Climb Bio 公布 budoprutug 治疗膜性肾病 PrisMN 二期初步数据：低剂量疗效与 1b 期一致，高剂量疗效数据要等 2027

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UNITED STATES
SECURITIES AND EXCHANGE COMMISSION
WASHINGTON, D.C. 20549
FORM
8-K
CURRENT REPORT
Pursuant to Section 13 or 15(d) of the Securities Exchange Act of 1934
Date of Report (Date of earliest event reported):
October 24, 2026
Climb Bio, Inc.
(Exact name of Registrant as Specified in Its Charter)
Delaware
001-40708
83-2273741
(State or Other Jurisdiction
of Incorporation)
(Commission File Number)
(IRS Employer
Identification No.)
20 William Street
Suite G50
Wellesley Hills
,
Massachusetts
02481
(Address of Principal Executive Offices)
(Zip Code)
Registrant’s Telephone Number, Including Area Code:
(866)
857-2596
Not Applicable
(Former Name or Former Address, if Changed Since Last Report)
Check the appropriate box below if the Form 8-K filing is intended to simultaneously satisfy the filing obligation of the registrant under any of the following provisions:
☐
Written communications pursuant to Rule 425 under the Securities Act (17 CFR 230.425)
☐
Soliciting material pursuant to Rule 14a-12 under the Exchange Act (17 CFR 240.14a-12)
☐
Pre-commencement communications pursuant to Rule 14d-2(b) under the Exchange Act (17 CFR 240.14d-2(b))
☐
Pre-commencement communications pursuant to Rule 13e-4(c) under the Exchange Act (17 CFR 240.13e-4(c))
Securities registered pursuant to Section 12(b) of the Act:
Title of each class
Trading
Symbol(s)
Name of each exchange on which registered
Common Stock, par value $0.0001 per share
CLYM
The Nasdaq Stock Market LLC
Indicate by check mark whether the registrant is an emerging growth company as defined in Rule 405 of the Securities Act of 1933 (§ 230.405 of this chapter) or Rule 12b-2 of the Securities Exchange Act of 1934 (§ 240.12b-2 of this chapter).
Emerging growth company
☒
If an emerging growth company, indicate by check mark if the registrant has elected not to use the extended transition period for complying with any new or revised financial accounting standards provided pursuant to Section 13(a) of the Exchange Act.
☐
Item 7.01 Regulation FD Disclosure.
On October 24, 2026, Climb Bio, Inc. (the “Company”) issued a press release announcing initial PrisMN Phase 2 data for budoprutug, its anti-CD19 monoclonal antibody, in primary membranous nephropathy (“pMN”) and a separate case study in minimal change disease, presented at the American Society of Nephrology (ASN) Kidney Week 2026. The Company also published an updated investor presentation, which includes a slide presenting competitive benchmarks for Week 12 PLA2R antibody reduction in pMN.
A copy of the press release and the updated investor presentation are furnished as Exhibit 99.1 and Exhibit 99.2, respectively, to this Current Report on Form 8-K and are incorporated by reference herein.
The information contained in Item 7.01 of this Current Report on Form 8-K, including the exhibits furnished under Item 7.01 of this Current Report on Form 8-K, shall not be deemed to be “filed” for purposes of Section 18 of the Securities Exchange Act of 1934, as amended (the “Exchange Act”), or otherwise subject to the liabilities of that section, nor shall it be deemed incorporated by reference in any filing under the Exchange Act or the Securities Act of 1933, as amended, regardless of any general incorporation language in such filing.
Item 8.01 Other Events.
On October 24, 2026, the Company announced initial PrisMN Phase 2 data for budoprutug, its anti-CD19 monoclonal antibody, in pMN and minimal change disease.
PrisMN is an ongoing Phase 2 dose-escalation trial evaluating budoprutug at three dose levels (200 mg, 600 mg and 1000 mg) in patients with moderate to severe pMN.
Patients enrolled in the reported cohorts were treatment-experienced, with high proteinuria and elevated anti-phospholipase A2 receptor (“PLA2R”) antibody levels at baseline.
At Week 12, the 200 mg cohort showed B-cell depletion, reductions in PLA2R antibody levels and immunologic remission.
The mean PLA2R antibody reduction was 70% at Week 12, and five of 13 patients (38%) achieved immunologic remission. Patients with baseline PLA2R antibody levels below 175 RU/mL had a mean reduction of 80% at Week 12. The Phase 2 Week 12 data in the 200 mg cohort were consistent with the Phase 1b Week 12 data across B-cell depletion, PLA2R antibody reduction and immunologic remission.
Initial data from the ongoing 600 mg cohort suggest greater drug exposure and deeper peripheral B-cell depletion compared with 200 mg, with mean peripheral CD20+ B-cell suppression at Week 4 of 98% at 600 mg, compared with 74% at 200 mg. A population pharmacokinetic analysis completed across all budoprutug studies (n≈120) found that patients with high proteinuria (median UPCR of 6.8 g/g) clear budoprutug ≥2-fold faster than non-proteinuric individuals, supporting the evaluation of higher doses in pMN.
Budoprutug has been generally well tolerated in the 200 mg and 600 mg cohorts, with follow-up through Week 12 for 200 mg and through Week 6 for 600 mg.
Most adverse events were mild to moderate (Grade 1 or 2), and no treatment-related serious adverse events, adverse events leading to treatment discontinuation or deaths were reported.
Enrollment is ongoing in the 1000 mg cohort. The Company anticipates additional data from the PrisMN Phase 2 trial in 2027.
Forward-Looking Statements
This Current Report on Form 8-K contains “forward-looking statements” including, without limitation, statements regarding: the anticipated timelines for announcing data from Climb Bio’s ongoing and planned clinical trials and other statements containing the words “anticipate,” “continue,” “could,” “expect,” “intend,” “may,” “plan,” “potential,” “should,” “suggest,” “target,” “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 to timely and successfully achieve or recognize the anticipated benefits of its technology transfer and exclusive license agreement with Beijing Mabworks Biotech Co., Ltd.; 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; managing expenses; changes in applicable laws or regulations; the possibility that Climb Bio may be adversely affected by other economic, business and/or competitive factors; and raising the substantial additional capital needed, on the timeline necessary, to continue development of budoprutug, CLYM116 and any other product candidates Climb Bio may develop. For a discussion of other risks and uncertainties, and other important factors, any of which could cause Climb Bio’s actual results to differ materially from those contained in the forward-looking statements, see the “Risk Factors” section, as well as discussions of potential risks, uncertainties and other important factors, in Climb Bio’s most recent filings with the U.S. Securities and Exchange Commission. In addition, the forward-looking statements included in this Current
Report on Form 8-K represent Climb Bio’s views as of the date hereof and should not be relied upon as representing Climb Bio’s views as of any date subsequent to the date hereof. Climb Bio anticipates that subsequent events and developments will cause Climb Bio’s views to change. However, while Climb Bio may elect to update these forward-looking statements at some point in the future, Climb Bio specifically disclaims any obligation to do so, except as required by law.
