Slide 1: Conditionally Active Biologics: Transforming Cancer Therapy
Corporate Presentation March 2026 Conditionally Active Biologics: Transforming Cancer Therapy
Slide 2: Important Notices & Disclaimers
Important Notices & Disclaimers This presentation (the “Presentation”) by BioAtla, Inc. (“we”, “us”, “our”, “BioAtla”, or the “Company”) contains “forward-looking statements” within the meaning of the Private Securities Litigation Reform Act of 1995 relating to our business, operations and financial
Slide 3: Leadership Team
Leadership Team Chris Vasquez Chief Financial Officer Sheri Lydick Chief Commercial Officer Jay Short, Ph.D. Chairman, CEO and Cofounder Eric Sievers, M.D. Chief Medical Officer Ji Hwan Lee VP Head of Portfolio Management Monica Sullivan Sr. VP, Intellectual Property & Contracts Susie Melody Sr. VP,
Slide 4: Board of Directors and Scientific Advisors
Board of Directors and Scientific Advisors Susan Moran, MD, MSCE Director Lawrence Steinman, MD Lead Director Mary Ann Gray, Ph.D. Director Sylvia McBrinn Director Scott Smith Director James Allison, Ph.D. MD Anderson Cancer Center Scientific Advisor Eddie Williams Director Lawrence Fong, MD Cancer
Slide 5: CAB technology binds acidic cancer cell surface
BioAtla discovered that acidic pH at the cancer cell surface unveils binding sites that are shielded at normal pH of healthy cells BioAtla invented CAB technology, creating antibodies that bind only to these unveiled sites on cancer cells CAB binding region is not masked or caged and thus different
Slide 6: CAB Platform Technology Summary
All cancer cells are acidic (pH5.3-pH6.7) The most acidic regions are oxygenated, not anaerobic Acidity is a result of the need for precursor molecules from glycolysis for continuous cell replication Cancer cells use acidity to promote metastasis and defend against immune response CAB mechanism Leve
Slide 7: Myths vs Facts of pH Therapies in Cancer
Myths vs Facts of pH Therapies in Cancer BioAtla’s Solution: Conditionally Active Biologics (CAB) Myth Fact Not all tumors are acidic ALL tumors and cancer cells are acidic (i.e. pH5.3-6.7). Cancer cells are ATP limited Cancer cells are NOT generally ATP deficient but are limited in other precursor
Slide 8: CAB Antibodies Bind Selectively and Reversibly Based on TME
CAB Antibodies Bind Selectively and Reversibly Based on the Tumor Microenvironment (TME) Note: OD450nm = optical density measurements using a microplate reader with a 450nm filter; TME = Tumor Micro Environment; mABs = monoclonal antibodies; Data above based on non-human primate studies CABs Bind Se
Slide 9: CAB Technology Eliminates On-target, Off-tumor Binding
CAB Technology Eliminates On-target, Off-tumor Binding Thus, widening the therapeutic index by 12.6-fold over cetuximab CAB Anti-EGFR mAb Enhanced Tumor Selectivity (12.6-fold increase in TI) Cetuximab Control PET scan images
Slide 10: Conditional Binding Approaches: Prodrug vs CAB Platform
Conditional Binding Approaches: Prodrug vs BioAtla's CAB Platform Technology Feature Proteolytic cleavage of prodrug Conditionally Active Biologic (CAB) Mechanism of Action Mask obscuring antibody binding site is cleaved by tumor-associated proteases Biologic is engineered to bind only in TME at low
