Bioatla, Inc. · NASDAQ:BCAB

Bioatla — Q1 2025 Earnings Presentation

66 slides from Bioatla's earnings presentation, May 6, 2025

  1. Slide 1: Conditionally Active Biologics: Transforming Cancer Therapy

    Conditionally Active Biologics: Transforming Cancer Therapy Corporate Presentation May 2025

  2. 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

  3. 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) Cash sufficient - 1H’26, Proprietary technology with beyond key clinical readouts over 500 issued patents Advancing clinical stage Advancing assets internally: BA3182: strategic col

  4. 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

  5. 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

  6. Slide 6: Selective and Targeted CAB Technology Widens Therapeutic Window

    Selective and Targeted CAB 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 shielded

  7. Slide 7: CAB Technology Summary

    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 to promote metastasis and defend against imm

  8. Slide 8: Pre-clinical Evidence Summary

    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 ⁻ Increased T1/2 and exposure in NHP (>2-fold increase in T1/2) ⁻ Reduced liver enzymes (>10-fold in ALT levels) • EpCAM DualCAB

  9. Slide 9: 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 patients • ROR2-ADC promising risk/benefit ra

  10. Slide 10: CAB Antibodies Bind Selectively and Reversibly Based on the Tumor Microenvironment

    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 ELISA Data Non-CAB Selective Focused Normal Cells Tumor Blood pH CABs Binding

  11. Slide 11: CAB ADCs Show Strong Selectivity and Have an Improved Therapeutic Window vs Traditional ADCs

    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 1000 AXL ADCs- 1mg/kg dose (12.6-fold increase in TI

  12. Slide 12: BioAtla’s Catalysts Expected to be Achieved through Internal Advancement

    BioAtla’s Catalysts Expected to be Achieved through Internal Advancement 2025 2026 Readout Readout BA3182 (EpCAM-TCE) – Phase 1 Dose Phase 2 Extension (n= up to 40) Adenocarcinomas Escalation (n=30) Readout Readout Mecbotamab vedotin (AXL-ADC) – Phase 2 (NSCLC) Phase 2 (mKRAS NSCLC ; n=up to 50) mKR

  13. Slide 13: BioAtla’s Catalysts Planned to be Achieved Through Corporate Partners

    BioAtla’s Catalysts Planned to be Achieved Through Corporate Partners 2025 2026 Readout Ozuriftamab vedotin (ROR2-ADC) – SCCHN Phase 2 √ Phase 3 (HPV+ SCCHN) In process of partnering Readout Evalstotug (CTLA4-IO) – √ Phase 2 Extension Phase 2 Phase 3 Melanoma (Project Optimus) Initiated partnering d

  14. Slide 14: BA3182 (EpCAM x CD3 Bispecific T-Cell Engager): Adenocarcinoma

    BA3182 (EpCAM x CD3 Bispecific T-Cell Engager): Adenocarcinoma

  15. Slide 15: CAB-EpCAM x CAB-CD3 Bispecific T-Cell Engager (BA3182)

    CAB-EpCAM x CAB-CD3 Bispecific T-Cell Engager (BA3182) Potential to address over one million patients with BA3182 given wide expression ACS estimate for EpCAM Expression 2024 in US2 (TIS 1 to 12)3 • EpCAM is an attractive therapeutic target expressed in most solid Breast Cancer 310,720 81% tumors, a

  16. Slide 16: Potent Lysis of EpCAM Positive Cancer Cells by BA3182

    Potent Lysis of EpCAM Positive Cancer Cells by BA3182 Dual CAB EpCAM x CAB CD3 Bispecific antibody In Vivo Efficacy and Dose Response of BA3182 Against HCT116 CDX Model in Humanized NOG Mice Lower EC50 at pH6.0 indicates markedly increased potency relative to pH7.4 EC50 (nM) pH6.0 EC50 (nM) pH7.4 HC

