Slide 1: Conditionally Active Biologics: Transforming Cancer Therapy
Conditionally Active Biologics: Transforming Cancer Therapy Corporate Presentation November 2025
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: BioAtla Is A Clinical Stage Company Focused on Transforming Cancer Therapy
BioAtla© Is A Clinical Stage Company Focused on Transforming Cancer Therapy with Conditionally Active Biologics (CABs) Initiation of the Oz-V P3 study Proprietary technology with in 2L+ OPSCC on-track to over 500 issued patents advance with a strategic Advancing P1 BA3182 (CAB- In advanced stages to
Slide 4: Leadership Team
Leadership Team Jay Short, Ph.D. Richard Waldron, M.B.A. Eric Sievers, M.D. Sheri Lydick Chairman, CEO and Cofounder Chief Financial Officer Chief Medical Officer Chief Commercial Officer GeneMedicine, Inc. William Boyle, Ph.D. Monica Sullivan Susie Melody Sr. Research Fellow Sr. VP, Intellectual Pr
Slide 5: Board of Directors and Scientific Advisors
Board of Directors and Scientific Advisors Jay Short, Ph.D. Chairman, Chief Executive Lawrence Steinman, MD Mary Ann Gray, Ph.D. Sylvia McBrinn Officer & Cofounder Lead Director Director Director Director Susan Moran, MD, MSCE Scott Smith Eddie Williams Director Director Director James Allison, Ph.D
Slide 6: Selective and Targeted CAB Platform Technology Widens Therapeutic Window
Selective and Targeted CAB Platform Technology Widens Therapeutic Window Thus has the potential to enhance clinical outcomes in multiple tumor types Alkaline Healthy Cell Membrane Acidic Cancer Cell Membrane BioAtla discovered that acidic pH at the cancer cell surface unveils binding sites that are
Slide 7: CAB Platform Technology Summary
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 ag
Slide 8: 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 NOT generally ATP deficient but are limited in other Cancer cells are ATP limited precursor
Slide 9: CAB Antibodies Bind Selectively and Reversibly Based on the Tumor Microenvironment
CAB Antibodies Bind Selectively and Reversibly Based on the Tumor Microenvironment (TME) - CAB technology generates a library of pH selective molecules from the original template - Enhancing exposure and reducing toxicity CABs Bind Selectively in the Lower pH TME Non-CABs Bind to Normal Non-CAB Tiss
Slide 10: 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 Enhanced ADC Tumor Selectivity (12.6-fold increase in TI) Cetuximab Control CAB Anti-EGFR mAb PET scan images BioAtla | Overview 10
Slide 11: Conditional Binding Approaches: Prodrug vs BioAtla's CAB Platform Technology
Conditional Binding Approaches: Prodrug vs BioAtla's CAB Platform Technology Feature Proteolytic cleavage of prodrug Conditionally Active Biologic (CAB) Mask obscuring antibody binding site is Biologic is engineered to bind only in Mechanism of Action cleaved by tumor-associated proteases TME at low
Slide 12: Preclinical Evidence Summary
Preclinical Evidence Summary ➢ 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 DualC
Slide 13: Clinical Evidence Summary
Clinical Evidence Summary ➢ Clinical evidence of CAB selectivity • AXL-ADC promising risk/benefit ratio ⁻ Two other companies' non-CAB AXL-targeting ADCs terminated in P1 due to toxicity ⁻ Potent and durable response with differentiated OS in mKRAS NSCLC and soft tissue sarcoma patients • ROR2-ADC p
Slide 14: 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
Slide 15: BioAtla's Catalysts Expected to be Achieved through Internal and Corporate Partnership Advancement
