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Investor Presentation Non-Confidential December 2024
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implied, as to the accuracy or completeness of the information contained in this Presentation. BioAtla | Overview 2
BioAtla Overview Clinical stage company harnessing the tumor
microenvironment for targeted cancer therapy Advancing a platform of targeted "Conditionally Active Biologics (CAB)" monoclonal antibodies that bind epitopes exposed in the acidic pH microenvironment of tumor cells, but are
otherwise shielded at normal pH of healthy cells Unlike prodrugs, no irreversible activation via enzymatic cleavage required for CAB antibody to bind in the acidic pH microenvironment CAB technology enables enhanced (1) therapeutic
exposure; (2) tumor selectivity; and (3) reduced toxicity relative to traditional antibodies Four clinical-stage and one pre-clinical stage programs will be advanced directly or via corporate partners Clinical readouts for multiple
indications with current runway into early 2026 Headquartered in San Diego, CA with approximately 60 employees BioAtla | Overview 3
Leadership Team Eric Sievers, M.D. Richard Waldron, M.B.A. Jay Short,
Ph.D. Sheri Lydick Chief Medical Officer Chief Financial Officer Chairman, CEO and Cofounder Chief Commercial Officer GeneMedicine, Inc. William Boyle, Ph.D. Monica Sullivan Susie Melody Sr. Research Fellow Sr. VP, Intellectual Property &
Contracts Sr. VP, Human Resources CapaIP BioAtla | Overview 4
Board of Directors and Scientific Advisors Jay Short, Ph.D. Lawrence
Steinman, MD Mary Ann Gray, Ph.D. Sylvia McBrinn Chairman, Chief Executive Officer & Cofounder Lead Director Director Director Director Susan Moran, MD, MSCE Scott Smith Eddie Williams Director Director Director James Allison, Ph.D. Padmanee
Sharma, MD, Ph.D. Lawrence Fong, MD MD Anderson Cancer Center MD Anderson Cancer Center Cancer Immunotherapy Program, UCSF Scientific Advisor Scientific Advisor Scientific Advisor BioAtla | Overview 5
CAB 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 promote metastasis and
defend against immune response CAB mechanism uses Protein-associated Chemical Switches (PaCS) PaCS typically are negatively charged, naturally occurring small molecules (e.g. bicarbonate, hydrogen sulfide) PaCS shield
positive charges on normal tissues, which are neutralized by hydrogen ions, displacing the PaCS molecule, thereby unveiling novel epitopes for antibody binding PaCS selective binding enables cancer-specific targeting of antibodies BioAtla |
Pre-clinical Evidence Summary Preclinical evidence of CAB
selectivity Differential EGFR tumor vs. skin binding (12.6-fold improved TI) AXL-ADC reduced TMDD yielding T and exposure in NHP (>2-fold increase in T ) 1/2 1/2 Reduced liver enzymes (>10-fold in ALT levels)
CTLA4 reduction of 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 EpCAM DualCAB TCE maintained efficacy with highly reduced toxicity MTD not reached >100-fold improvement in TI
B7H3 DualCAB TCE associated with high acidity via hyper-glycolysis MTD not reached in NHP Significantly improved safety profile compared to other B7H3 TCEs in development BioAtla | Overview 7
Clinical Evidence Summary Clinical evidence of CAB selectivity
AXL-ADC good risk/benefit ratio Two non-CAB AXL-targeting ADCs terminated in P1 Potent and durable response in mKRAS NSCLC patients ROR2-ADC good risk/benefit ratio Good tolerability with only 7%
treatment-related discontinuation rate Potent and durable response in SCCHN patients CTLA4 I/O enables higher and prolonged dosing with reduced immune-meditated 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, ongoing Reduced grade 3 AEs such as colitis; no grade 4 or 5 AEs, even at higher doses EpCAM DualCAB TCE
Non-CAB EpCAM TCE (BiTE) terminated in P1 Most advanced EpCAM TCE in the clinic showing tumor-reduction, ongoing in P1 MTD not yet reached CABs demonstrate universal clinical improvement in TI and enable therapeutic
