Slides
Page 1
Corporate Presentation November 2025 Conditionally Active Biologics: Transforming Cancer Therapy
Page 2
BioAtla | Overview 2 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 conditions, including but not limited to statements we make regarding BioAtla’s business plans and prospects; whether our clinical trials will support registration; achievement of milestones; results, progress and timing of our research and development programs and clinical trials; expectations with respect to enrollment and dosing in our clinical trials; the anticipated clinical benefits, safety, efficacy, and market potential of our product candidates; plans and expectations regarding future data updates, clinical trials, regulatory meetings and regulatory submissions; the timing of and the ability to establish collaborations or other strategic partnerships for selected assets; the potential regulatory approval path for our product candidates; and expectations about the sufficiency of our cash and cash equivalents to fund operations and expectations regarding R&D expenses and cash burn. Words such as, but not limited to, “anticipate”, “believe”, “could”, “estimate”, “expect”, “intend”, “may”, “plan”, “potential”, “predict”, “project”, “should”, “will”, “would” or the negative of those terms, and similar expressions that convey uncertainty of future events or outcomes, identify forward-looking statements. These forward-looking statements reflect management’s beliefs and views with respect to future events and are based on estimates and assumptions as of the date of this Presentation and are subject to risks and uncertainties, including those described in the Company's filings with the SEC, including but not limited to the Company's latest Annual Report on Form 10-K and any subsequently filed Quarterly Reports on Form 10-Q. Moreover, the Company operates in a very competitive and rapidly changing environment. New risks emerge from time to time. It is not possible for management to predict all risks, nor can the Company assess the impact of all factors on its business or the extent to which any factor, or combination of factors, may cause actual results to differ materially from those contained in any forward-looking statements we may make. Given these uncertainties, you should not place undue reliance on these forward-looking statements. The Company qualifies all the forward-looking statements in this Presentation by these cautionary statements. Except as required by law, the Company undertakes no obligation to publicly update any forward-looking statements, whether as a result of new information, future events or otherwise. Statements contained herein are made as of the date of this Presentation unless stated otherwise, and this Presentation shall not under any circumstances create an implication that the information contained herein is correct as of any time after such date or that the information will be updated or revisited to reflect information that subsequently becomes available or changes occurring after that date hereof. Certain information contained in this Presentation relates to or is based on statistical and other industry and market data obtained from independent industry publications and research, surveys and studies conducted by independent third parties as well as the Company’s own estimates of the prevalence of certain diseases and conditions. The market data used in this Presentation involves a number of assumptions and limitations, and you are cautioned not to give undue weight to such data. Industry publications and third-party research, surveys and studies generally indicate that their information has been obtained from sources believed to be reliable, although they do not guarantee the accuracy or completeness of such information. The Company’s estimates of the patient population with the potential to benefit from treatment with any product candidates the Company may develop include several key assumptions based on its industry knowledge, industry publications and third-party research, which may be based on a small sample size and may fail to accurately reflect the addressable patient population. While the Company believes that its internal assumptions are reasonable, no independent source has verified such assumptions. This Presentation may contain trademarks, trade names, or service marks belonging to other entities. The Company does not intend the use or display of other parties’ trade names, trademarks or service marks to imply a relationship with, or endorsement or sponsorship of, or by these other parties. None of the Company or any of its directors, officers, employees, contractors, agents, consultants, advisors or other representatives makes any representation or warranty, express or implied, as to the accuracy or completeness of the information contained in this Presentation.
Page 3
BioAtla | Overview 3 BioAtla© Is A Clinical Stage Company Focused on Transforming Cancer Therapy with Conditionally Active Biologics (CABs) Proprietary technology with over 500 issued patents CAB Platform maximizes therapeutic window Broad applicability in solid tumors Advancing P1 BA3182 (CAB- EpCAM x CAB-CD3 TCE): Updated P1 data expected 1H‘26 Dose-expansion expected later in 2026 In advanced stages to finalize a strategic transaction with a potential partner; on-track to complete the transaction by year end TCE – T-cell engager; OPSCC – Oropharyngeal Squamous Cell Carcinoma Initiation of the Oz-V P3 study in 2L+ OPSCC on-track to advance with a strategic partner in early 2026 Achieved milestone payment with Context TCE Collaboration which further validates our CAB T-cell engager platform, including BA3182
Page 4
BioAtla | Overview 4 Leadership Team Richard Waldron, M.B.A. Chief Financial Officer Sheri Lydick Chief Commercial Officer Jay Short, Ph.D. Chairman, CEO and Cofounder GeneMedicine, Inc. Eric Sievers, M.D. Chief Medical Officer William Boyle, Ph.D. Sr. Research Fellow Monica Sullivan Sr. VP, Intellectual Property & Contracts Susie Melody Sr. VP, Human Resources CapaIP
Page 5
BioAtla | Overview 5 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 Immunotherapy Program, UCSF Scientific Advisor Padmanee Sharma, MD, Ph.D. MD Anderson Cancer Center Scientific Advisor Jay Short, Ph.D. Chairman, Chief Executive Officer & Cofounder Director
Page 6
BioAtla | Overview 6 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 from prodrugs that require irreversible enzymatic cleavage to become activated CAB antibodies have the potential for increased efficacy with improved safety relative to traditional antibodies H+ H+ H+ H+ H+H+ H+ H+H+ H+ Alkaline Healthy Cell Membrane Acidic Cancer Cell Membrane CAB BindingNo CAB Binding Selective and Targeted CAB Platform Technology Widens Therapeutic Window Thus has the potential to enhance clinical outcomes in multiple tumor types Chang, H.W., Frey, G., Liu, H., Xing, C., Steinman, L, Boyle, B.J., & Short, J.M. (2021) PNAS 118(9): 1 -10, Suppl. 1-19.
Page 7
BioAtla | Overview 7 ➢ 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 • Leverages naturally occurring, negatively charged molecules (e.g. bicarbonate, hydrogen sulfide) to differentiate between targets on cancer cells versus normal cells • These physiological molecules underpin the CAB mechanism and are referred to as Protein- associated Chemical Switches (PaCS)TM • In normal tissues, PaCS shield epitopes, so CAB antibodies cannot bind. In contrast, cancer cells produce H+ ions that remove PaCS molecules from the epitopes, enabling cancer-specific binding. CAB Platform Technology Summary
Page 8
BioAtla | Overview 8 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 molecules whose synthesis depends upon glycolysis. pH technology will miss tumor cells because tumor pH is variable While tumor degree of pH acidity can vary, CABs are designed to bind any cancer cell at or below a predetermined pH. Tumor size influences the acidic environment so pH technology will not work • Larger tumors with larger anaerobic regions are not necessarily more acidic since oxygenated regions have higher acidity due to the higher concentration of hydrogen ions from rapid glycolysis. • Cancer cells – as opposed to the average pH of a tumor – are more acidic, especially at the membrane of the cancer cell.
