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Corporate Presentation AUGUST 2026 CLIMBBIO
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© 2026 Climb Bio 2 Forward Looking Statements This presentation contains “forward-looking statements” 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 initiating and conducting Climb Bio’s Phase 1b/2a clinical trial of budoprutug in systemic lupus erythematosus in China; the anticipated timelines for announcing data from Climb Bio’s ongoing and planned clinical trials and Beijing Mabworks Biotech Co., Ltd.’s (“Mabworks”) trial of CLYM116; the anticipated timelines for enrolling patients in Climb Bio’s ongoing and planned clinical trials; plans for the development strategy for budoprutug and CLYM116; potential commercial opportunity for budoprutug in primary membranous nephropathy, immune thrombocytopenia, and systemic lupus erythematosus and for CLYM116 in IgA nephropathy; expectations regarding cash runway and the sufficiency of Climb Bio’s cash resources for the period anticipated; and other statements containing the words “anticipate,” “believe,” “continue,” “could,” “expect,” “intend,” “may,” “plan,” “potential,” “should,” “target,” “would,” “will,” 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 totimely and successfully achieve or recognize the anticipated benefits of its technology transfer and exclusive license agreement 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; 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 theforward-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 representingClimb 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. Certain information contained in this presentation is based on studies, publications, surveys, and other data obtained from third-party sources and our own internal estimates and research. While we believe these third-party studies, publications, surveys, and other data to be reliable as of the date of this presentation, we have not independently verified, and make no representation as to the adequacy, fairness, accuracy or completeness of, any information obtained from third-party sources. In addition, no independent source has evaluated the reasonableness or accuracy of our internal estimates or research, and no reliance should be made on any information or statements made in this presentation relating to or based on such internal estimates and research. In addition, Climb Bio has not conducted any head-to-head clinical studies comparing its product candidates to any third-party products or candidates, whether investigational or approved. Information regarding other drug products in this presentation is meant to provide context for illustrative purposes only. Because there are no head-to-head studies, no conclusions should be made based on cross- study comparisons. Recipients are cautioned not to place undue reliance on these forward-looking statements which speak only as of the date such statements are made and should not be construed as statements of fact.
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© 2026 Climb Bio 3 © 2026 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 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; Fast Track and Orphan Drug Designation granted for pMN • CLYM116 - anti-APRIL mAb in development for IgAN Delivering Clinical Results and Advancing Development pMN = primary membranous nephropathy, ITP = immune thrombocytopenia, SLE = systemic lupus erythematosus, IgAN = IgA nephropathy Corporate Highlights Well-resourced to advance clinical programs through meaningful value-driving milestones, with runway anticipated into the second half of 2028