development undruggable targets BioAtla | Overview 8
Selective and Targeted CAB Technology Widens Therapeutic Window Thus has
the potential to enhance clinical outcomes in multiple tumor types Acidic Cancer Cell Membrane Alkaline Healthy Cell Membrane 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 No CAB Binding CAB Binding different from prodrugs that require irreversible
enzymatic + H + H + cleavage to become activated H + H + H + H + H + + H H CAB antibodies have the potential for increased efficacy + H with improved safety relative to traditional antibodies 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. BioAtla | Overview 9
CAB Antibodies Bind Selectively and Reversibly Based on the Tumor
Microenvironment (TME) Enhancing exposure and reducing toxicity CABs Bind Selectively in the Lower pH TME Non-CABs Bind to Normal Tissues, Causing Toxicity Non-CAB Normal Cells Focused Selective Tumor CABs Preserved Binding Tumor Killing pH CABs Do
Not Bind to Normal Tissues, Enhancing Safety 7.4 is pH of normal cell 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 BioAtla | Overview 10 ELISA Data Blood
CAB ADCs Show Strong Selectivity and Have an Improved Therapeutic
Window vs Traditional ADCs Unlike prodrugs, CABs are reversible and selective enhancing the therapeutic index 10000 Enhanced ADC Therapeutic Exposure Enhanced ADC Tumor Selectivity (12.6-fold increase in TI) 1000 AXL ADCs- 1mg/kg dose 10000 100
CAB-ADC male 1000 CAB-ADC female 100 10 CAB-ADC male AM-ADC male CAB-ADC female AM-ADC female 10 AM-ADC male 1 AM-ADC female 0 50 100 150 200 1 Time (Hours) 0 50 100 150 200 Time (Hours) Reduced ADC Toxicity CAB Post-Treatment AM Non-CAB AXL-ADC CAB
AXL-ADC Pre- Treatment CAB ADC resulted in minimal Normal (skin patch) versus Tumor Binding by anti-EGFR versus CAB-anti-EGFR increase in ALT, supporting that on- target, off-tumor toxicity is reduced Day -3 Day 3 with the CAB ADC Study Day
BioAtla | Overview 11 Note: OD450nm = optical density measurements using a microplate reader with a 450nm filter; Data above based on non-human primate studies; AM = affinity matched; ALT or alanine aminotransferase is a sign of liver toxicity [Ab]
ng/mL Ab-ADC (ng/mL) [Ab] ng/mL ALT (u/L)
Broad Applicability of BioAtla's CAB Platform Across Several
Antibody Types ADCs I/O Antibodies Bispecific TCE Targets: ROR2, AXL Target: CTLA-4 Target: EpCAM & CD3 Widely expressed in a variety of tumor CTLA-4 blockade activates effector Bispecific antibodies bridge cancer types, ROR2 and AXL
overexpression T cells, thereby enhancing anti- cells and cytotoxic T lymphocytes, correlates with poor prognosis, tumor immunity activating T cells and promoting metastasis, and drug resistance to PD-1 cancer cell lysis and EGFR therapies CAB-CTLA4
CAB-CTLA4 Tumor Cell Target CAB-Tumor Cell Target CAB-EpCAM Cytotoxic payload CAB-CD3 T Cell Target and linker BioAtla | Overview 12 ADC - antibody drug conjugate; IO - immuno-oncology; TCE - T-cell engager
Focused Pipeline with Broad Applicability of Differentiated CAB Assets
Designed to Deliver Near-term value IND Enabling Phase 1 Phase 2 CAB Program Target Indications Pre-Clinical Clinical Clinical Mecbotamab Vedotin NSCLC AXL BA3011 UPS CAB-ADCs Ozuriftamab Vedotin ROR2 SCCHN BA3021 Evalstotug Melanoma CAB-I/O CTLA-4
BA3071 NSCLC CAB- BA3182 EpCAM x CD3 Adenocarcinomas Bispecific TCE CAB- BA3142 B7H3 x CD3 Multiple tumor types Bispecific TCE BA3382 CAB- (Out-Licensed to Context Nectin4 x CD3 Multiple tumor types Therapeutics for up to Bispecific TCE $133.5
Million) BioAtla | Overview 13 IND, investigational new drug; UPS, Undifferentiated Pleomorphic Sarcoma; NSCLC, Non-small Cell Lung Cancer; SCCHN, Squamous Cell Carcinoma of the Head and Neck
BioAtla's Near-Term Catalysts 2025 2026 Readout BA3011 (AXL-ADC)