Item 9.01 Financial Statements and Exhibits.
(d) Exhibits
Exhibit
No.
Description
99.1
Press Release, dated October 24, 2026
99.2
Investor Presentation of Climb Bio, Inc. dated October 24, 2026
104
Cover Page Interactive Data File (embedded within the Inline XBRL document)
SIGNATURES
Pursuant to the requirements of the Securities Exchange Act of 1934, the registrant has duly caused this report to be signed on its behalf by the undersigned hereunto duly authorized.
Climb Bio, Inc.
Date:
October 26, 2026
By:
/s/ Aoife Brennan
Aoife Brennan, M.B., Ch.B.
President and Chief Executive Officer

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EX-99.1
2
clym-ex99_1.htm
EX-99.1
EX-99.1
Exhibit 99.1
Climb Bio Presents Initial PrisMN Phase 2 Data from Budoprutug in pMN at an Oral Session at ASN Kidney Week 2026
Low dose (200 mg) budoprutug demonstrated B-cell depletion, PLA2R Ab reduction, and immunologic remission at 12 weeks, consistent with Phase 1b data; additional data from the PrisMN Phase 2 study anticipated in 2027
200 mg and 600 mg doses have been generally well-tolerated
Separate MCD case study described three-year steroid-free remission following budoprutug treatment, supporting further investigation
WELLESLEY HILLS, Mass., October 24, 2026 (GLOBE NEWSWIRE) -- Climb Bio, Inc. (Nasdaq: CLYM), a clinical stage biotechnology company developing therapeutics for patients with immune-mediated diseases, today announced new clinical data for budoprutug, its anti-CD19 monoclonal antibody (mAb), in two immune-mediated renal diseases, primary membranous nephropathy (pMN) and minimal change disease (MCD). These data were presented at the American Society of Nephrology (ASN) Kidney Week 2026, which is taking place October 21-25, 2026, in Denver, Colorado.
PrisMN is an ongoing Phase 2 dose-escalation trial evaluating budoprutug at three dose levels (200 mg, 600 mg, and 1000 mg) in patients with moderate to severe pMN. Patients enrolled in the reported cohorts were treatment-experienced, with high proteinuria and elevated PLA2R antibody levels at baseline. At Week 12, the 200 mg cohort demonstrated B-cell depletion, reductions in PLA2R antibody levels, and immunologic remission. Initial data from the ongoing 600 mg cohort suggest greater drug exposure and deeper peripheral B-cell depletion compared with 200 mg. Budoprutug has been generally well tolerated in both cohorts to date, with follow-up through Week 12 for 200 mg and Week 6 for 600 mg. Enrollment is ongoing in the 1000 mg cohort.
In a separate case study presented yesterday, one patient with frequently relapsing MCD received 100 mg of budoprutug. The patient experienced three-year steroid-free remission and remained in remission for one year following B-cell reconstitution. This observation supports further investigation of budoprutug in MCD.
"Current treatment strategies fail to induce complete remission in most patients with pMN, underscoring the need for more effective treatments,” said Dr. Frank Cortazar, Director of the New York Nephrology Vasculitis and Glomerular Center. “While complete remission often takes more than a year to achieve, changes in PLA2R antibody levels can be appreciated much earlier in the treatment course and serve as an early indicator of therapeutic efficacy. Reductions in PLA2R antibody levels have been shown to correlate with downstream improvements in proteinuria, and ultimately complete remission. In the PrisMN study, the low-dose budoprutug cohort demonstrated encouraging PLA2R antibody reductions and immunologic remission rates in patients with moderate to severe pMN. These early results are highly promising, and I look forward to seeing how these data evolve as follow-up continues and higher-dose cohorts read out. These data provide further evidence that targeting CD19 with budoprutug may be a compelling approach in the treatment of pMN."
“These initial PrisMN results build on our Phase 1b findings, demonstrating early immunologic activity at 200 mg and the potential for increased activity at higher doses,” said Aoife Brennan, M.B., Ch.B., President and Chief Executive Officer of Climb Bio. “The observed pharmacokinetics confirm that patients with pMN have increased clearance of budoprutug compared to patients who do not have proteinuria. We are encouraged by the greater exposure and deeper B-cell depletion we are seeing at these early time points in the 600 mg cohort. As enrollment and follow-up continue, we look forward to sharing additional data. Beyond pMN, we are encouraged by the sustained steroid-free remission reported in the MCD case, supporting further investigation of budoprutug in additional glomerular diseases and highlighting its potential impact across different B-cell mediated diseases.”
Key highlights from the oral presentation:
•
Early immunologic activity at 200 mg
o
Mean PLA2R antibody reduction of 70% at Week 12; five of 13 patients (38%) achieved immunologic remission. Mean reduction of 80% at Week 12 for patients with baseline PLA2R antibody (Ab) <175 RU/mL
o
Phase 2 Week 12 data consistent with Phase 1b Week 12 data across B-cell depletion, anti-PLA2R antibody reduction, and immunologic remission rate
•
Population PK analysis and emerging 600 mg data support the evaluation of higher doses
o
Population PK analysis completed across all budoprutug studies (n≈120) found that patients with high proteinuria (median UPCR of 6.8 g/g) clear budoprutug ≥2-fold faster than non-proteinuric individuals, supporting the use of higher doses in pMN
o
Mean peripheral CD20+ B-cell suppression at Week 4 was 98% at 600 mg, compared with 74% at 200 mg
•
Safety and tolerability
o
Budoprutug was generally well tolerated in the 200 mg and 600 mg cohorts
o
Most adverse events were mild to moderate (Grade 1 or 2), with no treatment-related serious adverse events, adverse events leading to treatment discontinuation, or deaths reported
Following the oral presentation at 5:30 p.m. MT., the presentation and poster will be available on the Pipeline & Science—Publications page of the Company’s website
here.