BioAtla’s Catalysts Expected to be Achieved through Internal and Corporate Partnership Advancement 2025 2026 Readout Readout Readout BA3182 (EpCAM-TCE) – Phase 1 Dose Phase 1 Dose Escalation (n=30) Phase 2 Expansion (n= up to 40) Escalation (n=30) Adenocarcinomas Readout Ozuriftamab vedotin (ROR2-AD
Slide 16: BA3182 (Dual CAB EpCAM x CD3 Bispecific T-Cell Engager): Adenocarcinoma
BA3182 (Dual CAB EpCAM x CD3 Bispecific T-Cell Engager): Adenocarcinoma
Slide 17: 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) Challenges of targeting EpCAM Estimated Number of New EpCAM Expression Cancer Cases in 2025 (TIS 1 to 12)2 All normal epithelia express EpCAM which wi
Slide 18: 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 BioAtla | Overview 18 Mabs. 2024 Mar 6;16(1):2322562
Slide 19: BA3182 – First Dual-CAB T-cell Engager Targeting EpCAM
BA3182 – First Dual-CAB T-cell Engager Targeting EpCAM Potent Lysis of EpCAM Positive Cancer Cells by BA3182 pH Range ELISA HCT116 CDX Model Tetravalent T-cell TME Physiologic pH engager EpCAM Highly reduced binding to both Similar efficacy in mouse xenograft models targets at normal physiological p
Slide 20: CAB-EpCAM-TCE, BA3182, is Well Tolerated at High Doses in Non-human Primates
CAB-EpCAM-TCE, BA3182, is Well Tolerated at High Doses in Non-human Primates Cytokine Levels Associated with Toxicity Increase in Safety and Tolerability Non-CAB Parent BA3182 800 0.05 mg/kg 2.5 mg/kg 100 10000 TI IL-6 (pg/mL) 550 80 8000 MCP-1 (pg/mL) IL-6 (pg/mL) IL-2 (pg/mL) 300 60 6000 50 20 40
Slide 21: Phase 1 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 Part A: Dose Escalation (QW) Part B: Dose Expansion/Dose Optimization Two Priming Doses Continue Escalation Dose B (N~ 20-30) 0.1/0.6/1.8 mg One Priming Dose 0.1, 0.3
Slide 22: BA3182 Phase 1 Patient Demographics
BA3182 Phase 1 Patient Demographics Patients dosed SC per protocol as of September 10, 2025: N=35 Median # Patient Characteristic N=35 Carcinoma Type (n, %) N=35 of prior treatments Age, mean (SD), y 57 (10) Adenoid Cystic Carcinoma 1 (3) 2 Male (n, %) 19 (54) Appendiceal 1 (3) 2 Female (n
Slide 23: BA3182 Preliminary Prolonged Tumor Control With Increasing Doses
BA3182 Preliminary Prolonged Tumor Control With Increasing Doses Treatment Dose Average # (mg) of Doses All 8+ 1.2 3+ 0.6 11+ 0.3 9 0.1 8 0.032 6 *Pts with unconfirmed PD were treated beyond initial progression per protocol when pseudo-progression was suspected BioAtla | Overview 23 Presented at E
Slide 24: BA3182 Achieved Objective Tumor Size Reductions Across Multiple Tumor Types
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 be
Slide 25: BA3182 Adverse Events Generally Transient and Readily Manageable
BA3182 Adverse Events Generally Transient and Readily Manageable Preliminary safety of subcutaneous dosing Characteristic N=35 TRAE >10% (N=35) TRAE TRAE (n, %) Any (n, %) G3+ (n, %) Any Adverse Events (AEs) 29 (83) Alanine aminotransferase increased* 15 (42.9) 7 (20.0) Related AEs of Grad
Slide 26: Early, Transient Increases in Hepatic Analytes Resolved with Continued Dosing
Early, Transient Increases in Hepatic Analytes Resolved with Continued Dosing Patients primed with 0.1 mg prior to treatment dose (N=9; treatment doses: 0.3, 0.6, and 1.2 mg) Summary of hepatic analyte changes: • Early, transient, and asymptomatic • Enabling on-time weekly treatment dosing • Consist