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© 2026 Climb Bio 5© 2026 Climb Bio 5 Budoprutug ITP Initial Ph1b data – June B cell and platelets, low dose cohort ✓ Climb Bio: Data-Rich 2026 Continuing the ascent with initial readouts anticipated from all ongoing trials 2026 CLYM116 ITP = Immune Thrombocytopenia; SLE = Systemic Lupus Erythematosus; pMN = primary membranous nephropathy; SC = subcutaneous; HV = healthy volunteers; PK = pharmacokinetics, PD = pharmacodynamics; FPI = first patient in Initial Ph1 HV data – May PK, PD, bioavailability Initial Ph1 HV data – Sept PK, PD Budoprutug pMN Initial Ph2 data – Q4 B cell and PLA2R, low dose cohort Budoprutug ITP Additional Ph1b data – Q4 Budoprutug SLE Initial global Ph1b data – Q4 safety & biomarkers, low doses Budoprutug SC✓ Budoprutug SLE FPI China Ph1b – Q2 ✓ FPI Ph2 – Q3 CLYM116 Additional Ph1 HV data – Q4 CLYM116
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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, HV = healthy volunteers 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 PHASE 1 CLIMB RIGHTS Worldwide Worldwide Worldwide Outside Greater China* Initial Ph2 data Q4 ‘26 ANTICIPATED MILESTON ES Initial Global Ph1b data Q4 ‘26 Additional Ph1b data Q4 ‘26 FPI in Ph2 Q3 ‘26 Additional Ph1 data Q4 ‘26 PHASE 2 PHASE 3 Initial PK/PD Ph1 HV data Sept ‘26 PRECLINICAL Initiate multiple dose patient study Initial Ph1b data 2027
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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 (Stoneman JAMA 2026), ITP (Feudjo-Tepie 2008, U.S. Census Estimates 2020-2025), pMN (McGrogan Nephrol Dial Transplant 2011, ~1 per 100,000; U.S. Census Estimates 2020-2025, assumes 28-year duration of pMN), SLE (Izmirly Arthritis Rheumatol 2021, U.S. Census Estimates 2020-2025). TODAY Opportunity: >500k PATIENTS TOMORROW Opportunity: ~2M PATIENTS ITP ~85k pMN ~75k SLE ~240k Budoprutug, Anti-CD19 mAb CLYM116, Anti-APRIL mAb IgAN ~200k 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© 2026 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 Breanna O’Reilly, PhD Analyst, RA Capital Stephen Thomas, PhD CEO, Sera Medicines B O A R D O F D I R E C T O R S Chandra Adams, JD SVP, General Counsel Adam Villa, MBA, MS SVP, Tech Ops Ashley Jones SVP, People & Workforce Strategy Aoife Brennan, MB, ChB President and CEO Perrin Wilson, PhD CBO Edgar Charles, MD CMO Susan Altschuller, PhD, MBA CFO
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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 • Limited competition in CD19 mAb space • Administration profile intended to support outpatient and community use • Potential to address multiple B-cell mediated diseases • 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 may confer 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 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 while preserving protective antibody responses mediated by long-lived plasma cells 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 depletionCD38 depletionCD19 depletionCD20CD38CD19 Legend • Naked mAbs targeting CD20 have been shown to deplete B cells in tissue2 • Deeper depletion may be achieved by targeting CD19
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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 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 Potential for long-term disease remission based on initial clinical data; Fast Track Designation granted Primary Membranous Nephropathy (pMN) No approved therapies ~75,000 patients1,2 Potential to achieve durable response and disease remission in the previously treated population Poor QoL, with majority of previously treated patients failing to achieve durable platelet response6 Immune Thrombocytopenia (ITP) ~85,000 patients2,3 Potential for broad B-cell targeting and disease suppression with the safety and convenience of a mAb Majority of patients fail to achieve disease control with existing treatments7 Systemic Lupus Erythematosus (SLE) ~240,000 patients2,4 BUDOPRUTUG OPPORTUNITY 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 Progressive renal disease characterized by proteinuria, nephrotic syndrome and progressive loss of renal function.5 Chronic bleeding disorder characterized by the destruction of platelets.6 Chronic autoimmune condition with severe disease manifestations that can affect virtually any organ system.7