  17. Slide 17: Both EpCAM DualCAB TCE and EpCAM Wild-Type TCE Completely Eradicated Established Tumors in vivo

    Both EpCAM DualCAB TCE (BA3182) and EpCAM Wild-Type TCE Completely Eradicated Established Tumors in vivo Cell line-derived xenograft humanized mouse model of human colorectal cancer Non-CAB DualCAB (BA3182) EpCAM EpCAM TCE, T-Cell Engager BioAtla | Overview 17 Source: MABS 2024, VOL. 16, NO. 1, 2322

  18. Slide 18: BA3182 DualCAB is Safely Tolerated at High Doses in Nonhuman Primates

    BA3182 DualCAB is Safely Tolerated at High Doses in Nonhuman Primates Cytokine Levels Associated with Toxicity Non-CAB MonoCAB DualCAB TI BA3182 BA3182 BA3182 BA3182 BA3182 Source: MABS 2024, VOL. 16, NO. 1, 2322562 https://doi.org/10.1080/19420862.2024.2322562 BioAtla | Overview 18

  19. Slide 19: BA3182 Dose Escalation Schema: C and D Cohorts Enrolling Concurrently

    BA3182 Dose Escalation Schema: C and D Cohorts Enrolling Concurrently Animal data modeling suggests that tumor reduction may be observed at ~ 200 µg QW C7 100 / 2700 μg D4 30 / 100 / 2700 μg C6 100 / 900 μg D3 30 / 100 / 900 μg Dosed 3 patients* C5 30 / 300 μg D2 30 / 100 / 300 μg Dosing C4 10 / 100

  20. Slide 20: BA3182 Conclusions / Milestones

    BA3182 Conclusions / Milestones • Phase 1 dose escalation ongoing o Heavily pretreated adenocarcinoma population enrolled o Observed multiple patients with tumor reduction, including one colorectal cancer patient with stable disease for greater than one year o Maximally tolerated dose has not yet be

  21. Slide 21: Mecbotamab Vedotin (CAB-AXL-ADC): mKRAS Non-Small Cell Lung Cancer (NSCLC)

    Mecbotamab Vedotin (CAB-AXL-ADC): mKRAS Non-Small Cell Lung Cancer (NSCLC)

  22. Slide 22: 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-

  23. Slide 23: AXL Plays a Crucial Role in the Survival of mutated KRAS (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

  24. Slide 24: Confirmed Responses with Mec-V Across NSCLC mKRAS Variants

    Confirmed Responses with Mec-V Across NSCLC mKRAS Variants 1.8 mg/kg Q2W and 2Q3W regimens; heavily pre-treated, median of 3 prior lines of therapy Best % Change in TL Median 3 prior mKRAS mKRAS lines of therapy (Q2W only) (all dosing regimens) G13R G12S G12A Q61H G12D G12S G12V G12R G12Cⱡ G12A G12V

  25. Slide 25: Exceptional Overall Survival with 1.8 mg/kg Q2W Dosing Frequency with Mec-V

    Exceptional Overall Survival with 1.8 mg/kg Q2W Dosing Frequency with Mec-V 8 patients alive greater than 18 months Events n (%) Median (95% CI) Q2W 6 (35.3) NR (4.0- NE)* Median of 3 prior lines of therapy *Ongoing BioAtla | Overview 25 Data Cut Date: Live database as of 16Apr25

  26. Slide 26: Mec-V 1.8 mg/kg Q2W 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

  27. Slide 27: Docetaxel (expected control arm) has Modest Efficacy in 2L+ NSCLC

    Docetaxel (expected control arm) has Modest Efficacy in 2L+ NSCLC Median Overall Survival ranges from 6 to 11 months in mKRAS NSCLC when treated with docetaxel in the 2L+ Timing relative Study with to Immune Median Docetaxel in 2L+ Pts ORR Median OS checkpoint PFS NSCLC inhibitors REVEL1 Prior 625 1

  28. Slide 28: Ph2 Mec-V: Overall Safety Summary of NSCLC patients

    Ph2 Mec-V: Overall Safety Summary of NSCLC patients 1.8 mg/kg Q2W with or without nivolumab generally well-tolerated; only 7% discontinuation due to related AEs 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 14 (3

  29. Slide 29: 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 exceptional 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 increa

  30. Slide 30: 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

  31. Slide 31: Exceptional Overall Survival also Observed in Soft Tissue Sarcoma

    Exceptional 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.

