionality in development and may be a differentiating feature of budoprutug relative to other anti-CD19 mAbs Budoprutug SC concentration and volume targets defined by benchmark immunology mAbs • Patient and provider flexibility • Potential for at-home administration, reducing burden on healthcare facilities and improving patient convenience • Potential to broaden target patient populations or indications Potential Value of SC Administration Efgartigimod Dupilimab Belimumab Tezepelumab Secukinumab Ustekinumab Risankizumab Bimekizumab Ofatumumab Vedolizumab Benralizumab Mepolizumab Omalizumab Golimumab 0 50 100 150 200 250 0 1 2 3 4 5 6 Maximum Single Subcutaneous Delivery Volume (mL) Budoprutug SC Formulation Provides Optionality and Differentiation Concentration (mg/mL) Budoprutug
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© 2026 Climb Bio 31 IV = intravenous, NHP = nonhuman primates, SC = subcutaneous Note: Each line in the bioavailability figure represents an individual animal (n= 4/arm) • No local tolerance issues identified on histopathology • No safety findings • No observed anti-drug antibodies (ADAs) Favorable Tolerability Profile NHP Data Supports Viability of Budoprutug SC Formulation Budoprutug SC formulation demonstrated high bioavailability and favorable tolerability High concentration, low viscosity, and high bioavailability provide potential for a high concentration, single SC injection Bioavailability: >90% IV SC Matched doses
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© 2026 Climb Bio 32 Budoprutug SC Formulation Phase 1 Trial Enrolling Initial clinical data anticipated H1 2026 (NCT07090655) IV = intravenous, SC = subcutaneous. Follow-up will continue for subjects whose B cell count is not above 50% of baseline or above lower limit of normal by week 8 Population • N ~ 46 healthy volunteers Primary Objective • Safety and tolerability Secondary Objectives • Pharmacokinetic profile • Effects on B cell depletion (pharmacodynamic response) • Bioavailability of SC formulation Randomized, double-blind, placebo-controlled, single ascending dose study SINGLE ASCENDING DOSE COHORTS, N ~46 ~8 subjects per SC cohort (6 budoprutug: 2 placebo) ~14 subjects in the IV cohort (12 budoprutug: 2 placebo) Cohort 1 - SC Cohort 4 - SC Cohort 2 – SC Cohort 3 – matched IV dose Day 1 = Budoprutug SC injection, Day 1 IN -PATIENT Week 8Day 4 FOLLOW -UP
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© 2026 Climb Bio 33 CLYM116 Anti-APRIL mAb
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© 2026 Climb Bio 34 CLYM116: A Potential Best-in-Class anti-APRIL mAb APRIL = a proliferation-inducing ligand, HV = healthy volunteer, mAb = monoclonal antibody, NHP = nonhuman primate Initial clinical data expected mid-2026 • NHP data demonstrated potential for deep and durable IgA suppression, long half-life, and acceptable safety profile • Initiated dosing in Phase 1 clinical trial in healthy volunteers to evaluate safety and PK/PD • Initial Phase 1 HV data expected mid-2026 • CLYM116 has the potential to provide: Improved activity Less frequent dosing Favorable safety profile Strong Preclinical Data Differentiated Profile Phase 1 HV Data Mid-2026
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© 2026 Climb Bio 35 • Autoantibody mediated disease caused by deposition of immune complexes in the glomeruli, which leads to proteinuria, kidney injury and loss of kidney function • Diagnosed early in life (typically, ages 15-40)1; patients at risk for renal failure as disease progresses • Lifelong disease – patients likely to require chronic therapy • Accelerated approval based on reduction in proteinuria with full approval based on stabilization of eGFR • Biomarkers (APRIL, IgA) enable rapid assessment of clinical profile during early development Progressive, lifelong renal disease IgA Nephropathy (IgAN) APRIL = a proliferation-inducing ligand, eGFR = estimated glomerular filtration rate, mAb = monoclonal antibody US Prevalence: Tarpeyo CDER Integrated Review 2021, Filspari CDER Integrated Review 2022); 1 Schena Semin Nephrol 2018, 2 KIDGO 2025 Clinical Practice Guideline for the Management of IgAN, 3 