Slide 11: Preclinical evidence of CAB selectivity
Preclinical evidence of CAB selectivity Differential EGFR tumor vs. skin binding (12.6-fold improved TI) AXL-ADC reduced TMDD yielding Increased T1/2 and exposure in NHP (>2-fold increase in T1/2) Reduced liver enzymes (<10% of non-CAB ALT levels) EpCAM DualCAB TCE maintained efficacy with highly re
Slide 12: Clinical evidence of CAB selectivity
Clinical evidence of CAB selectivity AXL-ADC good risk/benefit ratio Two non-CAB AXL-targeting ADCs terminated in P1 due to toxicity Potent and durable response with differentiated OS in mKRAS NSCLC and sarcoma patients ROR2-ADC good risk/benefit ratio Good tolerability with only 7% treatment-relate
Slide 13: Key Advantages of the CAB Platform
Key Advantages of the CAB Platform Widening The Therapeutic Index Conditional and reversible binding increases clinical activity and improves safety Not dependent on enzymatic activation for selective binding Enhances pharmacologic properties Broadly applicable to antibody formats including ADCs, Bi
Slide 14: Clinical and Preclinical Pipeline of Differentiated CAB Assets
CAB Program Target Indications IND Enabling Pre-Clinical Phase 1 Clinical Phase 2 Clinical Phase 3 Clinical CAB- Bispecific TCE BA3182 EpCAM x CD3 Adenocarcinomas CT-202 (Out licensed to Context Therapeutics) Nectin-4 x CD3 Solid Tumors BA3142 B7H3 x CD3 Solid Tumors BA3241 Trop2 x CD3 Solid Tumors
Slide 15: BA3182 (Dual CAB EpCAM x CD3 Bispecific T-Cell Engager): Adenocarcinoma
BA3182 (Dual CAB EpCAM x CD3 Bispecific T-Cell Engager): Adenocarcinoma
Slide 16: Why EpCAM As a Target?
Why EpCAM (Epithelial Cell Adhesion Molecule) As a Target? Targeting EpCAM has potential to serve over 1 Million patients (potential Pan-cancer drug) Estimated Number of New Cancer Cases in 2025 EpCAM Expression (TIS 1 to 12)2 Breast Cancer 319,750 81% Prostate Cancer 313,780 99% Lung Cancer 226,650
Slide 17: Proposed Mechanism of Action of BA3182
Proposed Mechanism of Action of BA3182, a Dual-CAB EpCAM x CD3 bispecific T-cell Engager CAB-TCEs redirect all T cells in the TME to attack cancer cells, but not in healthy tissues Mabs. 2024 Mar 6;16(1):2322562
Slide 18: BA3182 – First Dual-CAB T-cell Engager Targeting EpCAM
pH Range ELISA TME Physiologic pH BA3182 – First Dual-CAB T-cell Engager Targeting EpCAM Potent Lysis of EpCAM Positive Cancer Cells by BA3182 HCT116 CDX Model Highly reduced binding to both targets at normal physiological pH Similar efficacy in mouse xenograft models compared to Non-CAB parent mole
Slide 19: BA3182 Well Tolerated at High Doses in Non-human Primates
CAB-EpCAM-TCE, BA3182, is Well Tolerated at High Doses in Non-human Primates Test Article Non-CAB Parent BA3182 Dose 0.05 mg/kg 5 mg/kg Clinical Outcome All Euthanized on Day 8 No Clinical Findings MCP-1 (pg/mL) IL-2 (pg/mL) IL-6 (pg/mL) Time (Hours) Non-CAB Parent 0.05 mg/kg BA3182 2.5 mg/kg Low cy
Slide 20: Dose Escalation Study of BA3182 in Advanced Adenocarcinomas
Phase 1 Dose Escalation Study of BA3182 in Advanced Adenocarcinomas Trial ongoing; evaluating various dosing and treatment schedules 0.003 to 0.1 mg 0.01/0.3 mg 0.01/0.6 mg 0.1, 0.3 or 0.6/1.2 mg 0.1/0.6/1.8 mg Continue Escalation No Priming Dose One Priming Dose Two Priming Doses Dose B (N~ 20-30)