About Primary Membranous Nephropathy (pMN)
Primary membranous nephropathy is an autoantibody mediated disease characterized by proteinuria, nephrotic syndrome, and progressive loss of renal function. Patients with uncontrolled disease may develop chronic kidney disease or end-stage kidney disease, requiring dialysis or transplantation. There are about 75,000 people in the U.S. living with pMN. Currently, there are no FDA approved therapies for pMN.
About Climb Bio, Inc.
Climb Bio, Inc. is a clinical-stage biotechnology company with a mission to deliver high impact, disease-modifying medicines for individuals living with immune-mediated diseases, including those affecting kidney health. The Company’s pipeline includes, budoprutug, an anti-CD19 monoclonal antibody that has potential to treat a broad range of B-cell mediated diseases, and CLYM116, an anti-APRIL monoclonal antibody being developed for IgA nephropathy. For more information, please visit
climbbio.com
.
About Budoprutug
Budoprutug is a clinical-stage, anti-CD19 monoclonal antibody with the potential to address a broad range of B-cell mediated, immune-driven diseases. Designed with enhanced effector function and low picomolar affinity, budoprutug targets and depletes CD19-expressing B cells, including plasmablasts and certain plasma cells, key sources of pathogenic autoantibodies. Early clinical data suggest budoprutug may offer durable B-cell depletion, rapid reductions in autoantibodies, and clinical remission in primary membranous nephropathy (pMN). Budoprutug is being evaluated in clinical trials for pMN, immune thrombocytopenia (ITP), and systemic lupus erythematosus (SLE). A subcutaneous formulation is also in development to enable broader patient access. Budoprutug has been granted Orphan Drug Designation and Fast Track Designation by the FDA for the treatment of pMN.
Forward-Looking Statements
This press release contains “forward-looking statements” 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; the anticipated timelines for announcing data from Climb Bio’s ongoing and planned clinical trials; the anticipated timelines for enrolling patients in planned clinical trials; and other statements containing the words “anticipate,” “continue,” “could,” “expect,” “intend,” “may,” “plan,” “potential,” “should,” “suggest,” “target,” “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 to timely and successfully achieve or recognize the anticipated benefits of its technology transfer and exclusive license agreement with Mabworks; 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; managing expenses; changes in applicable laws or regulations; the possibility that Climb Bio may be adversely affected by other economic, business and/or competitive factors; and raising the substantial additional capital needed, on the timeline necessary, to continue development of budoprutug, CLYM116 and any other product candidates Climb Bio may develop. For a discussion of other risks and uncertainties, and other important factors, any of which could cause Climb Bio’s actual results to differ materially from those contained in the forward-looking statements, see the “Risk Factors” section, as well as discussions of potential risks, uncertainties and other important factors, in Climb Bio’s most recent filings with the U.S. Securities and Exchange Commission. In addition, the forward-looking statements included in this press release represent Climb Bio’s views as of the date hereof and should not be relied upon as representing Climb Bio’s views as of any date subsequent to the date hereof. Climb Bio anticipates that subsequent events and
developments will cause Climb Bio’s views to change. However, while Climb Bio may elect to update these forward-looking statements at some point in the future, Climb Bio specifically disclaims any obligation to do so, except as required by law.
Investors and Media
Carlo Tanzi, Ph.D.
Kendall Investor Relations
ctanzi@kendallir.com

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EX-99.2
3
clym-ex99_2.htm
EX-99.2
Corporate Presentation OCTOBER 2026
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 enrolling patients in Climb Bio’s ongoing and planned clinical trials; plans for the development strategy for budoprutug and CLYM116; the anticipated timelines for announcing data from Climb Bio’s ongoing and planned clinical trials of budoprutug and CLYM116 and Beijing Mabworks Biotech Co., Ltd.’s (“Mabworks”) trial of CLYM116; potential commercial opportunity and limited competitive landscape for budoprutug in primary membranous nephropathy, immune thrombocytopenia, and systemic lupus erythematosus and for CLYM116 in IgA nephropathy; projections and estimates derived from pharmacokinetic and pharmacodynamic modeling; 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 to timely and successfully achieve or recognize the anticipated benefits of its technology transfer and exclusive license agreement with Mabworks; changes in applicable laws or regulations; 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; expectations regarding formulation and device readiness; 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; the possibility that models used in clinical development may be inaccurate; and raising the substantial additional capital needed, on the timeline necessary, to continue development of budoprutug, CLYM116 and any other product candidates Climb Bio may develop. For a discussion of other risks and uncertainties, and other important factors, any of which could cause Climb Bio’s actual results to differ materially from those contained in the forward-looking statements, see the “Risk Factors” section, as well as discussions of potential risks, uncertainties and other important factors, in Climb Bio’s most recent filings with the U.S. Securities and Exchange Commission. In addition, the forward-looking statements included in this presentation represent Climb Bio’s views as of the date hereof and should not be relied upon as representing Climb Bio’s views as of any date subsequent to the date hereof. Climb Bio anticipates that subsequent events and developments will cause Climb Bio’s views to change. However, while Climb Bio may elect to update these forward-looking statements at some point in the future, Climb Bio specifically disclaims any obligation to do so, except as required by law.
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, including estimates and other statistical data made by independent parties and by us relating to market size and other data about our industry. 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. These data involve a number of assumptions and limitations, and you are cautioned not to give undue weight to such estimates. In addition, projections, assumptions and estimates of our future performance and the future performance of the markets in which we operate are necessarily subject to a high degree of uncertainty and risk. 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.
Deliver high impact, disease-modifying medicines for individuals living with immune-mediated diseases Scaling New Heights in the Development of Transformative Immune Medicines 3 OUR MISSION
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 Wrapping up a data-rich 2026 with multiple clinical readouts across both 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
Budoprutug ITP Initial Ph1b data – June B cell and platelets, low dose cohort  Climb Bio: Data-Rich 2026 Delivered on 2026 data guidance, with budoprutug SLE and ITP readouts to close out the year 2026 FPI = first patient in, HV = healthy volunteers, ITP = immune thrombocytopenia, PD = pharmacodynamics, PK = pharmacokinetics, pMN = primary membranous nephropathy,
SC = subcutaneous, SLE = systemic lupus erythematosus Initial Ph1 HV data – May
PK, PD, bioavailability CLYM116 Initial Ph1 HV data – Sept PK, PD Budoprutug pMN Initial Ph2 data – Oct B cell and PLA2R, low dose cohort Budoprutug ITP Additional Ph1b data Budoprutug SLE Initial global Ph1b data
safety & biomarkers, low doses Budoprutug SC  Budoprutug SLE FPI China Ph1b – Q2  FPI Ph2 – Q3 CLYM116   Additional Ph1 HV data – Oct CLYM116   Expected in Q4
Pipeline of Highly Differentiated mAbs 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* Additional Ph2 data 2027 ANTICIPATED MILESTONES Initial Global Ph1b data Q4 ‘26 Additional Ph1b data Q4 ‘26 PHASE 2 PHASE 3 PRECLINICAL Initiate patient study Initial Ph1b data 2027 Initial Ph2 data H1 ‘27
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
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 Board of Directors 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
CLYM116 Anti-APRIL mAb
CLYM116: A Potential Best-in-Class anti-APRIL mAb *NAVIGATE-2 (NCT07375758) is being conducted in collaboration with our partner, Beijing Mabworks Biotech.