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© 2026 Climb Bio 14 Primary Membranous Nephropathy Seferiana, living with pMN
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© 2026 Climb Bio 15 • 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, but only 35% of patients achieve a complete remission (CR) by year 2 • 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; Couser CJASN 2017, Ronco J Clin Med 2021, Teisseyre Front Immunol 2022, KDIGO 2021 guidelines US Prevalence: McGrogan Nephrol Dial Transplant 2011, ~1 per 100,000; U.S. Census Estimates 2020-2025, assumes 28-year duration of pMN 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 ~75,000 patients in the US alone
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© 2026 Climb Bio 16 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 KDIGO 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
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© 2026 Climb Bio 17 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 18 LLOQ = lower limit of quantification, PLA2R = phospholipase A2 receptor, pMN = primary membranous nephropathy, 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 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) 0 10 20 30 40 50 60 70 80 90 0 8 16 24 32 40 48 56 64 72 80 Anti-PLA2R Autoantibodies (RU/mL)14 19.6 5.9 0 1 2 3 4 5 6 7 0 8 16 24 32 40 48 56 64 72 80 UPCR (g/g) 0.3 0.98 0.14 0.325 0.090.11 0 50 100 150 200 250 300 350 0 8 16 24 32 40 48 56 64 72 80 CD20+ cell count (cells/µL) NEGATIVE COMPLETE REMISSION LLOQ 5.02 WeekWeekWeek anti-PLA2R1 Proteinuria1B Cells1
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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 ; Phase 1b pMN: budoprutug (100-200 mg) administered in two IV infusions, 14 days apart, at Wk 0 and Wk 24 Budoprutug was generally well tolerated in the completed Phase 1b pMN trial at doses of up to 200 mg, supporting exploration of higher doses in ongoing and future studies 8 patients received at least one infusion 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 Compelling 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 NEJM 2026, 4 Madan KI Reports 2025, 5 Rovin KI Reports 2024 Budoprutug (based on completed pMN Ph1b1) Rituximab (MENTOR study2) Obinutuzimab (MAJESTY Ph3 study3) Povetacicept (RUBY-3 Ph1/2 study4) Felzartamab (Phase 1b/2a5) Target CD19 CD20 CD20 BAFF/APRIL CD38 Serologic remission (anti-PLA2R negativity) 100% (3/3) 48wks 64-95% (titer decrease), 6-24mo 70.4 % (38/54) 104wks 100% (4/4) 48wks 23% (6/26) 6mo Complete or partial clinical remission 100% (5/5) 48wks 60% (39/65) 24mo 50.8% (36/71) 104wks 100% (5/5) 48wks 35% (9/26) 12mo Complete remission 60% (3/5) UPCR ≤0.3 g/g, 48wks 14%, 35% (9/65, 23/65) UPCR ≤0.3 g/g; 12mo, 24mo 24%, 37% (17/72, 26/72) UPCR ≤0.3 g/g; 52 wks, 104wks 40% (2/5) UPCR <0.5 g/g; 48wks 0% (0/26) UPCR <0.5 g/g; 12mo 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 PrisMN: Budoprutug Phase 2 pMN Study Enrolling Biomarker endpoint provides potential to rapidly identify dose to carry forward into Phase 3; initial B cell and PLA2R data from low dose cohort anticipated in Q4 2026 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 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 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) DOSE ESCALATION TREATMENT PERIOD LTFU Week 0 Week 48Week 24 Week 36 = Budoprutug IV (2 doses, 14 days apart at Week 0 and Week 24) 600 mg 1000 mg 200 mg 15 patients per cohort, enrolled sequentially
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© 2026 Climb Bio 22 Immune Thrombocytopenia John, living with ITP