Slide 21: BA3182 Patient Demographics
BA3182 Phase 1 Patient Demographics Patients dosed SC per protocol as of September 10, 2025: N=35 Data cut as of 10Sep25 Presented at ESMO Berlin, 2025. Patient Characteristic N=35 Age, mean (SD), y 57 (10) Male (n, %) 19 (54) Female (n, %) 16 (46) ECOG performance status 0 (n, %) 24 (
Slide 22: BA3182 Preliminary Prolonged Tumor Control With Increasing Doses
BA3182 Preliminary Prolonged Tumor Control With Increasing Doses Live Data cut as of 10Sep2025 *Pts with unconfirmed PD were treated beyond initial progression per protocol when pseudo-progression was suspected Presented at ESMO Berlin, 2025. Treatment Dose (mg) Average # of Doses All 8+ 1.2 3+
Slide 23: BA3182 Achieved Objective Tumor Size Reductions
BA3182 Achieved Objective Tumor Size Reductions Across Multiple Tumor Types Preliminary assessment of anti-tumor activity among pts receiving treatment doses of ≥0.6 mg (N=24) 14 CRC pts: among 7 pts who had one scan – 5 achieved SD at 1st scan; among the 7 pts without scans –2 withdrew consent bef
Slide 24: BA3182 Adverse Events Generally Transient and Readily Manageable
BA3182 Adverse Events Generally Transient and Readily Manageable Preliminary safety of subcutaneous dosing Data cut as of 10Sep25 Presented at ESMO Berlin, 2025. 1Early, transient elevation of hepatic analytes: AST, ALT, bilirubin, and/or alkaline phosphatase 2Non-febrile, transient neutropenia, po
Slide 25: Early, Transient Increases in Hepatic Analytes Resolved
Early, Transient Increases in Hepatic Analytes Resolved with Continued Dosing Summary of hepatic analyte changes: Early, transient, and asymptomatic Enabling on-time weekly treatment dosing Consistent with cholestasis (not on target toxicity) Patients primed with 0.1 mg prior to treatment dose (N=9;
Slide 26: BA3182 Confirmed Partial Response in Cholangiocarcinoma
71-year-old male with stage IV cholangiocarcinoma previously treated on clinical trial with gemcitabine, cisplatin, durvalumab, and investigational agent. Confirmed Partial Response (31% Tumor Reduction) BA3182 at 0.6 mg in Patient with Intrahepatic Cholangiocarcinoma without Progression for >6 mont
Slide 27: BA3182 Summary / Upcoming Milestones
BA3182 Summary / Upcoming Milestones BA3182, a dual-conditionally binding CAB-EpCAM x CAB-CD3 T-cell engager continues to demonstrate a manageable safety profile with preliminary evidence of antitumor activity Early cytokine increases appear to cause brief, reversible cholestasis – consistent with
Slide 28: Ozuriftamab Vedotin (CAB-ROR2-ADC): OPSCC
Ozuriftamab Vedotin (CAB-ROR2-ADC): Oropharyngeal Squamous Cell Carcinoma (OPSCC)
Slide 29: Significant Opportunity for Oz-V in OPSCC
Significant Opportunity for Oz-V in OPSCC Rapidly Growing Patient Population OPSCC incidence is increasing, largely due to HPV-driven disease1,2 Up to 80% of OPSCC cases in the United States caused by HPV infection3 By 2030, OPSCC will be the most common subtype of head and neck cancer in the US1,2
Slide 30: OPSCC Incidence is Increasing