APRIL = a proliferation-inducing ligand, Gd = galactose deficient, HV = healthy volunteer, IgAN = IgA nephropathy, PFS = pre-filled syringe Initial data from NAVIGATE-2 Phase 2 trial expected in 1H 2027 Sweeper mechanism facilitates recycling of CLYM116 and degradation of APRIL CLYM116 is designed for improved activity, less frequent dosing, and favorable safety profile NAVIGATE-2 Phase 2 trial in IgAN* initial data expected 1H 2027 PFS development complete, autoinjector compatible drug product Phase 3 initiation anticipated in 2027, pending regulatory feedback CLYM116 Phase 1 data demonstrates potential best-in-class profile Deep & durable APRIL, IgA and Gd-IgA1 suppression Potential for every-12-week dosing Favorable safety & tolerability profile Differentiated MOA Compelling Phase 1 HV Data NAVIGATE-2 Ph2 Trial Underway
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, Gd-IgA1, 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, Gd-IgA1 = galactose-deficient IgA1, 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 The Climb Solution CLYM116 is a potential
best-in-class anti-APRIL mAb, designed for
improved activity and
less frequent dosing Significant opportunity 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
KDIGO Guidelines Highlight Impact of IgA Reduction in IgAN KDIGO commentary includes anti-APRIL therapies as a core pillar in the treatment of IgAN, reinforcing need for disease modifying treatments that stop production of pathogenic IgA (Gd-IgA1) APRIL = a proliferation-inducing ligand, IgAN = IgA nephropathy , KDIGO = Kidney Disease Improving Global Outcomes Rovin Kidney International 2026 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 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 Blood
pressure
control Reduce glomerular hyperfiltration, proteinuria and the impact of proteinuria on the tubulointerstitium Cardiovascular risk reduction Mycophenolate mofetil (China) Hydroxychloroquine (China) Tonsillectomy (Japan) Nefecon Systemic glucocorticoids Interventions with
reported efficacy in
specific populations APRIL inhibitors Dual APRIL/BAFF inhibitors Complement inhibitors
APPROVED BLA FILED @ APPROVED APRIL is a Validated Target in IgAN with Further Potential to Unlock Phase 3 results and recent approvals establish the APRIL class and create an opportunity for differentiated next-generation therapies *Phase 3 eGFR data not yet available. APRIL = a proliferation-inducing ligand, BAFF = B-cell activating factor, eGFR = estimated glomerular filtration rate, IgAN = IgA nephropathy, UPCR = urine protein creatinine ratio 1 Perkovic NEJM 2025, 2 Rizk GlomCon 2026, 3 Lafayette NEJM 2025, 4 Barratt NEJM 2026, 5 Vertex Press Release, March 9, 2026, 6 Madan KI Reports 2025 First Generation: Where We Are Now Next Generation: Where We’re Headed Atacicept3,4 BAFF/APRIL Povetacicept5,6 BAFF/APRIL Sibeprenlimab1,2 APRIL 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. 51.2% placebo-adjusted UPCR reduction 41.8% placebo-adjusted UPCR reduction Q1W Stabilization of eGFR through 2 years in Phase 3 Q4W Stabilization of eGFR through 2 years in Phase 3 49.8% placebo-adjusted UPCR reduction Q4W Stabilization of eGFR through 48 weeks in Phase 1/2* Depth and Durability of Suppression Near-complete APRIL suppression Robust IgA Response Reduced pathogenic forms of IgA and IgA immune complex formation Convenient Dosing Regimen Substantive decrease from 12 to 4 injections annually
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
CLYM116 “Sweeper” Designed for a Differentiated Clinical Profile pH-dependent binding and FcRn recycling allow CLYM116 to release captured APRIL for degradation and re-enter circulation to bind again APRIL = a proliferation-inducing ligand, mAb = monoclonal antibody Deeper target suppression
Repeated capture and clearance of APRIL Sustained activity
Antibody recycling enables continued target engagement Less frequent dosing
Prolonged pharmacology may support an extended maintenance interval beyond half-life extension alone pH 6.0 Low affinity to APRIL
at pH 5.8, promoting
APRIL degradation APRIL Endocytosis APRIL degradation pH 6.0 pH 6.0 FcRn CLYM116 Antibody recycling High affinity to APRIL at pH 7.4 Endothelial cell pH 7.4 High affinity to FcRn
at pH 5.8, promoting CLYM116 recycling Enhanced clearance beyond conventional neutralization:
Phase 1 Data Support Best-in-Class Potential of CLYM116 Data from healthy volunteer study demonstrate differentiation across key clinical attributes Luo ASN 2026; Liang ASN 2026 APRIL = a proliferation-inducing ligand, DLTs = dose limiting toxicities, Gd = galactose deficient, SAEs = serious adverse events, SC = subcutaneous Projected CLYM116 half-life based on 800 mg and 320 mg MAD. Target regimen: 800 mg loading dose, followed by 400 mg Q12W. Hypogammaglobulinemia defined as IgG < 300 mg/dL. Favorable Safety Profile SAFETY Generally well-tolerated No treatment-related SAEs
or DLTs No hypogammaglobulinemia Potential for Every 12-Week Dosing CONVENIENCE Half-life of ~33 days, ~3.5x longer than sibeprenlimab Low dosing burden with target regimen; 5 doses in year 1, then 4 doses per year Robust APRIL & IgA Suppression EFFICACY >90% free APRIL suppression through Week 12 after a single SC dose of ≥480 mg ~70% reduction in Gd-IgA1, the pathogenic form of IgA, and ~60% reduction in IgA at Week 12 after a single 800 mg dose
CLYM116 Global Phase 1 Strategy In Healthy Volunteers Data demonstrating deep, durable APRIL suppression and robust Gd-IgA1 reduction presented at ASN Kidney Week 2026 Luo ASN 2026; Liang ASN 2026