Slide 27: Confirmed Partial Response BA3182 at 0.6 mg in Patient with Intrahepatic Cholangiocarcinoma
Confirmed Partial Response (31% Tumor Reduction) BA3182 at 0.6 mg in Patient with Intrahepatic Cholangiocarcinoma without Progression for >6 months 71-year-old male with stage IV cholangiocarcinoma previously treated on clinical trial with gemcitabine, cisplatin, durvalumab, and investigational agen
Slide 28: 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 w
Slide 29: Ozuriftamab Vedotin (CAB-ROR2-ADC): Oropharyngeal Squamous Cell Carcinoma
Ozuriftamab Vedotin (CAB-ROR2-ADC): Oropharyngeal Squamous Cell Carcinoma (OPSCC)
Slide 30: Significant Opportunity for Oz-V in OPSCC
Significant Opportunity for Oz-V in OPSCC Steadily 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
Slide 31: OPSCC Incidence is Increasing
OPSCC Incidence is Increasing Proportion of new HPV+ OPSCC diagnoses now approach 80% in the US Oropharyngeal Cancer Burden by Infection Status Annual number of OPC Cases • Oropharyngeal cancer has now surpassed cervical cancer as the most common HPV-related malignancy • More than 21,000 U.S. cases
Slide 32: 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 BA3021 pH binding inflection point adjusted for tumor CAB-tumor cell target microenvironment selectivity Normal
Slide 33: 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 infection drives ROR2 overexpression • HPV driven cancers o Highest ROR2 expression among SCCHN o HPV E6 and E7 oncoproteins drive ROR2 overexpression o ROR2 overexpression r
Slide 34: Demographics and Baseline Clinical Characteristics
Demographics and Baseline Clinical Characteristics HPV p16 positive and all patients p16+ analysis Full analysis Median age, (range) years 64 (51-76) 65 (47-84) Sex Male 24 (92) 37 (90) Female 2 (8) 4 (10) ECOG 0 10 (39) 16 (39) 1 15 (58) 25 (61) Prior lines of Therapy 1 2 (8) 4 (10) 2 8 (31) 13 (33
Slide 35: Oz-V in SCCHN Continues to Demonstrate Clinical Responses in a Heavily Pretreated Population
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 Confirmed Response 1.8 mg/kg 2Q3W 1.8 mg/kg Q2W p16 + On Treatment CR ORR = 40%* DCR = 86%* CR * Response evaluable patients defined as patients tha
Slide 36: Oz-V in SCCHN p16+ OPSCC
Oz-V in SCCHN p16+^ OPSCC 1.8 mg/kg Q2W; Median of 3 prior lines of therapy Q2W Responders 45% (confirmed & unconfirmed) (5/11*) Responders 27% (confirmed) (3/11*) 100% DCR (11/11*) Median DOR 9.9 (months) ongoing Median PFS 4.7 (months) ongoing Median OS 11.6 (months) ongoing ^ p16 is strongly asso
Slide 37: 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 Median prior lines Cross trial comparisons** ORR (%) OS (months)*** of therapy Ozuriftamab vedotin monotherapy 45% ORR 11.6 3 (1.8 mg/kg Q2W) 27% cORR on
Slide 38: Confirmed Complete Response Oz-V in SCCHN – HPV Positive
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 39: Partial Response (-80%) Oz-V in SCCHN – HPV Positive
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 On Treatment – February 15, 2025 Baseline – December 4, 2025 BioAtla | Overview 3
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 1.8 mg/kg Total Q2W 2Q3W (N=40)3 (N=20) (N=20)3 Any Adverse Events (AEs) 18 (90%) 20 (100%) 38 (95%) Related AEs with CTCAE1 Grade 3 or 42 3 (15%)
Slide 41: Phase 2 Oz-V Safety Data
Phase 2 Oz-V Safety Data Most frequent treatment-emergent related adverse events 1.8 mg/kg Q2W 1.8 mg/kg 2Q3W Total (N=20) (N=20)^ (N=40)^ All Grades Grade 3-4 All Grades Grade 3-4 All Grades Grade 3-4 Preferred Term n (%) n (%) n (%) n (%) n (%) n (%) Number of subjects with at least one TRAE 13 (6