Cantor IgAN Report Mar 2025, 4 Goldman Sachs IgAN Report Aug 2025, 5 Oppenheimer IgAN Report Aug 2025. Growing market Rapid and defined path to approval T H E C L I M B S O L U T I O N CLYM116 is a potential best-in-class anti-APRIL mAb, designed for improved activity and less frequent dosing S I G N I F I C A N T O P P O R T U N I T Y Most common primary glomerular disease worldwide, ~170,000 patients in the US alone• Treatment goals are to normalize proteinuria and preserve kidney function (stabilize eGFR)2 • KDIGO 2025 Guideline updates likely to increase diagnosis rates, expand patient population requiring treatment, and increase proportion of patients receiving potential disease-modifying therapy • Market expected to reach ~ $10-20B annually3-5
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© 2026 Climb Bio 36 Proteinuria is an Established Surrogate Endpoint for IgAN Prior approvals provide precedent regarding study design and registrational endpoints, including proteinuria at 9 months for accelerated approval and stabilization of eGFR at 2 years for full approval eGFR = estimated glomerular filtration rate, IgAN = IgA nephropathy, RaDaR = UK National Registry of Rare Kidney Diseases Sources: Inker Am J Kidney Dis 2021, Inker Am J Kidney Dis 2016, Thompson CJASN 2019, FILSPARI Drugs@FDA, TARPEYO Drugs@FDA. UK RaDaR: Pitcher CJASN 2023. Proteinuria is associated with eGFR decline and kidney failure/death (UK RaDaR study)4 • Magnitude of proteinuria predicts development of kidney failure/death • Proteinuria improvement (6-12 month) correlates with long-term (6-30 month) kidney function improvement
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© 2026 Climb Bio 37 KDIGO 2025 Guideline Highlights Role for IgA Reduction in IgAN KDIGO updates reinforce need for disease modifying treatments that halt the production of pathogenic IgA, positioning anti-APRIL therapies as a core pillar in the treatment of IgAN APRIL = a proliferation-inducing ligand, IgAN = IgA nephropathy , KDIGO = Kidney Disease Improving Global Outcomes KIDGO 2025 Clinical Practice Guideline for the Management of IgAN Initiation of treatment with therapies that both prevent/reduce pathogenic IgA and immune complex formation and manage disease-induced nephron loss KDIGO 2025 Guidelines recommend important changes: • Lower threshold for biopsy (proteinuria >=0.5 g/day) to enable earlier diagnosis • Treatment initiation in patients with proteinuria >=0.5 g/day • Revised treatment goal: proteinuria maintained at <0.5 g/day, preferably <0.3 g/day • Use of multiple treatment strategies simultaneously Manage the IgAN-specific drivers for nephron loss Manage the generic responses to IgAN-induced nephron loss In all patients, these should be addressed simultaneously Stop synthesis of pathogenic forms of IgA and IgA-IC formation Stop IgA/IgA-IC mediated kidney injury Blood pressure control Reduce glomerular hyperfiltration, proteinuria and the impact of proteinuria on the tubulointerstitium Lifestyle modification RASi or DEARA ± SGLT2i Drivers for nephron loss Treatment goals Interventions with reported efficacy across populations IgAN at risk of progressive kidney function loss Always consider the option of a clinical trial Cardiovascular risk reduction Mycophenolate mofetil (China) Hydroxychloroquine (China) Tonsillectomy (Japan) Nefecon Systemic glucocorticoids Interventions with reported efficacy in specific populations
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© 2026 Climb Bio 38 APRIL is a Potentially Disease Modifying Approach in IgAN In IgAN, APRIL inhibition has been demonstrated to prevent the production of pathogenic IgA and the consequent immune complex formation that leads to kidney damage APRIL = a proliferation-inducing ligand, eGFR = estimated glomerular filtration rate, IgAN = IgA nephropathy Adapted from Mathur J Clin Med 2023. 1 Mathur KI Reports 2022, 2 Davies Clin Transl Sci 2024, 3 Kooienga Kid Intl 2025, 4 Thompson CJASN 2019, 5 Pitcher CJASN 2023 IgA and Gd-IgA1 serve as pharmacodynamic biomarkers in early clinical studies1-3 Clinical endpoints in IgAN assess key measures of disease activity HIT 1 Production of galactose- deficient IgA1 (Gd-IgA1) HIT 2 Synthesis of anti-Gd-IgA1 autoantibodies HIT 3 Autoantibodies bind Gd-IgA1 to form pathogenic immune complexes HIT 4 Deposition of immune complexes in the mesangium and initiation of kidney injury Plasma cell differentiation Antibody class-switching APRIL APRIL blocking therapy Proteinuria reductions and eGFR stabilization reflect potential to preserve kidney function and support accelerated and full approval, respectively4,5