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© 2026 Climb Bio 23 Immune Thrombocytopenia (ITP) • Autoantibody mediated disease characterized by the destruction of platelets • Results in bruising, bleeding episodes, hemorrhage and fatigue • Guidelines recommend corticosteroids as 1L treatment, TPO- RAs, rituximab, or splenectomy as 2L, however many experience treatment failure • Only ~20% of previously-treated patients achieve durable platelet response with available 3L therapies (BTK, SYK inhibitors) • 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 ITP = immune thrombocytopenia; 1L = first line; 2L = second line; 3L = third line US Prevalence: Feudjo-Tepie 2008; U.S. Census Estimates 2020-2025 StatPearls Pietras 2024, Gafter-Gvili A Euro J Int Med 2023, Lucchini Haematologica 2019, Internal Research
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© 2026 Climb Bio 24 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
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© 2026 Climb Bio 25 Strong Rationale for CD19 Approach in ITP Potent anti-CD19 approach offers the promise of sustained elimination of pathogenic B 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 treatment1 74.9% 2.4% 1.2% ITP = immune thrombocytopenia, mAbs = monoclonal antibodies, RTX = rituximab 1Adapted from Mahevas J Clin Invest 2013, 2Crickx Kidney Intl 2020, 3Lucchini 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
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© 2026 Climb Bio 26 TREATMENT PERIOD Week 0 Week 36Week 12 Week 48Week 24 LTFU = Budoprutug IV (2 doses, 14 days apart at Week 0 and Week 24) Budoprutug Phase 1b ITP Trial Ongoing Designed to define dose and regimen, and establish depth and duration of platelet response and B cell depletion NCT07043946; ITP = immune thrombocytopenia, LTFU = long term follow-up, LLN = lower limit of normal Population • N ~24 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 DOSE ESCALATION – N ~24 500 mg, n=9 1000 mg, n=9 250 mg, n=6 6-9 patients per cohort, enrolled sequentially
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© 2026 Climb Bio 27 ITP Phase 1b: Patient Demographics and Initial Safety Data Budoprutug was generally well tolerated in the 250 mg and 500 mg cohorts, which enrolled heavily pretreated patients with persistent or chronic ITP AE = adverse event, ITP = immune thrombocytopenia, SAE = serious adverse event, TPO-RA = thrombopoietin receptor agonist *Median (range) follow-up for participants in Cohort 1 and 2: 38 weeks (28-44), and 12 weeks (3-20), respectively Kazi EHA 2026; Phase 1b/2a ITP: budoprutug administered in two IV infusions, 14 days apart. Data as of June 1, 2026. 250 mg (N=6) 500 mg (N=9) Age (median, range) 42 (22-75) 41 (18-58) Gender (M/F) 2/4 5/4 Time since diagnosis (median, range) 6.5 years (0.5-12) 15 years (0.6-40) Prior lines of therapy (median, range) 7.5 (4-18) 6 (2-15) Prior therapy: Corticosteroids (n) 6 9 IVIg (n) 2 5 TPO-RA (n) 4 7 Rituximab (n) 4 2 Splenectomy (n) 0 1 Baseline: Platelet count x103/µL (median, range) 13 (4-29) 7 (2.5-12) CD19+ B-cells/µL (median, range) 117.5 (87-287) 156 (82-343) Median of 6 to 7.5 prior lines of therapy ● Disease duration ranging from 0.5 to 40 years ● 6 of 15 (40%) patients had prior rituximab exposure Safety Budoprutug was generally well tolerated in the ongoing Phase 1b/2a ITP trial at doses of 250 mg and 500 mg 15 patients received two infusions of budoprutug and were included in the safety analysis population in the initial Phase 1b data cut* No SAEs or deaths reported All AEs were Grade 1 or Grade 2; majority of AEs belonged to the gastrointestinal system organ class No discontinuations due to AEs No infusion-related reactions No participants had hypogammaglobulinemia