OPSCC Incidence is Increasing Proportion of new HPV+ OPSCC diagnoses now approach 80% in the US Years Annual number of OPC Cases Oropharyngeal Cancer Burden by Infection Status Damgacioglu H, Sonawane K, Chhatwal J, et al. Long-term impact of HPV vaccination and COVID-19 pandemic on oropharyngeal ca
Slide 31: Ozuriftamab Vedotin (Oz-V): CAB-ROR2-ADC
Ozuriftamab Vedotin (Oz-V): CAB-ROR2-ADC ROR2 is expressed in a variety of tumor types, with overexpression associated with metastasis, tumor resistance to chemotherapy, and poor prognosis CAB-tumor cell target Cytotoxic payload and linker BA3021 pH binding inflection point adjusted for tumor microe
Slide 32: ROR2 Overexpression is Driven by HPV E6 / E7 Oncoproteins
ROR2 Overexpression is Driven by HPV E6 / E7 Oncoproteins 80% of OPSCC cases in the United States caused by HPV infection HPV driven cancers Highest ROR2 expression among SCCHN HPV E6 and E7 oncoproteins drive ROR2 overexpression ROR2 overexpression results in increased proliferation and invasivenes
Slide 33: Demographics and Baseline Clinical Characteristics
Demographics and Baseline Clinical Characteristics HPV p16 positive and all patients Ozuriftamab vedotin 1.8 mg/kg OPSCC p16+a Full Analysis 2Q3W (n=10) Q2W (n=13) 2Q3W and Q2W (N=40) Age, mean (SD), y 65 (5) 62 (7) 65 (8) Sex, n (%) Male 10 (100) 12 (92) 36 (90) Female 0 1 (8) 4 (10) ECOG performan
Slide 34: Oz-V in SCCHN Continues to Demonstrate Clinical Responses
Oz-V in SCCHN Continues to Demonstrate Clinical Responses in a Heavily Pretreated Population 1.8 mg/kg Q2W and 2Q3W; Median of 3 prior lines of therapy CR CR Response evaluable patients defined as pts that had at least 1 scan after treatment with study drug Not evaluable prior to first scan: 3 pts h
Slide 35: Oz-V in SCCHN p16+ OPSCC
Oz-V in SCCHN p16+^ OPSCC 1.8 mg/kg Q2W; Median of 3 prior lines of therapy * Response evaluable patients defined as patients that had at least 1 scan after treatment with study drug Not evaluable prior to first scan: 1 patients had clinical progression Q2W Responders (confirmed & unconfirmed) 42% (
Slide 36: 2L+ HPV+ OPSCC: Cross Trial Comparisons of ORR and OS
2L+ HPV+ OPSCC: Cross Trial Comparisons of ORR and OS Considerably improved response rate and survival among a heavily pretreated trial population Cross trial comparisons** Median prior lines of therapy ORR (%) OS (months)*** Ozuriftamab vedotin monotherapy (1.8 mg/kg Q2W) Study Ongoing* 3 42% ORR 2
Slide 37: Confirmed Complete Response Oz-V in SCCHN
Confirmed Complete Response Oz-V in SCCHN (1.8 mg/kg Q2W) – HPV Positive 76-year-old male, stage IV – recurred after surgery and radiation therapy; prior treatments: pembrolizumab; clinical trial bispecific anti-PD1/CD47; patient remains in complete response >16 months after Oz-V treatment initiatio
Slide 38: Partial Response (-80%) Oz-V in SCCHN
Partial Response (-80%) Oz-V in SCCHN (1.8 mg/kg Q2W) – HPV Positive 63-year-old male, stage IV – recurred after surgery and radiation therapy; prior treatments: platinum, investigational agents including pembrolizumab Baseline – December 4, 2025 On Treatment – February 15, 2025
Slide 39: Most frequent AEs of any grade