Page 9
BioAtla | Overview 9 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 MicroEnvironment; mABs = monoclonal antibodies; Data above based on non-human primate studies CABs Bind Selectively in the Lower pH TME Selective Binding Focused Tumor Killing Normal Cells Preserved ≥7.4 is pH of normal cell CABs Reduce or Eliminate, as needed, Binding to Normal Tissues, Enhancing Safety and Clinical Activity Non-CABs Bind to Normal Tissues, Causing Toxicity Tumor pH Blood Non-CAB Parent CABs - CAB technology generates a library of pH selective molecules from the original template - Enhancing exposure and reducing toxicity
Page 10
BioAtla | Overview 10 CAB Technology Eliminates On-target, Off-tumor Binding Thus, widening the therapeutic index by 12.6-fold over cetuximab CAB Anti-EGFR mAb Enhanced ADC Tumor Selectivity (12.6-fold increase in TI) Cetuximab Control PET scan images
Page 11
BioAtla | Overview 11 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 pH* Trigger Type Enzymes overexpressed in tumors TME (i.e., low pH) Bioengineering Addition of foreign sequence No foreign sequences Activation Precision Requires activation; dependent on expression and enzymatic efficiency No activation required – maximizes potency Risk of Off-Target Effects Irreversible activation - can bind target in normal tissues Reversible binding - will not bind target in normal tissues TME = Tumor microenvironment *Warburg effect
Page 12
BioAtla | Overview 12 ➢ 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 reduced toxicity ⁻ MTD not reached in NHP ⁻ >100-fold improvement in TI • B7H3 Dual CAB TCE; target expression associated with high acidity via hyper-glycolysis ⁻ MTD not reached in NHP ⁻ Encouraging safety profile compared to other B7H3 TCEs in development • CTLA4 reduced peripheral immune response while maintaining efficacy - Maintains efficacy at same dose, while enabling higher and extended dosing ⁻ Significant reduction in colitis in NHP compared to ipi ⁻ MTD not reached at 30 mg/kg in NHP ⁻ Selective reduction of activated T cells in the periphery or normal tissues Preclinical Evidence Summary CAB, Conditionally Active Biologics; TI, Therapeutic Index; T 1/2, Half-life; TMDD, Target—Mediated Drug Disposition; NHP, Non-Human Primate; ALT, Alanine Aminotransferase; TCE, T-Cell Engager; MTD, Maximally Tolerated Dose; ipi, ipilimumab
Page 13
BioAtla | Overview 13 ➢ 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 promising risk/benefit ratio ⁻ Good tolerability ⁻ Potent and durable response in SCCHN patients, including in refractory HPV+ patients ⁻ Alignment with FDA for initiating P3 pivotal study in OPSCC • EpCAM Dual CAB TCE ⁻ One other company with non-CAB EpCAM TCE (BiTE) terminated in P1 ⁻ Most advanced EpCAM TCE in the clinic showing confirmed PR and manageable safety, ongoing in P1 ⁻ MTD not yet reached • CTLA4 I/O enables higher and prolonged dosing with reduced immune-mediated AEs ⁻ Maintains PK and efficacy at similar dose, while enabling more intensive dosing ⁻ MTD not reached at 14.3 mg/kg ⁻ Extended dosing (>2x over ipi) and at higher doses and more refractory patients ⁻ Reduced grade 3 AEs such as colitis; no grade 4 or 5 AEs, even at higher doses Clinical Evidence Summary CABs demonstrate universal improvement in TI and enable therapeutic development for "undruggable" targets
Page 14
BioAtla | Overview 14 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, Bispecific TCEs, CAR-Ts and other proteins ✓Provides ability to create new therapies and combinations against targets that had previously been limited due to toxicity
Page 15
BioAtla | Overview 15 BioAtla’s Catalysts Expected to be Achieved through Internal and Corporate Partnership Advancement 2025 2026 Mecbotamab vedotin (AXL-ADC) – mKRAS NSCLC Advancement anticipated through corporate partnership BA3182 (EpCAM-TCE) – Adenocarcinomas Readout Phase 1 Dose Escalation (n=30) Phase 2 Expansion (n= up to 40) Readout Phase 2 (NSCLC) Phase 1 Dose Escalation (n=30) Readout Evalstotug (CTLA4-IO) – Melanoma BA3362 (Nectin4-TCE) – Solid Tumors Out-Licensed to Context Therapeutics for up to $133.5 Million IND Submission Pre-clinical and IND-enabling Studies√ = Completed or asset partnered Advancement anticipated through corporate partnershipPhase 2 √ √ √ Readout Readout Phase 2 Phase 3 (2L+ OPSCC) * (Planned Collaboration with a Partner) Ozuriftamab vedotin (ROR2-ADC) – 2L+ OPSCC √ Readout Phase 2 (STS / Bone Sarcoma) √ Readout √ Milestone payment Milestone *Dual primary endpoints – ORR for accelerated approval; OS for full approval
Page 16
BA3182 (Dual CAB EpCAM x CD3 Bispecific T-Cell Engager): Adenocarcinoma
Page 17
BioAtla | Overview 17 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 93% NSCLC 80% SCLC Colon Cancer 154,270 100% Pancreatic Cancer 67,440 99% Thyroid Cancer 44,020 97% Ovarian 20,890 92% Gallbladder & other biliary 12,610 97% 1Siegel RL, Kratzer TB, Giaquinto AN, Sung H, Jemal A. Cancer statistics, 2025. CA Cancer J Clin. 2025. 2G. Spizzo, et al. J Clin Pathol 2011;64:415e420. Normal Colon Colon Cancer Challenges of targeting EpCAM All normal epithelia express EpCAM which with traditional antibodies would lead to on-target, off-tumor toxicities CABs are essential for targeting EpCAM EpCAM IHC