APRIL = a proliferation-inducing ligand, IgAN = IgA nephropathy, MAD = multiple ascending dose, SAD = single ascending dose Australia Ph1: NCT07248865; China Ph1: NCT07375758 conducted by our partner, Beijing Mabworks Biotech Population Healthy volunteers Primary Objective Safety and tolerability Secondary Objectives Pharmacokinetic profile Pharmacodynamics, including effects on serum APRIL and immunoglobulins (IgA, IgM, IgG, Gd-IgA1) Strategy: Parallel Australia and China SAD datasets will yield a robust population PK foundation with built-in ethnic sensitivity assessment to de-risk next phase dose selection ASCENDING DOSE COHORTS, N=46 Subcutaneous administration ~8 subjects per cohort (6 CLYM116: 2 placebo) Australia Phase 1 320 mg x 2* MAD *dosed on Day 1 and Day 15 80 mg 160 mg 25 mg 320 mg 480 mg SAD ASCENDING DOSE COHORTS, N=42 Subcutaneous administration ~8 subjects per cohort (6 CLYM116: 2 placebo) China Phase 1 Mabworks sponsored study Climb Bio sponsored study SAD 160 mg 320 mg 40 mg (n=2) 480 mg 800 mg 1280 mg
Safety CLYM116 Demonstrated Favorable Safety and Tolerability in HV Well-tolerated across 25-1280 mg, with no treatment-related SAEs or hypogammaglobulinemia Pooled across Australia Phase 1 (25-480 mg SAD; 320 mg Day 1 and Day 15 MAD) and China Phase 1 (40-1280 mg SAD). Source: Luo ASN 2026; Liang ASN 2026
AE = adverse event, DLT = dose-limiting toxicity, HV = healthy volunteers, SAE = serious adverse event, TEAE = treatment-emergent AE; TRAE = treatment related AE; hypogammaglobulinemia defined as IgG < 300 mg/dL 67 participants received CLYM116 across both studies No dose-limiting toxicities No treatment-related SAEs No discontinuations due to AEs No hypogammaglobulinemia Injection-site reactions observed in 5 patients, all Grade 1 CLYM116 (pooled, N=67) Placebo (pooled, N=21) Any TEAE, n (%) 42 (63%) 10 (48%) Any TRAE, n (%) 15 (22%) 6 (29%) Grade ≥3 TRAE, n (%) 0 0 Treatment-related SAE, n 0 0 Discontinuation due to AE, n 0 0
CLYM116 Exposure Profile Supports Long Dosing Interval ~33-day half-life, ~3.5x longer than sibeprenlimab, with dose-proportional exposure and consistent PK across the Australia and China studies Mean serum concentration after a single SC dose (n=6 per cohort); error bars show +SEM. Projected half-life based on 320 mg MAD and 800 mg; half-life dependent on dose and dose interval. Source: Luo ASN 2026; Liang ASN 2026.
APRIL = a proliferation-inducing ligand, EC75 = concentration producing 75% of maximal APRIL suppression, SC = subcutaneous, TMDD = target-mediated drug disposition.
1 Zhang Clin Pharm Drug Dev 2023, 2 Sibeprenlimab US Prescribing Information, 3 Based on a PK/PD model developed from individual subject Ph1 data Serum Concentration Mean (SEM) (µg/mL) APRIL EC75 = 2.83 µg/mL3 Australia Phase 1 China Phase 1 Pharmacokinetic Profile Half-life of ~33 days vs. 9.3 days for sibeprenlimab1,2 Dose-proportional exposure across the dose range Linear clearance above 1 µg/mL; no TMDD at doses ≥160 mg over 12 weeks Data consistent across Australia and China studies 320 mg 480 mg 800 mg
CLYM116 Achieved Rapid and Sustained Free APRIL Suppression ≥90% free APRIL suppression through Week 12 with single doses ≥480 mg, consistent across the Australia and China studies Median % change from baseline after a single SC dose; error bars show the upper quartile (Q3); MAD = 320 mg on Day 1 and Day 15 (Australia).
Source: Luo ASN 2026; Liang ASN 2026 APRIL = a proliferation-inducing ligand, CFB = change from baseline, MAD = multiple ascending dose, SC = subcutaneous APRIL Suppression ≥98% suppression by Day 4 at doses ≥160 mg ≥90% suppression through Week 12 at doses ≥480 mg Data consistent across Australia and China studies Free APRIL % Change from Baseline Australia Phase 1 China Phase 1 320 mg 480 mg 800 mg
Above reflects cross-trial comparisons of observed single-dose healthy-volunteer data and not data from head-to-head studies; cross-trial comparisons are limited by differences in study design, populations, assays, regimens, and follow-up. CLYM116 free APRIL shown as median and sibeprenlimab as mean (as published). APRIL = a proliferation-inducing ligand, CFB = change from baseline, PD = pharmacodynamic, PK = pharmacokinetic, SC = subcutaneous, TMDD = target-mediated drug disposition. 1 Luo ASN 2026, 2 Based on a PK/PD model developed from individual subject Ph1 data, 3 Adapted from Zhang Clin Pharm Drug Dev 2023, 4 Based on a PK/PD model developed from published mean cohort Ph1 data (Mathur KI Reports 2022; Zhang Clin Pharm Drug Dev 2023) CLYM116: Longer APRIL Suppression vs. Sibeprenlimab CLYM116 showed greater in vivo potency and maintained ≥90% free APRIL suppression through Week 12 at 480 mg, while sibeprenlimab suppression waned after Week 6 0 2 4 6 8 10 12 0.1 1 10 100 -90 -70 -50 -30 -10 APRIL EC75 = 2.83 µg/mL2 Concentration, µg/mL (mean) Free APRIL, % CFB (median) Week CLYM1161 480 mg SC (single dose) serum concentration free APRIL 0 2 4 6 8 10 12 0.1 1 10 100 -90 -70 -50 -30 -10 APRIL EC75 = 7.11 µg/mL4 Concentration, µg/mL (mean) Free APRIL, % CFB (mean) Week Sibeprenlimab3 400 mg SC (single dose) serum concentration free APRIL
CLYM116 Demonstrated ~70% Reduction in Gd-IgA1 Deep, durable reductions in Gd-IgA1, IgA and IgM Source: Liang ASN 2026; Luo ASN 2026 Left: China Phase 1, 800 mg SAD, Right: Australia Phase 1 SAD (placebo pooled, n=11) and China Phase 1 SAD. Australia MAD cohort (320 mg Day 1 and Day 15) achieved 78% Gd-IgA1 reduction at Week 12; CFB = change from baseline, Gd-IgA1 = galactose-deficient IgA1, MAD = multiple ascending dose, SAD = single ascending dose 800 mg Single Dose % change from baseline, mean ± SEM Gd-IgA1 at Week 12 % change from baseline, mean IgG reductions did not exceed 30% at any dose; lowest individual IgG 5.8 g/L vs. 3 g/L hypogammaglobulinemia threshold; no meaningful change in IgE IgA IgM Gd-IgA1
CLYM116 PK/PD Modeling Supports Q12W Dosing 400 mg Q12W regimen predicted to keep median trough concentrations ~4x above APRIL EC75 and maintain near-complete APRIL suppression through 48 weeks Source: Luo ASN 2026; Liang ASN 2026. Simulated serum concentrations are derived from a population pharmacokinetic model, and free APRIL levels are derived from a population pharmacokinetic / pharmacodynamic model. Both models were developed with interim data from two Phase 1 studies in healthy subjects. The simulations show the median and 25-75th percentiles of 1000 virtual subjects with the indicated dosing regimen.