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© 2026 Climb Bio 28 • >90% mean B-cell depletion at Week 4 • 66% (4/6) patients achieved a durable platelet response • 33% (2/6) patients achieved a complete platelet response - Participants with complete response maintained platelet levels ≥100 x 103/µL for ≥24 weeks; both previously relapsed on rituximab • 75% (3/4) participants who had prior rituximab responded, two of whom had durable complete responses Clinical Proof-of-Concept Demonstrated in ITP Phase 1b Cohort 1 Initial data from ongoing Phase 1b demonstrated durable B-cell depletion and platelet response following administration of budoprutug (low dose, 250 mg) ITP = immune thrombocytopenia; LLOQ = lower limit of quantification; BL = baseline Durable Response: ≥30 × 103/µL and ≥2x BL at 6 months; Complete Response: ≥100 × 103/ µL and absence of bleeding; Responses require confirmation on two separate occasions at least 7 days apart through Week 24. Kazi EHA 2026; Phase 1b/2a ITP: budoprutug administered in two IV infusions, 14 days apart. Data as of June 1, 2026: B-cell and platelet counts presented up to Week 24, last date with data point for all 6 participants. High sensitivity assay, LLOQ of 0.4 cells/µL At Week 24, mean (SEM) increase in platelet count from baseline was 111 (66) x 103 platelets/µL Platelet Response AssessmentsB-Cell Depletion 0 2 4 6 8 10 12 14 16 18 20 22 24 0 20 40 60 80 100 120 140 160 180 200 220 240 260 280 300 320 340 Week CD20+ B-cell Count (cells/mL) Participant 1 Participant 2 Participant 3 Participant 4 Participant 5 Participant 6 Budoprutug Dose Participants continue to be followed 0 2 4 6 8 10 12 14 16 18 20 22 24 26 28 -10 10 30 50 70 90 110 130 150 170 190 Week Mean (SEM) Change in Platelet Count vs Baseline (Day 1) (x10^3/mL) D 30x10^3 platelets/mL D 50x10^3 platelets/mL D 100x10^3 platelets/mL Budoprutug dose
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© 2026 Climb Bio 29 Systemic Lupus Erythematosus Marisa, living with SLE
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© 2026 Climb Bio 30 • 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; U.S. Census Estimates 2020-2025, 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 31 Strong Rationale for Anti-CD19 mAb in SLE CD19 mAb approach could provide optimal profile of disease control, safety, and broad patient accessibility 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 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 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
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© 2026 Climb Bio 32 Parallel Global and China SLE Studies Enrolling Designed to assess safety, tolerability, B-cell depletion, and kinetics of B-cell subset repopulation 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 StudyGlobal 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 2026 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 and Day 15 TREATMEN T PERIOD Week 0 Week 28 LTFU SINGLE ASCENDING DOSE COHORTS, N ~30 30 mg 100 mg 10 mg 200 mg Up to 6 patients per cohort enrolled sequentially Subtherapeutic doses = Budoprutug IV Day 1 TREATMEN T PERIOD Week 24 LTFU Week 0
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© 2026 Climb Bio 33 Budoprutug – Subcutaneous (SC) Formulation Anti-CD19
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© 2026 Climb Bio 34 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 Dupilumab 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 Potential to deliver 350 mg of budoprutug in a single, 2 mL SC injection
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© 2026 Climb Bio 35 AUC = area under the curve, HV = healthy volunteers, IV = intravenous, SC = subcutaneous Company data on file from Phase 1 placebo-controlled, single ascending dose study in HV (NCT07090655); 3 cohorts: SC 3 mg, SC 6 mg, IV 6 mg, with 8 subjects per SC cohort (6 budoprutug: 2 placebo) and 14 subjects in IV cohort (12 budoprutug: 2 placebo). Low doses of budoprutug were chosen to achieve non-complete (~50%) peripheral B cell depletion in HV. 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 mg6 mg3 mgPlacebo SC IV 6 mg6 mg3 mgPlacebo SC IV
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© 2026 Climb Bio 36 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 with initial data expected in 2027 NHPs = nonhuman primates, PD = pharmacodynamic, SC = subcutaneous Healthy Volunteers (low dose) Next Steps Non-Human Primates Data confirmed bioavailability and favorable safety/ tolerability Evaluation of SC formulation at full B-cell depleting dose regimen in patients with autoimmune diseases Robust PD effects support continued clinical development