Page 18
BioAtla | Overview 18 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
Page 19
BioAtla | Overview 19 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 molecule Tetravalent T-cell engager EpCAM Mabs. 2024 Mar 6;16(1):2322562
Page 20
BioAtla | Overview 20 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 0 2 4 6 24 0 2 4 6 24 0 5 10 15 20 50 300 550 800 Time (Hours) IL-6 (pg/mL) 0 2 4 6 24 0 2 4 6 24 0 20 40 60 80 100 Time (Hours) IL-2 (pg/mL) 0 2 4 6 24 0 2 4 6 24 0 2000 4000 6000 8000 10000 Time (Hours) MCP-1 (pg/mL) NonCAB Parent DualCAB BA3182 0 2 4 6 24 0 2 4 6 24 0 5 10 15 20 50 300 550 800 Time (Hours) IL-6 (pg/mL) 0 2 4 6 24 0 2 4 6 24 0 20 40 60 80 100 Time (Hours) IL-2 (pg/mL) 0 2 4 6 24 0 2 4 6 24 0 2000 4000 6000 8000 10000 Time (Hours) MCP-1 (pg/mL) NonCAB Parent DualCAB BA3182 0 2 4 6 24 0 2 4 6 24 0 5 10 15 20 50 300 550 800 Time (Hours) IL-6 (pg/mL) 0 2 4 6 24 0 2 4 6 24 0 20 40 60 80 100 Time (Hours) IL-2 (pg/mL) 0 2 4 6 24 0 2 4 6 24 0 2000 4000 6000 8000 10000 Time (Hours) MCP-1 (pg/mL) NonCAB Parent DualCAB BA3182 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 cytokine levels with DualCAB vs Non-CAB Parent even at significantly higher doses Cytokine Levels Associated with Toxicity TI Increase in Safety and Tolerability Mabs. 2024 Mar 6;16(1):2322562
Page 21
BioAtla | Overview 21 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) Dose A (N~ 20-30) R Part A: Dose Escalation (QW) Part B: Dose Expansion/Dose Optimization Treatment notes: • Prophylactic acetaminophen and diphenhydramine delivered prior to all doses and prophylactic tocilizumab (no corticosteroids) given prior to Cycle 1 Day 1 treatment dose • Post treatment ondansetron guided for nausea • Ongoing weekly treatment dosing continued after DLT observation interval concluded Presented at ESMO Berlin, 2025.
Page 22
BioAtla | Overview 22 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 (69) 1 (n, %) 11 (31) Presence of liver metastases (n, %) 22 (63) Carcinoma Type (n, %) N=35 Median # of prior treatments Adenoid Cystic Carcinoma 1 (3) 2 Appendiceal 1 (3) 2 Cholangiocarcinoma 2 (6) 1 Colorectal 22 (63) 4 Gallbladder 1 (3) 3 Ovarian 1 (3) 8 Pancreas 7 (20) 3
Page 23
BioAtla | Overview 23 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+ 0.6 11+ 0.3 9 0.1 8 0.032 6
Page 24
BioAtla | Overview 24 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 before the 1st scan and 5 are pending 1st scan • 6 pancreatic cancer pts: 2 pts had SD at 1st scan and 2 pts continued treatment beyond potential pseudo-progression • 2 cholangiocarcinoma pts: 1 pt achieved a confirmed PR and 1 pt is pending first scan • 1 ACC pt experienced SD • Among pts treated with ≥0.6 mg , 9/10 pts achieved SD at a higher rate and remained on active treatment for prolonged intervals, generally longer than those who received lower doses Presented at ESMO Berlin, 2025. Live Data cut as of 10Sep2025 CRC, colorectal cancer; SD, stable disease; PR, partial response; ACC, adenoid cystic carcinoma
Page 25
BioAtla | Overview 25 BA3182 Adverse Events Generally Transient and Readily Manageable Preliminary safety of subcutaneous dosing Data cut as of 10Sep25Presented at ESMO Berlin, 2025. 1Early, transient elevation of hepatic analytes: AST, ALT, bilirubin, and/or alkaline phosphatase 2Non-febrile, transient neutropenia, possibly related to tocilizumab 3G2 pancreatitis, G2 atrial fibrillation, G3 diarrhea, G3 acute kidney injury, and G2 CRS 4G3 diarrhea; G3 diarrhea/lymphocyte count decrease; G3 acute kidney injury/white blood cell count decrease Characteristic N=35 (n, %) Any Adverse Events (AEs) 29 (83) Related AEs of Grade 3-4 14 (40) Related AEs of Grade 3 hepatic analytes1 11 (31) Related AEs of Grade 4 hepatic analytes1 1 (3) Related AEs of Grade 3-4 non-febrile neutropenia2 2 (6) Related AEs of Grade 3 excluding hepatic analytes1 and non-febrile neutropenia2,4 3 (9) Any related serious AEs3 5 (14) Related CRS of any grade (per ASTCT grading) 2 (6) Related AEs leading to death 0 Related AEs leading to treatment discontinuation 1 (3) TRAE >10% (N=35) TRAE Any (n, %) TRAE G3+ (n, %) Alanine aminotransferase increased* 15 (42.9) 7 (20.0) Aspartate aminotransferase increased* 15 (42.9) 9 (25.7) Nausea 14 (40.0) 0 Injection site reaction 12 (34.3) 0 Diarrhea 11 (31.4) 2 (5.7) Fatigue 9 (25.7) 0 Blood bilirubin increased* 8 (22.9) 0 Neutrophil count decreased 7 (20.0) 2 (5.7) Blood alkaline phosphatase increased* 6 (17.1) 1 (2.9) Decreased appetite 6 (17.1) 0 Dysgeusia 5 (14.3) 0 Vomiting 5 (14.3) 0 Abdominal pain 4 (11.4) 0 Constipation 4 (11.4) 0 *Transient laboratory changes; resolved
Page 26
BioAtla | Overview 26 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; treatment doses: 0.3, 0.6, and 1.2 mg) Grade 3 Grade 2 Grade 1 Normal Range 0.1 / 1.2 mg (n=4) 0.1 / 0.6 mg (n=3) 0.1 / 0.3 mg (n=2) Live Data cut as of 10Sep2025 Presented at ESMO Berlin, 2025.