Most frequent AEs of any grade (>15% of patients) (N=40) 2Q3W (n=20) Treatment-Related Adverse Events Related Grade 3 6 (30%) Related Grade 4 2 (10%) Related Serious 2 (10%) Treatment-Related Adverse Events Related Grade 3 3 (15%) Related Grade 4 0 (0%) Related Serious 0 (0%) Q2W (n=20) Related AEs
Slide 40: Ph2 Oz-V: Overall Safety Summary of SCCHN patients
Ph2 Oz-V: Overall Safety Summary of SCCHN patients Investigator Choice3 related AEs G3 or 4 = 35% - Considerably higher than Oz-V 1.8 mg/kg Q2W 1.8 mg/kg Q2W (N=20) 1.8 mg/kg 2Q3W (N=20)4 Total (N=40)4 Any Adverse Events (AEs) 19 (95%) 20 (100%) 38 (95%) Related AEs with CTCAE1 Grade 3 or 42 3 (
Slide 41: Oz-V Safety Data
Phase 2 Oz-V Safety Data Most frequent treatment-emergent related adverse events (>15%) 1.8 mg/kg Q2W (N=20) 1.8 mg/kg 2Q3W (N=20)^ Total (N=40)^ Preferred Term All Grades n (%) Grade 3-4 n (%) All Grades n (%) Grade 3-4 n (%) All Grades n (%) Grade 3-4 n (%) Number of subjects with at least one TRA
Slide 42: FDA End of Phase Meeting: Key Outcomes
FDA End of Phase 2 Meeting: Key Outcomes Dual primary endpoints of ORR and OS to support potential accelerated approval followed by full approval Pivotal Trial Design: For full approval, approximately 300 patients prospectively randomized and stratified, one to one between two open label treatment a
Slide 43: Mecbotamab Vedotin (CAB-AXL-ADC): mKRAS NSCLC
Mecbotamab Vedotin (CAB-AXL-ADC): mKRAS Non-Small Cell Lung Cancer (NSCLC)
Slide 44: Mecbotamab Vedotin (Mec-V): CAB-AXL-ADC
Mecbotamab Vedotin (Mec-V): CAB-AXL-ADC AXL is expressed in a variety of tumor types, with overexpression associated with metastasis, tumor resistance to chemotherapy, and poor prognosis 1. Gay CM, Balaji K, Byers LA. Br J Cancer. 2017;116(4):415-423. 2. Zhang G, Wang M, Zhao H, Cui W. Oncol Lett. 2
Slide 45: AXL Plays a Crucial Role in mKRAS NSCLC Cells
AXL Plays a Crucial Role in the Survival of mutated KRAS (mKRAS) NSCLC Cells Adapted from Morimoto et al. Cancer Letters 587 (April 2024) mKRAS leads to upregulation and activation of AXL expression Tumor resistance mechanism mKRAS represents 30% of all NSCLC patients 70% to 85% of mKRAS NSCLC expre
Slide 46: Mec-V Overall Survival mKRAS vs wtKRAS NSCLC
Mec-V 1.8 mg/kg Q2W Overall Survival mKRAS vs wtKRAS NSCLC Median of 3 prior lines of tx Events n (%) Median (95% CI) mKRAS 7 (41) NR (4.0 – NE) wtKRAS 20 (74) 8.3 (3.5-10.2) ^Response evaluable patients defined as patients that had at least 1 scan after treatment with study drug Prior to first scan
Slide 47: Mec-V Associated with Exceptional Overall Survival in mKRAS NSCLC
Mec-V 1.8 mg/kg Q2W Associated with Exceptional Overall Survival in mKRAS NSCLC Overall survival cross trial comparison1 mecbotamab vedotin (1.8 mg/kg Q2W) Docetaxel3 Population mKRAS mKRAS Number of patients 17 256 Prior Lines of tx 2 1 Prior Taxane 53% 0% ORR 31%2 14% PFS (months) 4.5 2.8 OS (mont
Slide 48: Competitive Response Rate in 2L+ mKRAS NSCLC
Competitive Response Rate in 2L+ mKRAS NSCLC Median Overall Survival ranges from 6 to 11 months in mKRAS NSCLC when treated with docetaxel in the 2L+ Cross trial comparisons** Pts Median prior lines of therapy ORR Median OS (months) Mecbotamab Vedotin (1.8 mg/kg Q2W regimen) Study Ongoing* 17 3 31%*
Slide 49: Ph2 Mec-V: Overall Safety Summary of NSCLC patients