APRIL = a proliferation-inducing ligand, PD = pharmacodynamic, PK = pharmacokinetic Median 25-75% Percentile Simulated Serum Concentration Over Time 800 mg loading dose on Day 1, then 400 mg Q12W starting Week 12 Simulated Free APRIL Over Time 800 mg loading dose on Day 1, then 400 mg Q12W starting Week 12 APRIL EC75 = 2.83 µg/mL
RANDOMIZED, OPEN-LABEL STUDY, N ~30 / COHORT Initial data anticipated in H1 2027; designed to confirm integrated Phase 1 PK/PD modeling and support advancing Q12W regimen into Phase 3 CLYM116 NAVIGATE-2 Phase 2 Study in IgAN Ongoing Population: Adults with biopsy-proven IgAN 24-hour UPCR ≥ 0.5 g/g or 24-hour urine protein ≥ 0.75 g eGFR ≥ 30 mL/min/1.73 m² Stable, maximum tolerated ACEi/ARB for
≥ 12 weeks Designed to evaluate: Safety and tolerability Gd-IgA1 24-hour UPCR eGFR slope Serum immunoglobulin profile Free APRIL ACEi = angiotensin-converting enzyme inhibitor, APRIL = a proliferation-inducing ligand, ARB = angiotensin II receptor blocker, eGFR = estimated glomerular filtration rate, Gd = galactose deficient, IgAN = IgA nephropathy, PD = pharmacodynamics, PK = pharmacokinetics, R = randomization, UPCR = urine protein creatinine ratio; NCT07375758; Dose regimens are 800 mg loading dose on Day 1, then 400 mg Q12W starting Week 12, and 800 mg loading dose on Day 1, then 400 mg Q8W starting Week 8; Lv ISN Frontiers 2026 Screening Loading Dose | 800 mg Q12W | 400 mg (72 weeks) Loading Dose | 800 mg Q8W | 400 mg (72 weeks) Follow-Up Observation or Extended Treatment (32 weeks) Optional 3rd Cohort R 1:1 Climb Bio / Mabworks collaborative, multi-center study being conducted in China NAVIGATE-2 Phase 2
CLYM116: Compelling Phase 1 Data, Clear Path Ahead CLYM116 offers the potential for durable disease control with convenient Q12W dosing;
NAVIGATE-2 Phase 2 ongoing and device development advancing HV = healthy volunteer, PD = pharmacodynamics, PFS = pre-filled syringe Pivotal Study & Commercial Device Readiness Phase 1 HV Favorable safety and deep, durable PD support best-in-class potential PFS ready for Phase 3; autoinjector in development for a patient-friendly launch presentation NAVIGATE-2 Phase 2 Ongoing Potential to move rapidly to Phase 3 with a single dose regimen
Budoprutug Anti-CD19
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 3 1
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 depletion CD38 depletion CD19 depletion CD20 CD38 CD19 Legend Naked mAbs targeting CD20 have been shown to deplete B cells in tissue2 Deeper depletion may be achieved by targeting CD19
Budoprutug is a Highly Potent, Fc-Enhanced Anti-CD19 mAb Designed for optimal biological activity, with potential for both IV and subcutaneous administration ADCC = antibody-dependent cellular cytotoxicity, 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
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
Primary Membranous Nephropathy Seferiana, living with pMN
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 FDA-approved therapies for pMN as of October 2026; FDA decision on obinutuzumab (Gazyva) for pMN expected November 2026 No approved therapies Clear path to approval The Climb Solution Budoprutug demonstrated compelling proof-of-concept in a pilot Phase 1b clinical study in pMN Significant opportunity ~75,000 patients
in the US alone
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
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 LTFU DOSING REGIMEN Week 0 Week 72 Week 48 Week 24 (induction) (maintenance) = Budoprutug IV infusion (2 doses, 14 days apart)
AEs = adverse events, DLTs = dose limiting toxicities, LLOQ = lower limit of quantification, PLA2R = phospholipase A2 receptor, pMN = primary membranous nephropathy, SAEs = serious adverse events, UPCR = urine protein creatinine ratio . 1 Cortazar ASN 2024, 2 Cortazar ASN 2025; Phase 1b pMN: budoprutug (100-200 mg) administered in two IV infusions, 14 days apart, at Wk 0 and Wk 24 Rapid and complete circulating B cell depletion observed in 100% (5/5)
patients at doses of 100-200 mg Sustained reductions out to 1 year +
after two dose cycles Anti-PLA2R antibody negativity achieved
in 100% (3/3) evaluable patients All patients achieved complete (3/5) or
partial (2/5) clinical remission by Week 48 Long-term control up to 3 years after initial dosing observed in 4 patients who received
up to 4 doses2 Clinical Proof-of-Concept Demonstrated in Pilot Study in pMN Budoprutug administration resulted in durable B-cell depletion, serologic remission, and clinical remission (as measured by proteinuria) Anti-PLA2R Autoantibodies (RU/mL) 14 19.6 5.9 UPCR (g/g) 0.3 0.98 0.14 0.325 0.09 0.11 CD20+ cell count (cells/µL) NEGATIVE COMPLETE REMISSION LLOQ
5.02 Week Week Week anti-PLA2R1 Proteinuria1 B Cells1 Generally well-tolerated with no deaths, no drug-related SAEs, no discontinuations due to AEs, no DLTs
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) Obinutuzumab (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 No FDA-approved therapies for pMN to date (FDA decision on obinutuzumab expected November 2026) Table above reflects cross-trial comparisons and not data from head-to-head studies; differences exist between trial designs and participant characteristics, and caution should be exercised when comparing data across trials.