Page 27
BioAtla | Overview 27 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 months Presented at ESMO Berlin, 2025. Data cut as of 10Sep25
Page 28
BioAtla | Overview 28 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 tumor- selective targeting • BA3182 treatment achieved an ongoing, confirmed partial response and multiple patients have experienced prolonged tumor control; currently testing dose levels up to 1.8mg and dose varying frequencies • Dose escalation read out anticipated 1H’26 • Phase 2 dose expansion (up to 40 pts) anticipated later in 2026
Page 29
Ozuriftamab Vedotin (CAB-ROR2-ADC): Oropharyngeal Squamous Cell Carcinoma (OPSCC)
Page 30
BioAtla | Overview 30 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 US1,2 Potential to Address Significant Unmet Need • OPSCC poorly served by SOC, including EGFR inhibitors4-10 • Oz-V has a compelling and differentiated profile in HPV+ OPSCC OPSCC, Oropharyngeal Squamous Cell Carcinoma; SOC, Standard of Care; WW, worldwide 1Med Sci (Basel). 2023 Jun 13;11(2):42.; 2Oral Oncol. 2021 Apr:115:105177.; 3Dela J Public Health. 2023 Apr 22;9(1):26-28. 4N Engl J Med 2016;375:1856-1867. 5Journal of Clinical Oncology 2018; 36(15): 1551- 1558. 6Cohen E, et al. (2019) Lancet 393, 156–167. 7British Journal of Cancer (2018) 119:153–159; https://doi.org/10.1038/s41416-018-0131-9. 82008 Jun 15;112(12):2710-9. doi: 10.1002/cncr.23442, 9Erbitux USPI accessed 2024., 10INTERLINK-1: Phase 3 study of cetuximab ± monalizumab /Volume 34, Supplement 2S554-S555 October 2023., 11Internal BioAtla projections.; 12https://www.coherentmi.com/industry- reports/oropharyngeal-cancer-market; 13Cervical Cancer Therapeutics Market Size, Demand, Report to 2033; 23-cervix-uteri-fact-sheet.pdf Large Commercial Opportunity with Potential to Expand • $800mm WW peak sales projections in 2L+ OPSCC11 • Total WW OPSCC market value projected to be ~$3Bn by 203212 • Total HPV+ solid tumors (i.e., cervical) worldwide market valued at >$7Bn13
Page 31
BioAtla | Overview 31 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 cancer incidence and burden among men in the USA: A modeling Study. The Lancet Regional Health – Americas. 2022;8:100143. *CDC report. • Oropharyngeal cancer has now surpassed cervical cancer as the most common HPV-related malignancy • More than 21,000 U.S. cases yearly compared to nearly 12,000 cervical cancer cases*
Page 32
BioAtla | Overview 32 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 microenvironment selectivity 7.4 is pH of normal cell Blood 6.00 6.25 6.50 6.75 7.00 7.25 7.50 0 25 50 75 100 pH value Normalized Binding (%) BA3021 Non-CAB Parent • MMAE-containing ADC (DAR4) with cleavable linker • Humanized anti-ROR2 (N-terminal) IgG1 • ~2nM affinity (pH 6) • MMAE-containing ADC (DAR4) with cleavable linker • Epitope in Ig loop region
Page 33
BioAtla | Overview 33 ROR2 Overexpression is Driven by HPV E6 / E7 Oncoproteins 80% of OPSCC cases in the United States caused by HPV infection • HPV driven cancers o Highest ROR2 expression among SCCHN o HPV E6 and E7 oncoproteins drive ROR2 overexpression o ROR2 overexpression results in increased proliferation and invasiveness • Oz-V conditionally and selectively eliminates ROR2-expressing cells HPV infection drives ROR2 overexpression ROR2 expression Carrero, et al. Oncogene (2019) 38:3551–3568; https://doi.org/10.1038/s41388-018-0659-4 Avincsal, et al. Oncol Rep. 2021 Jul;46(1):148. doi: 10.3892/or.2021.8099. Epub 2021 Jun 3. PMID: 34080643. Figure adapted from Z. Lu, et al. Cancers. 2024, 16, 3474.
Page 34
BioAtla | Overview 34 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) 3+ 16 (61) 22 (57) PD-(L)1 inhibitor 26 (100) 41 (100) Platinum-based therapy 23 (88) 34 (83) Taxanes 13 (65) Cetuximab 8 (31) 20 (49) Smoking Status Yes 0 1 (3) Ex-smoker 14 (54) 22 (55) Never 12 (46) 17 (43) Data Cut Date: Live Database as of May 13, 2025
Page 35
BioAtla | Overview 35 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 * Response evaluable patients defined as patients that had at least 1 scan after treatment with study drug – includes confirmed and unconfirmed responses) Not evaluable prior to first scan: • 3 patients had clinical progression • 2 patients withdrew consent • 1 patients pending first scan CR Confirmed Response 1.8 mg/kg 2Q3W 1.8 mg/kg Q2W p16 + On Treatment CR Data Cut Date: Live Database as of May 13, 2025 ORR = 40%* DCR = 86%*
Page 36
BioAtla | Overview 36 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) 45% (5/11*) Responders (confirmed) 27% (3/11*) DCR 100% (11/11*) Median DOR (months) 9.9 ongoing Median PFS (months) 4.7 ongoing Median OS (months) 11.6 ongoing Data Cut Date: Live Database as of 14 May 2025 ^ p16 is strongly associated with HPV; HPV testing in progress for unknown patients ASCO 2025
Page 37
BioAtla | Overview 37 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 45% ORR 27% cORR 11.6 ongoing SOC (methotrexate, docetaxel, or cetuximab)1,2 2 3.4% 4.4 Cetuximab monotherapy3,4,5 1 0% NA Not approved Petosemtamab (1500 mg Q2W) 2 13% NA Data Cut Date: Live Database as of 14 May 2025 1N Engl J Med 2016;375:1856-1867. 2 Journal of Clinical Oncology 2018; 36(15): 1551-1558. 32008 Jun 15;112(12):2710-9. doi: 10.1002/cncr.23442, 4Erbitux USPI accessed 2024., 5INTERLINK-1: Phase 3 study of cetuximab ± monalizumab /Volume 34, Supplement 2S554-S555 October 2023 SOC, Standard of Care (Cetuximab, Methotrexate or Docetaxel); NA, not available **The comparisons above are not based on data resulting from a head-to-head trial and are not direct comparisons. Different protocol designs, trial designs, patient selection and populations, number of patients, trial endpoints, trial objectives and other parameters that are not the same between the relevant trials may lead to bias in the results causing comparisons from different trials to be unreliable. *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 Anti-EGFR therapies have inferior therapeutic outcomes among HPV+ patients Accelerated Approval Opportunity (ORR) ***From Dr. Alan Ho at MSKCC: “…extrapolating the OS of CheckMate 141 patients after progression on Nivo, we are figuring the OS of these patients to be about 7 months (OS of 9 -PFS of 2 months) post PD-1. Some of the retrospective papers (https://pubmed.ncbi.nlm.nih.gov/31574417/ & https://pubmed.ncbi.nlm.nih.gov/31864957/ we reviewed post-PD1 saw that upper limit of OS was of about 7-8.5 months post PD-1. Figuring what the upper and lower estimates are, we think 6 months OS is a fair estimate for the null.”