Ph2 Mec-V: Overall Safety Summary of NSCLC patients 1.8 mg/kg Q2W with or without nivolumab generally well-tolerated; only 7% discontinuation due to related AEs Data Cut Date: 19Aug2025 N=45 (%) Any Adverse Events (AEs) 45 (100) Related AEs with CTCAE1 Grade 3 or 42 14 (31) Any Related Serious AEs2
Slide 50: Potential for Mec-V to Address All mKRAS NSCLC
Potential for Mec-V to Address All mKRAS NSCLC 1.8 mg/kg Q2W associated with improved overall survival and favorable benefit / risk profile Promising anti-tumor activity among patients whose tumors express KRAS mutations mKRAS represents 30% of all NSCLC patients and is associated with increased AXL
Slide 51: Opportunity for Mec-V to Expand Beyond mKRAS NSCLC
Significant Opportunity for Mec-V to Expand Beyond mKRAS NSCLC KRAS mutations most commonly found in CRC, NSCLC and PDAC Estimated US incidence of select mKRAS cancers and distribution of selected mKRAS variants Lee J., Sivakumar S., Schrock A., et al. NPJ Precision Oncology, 2022. PMID: 36494601. C
Slide 52: Improved Overall Survival also Observed in Soft Tissue Sarcoma
Improved Overall Survival also Observed in Soft Tissue Sarcoma Mirrors Overall Survival Observed in mKRAS NSCLC LMS, UPS, and Liposarcoma: 1.8 mg/kg Q2W Mono and anti-PD-1 Combo; cross-trial comparison* Data Cut Date: 24Mar2025 placebo eribulin dacarbazine trabectedin mecbotamab vedotin 21.5 (14.2 –
Slide 53: Evalstotug (CAB-CTLA-4)
Evalstotug (CAB-CTLA-4) Brita
Slide 54: Evalstotug is a Next Generation Adaptation of Ipilimumab
Evalustotug is a Next Generation Adaptation of Ipilimumab CAB-CTLA4 selectively active in tumor microenvironment, thereby reducing immune mediated adverse events (imAEs) Ipilimumab Evalstotug CAB CDR Engineering Inability to distinguish between normal and tumor tissue Similar efficacy and PK enhance
Slide 55: Evalstotug is a CABified Ipilimumab
Evalstotug is a “CABified” Ipilimumab: A Next Generation CTLA-4 Inhibitor Preserved efficacy with reduced toxicity in combination with PD-1 Ipilimumab (ipi) CDRs modified to bind at tumor cell acidic pH, but not at normal pH leading to evalstotug: Preserved affinity and epitope Equivalent EMax and E
Slide 56: Reversible Binding in the TME
Reversible Binding in the TME Comparison of evalstotug binding to CTLA-4 in different pH conditions Abbreviations: CTLA-4, cytotoxic T-lymphocyte associated protein 4; ICI, immune checkpoint inhibitor; IgG, immunoglobulin G; OD450, optical density at 450 nm; TME, tumor microenvironment. Note: Figure
Slide 57: Evalstotug Reduced GI Toxicity in Primates
Study Date 10 20 30 0 0 5 10 15 20 KI67+ CD4+ T cells Ratio to Baseline Vehicle Ipilimumab + nivolumab Evalstotug + nivolumab Evalstotug Reduced GI Toxicity in Primates Abbreviations: CD, cluster of differentiation; Cyno, cynomolgus macaque; GI, gastrointestinal; QW, once weekly. Note: Ipilimumab an
Slide 58: Evalstotug Across Multiple Tumor Types
Evalstotug Across Multiple Tumor Types
Slide 59: Evalstotug 350mg Q3W with PD1: Demographics
Evalstotug at 350mg Q3W (5mg/kg based on 70 kg pt) in Combination With PD1: Demographics – Across Multiple Tumor Types; n=17 82% patients experienced failure of prior PD-1 treatment Total (N=17) Total (N=17) Prior # of treatments Age, y, mean (SD) 60 (14) Tumor type, n (%) Sex, n (%) Melanoma 11 0 -