  32. Slide 32: Programs to be Advanced Through Corporate Partnerships

    Programs to be Advanced Through Corporate Partnerships

  33. Slide 33: BioAtla’s Catalysts Planned to be Achieved Through Corporate Partners

    BioAtla’s Catalysts Planned to be Achieved Through Corporate Partners 2025 2026 Ozuriftamab vedotin (ROR2-ADC) – SCCHN Phase 2 √ Phase 3 (HPV+ SCCHN) In process of partnering Evalstotug (CTLA4-IO) – √ Phase 2 Extension Phase 2 Phase 3 Melanoma (Project Optimus) Initiated partnering discussions IND √

  34. Slide 34: Ozuriftamab Vedotin (CAB-ROR2-ADC): Squamous Cell Carcinoma of the Head and Neck (SCCHN)

    Ozuriftamab Vedotin (CAB-ROR2-ADC): Squamous Cell Carcinoma of the Head and Neck (SCCHN)

  35. Slide 35: Potential Market Opportunity in 2L+ HPV+ SCCHN

    Potential Market Opportunity in 2L+ HPV+ SCCHN No current approved worldwide new the majority of therapy specifically for 660K cases of SCCHN By 2030 SCCHN will be HPV+ population annually1 HPV associated2 Limited benefit with SOC (cetuximab, methotrexate, approved HPV+ docetaxel)4-10: therapies dri

  36. Slide 36: 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

  37. Slide 37: HPV+ E6/E7 proteins upregulate ROR2 and drive proliferation and invasion

    HPV+ E6/E7 proteins upregulate ROR2 and drive proliferation and invasion Provides compelling rationale for targeting ROR2 with Oz-V HPV infection drives ROR2 overexpression • ROR2 is expressed by SCCHN at high rates • HPV driven cancers o Highest ROR2 expression among SCCHN o Recently shown that HPV

  38. Slide 38: 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) 14 (34) 1 15 (58) 25 (61) Prior lines of therapy 1 2 (8) 4 (10) 2 8 (31) 13 (33

  39. Slide 39: 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 Q2W Total p16 + On Treatment Responders 40% 40% (confirmed & CR unconfirmed) (6/15*) (14/35*) Respon

  40. Slide 40: Oz-V in SCCHN HPV positive oropharyngeal

    Oz-V in SCCHN HPV positive oropharyngeal 1.8 mg/kg Q2W; Median of 3 prior lines of therapy Q2W Responders 45% (confirmed & unconfirmed) (5/11*) CR Responders 27% (confirmed) (3/11*) 100% DCR (11/11*) DOR ongoing (months) PFS ongoing (months) OS ongoing (months) * Response evaluable patients defined

  41. Slide 41: 2L+ SCCHN Oz-V Mono vs Petosemtamab Mono

    2L+ SCCHN Oz-V Mono vs Petosemtamab Mono 3 vs 1 – 2 median prior lines of therapy; Cross Trial Comparisons** Ozuriftamab vedotin (1.8 mg/kg Q2W) Petosemtamab (1500 mg Q2W) Study Ongoing* Median prior lines (range) 3 (1 – 6) 2 (1 – 4) No previous exposure EGFR Inclusion No restriction on EGFR or prio

  42. Slide 42: Oz-V Monotherapy Has Promising Clinical Profile in 2L+ SCCHN

    Oz-V Monotherapy Has Promising Clinical Profile in 2L+ SCCHN Cross trial comparisons** between 3 vs 1 – 2 median prior lines of therapy Ozuriftamab vedotin monotherapy 1.8mg/kg IC monotherapy IC monotherapy Cetuximab Q2W (Checkmate-141)1,2 (Keynote-040)3 monotherapy5,6,7 (all PD-1 failures) Study, o

  43. Slide 43: Confirmed Complete Response Oz-V in SCCHN (1.8 mg/kg Q2W) – 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

  44. Slide 44: Partial Response (-80%) Oz-V in SCCHN (1.8 mg/kg Q2W) – 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 4