Page 38
BioAtla | Overview 38 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 initiation Baseline - July 14, 2023 On Treatment – December 8, 2023
Page 39
BioAtla | Overview 39 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
Page 40
BioAtla | Overview 40 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)3 Total (N=40)3 Any Adverse Events (AEs) 18 (90%) 20 (100%) 38 (95%) Related AEs with CTCAE1 Grade 3 or 42 3 (15%) 9 (45%) 12 (30%) Any related serious AEs2 1 (5%) 4 (20%) 5 (13%) Possibly Related AEs leading to death2 0 0 0 Related AEs leading to treatment discontinuation2 1 (5%) 1 (5%) 2 (5%) 1CTCAE: Common Terminology Criteria for Adverse Events. The NCI Common Terminology Criteria for Adverse Events is a descriptive terminology which is utilized for Adverse Event (AE) reporting. A grading (severity) scale is provided for each AE term. 2As assessed by the investigator. Missing responses are counted as related. 3N Engl J Med 2016;375:1856-1867. 2 Journal of Clinical Oncology 2018; 36(15): 1551-1558 Data Cut Date: Live Database as of March 26, 2025
Page 41
BioAtla | Overview 41 Phase 2 Oz-V Safety Data Most frequent treatment-emergent related adverse events 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 TRAE 13 (65) 3 (15%) 19 (95%) 9 (45%) 32 (80%) 12 (30%) Fatigue 5 (25%) 0 9 (45%) 0 14 (35%) 0 Nausea 3 (15%) 1 (5%) 6 (30%) 0 9 (23%) 1 (3%) Lymphocyte count decreased 3 (15%) 1 (5%) 5 (25%) 5 (25%) 8 (20%) 6 (15%) Diarrhoea 1 (5%) 0 6 (30%) 1 (5%) 7 (18%) 1 (3%) Anaemia 3 (15%) 0 3 (15%) 0 6 (15%) 0 White blood cell count decreased 3 (15%) 0 3 (15%) 0 6 (15%) 0 Decreased appetite 1 (5%) 0 3 (15%) 0 4 (10%) 0 Localised oedema 1 (5%) 0 2 (10%) 0 3 (8%) 0 Hyponatraemia 0 0 3 (15%) 1 (5%) 3 (8%) 1 (3%) Arthralgia 1 (5%) 0 2 (10%) 0 3 (8%) 0 Weight decreased 1 (5%) 0 2 (10%) 0 3 (8%) 0 Aspartate aminotransferase increased 1 (5%) 1 (5%) 2 (10%) 0 3 (8%) 1 (3%) Myalgia 1 (5%) 0 2 (10%) 0 3 (8%) 0 Vomiting 2 (10%) 0 1 (5%) 0 3 (8%) 0 ^ One patient from Phase 1 not included * Derived from neutropenia, and neutrophil count decreased ¥ Derived from neuropathy peripheral, peripheral motor neuropathy, and peripheral sensory neuropathy Data Cut Date: Live Database as of March 24, 2025
Page 42
BioAtla | Overview 42 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 arms • Oz-V Dose and Regimen: Patients randomized to the investigational arm will receive 1.8 mg/kg every other week • Investigator’s Choice (IC) control arm: Patients randomized to the control arm will receive either cetuximab, docetaxel, or methotrexate monotherapy • Accelerated Approval Endpoint: Based on interim analysis of enrolled patients, statistically significant improvement of confirmed Overall Response Rate (ORR) by Blinded Independent Central Review (BICR) supported by an adequately characterized Duration of Response (DOR) without detriment in OS • Full Approval Endpoint: Statistically significant improvement of OS
Page 43
Mecbotamab Vedotin (CAB-AXL-ADC): mKRAS Non-Small Cell Lung Cancer (NSCLC)
Page 44
BioAtla | Overview 44 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. 2018;15(3):2726-2734. Abbreviations: ADC, antibody-drug conjugate; AM, affinity matched; CAB, conditionally active biologic; DAR, drug antibody ratio; ELISA, enzyme linked immunosorbent assay; Ig, immunoglobulin; OD, optical density; VC-MMAE, valine-citrulline monomethylauristatin E. CAB-tumor cell target Cytotoxic payload and linker BA3011 pH binding inflection point adjusted for tumor microenvironment selectivity ≥7.4 is pH of normal cell pH value Blood Non-CAB AM CAB AM 6.00 6.25 6.50 6.75 7.00 7.25 7.50 0 25 50 75 100 Non-CAB BA3011 Normalized ELISA Data (OD 450 nm) • Humanized anti-AXL IgG1 • ~100 pM affinity (pH 6.5) • VC-MMAE (DAR 4) linker and payload • Epitope in Ig loop region
Page 45
BioAtla | Overview 45 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 express AXL by IHC and higher by mRNA analysis • AXL over-expression drives aggressive tumor characteristics, resistance to therapies, and poor patient outcomes • Significant opportunity for Mec-V (CAB-AXL-ADC) * Morimoto et al., Cancer Letters 587 (2024) 216692 and BioAtla study BA3011-002 IHC- Immunohistochemical assay
Page 46
BioAtla | Overview 46 Mec-V 1.8 mg/kg Q2W Overall Survival mKRAS vs wtKRAS NSCLC Median of 3 prior lines of tx Data Cut Date: Live database as of 16Apr25 Events n (%) Median (95% CI) mKRAS 6 (35) NR (4.0 – NE) wtKRAS 20 (74) 8.3 (3.5-10.2) Median 3 prior lines of therapy mKRAS (Q2W only) Responders (confirmed & unconfirmed) 31% (5/16^) Responders (confirmed) 25% (4/16^) DCR 81% (13/16^) Median DOR 5.9 months Median PFS 4.5 months One-year landmark OS 67% ^Response evaluable patients defined as patients that had at least 1 scan after treatment with study drug Prior to first scan: one patients withdrew consent
Page 47
BioAtla | Overview 47 Mec-V 1.8 mg/kg Q2W Associated with Exceptional Overall Survival in mKRAS NSCLC Overall survival cross trial comparison* Data Cut Date: Live database as of 16Apr25 FDA guidance: 2L+ NSCLC Phase 3 trial will be randomized mecbotamab vedotin versus docetaxel (full-approval = OS) *The comparisons above are not based on data resulting from a head-to-head trial and are not direct comparisons. Different protocol designs, trial designs, patient selection and populations, number of patients, trial endpoints, trial objectives and other parameters that are not the same between the relevant trials may lead to bias in the results causing comparisons from different trials to be unreliable. mecbotamab vedotin (KRAS) RMC-6236 (RAS G12X) Docetaxel (SOC in G12C) Sotorasib (G12C) 12 months 24 months mecbotamab vedotin (1.8 mg/kg Q2W) RMC-62361 Sotorasib2 Docetaxel3 Population mKRAS RAS G12X G12C mKRAS Number of patients 17 73 171 256 Prior Lines of tx 3 2 2 1 Median OS Not reached 17.7 months 10.6 months 7.9 months Survival at 12 months 67% 69% 51% <40% Survival at 24 months 59% Not Reported 33% <20% Docetaxel + Placebo (SOC in KRAS)Selumetinib + Docetaxel (mKRAS) 1Revolution Medicines Corporate Presentation February 2025; 2Lancet 2023; 401: 733–46.; 3JAMA. 2017 May 9;317(18):1844–1853.