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© 2026 Climb Bio 39 Selective APRIL Inhibition Has Been Clinically Validated in IgAN Anti-APRIL mAb, sibeprenlimab, demonstrated numerically better proteinuria (UPCR) reductions as compared to anti-BAFF/APRIL antagonist, atacicept, in Phase 3 IgAN studies 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. • Dual BAFF/APRIL inhibition does not appear to provide an efficacy benefit beyond APRIL inhibition alone in IgAN • APRIL only approach avoids potential immunosuppression associated with BAFF inhibition 400 mg SC, Q4W 320* -50.2% vs. +2.1% for placebo 51.2% p<0.0001 Atacicept2 (TACI-IgG Fc) 150 mg SC, QW 203** -46% vs. +7% for placebo 42% p<0.0001 Dose N UPCR change at 9 months UPCR reduction at 9 months (placebo-adjusted) Sibeprenlimab1 (anti-APRIL mAb) *Interim analysis of 320 patients, total of 530 enrolled; **Interim analysis of 203 patients, total of 431 enrolled; 1 Perkovic ERA 2025, 40 week endpoint, 2Vera Corporate Presentation, June 2025, 36 week endpoint. APRIL = a proliferation-inducing ligand, BAFF = B-cell activating factor, IgAN = IgA nephropathy, mAb = monoclonal antibody, QW = once weekly, Q4W = once every four weeks, SC = subcutaneous, UPCR = urine protein creatinine ratio
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© 2026 Climb Bio 40 Next Gen Anti-APRILs Have Potential to Deliver Improved Profiles *Adapted from Mathur NEJM 2024. Sibeprenlimab Phase 3 dose (400 mg SC) equivalency based on average 80 kg weight and 75% bioavailability (Zhang Clin Pharm Drug Dev 2023). APRIL = a proliferation-inducing ligand, IV = intravenous, mo = months, Q4W = once every four weeks, SC = subcutaneous, UPCR = urine protein creatinine ratio, wks = weeks Sibeprenlimab Phase 2 Results* Opportunity for next generation approach • Improved efficacy: more robust proteinuria reductions through deeper APRIL suppression, getting more patients to clinical remission • Less frequent dosing: reduced injection frequency through more prolonged APRIL suppression • Favorable safety profile: supporting chronic administration Sibeprenlimab Phase 3 dose (400 mg SC, Q4W) roughly equivalent to 4 mg/kg IV Dose (IV, Q4W) APRIL levels over 16 wks Change in UPCR at 12 mo Clinical Remission % patients with UPCR < 0.3 g/d at 12 mo 2 mg/kg -47.2% 7.9% 4 mg/kg -58.8% 12.2% 8 mg/kg -62.0% 26.3% 8000 6000 4000 2000 0 0 4 8 12 16 8000 6000 4000 2000 0 0 4 8 12 16 8000 6000 4000 2000 0 0 4 8 12 16 Clinical data suggest that Phase 3 sibeprenlimab dose may not completely suppress APRIL or provide optimal proteinuria control, leaving opportunity for next generation agents
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© 2026 Climb Bio 41 CLYM116 Is The Only Known “Sweeper” Anti-APRIL In Development Potential best-in-class anti-APRIL mAb, designed for improved activity, less frequent dosing, and favorable safety profile APRIL = a proliferation-inducing ligand, mAb = monoclonal antibody pH-dependent binding to APRIL Clinically validated Fc mutations to increase serum half-life and diminish effector function Facilitates recycling of CLYM116 and elimination of APRIL FC -ENGINEERED KEY FEATURES HIGH AFFINITY SWEEPER MECHANISM
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© 2026 Climb Bio 42 APRIL Endocytosis APRIL degradation pH 6.0 pH 6.0 pH 6.0 FcRn pH 7.4 CLYM116 Antibody recycling CLYM116 “Sweeper” MoA Provides Potential for Clinical Benefits CLYM116’s recycling degrader ‘sweeper’ mechanism of action provides potential for improved activity and less frequent dosing vs. first generation approaches or half-life extension alone APRIL = a proliferation-inducing ligand, MoA = mechanism of action pH-dependent binding to APRIL provides potential for enhanced APRIL elimination through both: potent blocking of APRIL binding to its receptors and promotion of APRIL degradation in the lysosome Efficient antibody recycling reduces clearance of CLYM116, resulting in potentially longer half-life Low affinity to APRIL at pH 5.8, promoting APRIL degradation 2 1 High affinity to APRIL at pH 7.4 Endothelial cell a High affinity to FcRn at pH 5.8, promoting CLYM116 recycling 3 1 2 3