Slide 42: FDA End of Phase 2 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
Slide 43: Mecbotamab Vedotin (CAB-AXL-ADC): mKRAS Non-Small Cell Lung Cancer
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 BA3011 pH binding inflection point adjusted for tumor CAB-tumor cell target microenvironment selectivity 100 Non-
Slide 45: AXL Plays a Crucial Role in the Survival of mKRAS NSCLC Cells
AXL Plays a Crucial Role in the Survival of mutated KRAS (mKRAS) NSCLC Cells mKRAS leads to upregulation and activation of AXL expression • mKRAS represents 30% of all NSCLC patients • 70% to 85% of mKRAS NSCLC express AXL by IHC and higher by mRNA analysis Tumor resistance • AXL over-expression dri
Slide 46: Mec-V 1.8 mg/kg Q2W 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) Median 3 prior mKRAS mKRAS 6 (35) NR (4.0 – NE) lines of therapy (Q2W only) wtKRAS 20 (74) 8.3 (3.5-10.2) Responders (confirmed & 31% (5/16^) unconfirmed) Responders 25% (4/16^) (con
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 comparison* 12 months 24 months mecbotamab vedotin RMC-62361 Sotorasib2 Docetaxel3 (1.8 mg/kg Q2W) Population mKRAS RAS G12X G12C mKRAS mecbotamab vedotin (KRAS) Number of 17 73 171 256 patie
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+ Median Cross trial comparisons** Pts prior lines ORR Median OS (months) of therapy Mecbotamab Vedotin Not Reached (1.8 mg/kg Q2W regimen) 17 3 31%***
Slide 49: Phase 2 Mec-V: Overall Safety Summary of NSCLC patients
Phase 2 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 Most frequent AEs any grade occurring at a rate >15% N=45 (%) Any Adverse Events (AEs) 45 (100) Related AEs with CTCAE1 Grade 3 or 42 1
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 o mKRAS represents 30% of all NSCLC patients and is associated with increased
Slide 51: Significant 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 NSCLC 50K patients/year PDAC 50K patients/year CRC 75K patients/year G12C G12D G12V G12A
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* mecbotamab vedotin 21.5 (14.2 – 29.9) trabectedin 13.6 (7.1 – 17.3) pazopanib 12.5 (10.6 – 12.8)
Slide 53: Evalstotug (CAB-CTLA-4)
Evalstotug (CAB-CTLA-4)
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 Similar efficacy and PK between normal and enhanced with select
Slide 55: Evalstotug is a “CABified” Ipilimumab: A Next Generation CTLA-4 Inhibitor
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
Slide 56: Reversible Binding in the TME
Reversible Binding in the TME Comparison of evalstotug binding to CTLA-4 in different pH conditions CAB-CTLA4 Shows Potent Anti-Tumor Activity in pH range ELISA MC38/hCTLA4 KI Model 3000 IgG control Evalstotug Tumor volume (mm3) Ipilimumab Mean ± SEM 2000 1000 0 0 7 14 21 Days after the start of tre
Slide 57: Evalstotug Reduced GI Toxicity in Primates
Evalstotug Reduced GI Toxicity in Primates Vehicle Control GI Symptoms Ipilimumaba + nivolumab Liquid feces 15 mg/kg + 20 mg/kg Non-formed feces Other GI symptoms Evalstotuga + nivolumab 15 mg/kg + 20 mg/kg 20 15 KI67+ CD4+ T cells Ratio to Baseline Vehicle 10 Ipilimumab + nivolumab 5 Evalstotug + n
Slide 58: Evalstotug at 350 mg in Combination With PD1: Demographics