Page 48
BioAtla | Overview 48 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%*** Not Reached (1 year landmark at 67%) SELECT-11 (all mKRAS variants) 256 1 13.7% 7.9 Real-life ESME cohort2 (all mKRAS variants) 1000+ 1 NA 6.1 to 10.6* Codebreak 2003 (mKRAS G12C) 174 2 13.2% 11.3 KRYSTAL-124 (mKRAS G12C) 152 2 9.2% NA 1. Janne, P et al. JAMA. 2017 May 9;317(18):1844–1853. (2) Thomas QD, et al. ESMO Open, Volume 9, Issue 6, 103473. (3) de Langen AJ, et al. Lancet 2023; 401:733-746; (4) Mok TS, Journal Clinical Oncology 2024; 42(17_suppl):LBA8509. * PD-1/PD-L1 monotherapy, PT-based CT without a PD-1/PD-L1, or Docetaxel monotherapy or combination **The comparisons above are not based on data resulting from a head-to-head trial and are not direct comparisons. Different protocol designs, trial designs, patient selection and populations, number of patients, trial endpoints, trial objectives and other parameters that are not the same between the relevant trials may lead to bias in the results causing comparisons from different trials to be unreliable. ***Confirmed and Unconfirmed Docetaxel Studies
Page 49
BioAtla | Overview 49 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 1CTCAE: Common Terminology Criteria for Adverse Events. The NCI Common Terminology Criteria for Adverse Events is a descriptive terminology which is utilized for Adverse Event (AE) reporting. A grading (severity) scale is provided for each AE term. 2As assessed by the investigator. Missing responses are counted as related. Data Cut Date: 18Jan2025 N=45 (%) Any Adverse Events (AEs) 45 (100) Related AEs with CTCAE1 Grade 3 or 42 14 (31) Any Related Serious AEs2 5 (11) Possibly Related AEs leading to death2 0 Related AEs leading to treatment discontinuation2 3 (7) Most frequent AEs any grade occurring at a rate >15%
Page 50
BioAtla | Overview 50 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 AXL expression o 1.8 mg/kg Q2W associated with exceptional overall survival even in heavily pretreated patients o 67% alive at a landmark of one year o 59% alive at a landmark of two years; standard of care agents result in less than 20% alive at the two year* o Anti-tumor activity across nine different KRAS mutation variants • Partial response observed in a patient who had experienced prior failure of sotorasib • Patient treated with mecbotamab vedotin + anti-PD-1 antibody remains in complete response for >2 years • Potential for a pan mKRAS strategy in NSCLC; currently positioning for a future pivotal trial *The comparisons above are not based on data resulting from a head-to-head trial and are not direct comparisons. Different protocol designs, trial designs, patient selection and populations, number of patients, trial endpoints, trial objectives and other parameters that are not the same between the relevant trials may lead to bias in the results causing comparisons from different trials to be unreliable.
Page 51
BioAtla | Overview 51 Significant Opportunity for Mec-V to Expand Beyond mKRAS NSCLC KRAS mutations most commonly found in CRC, NSCLC and PDAC CRC PDAC NSCLC G12C G12D G12V G12A G12R Multiple Other 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. CRC: colorectal cancer; NSCLC: non-small cell lung cancer; PDAC: pancreatic ductal adenocarcinoma 75K patients/year 50K patients/year 50K patients/year
Page 52
BioAtla | Overview 52 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 dacarbazine trabectedin mecbotamab vedotin 21.5 (14.2 – 29.9) trabectedin 13.6 (7.1 – 17.3) pazopanib 12.5 (10.6 – 12.8) eribulin 13.5 (10.9 – 15.6) dacarbazine 11.5 (9.6 – 13.0) best supportive care 10.8 (6.0 – 18.8) anti-PD1 12.5 (7.7-17.3) placebo 10.7 (8.7 – 12.8) mecbotamab vedotin Best supportive care pazopanib Graaf, Winette van der et al. The Lancet 379 (2012): 1879-1886. Le Cesne, A. et al Annals of Oncology, Volume 32, Issue 8, 1034 - 1044 Schöffski, Patrick et al. The Lancet, Volume 387, Issue 10028, 1629 – 1637 Miao, R. Cancer Immunol Immunother 72, 2521–2527 (2023) Responders, n (%) 2 (5) DCR, n (%) 23 (52) Mec-V in Sarcoma: Median of 2 prior lines of Tx Median OS of 21.5 months Landmark OS at 1 year 73% (54-85) Anti-PD1 monotherapy *The comparisons above are not based on data resulting from a head-to-head trial and are not direct comparisons. Different protocol designs, trial designs, patient selection and populations, number of patients, trial endpoints, trial objectives and other parameters that are not the same between the relevant trials may lead to bias in the results causing comparisons from different trials unreliable.