- Phase 2 (n=50) mKRAS NSCLC Readout Readout BA3182 (EpCAM-TCE) - Phase 1 Dose Phase 2 Extension (n=40) Escalation (n=30) Adenocarcinomas BCAB OPEX (including G&A, IP, etc.) Operations BioAtla | Overview 14
BioAtla's Near-Term Catalysts with Potential Partnering
Opportunities 2025 2026 BA3021 (ROR2-ADC) - Phase 2 Extension (n=40) Phase 3 SCCHN BA3071 (CTLA4-IO) - Phase 2 (n=60) Phase 3 Melanoma Submission BA3362 (Nectin4-TCE) - Pre-clinical and IND-enabling Studies Solid Tumors
Out-Licensed to Context Therapeutics for up to $133.5 Million BioAtla | Overview 15
Mecbotamab Vedotin (CAB-AXL-ADC): mKRAS Non-Small Cell Lung Cancer
Mecbotamab Vedotin: 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-CAB AM Cytotoxic 75 payload
and linker Non-CAB BA3011 50 25 Humanized anti-AXL IgG1 CAB AM ~100 pM affinity (pH 6.5) 0 VC-MMAE (DAR 4) linker and payload 6.00 6.25 6.50 6.75 7.00 7.25 7.50 Epitope in Ig loop region pH value 7.4 is pH of
normal cell BioAtla | Overview 17 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. Normalized ELISA Data (OD 450 nm) Blood
Co-expression of mutant KRAS and AXL is Significant and Functionally
Linked In lung cancer cells, AXL over-expression is involved in resistance to chemotherapy and targeted therapies and drives epithelial to mesenchymal transition Prevalence of AXL expression in KRAS mutant NSCLC is significant, the
majority of these tumors exhibit high levels of AXL o Upregulation is associated with aggressive tumor characteristics, resistance to therapies, and poor patient outcomes. AXL signaling mediates the adaptive resistance to mKRAS inhibitors
adagrasib and sotorasib (G12C) in lung cancer (85% AXL positive) (Morimoto et al., Cancer Letters 587 (2024) 216692) Potential significant opportunity for mecbotamab vedotin to improve outcomes in the mKRAS population across mKRAS variants
BioAtla | Overview 18 confidential
AXL Plays a Crucial Role in the Survival of KRAS G12C mutant NSCLC
Cells Treated with KRAS G12C Inhibitors AXL driving resistance to KRAS inhibitors KRAS inhibition leads to upregulation and activation of AXL expression o Autocrine/paracrine of increased GAS6 expression AXL inhibition alone does not
lead to tumor killing, but potentiates anti- tumor effects of KRAS inhibition o These results indicated pivotal roles for the YAP-GAS6-AXL axis and its inhibition in the intrinsic resistance to KRAS G12C inhibitors AXL-ADC improves outcomes
via tumor killing No Treatment KRAS G12C inhibitor p = Phosorylated form of protein BioAtla | Overview 19 Morimoto et al. Cancer Letters 587 (April 2024) AXL-resistance mechanism
Docetaxel (expected control arm) has modest efficacy in 2L+ NSCLC
Codebreak and Krystal has G12C docetaxel 2L+ data 234,580 new cases of NSCLC expected in US for 2024 No pan-KRAS docetaxel 2L+ data Timing relative to Study with 30% or 70,374 new cases of NSCLC with RAS Median Median Immune
Docetaxel in 2L+ Pts ORR checkpoint PFS OS mutations in US for 2024 NSCLC inhibitors RAS Genotypes in NSCLC 1 REVEL Prior 625 14% 3.0 9.1 G13 and Q61 G12 Other 5% 2 3% CheckMate 057 Prior 290 12% 4.2 9.4 G12V 6% 3 OAK Prior 425 13% 4.0 9.6 G12D 4% 4
POPLAR Prior 143 14.7% 3.0 9.7 TROPION-Lung- After 305 13% 3.7 11.8 G12C 6 01 12% 5 Codebreak 200 After 174 13.2% 4.5 11.3 (KRAS G12C) 7 KRYSTAL-12 After 152 9.2% 3.8 NA (KRAS G12C) WT 70% WT G12C G12D G12V G12 Other G13 and Q61 BioAtla | Overview
Emerging Opportunity for Mecbotamab Vedotin in Patients with Mutated
KRAS (mKRAS) Variants mKRAS constitutes 30% of all NSCLC patients mutant KRAS; all NSCLC (SQ+NSQ); median of approximately 3 prior lines of tx for both mKRAS and wtKRAS Total (N=78) Age, y, mean (range) 67 (46-82) KRAS Status, n (%) WtKRAS 50 (64)
mKRAS 24 (31) Unknown KRAS status 4 (5)* * Two responders with no additional biopsy sample for KRAS mutation assessment Data Cut Date: Live database as of 24Oct2024 BioAtla | Overview 21
Confirmed Responses with Mecobotamab Vedotin Across mKRAS Variants -