PrisMN: Budoprutug Phase 2 pMN Study Enrolling Biomarker endpoint provides potential to rapidly identify dose to carry forward into
Phase 3; initial data presented at ASN with additional data anticipated in 2027 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
Cortazar ASN 2026 Population 18-75 years of age UPCR ≥ 2.0 g/g; designed to ensure adequate enrollment of patients with UPCR > 5.0 g/g PLA2R antibody positive or negative if other features of chronic disease present, e.g. nephrotic range proteinuria Primary Objective Safety and tolerability Secondary Objectives Preliminary PK and PK/PD PD markers (B cells, anti-PLA2R, total Ig) Preliminary efficacy: complete and partial remission at week 48 (UPCR and eGFR) DOSE ESCALATION TREATMENT PERIOD LTFU Week 0 Week 48 Week 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 Open-label, dose escalation study
PrisMN: Patient Demographics and Initial Safety Data Budoprutug was generally well tolerated in the 200 mg and 600 mg cohorts, which enrolled patients with high proteinuria and PLA2R Ab levels at baseline *downgraded from initial SAE assignment 600 mg baseline data incomplete (UPCR n=13; anti-PLA2R n=9, one patient with anti-PLA2R <2 RU/mL; prior therapy n=13). Source: Cortazar ASN 2026
ACEi = angiotensin-converting enzyme inhibitor, ARB = angiotensin receptor blocker, eGFR = estimated glomerular filtration rate, PLA2R = phospholipase A2 receptor, UPCR = urine protein-creatinine ratio, SAE = serious adverse event, AE = adverse event Safety Budoprutug was generally well tolerated in the ongoing Phase 2 trial at doses of 200 mg and 600 mg No treatment-related SAEs or deaths reported Most AEs were mild to moderate (Grade 1-2) No dose-limiting toxicities or discontinuations due to AEs No hypogammaglobulinemia observed; one patient experienced two events of neutropenia in the 200 mg cohort* 200 mg (n=14) 600 mg (n=15) Proteinuria 24-hr UPCR, g/g, median 6.8
range 2.8-13.4 5.2
range 2.4-11.1 (n=11) Anti-PLA2R RU/mL, mean 348.4
SD ± 395.3 244.5
SD ± 231.0 (n=9) Prior rituximab n (%) 4 (29%)
of 14 participants 3 (23%)
of 13 participants
CD20+ mean (SEM); absolute count (cells/mL) PrisMN: PK/PD Data Support Rapid, Deep B Cell Depletion Higher rate of clearance and deeper B-cell depletion observed with 600 mg 1 Data on file.
Source: Cortazar ASN 2026. PK = pharmacokinetics, PopPK = population PK, UPCR = urine protein-creatinine ratio Serum Concentration 200 mg D 1, 15; 8 weeks of follow-up Peripheral CD20+ B-cell depletion 200 mg D 1, 15; 12 weeks of follow-up 200 mg (n=13): Mean 86% peripheral CD20+ B-cell depletion by Week 8 600 mg (preliminary, n=12 at Week 4): 98% B-cell depletion at Week 4 compared to 74% at Week 4 with 200 mg In PrisMN patients with nephrotic-range proteinuria (median baseline 24hr UPCR 5-7 g/g), linear clearance estimated to be ≥2-fold higher than in non-proteinuric individuals Findings support evaluation of higher doses (600 / 1000 mg) in pMN to achieve exposures comparable to those in non-proteinuric populations PopPK analysis across 6 budo studies
(N ≈ 120) identified baseline UPCR as a significant covariate on clearance.1 Week 200 mg 600 mg 200 mg 600 mg 0 0.1 1 10 100 1000 1 2 4 8 3 Week Serum Concentration, mean (SEM) 0 -80 -60 -40 -20 0 4 8 12
0 -80 -60 -40 -20 0 2 4 8 12 PrisMN: Encouraging Reductions in Anti-PLA2R Low-dose budo demonstrated promising impact on anti-PLA2R Ab levels and early positive signal for 24hr UPCR at Week 12 Anti-PLA2R at Week 12 %CFB, individual participants Immunologic remission achieved in 5/13 (38%) overall and in 5/7 (71%) of pts with <175 RU/mL anti-PLA2R at BL Anti-PLA2R % CFB mean (SEM) ≥50% reduction in anti-PLA2R observed in 69% of pts overall, and in 86% of pts with <175 RU/mL anti-PLA2R at BL 24hr UPCR at Week 12: ≥25% reduction observed in 5/12 (42%) overall and in 3/7 (43%) with anti-PLA2R <175 RU/mL at BL Immunologic remission = <14 RU/mL N=13 for all time points for anti-PLA2R; N=12 for 24hr UPCR (one patient is missing baseline 24hr UPCR); BL = baseline; CFB = change from baseline; 200 mg D 1, 15; 12 weeks of follow-up Source: Cortazar ASN 2026 BL Anti-PLA2R <175 RU/mL All patients % CFB (mean, SEM) Week % CFB anti-PLA2R, Week 12 70% 80%
Low-Dose Budoprutug Week 12 PLA2R Rivals Obinutuzumab RP3D At just 200 mg, budoprutug reduced anti-PLA2R by 70% at Week 12, in line with prior Phase 1b results, and within range of other agents at Phase 3 or expected labeled doses (−22% to −85%) BL = baseline, EXP = expected, NR = not reported; PLA2R = phospholipase A2 receptor, RP3D = recommended Phase 3 dose;
1 Cortazar ASN 2026, 2 Fervenza NEJM 2026, 3 Madan KI Rep 2026, 4 Rovin KI Rep 2024, 5 Company data on file Data 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. Budoprutug Other agents PLA2R <175 subgroup Program Population Dose studied Mean change in
anti-PLA2R Week 12 Immunologic remission* Week 12 Anti-PLA2R+ Anti-PLA2R+ Anti-PLA2R+ N 54 10 26 Mean baseline PLA2R (RU/mL) 263 140 247 Obinutuzumab2 (anti-CD20) Ph3 Povetacicept3 (BAFF/APRIL) Ph1/2 Felzartamab4 (anti-CD38) Ph1/2 NR at Week 12 PrisMN Low-Dose Highlights† 200 mg Budoprutug low-dose cohort;
two infusions (D1, D15) before the Week 12 readout −70% Anti-PLA2R at Week 12, on par with povetacicept Phase 3 dose (−73%) and >3× felzartamab (−22%) 71% Immunologic remission at Week 12 in patients with BL PLA2R <175; 38% across all anti-PLA2R+ *Immunologic remission = anti-PLA2R <14 RU/mL among patients ≥14 RU/mL at baseline; **Weighted average † Low-dose results in line with prior Phase 1b, which demonstrated 75% reduction in PLA2R and 33% immunologic remission at Week 121,5 D1, W2, W24, W26 EXP. LABEL DOSE 1000 mg IV Q4W PHASE 3 DOSE 80 mg SC ×9 over 24 wk PHASE 3 DOSE 16 mg/kg IV 96% 49 PLA2R <175 24 NR at Week 12 72% 44% -85% Anti-PLA2R+ PLA2R <175 13 7 348 93 Budoprutug1 (anti-CD19) PrisMN Ph2 D1, D15, W24, W26 LOW DOSE 200 mg IV 71% 38% -80% -70% -73% -22%**