Page 53
Evalstotug (CAB-CTLA-4)
Page 54
BioAtla | Overview 54 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 enhanced with selective pH- dependent tumor binding
Page 55
BioAtla | Overview 55 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 EC50 in preclinical models ▪ However, observed substantially reduced G.I. toxicity in primates • CAB CTLA-4, evalstotug, enables targeted exposure in TME enabling lower imAE relative to ipi Abbreviations: ADCC, antibody-dependent cellular cytotoxicity; CAB, Conditionally Active Biologic; CD, cluster of differentiatio n; CDR, complementarity-determining region; CTLA-4, cytotoxic T-lymphocyte associated protein 4; EC50, concentration producing 50% Emax; Emax, maximum effect; imAE, immune mediated adverse event; PD-1, programmed cell death protein 1; t1/2, half-life; Treg, regulatory T cells. 1. Chang HW, et al. Proc Natl Acad Sci USA. 2021;118(9):e2020606118.
Page 56
BioAtla | Overview 56 Reversible Binding in the TME Comparison of evalstotug binding to CTLA-4 in different pH conditions 56 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: Figures modified from Chang HW, et al. Proc Natl Acad Sci USA. 2021;118(9):e2020606118. CAB-CTLA4 Shows Potent Anti-Tumor Activity in MC38/hCTLA4 KI Model BA3071 induces complete tumor regression in mouse tumor model. Mice were dosed with IgG control and anti-CTLA antibodies at 10mg/kg (equivalent to 1mg/kg anti-CTLA-4 human dose), IP, BIW, N=12 mice/group. pH range ELISA 0 7 14 21 0 1000 2000 3000 Days after the start of treatment Tumor volume (mm3) Mean ± SEM Evalstotug IgG control Ipilimumab
Page 57
BioAtla | Overview 57 Study Date10 20 300 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 and evalstotug had the same half-life and exposure in this model. Figure modified from Chang HW, et al. Proc Natl Acad Sci USA. 2021;118(9):e2020606118. aIpilimumab analog or evalstotug 15 mg/kg (≈11 mg/kg human dose) + nivolumab 20 mg/kg (≈14.6 mg/kg human dose) both administered QW for 4 weeks. 57 Liquid feces Non-formed feces Other GI symptoms GI Symptoms Vehicle Control Ipilimumaba + nivolumab 15 mg/kg + 20 mg/kg Evalstotuga + nivolumab 15 mg/kg + 20 mg/kg
Page 58
BioAtla | Overview 58 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 (N=17) Total (N=17) Prior # of treatments Age, y, mean (SD) 60 (14) Tumor type, n (%) Sex, n (%) Melanoma 11 0 - 1 Female 8 (47) Gastric 2 3 - 5 Male 9 (53) Renal cell 1 3 White race, n (%) 13 (76) Cervical 1 3 ECOG, n (%) NSCLC 1 3 0 12 (71) aHCC 1 5 1 5 (29) Prior Anti-PD-1 Therapy, n (%) 14 (82) Data Cut Date: 26Jul24
Page 59
BioAtla | Overview 59 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 700 mg are dose-equivalent to ipilimumab 5 mg/kg and 10 mg/kg, respectively. *Mohr P, et al. J Eur Acad Dermatol Venereol. 2018;32(6):962-971. Evalstotug 350 mg (5 mg/kg) N=17 Ipilimumab 3 mg/kg* Number of doses 3.4 7.8 0 2 4 6 8 Live Database 21Feb2025
Page 60
BioAtla | Overview 60 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 (confirmed & unconfirmed) 44% (7/171) Responders (confirmed) 41% (7/171) DCR 76% (13/171) DOR ongoing OS ongoing 1Response evaluable patients defined as patients that had at least 1 scan after treatment with study drug Live Database 28Apr2025
Page 61
BioAtla | Overview 61 Evalstotug: 7 of 17 Achieved Response in the 5 mg/kg Q3W + PD1 Durable antitumor activity across multiple solid tumor types Live Database 28Apr2025 70 mg Q3W + PD1 210 mg Q3W + PD1 350 mg Q3W + PD1 1 year
Page 62
BioAtla | Overview 62 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 (mg) Age (yrs) Sex ECOG Prior Treatment Prior PD1 exposure < 6 months Best change in target lesion (%) Response to evalstotug 350 34 M 0 None No -100% CR* 350 54 F 0 Adjuvant anti-PD-1 for 3mos Yes -100% cCR 350 63 M 0 Adjuvant anti-LAG-3/anti-PD-1 for 11mos Yes -9% SD 350 59 F 0 Adjuvant anti-PD-1 for 12mos No -75% cPR 350 67 F 0 Adjuvant anti-PD-1 for 12mos Yes -100% cCR 350 89 F 0 None No 0% SD 350 34 M 0 Adjuvant anti-PD-1 for 6mos No - PD 700 73 M 0 Adjuvant anti-PD-1 for 7mos Yes -50% cPR 700 57 F 1 Neo-adjuvant anti-PD-1 for 12mos No -8% SD 700 72 F 0 Adjuvant anti-PD-1 for 11mos No -34% cPR 70 ➢210 ➢350 75 F 1 Adjuvant anti-PD-1 for 11mos Yes -46% cPR 700 ➢1000 57 M 0 Adjuvant anti-LAG-3/anti-PD-1 for 3mos Yes -39% PR** *Patient with 73% tumor reduction initially experienced tumor growth with new lesions and Investigator continued treatment per protocol resulting in complete metabolic response based on PET scan (May 5, 2025) **Pending confirmation Live Database 28Apr2025
Page 63
BioAtla | Overview 63 Evalstotug in Combination with PD1 Across Prior IO 1L Melanoma All patients living as of data cut date Data Cut Date: 22Jul25
Page 64
BioAtla | Overview 64 Evalstotug vs Ipilimumab TRAE, imAE, and Response Lower imAE rate vs Ipilimumab despite more patients previously treated with ICI Treatment Evalstotug (5 mg/kg) + PD1 Q3W N=17 Ipilimumab (3 mg/kg) + nivolumab Q3W N=178-3141,2,3 Doses 1 – ≤18 weeks exposure (≤6 doses) 1 – ≤12 weeks exposure (≤4 doses) Tumor Types Multiple tumor types 90% with prior tx Melanoma 15% with prior tx4 imAE (G3-4) 18% (no G4) 40% 1Wolchok, J; Five-Year Survival with Cmbined Nivolumab and Ipilimumab in Advanced Melanoma; N Engl J Med 2019;381:1535 -1546; 2Lebbe, C; Evaluation of Two Dosing Regimens for Nivolumab in Combination With Ipilimumab in Patients With Advanced Melanoma: Results Fr om the Phase IIIb/IV CheckMate 511 Trial; J Clin Oncol. 2019 Feb 27;37(11):867 –875; 3Larkin, J. Combined Nivolumab and Ipilimumab or Monotherapy in Untreated Melanoma; N Engl J Med 2015;373:23-34; 4Allouchery, M; Safety of immune checkpoint inhibitor rechallenge after discontinuation for grade ≥2 immune-related adverse events in patients with cancer; J Immunother Cancer. 2020 Dec;8(2):e001622. Live Database 21Feb2025