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© 2026 Climb Bio 37 CLYM116 Anti-APRIL mAb
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© 2026 Climb Bio 38 CLYM116: A Potential Best-in-Class anti-APRIL mAb *CLYM116 is being developed as MIL116 in Greater China by our partner, Beijing Mabworks Biotech (NCT07375758) APRIL = a proliferation-inducing ligand, HV = healthy volunteer, mAb = monoclonal antibody, NHP = nonhuman primate Initial PK/PD data in HVs expected in Sept; FPI in Phase 2 trial in IgAN patients anticipated in Q3 ‘26 • NHP data demonstrated potential for deep and durable IgA suppression, long half-life, and acceptable safety profile • Phase 1 clinical trial in HV ongoing, with initial PK/PD data expected at September R&D Spotlight Event • Mabworks Phase 1 in HV ongoing; Phase 2 portion in IgAN patients now enrolling* • CLYM116 has the potential to provide: Improved activity Less frequent dosing Favorable safety & immunogenicity profile Strong Preclinical Data Differentiated Profile Phase 1 HV Data September R&D Spotlight Event
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© 2026 Climb Bio 39 • 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; with potential for a further streamlined path based on recent NKF/FDA workshop6 • 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: Stoneman JAMA 2026; 1 Schena Semin Nephrol 2018, 2 KDIGO 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. 6 Vera press release June 2, 2026 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, ~200,000 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 • US market expected to reach ~ $10-20B annually3-5
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© 2026 Climb Bio 40 Magnitude of Proteinuria Predicts Development of Kidney Failure Proteinuria improvement correlates with long-term kidney function stabilization eGFR = estimated glomerular filtration rate, IgAN = IgA nephropathy, RaDaR = UK National Registry of Rare Kidney Diseases Pitcher CJASN 2023 Proteinuria is associated with eGFR decline and kidney failure/death (UK RaDaR study)
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© 2026 Climb Bio 41 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 KDIGO 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 42 Selective APRIL Inhibition Has Been Clinically Validated in IgAN In Phase 3, sibeprenlimab matched or outperformed BAFF/APRIL agents on proteinuria (UPCR) reduction and achieved statistically significant eGFR improvement at 2 years 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 APRIL = a proliferation-inducing ligand, BAFF = B-cell activating factor, IgAN = IgA nephropathy, mAb = monoclonal antibody, UPCR = urine protein creatinine ratio 1Perkovic NEJM 2025; 2Lafayette NEJM 2025; 3Vertex Press Release, March 9, 2026; 4Otsuka Press Release, July 2, 2026; 5Lafayette Kidney International 2024; 6Madan KI Reports 2025 7Maillard, Adv Ther. Jan 2026 51.2% 1 p<0.0001 Atacicept 42% 2 p<0.0001 UPCR reduction at 9 months (placebo-adjusted) Sibeprenlimab Povetacicept 49.8% 3 p<0.0001 In patients with IgAN, depth of proteinuria reduction has been correlated with better long-term kidney outcomes, including slower eGFR decline and reduced risk of kidney failure7 eGFR* Stabilization of eGFR through 2 years in Phase 34 Stabilization of eGFR at 36 weeks in Phase 25 Stable eGFR through 48 weeks observed in Phase 1/26 SELECTIVE APRIL INHIBITION DUAL BAFF/APRIL INHIBITION DUAL BAFF/APRIL INHIBITION