Slide 60: Patients Treated with Evalstotug Received More Doses vs Ipi
Patients Treated with Evalstotug Received More Than Twice as Many Doses Compared with Reported Ipi Dosing Mean number of evalstotug 350 mg doses vs ipilimumab when in combination with PD1 Note: Mean number of doses for ipilimumab is based on a retrospective observational study. Evalstotug 350 mg and
Slide 61: Evalstotug with PD1 Across Multiple Tumor Types
Evalstotug at 350mg Q3W (5mg/kg based on 70 kg pt) in Combination with PD1 Across Multiple Tumor Types 3 Complete Responders with 2 in melanoma and 1 in cervical cancer Total Responders (confirmed & unconfirmed) 44% (7/171) Responders (confirmed) 41% (7/171) DCR 76% (13/171) OS ongoing 1Response eva
Slide 62: Evalstotug with PD1: Durability of Response
Evalstotug in Combination with PD1: 7 of 17 Achieved Response Durable antitumor activity across multiple solid tumor types 70 mg Q3W + PD1 210 mg Q3W + PD1 350 mg Q3W + PD1 1 year Data Cut Date: 31Oct25
Slide 63: Evalstotug Melanoma
Evalstotug Melanoma (with or without prior ICI treatment)
Slide 64: Evalstotug with PD1 in Melanoma: Demographics
Evalstotug In Combination with PD1 in Melanoma (with or without prior ICI treatment; n=16): Demographics Evalstotug 350 mg or 700 mg Q3W (5 mg/kg or 10 mg/kg based on 70 kg patient) Total (N=16) Age, y, mean (SD) 61 (14) Sex, n (%) Female 10 (62) Male 6 (38) White race, n (%) 16 (100) ECOG, n (%) 0
Slide 65: Evalstotug with PD1 in Melanoma
Evalstotug in Combination with PD1 in Melanoma (with or without prior ICI treatment) 8 responders among 16 patients; 81% of patients had prior ICI Total Responders (confirmed & unconfirmed) 50% (8/161) Responders (confirmed) 50% (8/161) DCR 94% (15/161) PFS Not Reached OS Not Reached 1Response evalu
Slide 66: 50% ORR and 94% DCR in Melanoma
50% ORR and 94% DCR in Melanoma (with or without prior ICI treatment) 81% patients had received prior PD1 Data Cut Date: 31Oct25 Evalstotug
Slide 67: Evalstotug 1L Melanoma
Evalstotug 1L Melanoma – prior adjuvant therapy or no prior ICI treatment
Slide 68: Evalstotug in 1L Melanoma: Demographics and Waterfall
Total (N=16) Age, y, mean (SD) 61 (14) Sex, n (%) Female 10 (62) Male 6 (38) White race, n (%) 16 (100) ECOG, n (%) 0 12 (75) 1 4 (25) Prior ICI Therapy Status, n (%) No prior ICI treatment 3 (19) Adjuvant 10 (62) Metastatic setting 3 (19) Evalstotug In Combination with PD1 in Melanoma (no prior tre
Slide 69: 62% ORR and 92% DCR in Melanoma
62% ORR and 92% DCR in Melanoma (with or without prior ICI treatment; n=13) Evalstotug in Combination with PD1 81% patients had received prior PD1 adjuvant treatment Data Cut Date: 31Oct25 All 13 melanoma pts living as of data cut date Evalstotug Evalstotug
Slide 70: Evalstotug 1L and 2L+ Melanoma with prior ICI
Evalstotug 1L and 2L+ Melanoma who received prior ICI treatment
Slide 71: Evalstotug in Melanoma with Prior ICI: Demographics and Waterfall
Total (N=16) Age, y, mean (SD) 61 (14) Sex, n (%) Female 10 (62) Male 6 (38) White race, n (%) 16 (100) ECOG, n (%) 0 12 (75) 1 4 (25) Prior ICI Therapy Status, n (%) No prior ICI treatment 3 (19) Adjuvant 10 (62) Metastatic setting 3 (19) Evalstotug In Combination with PD1 in Melanoma (received pri