  45. Slide 45: Partial Response (-91%) Oz-V in SCCHN (1.8 mg/kg Q2W) – HPV negative

    Partial Response (-91%) Oz-V in SCCHN (1.8 mg/kg Q2W) – HPV negative 69-year-old female, stage III – recurred after surgery and radiation therapy; prior treatments: platinum / taxane / pembrolizumab, cetuximab Baseline – 19 November 2024 On Treatment – 09 January 2025 BioAtla | Overview 45

  46. Slide 46: Ph2 Oz-V: Overall Safety Summary of SCCHN patients

    Ph2 Oz-V: Overall Safety Summary of SCCHN patients Q2W dosing regimen was well-tolerated 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%) 9 (45%) 12 (30%) Any related serious AEs2 1 (5%) 4 (20

  47. Slide 47: 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

  48. Slide 48: FDA Actionable Guidance Received on Pivotal Trial in Second-Line Plus SCCHN

    FDA Actionable Guidance Received on Pivotal Trial in Second-Line Plus SCCHN Oz-V has Fast Track Designation • Supportive of: • Proposed pivotal randomized, controlled trial of Oz-V monotherapy vs investigator’s choice (cetuximab, docetaxel, or methotrexate) • Dual primary endpoints • Overall Respons

  49. Slide 49: Ozuriftamab vedotin next steps

    Ozuriftamab vedotin next steps Oz-V has Fast Track Designation • BioAtla recommended dose of Oz-V is 1.8 mg/kg Q2W for planned pivotal trial • Confirming with FDA that the selected lower dose intensity meets requirements for Project Optimus • Partnering discussions ongoing with updated Oz-V data; fo

  50. Slide 50: Evalstotug (CAB-CTLA-4)

    Evalstotug (CAB-CTLA-4)

  51. Slide 51: Evalustotug 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

  52. Slide 52: Evalstotug is a CAB-Derivative of Ipilimumab

    Evalstotug is a CAB-Derivative of Ipilimumab Preserved efficacy with reduced toxicity in combination with PD-1 • Ipilimumab (ipi) CDR’s modified to bind at tumor cell acidic pH, but not at normal pH leading to evalstotug: ▪ Preserved affinity and epitope Normal Tumor Normal Tumor ▪ Equivalent EMax a

  53. Slide 53: Reversible Binding in the TME

    Reversible Binding in the TME Comparison of evalstotug binding to CTLA-4 in different pH conditions Abbreviations: CTLA-4, cytotoxic T-lymphocyte associated protein 4; ICI, immune checkpoint inhibitor; IgG, immunoglobulin G; OD450, optical density at 450 nm; TME, tumor microenvironment. Note: Figure

  54. Slide 54: 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

  55. Slide 55: Evalstotug at 350 mg in combination with PD1: Demographics – Tumor Types

    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

  56. Slide 56: Patients Treated with Evalstotug Received More Than Twice as Many Doses Compared with Reported Ipi Dosing

    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

  57. Slide 57: 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

  58. Slide 58: Evalstotug: Responders in the 5 mg/kg Q3W + PD1

    Evalstotug: 7 of 16 Responders 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 58 Live Database 28Apr2025

  59. Slide 59: 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

  60. Slide 60: 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 ^Two patients dose escalated Doses 1 – ≤18 weeks 1 - >100 weeks 1 – ≤12 weeks - 70 mg to 350 mg exposure exposure exposure - 210 mg to 350 mg (≤6 doses) (1 - >33 doses) (

  61. Slide 61: 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

  62. Slide 62: 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

  63. Slide 63: 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 (ADC targeting ROR2) + evalstotug + PD1 69 yo M with oral cavity, floor of mouth/ mandibular, mucoepidermoid carcinoma; neo-adjuvant patient Disease had recurred after prior surgery and chemoradia

  64. Slide 64: FDA Guidance Regarding Evalstotug Pivotal Trial in 1L Unresectable and / or Metastatic 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

  65. Slide 65: Conclusions

    Conclusions • 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 9

  66. Slide 66: 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) Cash sufficient - 1H’26, Proprietary technology with beyond key clinical readouts over 500 issued patents Advancing clinical stage Advancing assets internally: strategic collaborati

BioAtla — Q1 2025 Earnings Presentation on 6ix