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© 2026 Climb Bio 43 Next Gen Anti-APRILs Have Potential to Deliver Improved Profiles APRIL = a proliferation-inducing ligand, IV = intravenous, mo = months, Q4W = once every four weeks, SC = subcutaneous, UPCR = urine protein creatinine ratio, wks = weeks 1 Chart adapted from Mathur NEJM 2024 (Ph2 study results), 2 Sibeprenlimab prescribing information, 3 Equivalency based on average 80 kg weight and 75% bioavailability (Zhang Clin Pharm Drug Dev 2023). Opportunity for next generation anti-APRIL agents to demonstrate improved efficacy, less frequent dosing, and reduced immunogenicity Immunogenicity was observed in the Phase 3 sibeprenlimab study, which resulted in an impact on drug exposure and proteinuria reductions 2 Clinical data1 suggest that sibeprenlimab recommended dosage2 may not completely suppress APRIL or provide optimal proteinuria control 34% evaluable patients developed ADA In patients who developed ADA: • Drug exposure was ~40% lower • UPCR reductions at Month 9 were lower (41.6% vs. 52.7%) 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, with reduced immunogenicity: supporting chronic administration Sibeprenlimab recommended dosage (400 mg SC) roughly equivalent to 4 mg/kg IV3 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
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© 2026 Climb Bio 44 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 45 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 46 ADA = anti-drug antibody, NHPs = nonhuman primates, SC = subcutaneous *Data from a head-to-head study in nonhuman primates, 4-6 animals per cohort, single SC administration. †Toxicity study in nonhuman primates, 10-14 animals per cohort, SC administration on days 1, 15, 29. A subset were observed through an 8-wk recovery; 4 in the control and 100 mg/kg cohort were observed through an extended 6-mo recovery. Luo ERA 2026; Beeck ASN 2025 CLYM116 demonstrated deep and durable IgA suppression CLYM116 Showed a Differentiated PK/PD Profile in NHPs CLYM116 demonstrated deep and durable IgA suppression and a ~2-3 fold longer half-life vs. sibeprenlimab in NHPs In a head-to-head study in NHPs, CLYM116 SC demonstrated: • ~2-3x longer serum half-life vs. sibeprenlimab • Deeper IgA suppression with a longer duration of effect vs. sibeprenlimab • ~85% bioavailability and favorable tolerability Deep IgA suppression, with longer duration of effect vs. sibeprenlimab after a single SC administration* Similar magnitude of IgA suppression (~70%) observed in a repeat dose toxicology study† Confirmed ADA+ animals were excluded from the analysis
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© 2026 Climb Bio 47 Clear Translation of Data from NHPs to HV to IgAN Patients Emerging CLYM116 data support potential to have a best-in-class profile in IgAN Sibeprenlimab (anti-APRIL mAb) Povetacicept (BAFF/APRIL inhib) IgA – Percent Reduction From Baseline UPCR Reduction, 9 months* 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. Reported as 9 months and Week 40 for sibeprenlimab Phase 2 and Phase 3, respectively, and Week 36 for povetacicept Phase 2 and Phase 3. Sibeprenlimab: Myette Kid Intl 2019, Mathur Kid Intl Reports 2022, Mathur NEJM 2024. Povetacicept: Evans Arthritis & Rheumatology 2023, Davies Clin Transl Sci 2024, Madan KI Reports 2026, Vertex Press Release, Mar 9, 2026. APRIL = a proliferation-inducing ligand, BAFF = B-cell activating factor, HV = healthy volunteers, IgAN = IgA nephropathy, inhib = inhibitor, 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 Sept ‘26 max % reduction observed IgAN PHASE 2 % reduction Gd-IgA1 @ 12 weeks ~60% (4 mg/kg IV, Q4W) ~65% (80 mg SC, Q4W) IgAN PHASE 2 58% (4 mg/kg IV, Q4W) 58% (80 mg SC, Q4W) CLYM116 development ongoing potential for improved activity, less frequent dosing, and favorable safety profile IgAN PHASE 3 51% (placebo adjusted) (4 mg/kg IV, Q4W) 50% (placebo adjusted) (80 mg SC, Q4W)