Evalstotug at 350 mg (5mg/kg based on 70 kg pt) in Combination With PD1: Demographics – Tumor Types 82% patients experienced failure of prior PD-1 treatment Total Total Prior # of (N=17) (N=17) treatments Age, y, mean (SD) 60 (14) Tumor type, n (%) Sex, n (%) Melanoma 11 0-1 Female 8 (47) Gastric 2
Slide 59: Patients Treated with Evalstotug Received More Than Twice as Many Doses
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 Ipilimumab 3 mg/kg* 3.4 Evalstotug 350 mg (5 mg/kg) 7.8 N=17 0 2 4 6 8 Number of doses Note: Mean number of dose
Slide 60: Evalstotug at 350 mg in Combination with PD1 Across Multiple Tumor Types
Evalstotug at 350 mg in Combination with PD1 Across Multiple Tumor Types 17 patients treated at 350 mg; 3 Complete Responders with 2 in melanoma and 1 in cervical cancer Total Responders 44% (7/171) (confirmed & unconfirmed) Responders 41% (7/171) (confirmed) DCR 76% (13/171) DOR ongoing OS ongoing
Slide 61: Evalstotug: 7 of 17 Achieved Response in the 5 mg/kg Q3W + PD1
Evalstotug: 7 of 17 Achieved Response in the 5 mg/kg Q3W + PD1 Durable antitumor activity across multiple solid tumor types 70 mg Q3W + PD1 1 year 210 mg Q3W + PD1 350 mg Q3W + PD1 BioAtla | Overview 61 Live Database 28Apr2025
Slide 62: 67% ORR and 92% DCR in Unresectable and/or Metastatic Cutaneous Melanoma
67% ORR and 92% DCR in Unresectable and/or Metastatic Cutaneous Melanoma Patients Treated with Evalstotug (5―14.3 mg/kg) in combination PD-1 Antibody 10/12 patients had received prior PD1 adjuvant or neoadjuvant treatment Evalstotug dose Age Sex ECOG Prior Treatment Prior PD1 Best change in Response
Slide 63: Evalstotug in Combination with PD1 Across Prior IO 1L Melanoma
Evalstotug in Combination with PD1 Across Prior IO 1L Melanoma All patients living as of data cut date Data Cut Date: 22Jul25 BioAtla | Overview 63
Slide 64: Evalstotug vs Ipilimumab TRAE, imAE, and Response
Evalstotug vs Ipilimumab TRAE, imAE, and Response Lower imAE rate vs Ipilimumab despite more patients previously treated with ICI Treatment Evalstotug Ipilimumab (5 mg/kg) + PD1 Q3W (3 mg/kg) + nivolumab Q3W N=17 N=178-3141,2,3 Doses 1 – ≤18 weeks exposure 1 – ≤12 weeks exposure (≤6 doses) (≤4 doses
Slide 65: Evalstotug in Combination with PD1 Safety Data
Evalstotug in Combination with PD1 Safety Data Treatment-emergent related adverse events Total (N=17) Total (N=17) All Grades Grade 3 Grade 4 All Grades Grade 3 Grade 4 Preferred Term Preferred Term [n (%)] [n (%)] [n (%)] [n (%)] [n (%)] [n (%)] Number of subjects with at least Chronic gastritis 1
Slide 66: Evalstotug in Combination with PD1: Overall Safety Summary
Evalstotug in Combination with PD1: Overall Safety Summary Generally well-tolerated; All G3 and G4 resolved Total Related AE Summary (N=17) Any Related Adverse Events (AEs) 16 (94%) Related AEs with CTCAE1 Grade 32 6 (36%) Grade 42 transient hypercalcemia 1 (6%) Any related serious AEs2 5 (29%) Poss
Slide 67: Evalstotug Enables the 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 68: 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
Slide 69: Summary
Summary Lower imAE rate vs Ipilimumab despite more patients previously treated with ICI • 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 enviro
Slide 70: BioAtla Is A Clinical Stage Company Focused on Transforming Cancer Therapy
BioAtla© Is A Clinical Stage Company Focused on Transforming Cancer Therapy with Conditionally Active Biologics (CABs) Initiation of the Oz-V P3 study Proprietary technology with in 2L+ OPSCC on-track to over 500 issued patents advance with a strategic Advancing P1 BA3182 (CAB- In advanced stages to