PrisMN: Encouraging Preliminary Data at Lowest Dose Enrollment and follow-up are ongoing; additional data expected in 2027 Promising PLA2R Ab reduction and immunologic remission rate consistent with Phase 1b observations at Week 12 BIOMARKERS Budoprutug has been generally well tolerated at doses of up to 600 mg SAFETY Dose dependent increases in exposure and B-cell depletion observed; confirmed higher clearance in proteinuric population justifies exploration of higher doses DOSING
Immune Thrombocytopenia John, living with ITP
Immune Thrombocytopenia (ITP) Autoantibody mediated disease characterized by the destruction of platelets  Results in bruising, bleeding episodes, hemorrhage and fatigue Chronic bleeding disorder 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) Limited treatment options Platelet response can demonstrate early proof-of-concept and served as primary endpoint measure for approvals in ITP Defined
endpoint The Climb Solution Budoprutug has the potential to achieve disease remission in this high unmet need population Significant opportunity ~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
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
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 CD19+/CD20- plasma cells expand within B cell niches post anti-CD20 treatment1 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 2.4% 1.2%
TREATMENT PERIOD Week 0 Week 36 Week 12 Week 48 Week 24 LTFU = Budoprutug IV (2 doses, 14 days apart at Week 0 and Week 24) Budoprutug Phase 1b ITP Trial Ongoing Designed to define dose and regimen, and establish depth and duration of platelet response and
B cell depletion; additional data from 500 and 1000 mg cohorts expected in Q4 2026 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
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; Source: Kazi EHA 2026; Phase 1b/2a ITP: budoprutug administered in two IV infusions, 14 days apart. 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 Also at baseline: median disease duration 6.5 (250 mg) / 15 years (500 mg); prior TPO-RA 4 patients (250 mg) / 7 patients (500 mg); 1 prior splenectomy (500 mg) 250 mg (n=6) 500 mg (n=9) Prior lines of therapy Median 7.5
range 4-18 6
range 2-15 Prior rituximab n (%) 4 (67%)
of 6 participants 2 (22%)
of 9 participants Baseline platelets ×10³/µL, median 13
range 4-29 7
range 2.5-12
>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; Source: Kazi EHA 2026; Phase 1b/2a ITP: budoprutug administered in two IV infusions, 14 days apart. 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 Assessments B-Cell Depletion Participants continue to be followed
Systemic Lupus Erythematosus Marisa, living with SLE
High unmet need 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 Chronic autoimmune condition 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 Established PoC for CD19 CD19 CAR T-cell therapies have demonstrated potential for remission; but modality limits broad utility and patient access 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 Notes 2022, Marinho Front Immunol 2023, Wu J Manag Care Spec Pharm 2023. The Climb Solution Budoprutug offers potential for broad
B-cell targeting with the safety and convenience
of a mAb Significant opportunity ~240,000 patients
in the US alone
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 approved for LN; rituximab off-label CD19 CAR Ts demonstrate strong efficacy B-cell targeting has promise but have significant risks and access challenges 8/8 SLE patients treated with anti-CD19 CAR T-cells achieved disease remission by 6 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
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 Study Global Phase 1b Study Enrolling adults with seropositive SLE; SLEDAI ≥ 8; refractory
to adequate trials of at least 2 therapies Enrolling adults with seropositive SLE; SLEDAI ≥ 6; refractory
to adequate trial of at least 1 therapy Initial data from low dose cohorts in the Global Study anticipated in Q4 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 TREATMENT 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 TREATMENT PERIOD Week 24 LTFU Week 0
Budoprutug – Subcutaneous (SC) Formulation Anti-CD19
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 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
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 mg 6 mg 3 mg Placebo SC IV 6 mg 6 mg 3 mg Placebo SC IV
Budoprutug SC: Future Direction Data in NHPs and healthy volunteers support continued development of SC formulation, with plans to advance to a study in patients to confirm dose and regimen with initial data expected in 2027 NHPs = nonhuman primates, PD = pharmacodynamic, SC = subcutaneous 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 Healthy Volunteers (low dose) Robust PD effects support continued clinical development
Looking ahead
Climb Bio: Continuing the Ascent Into 2027 Numerous milestones across both assets through 2027, funded into 2H 2028 2026 79.8M† FULLY DILUTED SHARES OUTSTANDING *Cash, cash equivalents, and marketable securities as of June 30, 2026; †57.3 million common shares outstanding as of June 17, 2026 HV = healthy volunteers, IgAN = IgA nephropathy, ITP = immune thrombocytopenia, pMN = primary membranous nephropathy, SC = subcutaneous, SLE = systemic lupus erythematosus $239.2M* RUNWAY
INTO 2H 2028 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 2027   CLYM116 Initial Ph2 IgAN data – 1H 2027 Ph3 initiation, pending regulatory feedback – 2027 Budoprutug pMN all dose cohorts
and CR data – 2027 Initial Ph1b SC data – 2027