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© 2026 Climb Bio 43 c CLYM116 In Vitro and In Vivo Data Support Sweeper Mechanism Preclinical data demonstrate the potential for CLYM116 to provide a differentiated activity profile APRIL = a proliferation-inducing ligand, mAbs = monoclonal antibodies; pH dependent binding assay: Binding profiles of CLYM116 and sibeprenlimab were assessed via ELISA (enzyme-linked immunosorbent assay) at neutral and acidic pH. APRIL degradation assay: Wild type C57BL/6 mice were administered 10 mg/kg of antibody sc at time 0 and human APRIL (15 mg/kg sc) at 36 hours; APRIL concentration assessed every 2 hours thereafter. Antibody exposure assay: Humanized FcRn transgenic mice were administered 10mg/kg of antibody sc at time 0 and human APRIL (15 mg/kg sc) at 48 hours. Antibody concentration assessed thereafter. Sibeprenlimab and zigakibart analogs generated from publicly available sequences. CLYM116 demonstrated: Potent, pH-dependent binding of APRIL in an in vitro binding assay, as compared to first-generation anti-APRIL mAbs (sibeprenlimab and zigakibart) which did not demonstrate this profile More effective APRIL depletion and clearance as compared to first-generation anti-APRIL mAbs (sibeprenlimab and zigakibart) in APRIL degradation assay in a C57BL/6 mouse model More efficient antibody recycling as compared to first-generation anti-APRIL mAbs (sibeprenlimab and zigakibart) in an antibody exposure humanized FcRN transgenic mouse model
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© 2026 Climb Bio 44 -80 -70 -60 -50 -40 -30 -20 -10 0 10 Study Day IgA (% Change from Baseline, Mean ± SEM) sibeprenlimab 1 8 43 50 57 64 15 22 29 36 CLYM116 71 78 85 92 ADA = anti-drug antibody, NHPs = nonhuman primates, SC = subcutaneous Data from a head-to-head study in nonhuman primates; single subcutaneous administration. Sibeprenlimab analog generated from publicly available sequence. Beeck ASN 2025 CLYM116 demonstrated >70% maximal reduction in IgA after a single 6 mg/kg SC dose, with >50% reduction in IgA maintained out to 3 months CLYM116 Showed a Differentiated PK/PD Profile in NHPs CLYM116 demonstrated high bioavailability, a ~2-3 fold longer half-life vs. sibeprenlimab and deep and durable suppression of IgA after a single SC dose in NHPs Confirmed ADA+ animals were excluded from the analysis In a head-to-head study in NHPs, CLYM116 SC demonstrated: • ~85% bioavailability and favorable tolerability, with a formulation designed to support potential for convenient, at-home dosing • ~2-3x longer half-life across doses as compared to sibeprenlimab, supporting potential for improved exposure and less frequent dosing in humans • Deeper and more prolonged IgA reduction compared to sibeprenlimab after a single subcutaneous administration at equivalent doses (6 mg/kg), supporting potential to demonstrate a differentiated activity profile
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© 2026 Climb Bio 45 ADA = anti-drug antibody, NHPs = nonhuman primates 28-day toxicity study in NHPs, 10-14 animals per cohort, subcutaneous dosing on days 1, 15, 29. Subset of animals observed through an 8-week recovery period; 4 animals in the control and 100 mg/kg cohort observed through an extended 6-month recovery period. Beeck, ASN 2025 CLYM116 Tox Study Showed IgA Reduction and Favorable Tolerability In a 28-day repeat-dose toxicity study in NHPs, CLYM116 demonstrated a >70% reduction of IgA through the recovery period and a favorable tolerability profile Confirmed ADA+ animals were excluded from the analysis CLYM116 showed deep and durable IgA suppression through the recovery period • CLYM116 100 mg/kg cohort observed through the extended recovery period demonstrated sustained IgA suppression (>70% from baseline) through Day 183 Favorable tolerability observed • No local tolerance issues identified on histopathology • No CLYM116-related toxicity findings IgA