Slide 72: 54% ORR and 85% DCR in Melanoma with Prior ICI
54% ORR and 85% DCR in 1L and 2L+ Melanoma who received Prior ICI All 13 patients received prior ICI; evalstotug at higher doses achieves greater efficacy ipilimumuab (3mg/kg) ipilimumab (3mg/kg) + nivolumab Evalstotug (5mg/kg or 10mg/kg) + pembrolizumab Evalstotug + pembrolizumab lifileucel ipilimu
Slide 73: Safety
Safety
Slide 74: Evalstotug vs Ipilimumab: Cross Trial Comparison
Evalstotug vs Ipilimumab: Cross Trial Comparison Lower imAE rate vs Ipilimumab despite more patients previously treated with ICI Treatment Evalstotug (5 mg/kg) + PD1 Q3W N=17 Evalstotug (5 mg/kg or 10 mg/kg) + PD1 Q3W N=25 Ipilimumab (3 mg/kg) + nivolumab Q3W N=178-3141,2,3 Doses 1 – ≤18 weeks expos
Slide 75: Evalstotug with PD1: Overall Safety Summary
Evalstotug in Combination with PD1: Overall Safety Summary Generally well-tolerated; All G3 and G4 resolved Related AE Summary Total (N=17) Total (N=8) Total (N=25) Any Related Adverse Events (AEs) 16 (94%) 8 (100%) 24 (96%) Related AEs with CTCAE1 Grade 32 6 (36%) 4 (50%) 12 (48%) Grade 42 transien
Slide 76: Evalstotug with PD1 Safety Data
Evalstotug in Combination with PD1 Safety Data Treatment-emergent related adverse events >15% Data Cut Date: 31Oct25 Evalstotug 350 mg + PD1 (N=17) Evalstotug 700 mg + PD1 (N=8) Total (N=25) AE All Gr3+ All Gr3+ All Gr3+ Chills 11 (64.7) 0 4 (50.0) 0 15 (60.0) 0 Fatigue 11 (64.7) 0 3 (37.5) 1 (12.5)
Slide 77: Confirmed PR - Gastro-esophageal Cancer
Confirmed PR - Gastro-esophageal Cancer 63-year-old male, stage IV gastro-esophageal cancer HER2 negative, post-FOLFOX, taxane, TKI, anti-PD1 and anti-VEGFl Baseline - July 31,2023 On Treatment - October 23, 2023
Slide 78: Confirmed CR - Cervical Cancer
Confirmed CR - Cervical Cancer 43-year-old female, stage IV cervical cancer HPV+16 positive, post-platinum, taxane, anti-PD1 and anti-VEGF “No enlarged mediastinal, hilar or axillary lymph nodes are present. There is persistent resolution of previously noted enlarged mediastinal and paraesophageal l
Slide 79: Evalstotug Enables Combination with ADC and PD1 Antibodies
Evalstotug Enables the Combination with ADC and PD1 Antibodies PR (-50%) – Well Tolerated Triplet; Oz-V + Evalstotug + PD1 69 yo M with oral cavity, floor of mouth/ mandibular, mucoepidermoid carcinoma; neo-adjuvant patient Disease had recurred after prior surgery and chemoradiation (platinum / taxa
Slide 80: FDA Guidance Regarding Evalstotug Pivotal Trial in 1L Melanoma
FDA Guidance Regarding Evalstotug Pivotal Trial in 1L Unresectable and / or Metastatic Melanoma Centrally reviewed PFS acceptable as primary endpoint General agreement with proposed study population and sample size Additional guidance received on ongoing dose optimization and control arm: IO-based c
Slide 81: Overall Summary: Evalstotug + PD1
Overall Summary: Evalstotug + PD1 Greater efficacy and lower imAE rate vs ipilimumab + PD1 Preclinical & clinical data demonstrate that ipi & evalstotug are similar, i.e. epitope, affinity, T1/2 and tumor exposure, and efficacy ipi & evalstotug are NOT similar with respect to normal tissue environme
Slide 82: Gita
www.bioatla.com Gita