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© 2026 Climb Bio 48 HV = healthy volunteer, mAbs = monoclonal antibodies, MAD = multiple ascending dose, NHP = nonhuman primate, PD = pharmacodynamic, PK = pharmacokinetic, SAD = single ascending dose, TMDD = target-mediated drug disposition Luo ERA 2026. Modeling based on pooled data from 4 SAD and MAD NHP studies (0.5−100 mg/kg SC, 6 mg/kg IV) Translational Model Projects Dose-Dependent IgA Suppression in HV CLYM116-specific PK/PD modeling derived from NHP data projected HV exposure and dose- dependent IgA suppression across the Ph1 dose range, with potential for less frequent dosing Modeling Workflow Cyno PK/PD modeling (2-compartment + TMDD; Indirect-response IgA, IgG, IgM) Allometric extrapolation to human using exponents tuned for half-life- extended mAbs Healthy-volunteer SAD/MAD simulations (PK, IgA, Gd-IgA1, IgG, IgM) Validation against emerging Phase 1 observations Extended Half-Life Supports Durable, Dose-Dependent IgA Suppression
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© 2026 Climb Bio 49 CLYM116 Global Phase 1 Strategy In Healthy Volunteers Pharmacodynamic biomarker data (APRIL, IgA) expected to guide dose and dose frequency for studies in IgAN patients; initial PK/PD data expected at September R&D Spotlight Event Randomized, double-blind, placebo- controlled, ascending dose studies APRIL = a proliferation-inducing ligand, IgAN = IgA nephropathy, MAD = multiple ascending dose, SAD = single ascending dose Lou ERA 2026. Australia Ph1: NCT07248865; China Ph1 (NCT07375958) conducted by our partner, Beijing Mabworks Biotech Australia Phase 1 80 mg 160 mg 25 mg 320 mg 480 mg 320 mg x 2* China Phase 1 160 mg 320 mg 40 mg (n=2) 480 mg 640 mg ASCENDING DOSE COHORTS, N ~80 Subcutaneous administration 8 subjects per cohort (6 CLYM116: 2 placebo) SADPopulation • Healthy volunteers Primary Objective • Safety and tolerability Secondary Objectives • Pharmacokinetic profile • Effect on immunoglobulins (IgA, IgM, and IgG) and APRIL levels (pharmacodynamic response) Strategy: Parallel ex-China and China SAD datasets will yield a robust population PK foundation with built-in ethnic sensitivity assessment to de-risk next phase dose selection MAD SAD *dosed on Day 0 and Day 14
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© 2026 Climb Bio 50 No dose-limiting toxicities, serious adverse events, Grade ≥3 adverse events, or AE-related discontinuations All AEs mild to moderate (Grade 1-2), transient, and self-resolving Injection site reactions observed in 2 patients, both Grade 1, resolved without intervention Safety AE = adverse event; HV = healthy volunteers Luo ERA 2026 CLYM116 has been generally well tolerated in HV to date, with no unexpected safety findings Ongoing Studies in Australia and China: Preliminary Safety Data from Single Doses up to 320 mg (n=49)* *China Phase 1 study is placebo-controlled and remains blinded. The reported population (n=49) includes participants who received CLYM116 (n=39) or placebo (n=10)
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© 2026 Climb Bio 51 Looking ahead
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© 2026 Climb Bio 52© 2026 Climb Bio 52 Climb Bio: Data-Rich 2026 Continuing the ascent with readouts anticipated from all ongoing trials 2026 79.8M† FULLY DILUTED SHARES OUTSTANDING Budoprutug SLE FPI China Ph1b – Q2 CLYM116 *Cash, cash equivalents, and marketable securities as of June 30, 2026; †57.3 million common shares outstanding as of June 17, 2026; ITP = immune thrombocytopenia; SLE = systemic lupus erythematosus; pMN = primary membranous nephropathy; SC = subcutaneous; HV = healthy volunteers; PK = pharmacokinetics, PD = pharmacodynamics; FPI = first patient in $239.2M* RUNWAY INTO 2028 Initial Ph1 HV data – May PK, PD, bioavailability Initial Ph1 HV data – Sept PK, PD Budoprutug SC✓ Budoprutug ITP Initial Ph1b data – June B cell and platelets, low dose cohort ✓ ✓ Budoprutug pMN Initial Ph2 data – Q4 B cell and PLA2R, low dose cohort Budoprutug ITP Additional Ph1b data – Q4 Budoprutug SLE Initial global Ph1b data – Q4 safety & biomarkers, low doses Additional Ph1 HV data – Q4 CLYM116 FPI Ph2 – Q3 CLYM116
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© 2026 Climb Bio 53 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 Designation 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 the second half of 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