Page 65
BioAtla | Overview 65 Evalstotug in Combination with PD1 Safety Data Treatment-emergent related adverse events Total (N=17) Preferred Term All Grades [n (%)] Grade 3 [n (%)] Grade 4 [n (%)] Number of subjects with at least one TEAE 16 (94%) 6 (36%) 1 (6%) Chills 12 (71%) 0 (0%) 0 (0%) Nausea 6 (35%) 0 (0%) 0 (0%) Vomiting 5 (29%) 0 (0%) 0 (0%) Fatigue 5 (29%) 0 (0%) 0 (0%) Cytokine release syndrome 5 (29%) 0 (0%) 0 (0%) Pyrexia 4 (24%) 0 (0%) 0 (0%) Arthralgia 4 (24%) 0 (0%) 0 (0%) Infusion related reaction 4 (24%) 0 (0%) 0 (0%) Rash 4 (24%) 0 (0%) 0 (0%) Lipase increased 3 (18%) 2 (12%) 0 (0%) Headache 3 (18%) 0 (0%) 0 (0%) Pruritus 3 (18%) 0 (0%) 0 (0%) Colitis 2 (12%) 2 (12%) 0 (0%) Pancreatitis 2 (12%) 2 (12%) 0 (0%) Diarrhoea 2 (12%) 0 (0%) 0 (0%) Hypotension 2 (12%) 0 (0%) 0 (0%) Influenza like illness 2 (12%) 0 (0%) 0 (0%) Rash maculo-papular 2 (12%) 0 (0%) 0 (0%) Hypercalcaemia 1 (6%) 0 (0%) 1 (6%)* Total (N=17) Preferred Term All Grades [n (%)] Grade 3 [n (%)] Grade 4 [n (%)] Chronic gastritis 1 (6%) 1 (6%) 0 (0%) Hypertension 1 (6%) 1 (6%)* 0 (0%) Autoimmune encephalopathy 1 (6%) 1 (6%) 0 (0%) Abdominal pain 1 (6%) 0 (0%) 0 (0%) Decreased appetite 1 (6%) 0 (0%) 0 (0%) Asthenia 1 (6%) 0 (0%) 0 (0%) Troponin increased 1 (6%) 0 (0%) 0 (0%) Muscle spasms 1 (6%) 0 (0%) 0 (0%) Pain 1 (6%) 0 (0%) 0 (0%) Immune-mediated adrenal insufficiency 1 (6%) 0 (0%) 0 (0%) Dizziness 1 (6%) 0 (0%) 0 (0%) Autoimmune thyroiditis 1 (6%) 0 (0%) 0 (0%) Skin lesion 1 (6%) 0 (0%) 0 (0%) Alanine aminotransferase increased 1 (6%) 0 (0%) 0 (0%) Aphthous ulcer 1 (6%) 0 (0%) 0 (0%) Thyroiditis 1 (6%) 0 (0%) 0 (0%) Aspartate aminotransferase increased 1 (6%) 0 (0%) 0 (0%) Tachycardia 1 (6%) 0 (0%) 0 (0%) Tongue geographic 1 (6%) 0 (0%) 0 (0%) Hyperthyroidism 1 (6%) 0 (0%) 0 (0%) Hyperhidrosis 1 (6%) 0 (0%) 0 (0%) Live Database 21Feb2025 *G4 Hypercalcaemia and G3 Hypertension are not imAE based on SITC criteria.
Page 66
BioAtla | Overview 66 Evalstotug in Combination with PD1: Overall Safety Summary Generally well-tolerated; All G3 and G4 resolved Related AE Summary Total (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%) Possibly Related AEs leading to death2 0 Related AEs leading to treatment discontinuation2 5 (29%) 1CTCAE: Common Terminology Criteria for Adverse Events. The NCI Common Terminology Criteria for Adverse Events is a descriptive terminology which is utilized for Adverse Event (AE) reporting. A grading (severity) scale is provided for each AE term. 2As assessed by the investigator. Missing responses are counted as related. Live Database 21Feb2025
Page 67
BioAtla | Overview 67 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 / taxane / pembrolizumab as well as cetuximab). Prior to Oz-V triplet patient had tumor filling the maxillary sinus measuring 5.3cm in longest diameter. After triplet, the tumor nearly resolved and is difficult to measure. A transient, clinically asymptomatic elevation of hepatic transaminases was documented that didn't recur with subsequent dosing.
Page 68
BioAtla | Overview 68 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 combination regimen should be included in the control arm • Project Optimus should guide determination of Phase 3 evalstotug dose IO – immuno-oncology
Page 69
BioAtla | Overview 69 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 environment and safety; e.g., reduced irAEs and extended treatment • 67% ORR and 92% DCR in unresectable and/or metastatic cutaneous melanoma patients treated with evalstotug (5 – 14.3 mg/kg) in combination with PD-1 antibody • Higher and longer dosing relative to ipi yields encouraging efficacy with low incidence and severity of imAEs, consistent with CAB-driven tumor selectivity for potential best-in-class CTLA4 • Significant opportunity for an effective and better tolerated CTLA-4 in combination regimens • Partnering discussions ongoing 69
Page 70
BioAtla | Overview 70 BioAtla© Is A Clinical Stage Company Focused on Transforming Cancer Therapy with Conditionally Active Biologics (CABs) Proprietary technology with over 500 issued patents CAB Platform maximizes therapeutic window Broad applicability in solid tumors Advancing P1 BA3182 (CAB- EpCAM x CAB-CD3 TCE): Updated P1 data expected 1H‘26 Dose-expansion expected later in 2026 In advanced stages to finalize a strategic transaction with a potential partner; on-track to complete the transaction by year end TCE – T-cell engager; OPSCC – Oropharyngeal Squamous Cell Carcinoma Initiation of the Oz-V P3 study in 2L+ OPSCC on-track to advance with a strategic partner in early 2026 Achieved milestone payment with Context TCE Collaboration which further validates our CAB T-cell engager platform, including BA3182