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© 2026 Climb Bio 46 CLYM116 Has The Potential For A Best-in-Class Profile in IgAN CLYM116 development ongoing, NHP data support potential for a differentiated profile Sibeprenlimab (anti-APRIL mAb) Povetacicept (BAFF/APRIL trap) IgA – Percent Reduction From Baseline UPCR Reduction, Week 36* CLYM116 (anti-APRIL mAb) Table above reflects cross-study and 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. *Primary endpoint for accelerated approval. Sibeprenlimab: Myette Kid Intl 2019, Mathur Kid Intl Reports 2022, Mathur NEJM 2024. Povetacicept: Evans Arthritis & Rheumatology 2023, Davies Clin Transl Sci 2024, Tumlin WCN 2024. APRIL = a proliferation-inducing ligand, BAFF = B-cell activating factor, HV = healthy volunteers, IgAN = IgA nephropathy, IV = intravenous, mAb = monoclonal antibody, NHPs = nonhuman primates, QW = once weekly, Q4W = once every 4 weeks, SC = subcutaneous, UPCR = urine protein creatinine ratio, wks = weeks. NHP max % reduction observed 60-70% (2.5-10 mg/kg IV, QW for 4wks) 50% (9 mg/kg IV, single dose) >70% (6 mg/kg SC, single dose) HV 52% (6 mg/kg IV, single dose) 50% (80 mg SC, single dose) Initial data mid ’26 max % reduction observed IgAN PHASE 2 % reduction Gd-IgA1 @ 12 weeks ~60% (4 mg/kg IV, Q4W) ~58% (80 mg SC, Q4W) IgAN PHASE 2 58% (4 mg/kg IV, Q4W) 64% (80 mg SC, Q4W) CLYM116 development ongoing potential for improved activity, less frequent dosing, and favorable safety profile
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© 2026 Climb Bio 47 CLYM116 Phase 1 Study In Healthy Volunteers Pharmacodynamic biomarker data (APRIL, IgA) expected to guide dose and dose frequency for studies in IgAN patients; initial data expected mid-2026 Population • Healthy volunteers Primary Objective • Safety and tolerability Secondary Objectives • Pharmacokinetic profile • Effect on immunoglobulins (IgA, IgM, and IgG) and APRIL levels (pharmacodynamic response) Randomized, double-blind, placebo- controlled, ascending dose study ASCENDING DOSE COHORTS APRIL = a proliferation-inducing ligand, IgAN = IgA nephropathy, MAD = multiple ascending dose, SAD = single ascending dose (additional cohorts may be included as study progresses) Cohort 3 Cohort 4 Cohort 2 Cohort 1 SAD MAD Subcutaneous administration 8 subjects per cohort (6 CLYM116: 2 placebo)
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© 2026 Climb Bio 48 Looking ahead
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© 2026 Climb Bio 49© 2025 Climb Bio 49 Climb Bio is Poised for a Data-Rich 2026 Continuing the ascent with initial readouts anticipated from all ongoing trials Budoprutug SC Budoprutug pMN Budoprutug ITP Budoprutug SLE 2026 68.2M† FULLY DILUTED SHARES OUTSTANDING Budoprutug SLE FPI China Ph1b – H1 ‘26 CLYM116 *As of September 30, 2025; †47.7 million common shares outstanding; on December 11, 2025, RA Capital converted 20.4 million common shares to pre-funded warrants ITP = Immune Thrombocytopenia; SLE = Systemic Lupus Erythematosus; pMN = primary membranous nephropathy; SC = subcutaneous; HV = healthy volunteers; PK = pharmacokinetics, PD = pharmacodynamics; FPI = first patient in $175.8M* RUNWAY INTO 2028 Initial Ph1 HV data – H1 ‘26 PK, PD, bioavailability Initial Ph2 data – H2 ‘26 Initial Ph1b data – H2 ‘26 Preliminary efficacy Initial global Ph1b data – H2 ‘26 Preliminary efficacy Initial Ph1 HV data – mid ‘26 PK, PD
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© 2026 Climb Bio 50 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 • CLYM116 - anti-APRIL mAb in development for IgAN Well-resourced to advance clinical programs through meaningful value-driving milestones, with runway anticipated into 2028 Climb Bio is Well Positioned for Success pMN = primary membranous nephropathy; ITP = Immune Thrombocytopenia; SLE = Systemic Lupus Erythematosus; IgAN = IgA Nephropathy Multiple clinical readouts within cash runway