Black Diamond Therapeutics, Inc. · NASDAQ:BDTX

Black Diamond Therapeutics — AACR Annual Meeting 2024

15 slides from Black Diamond Therapeutics's conference presentation, Apr 5, 2024

  1. Slide 1: BDTX-1535 – A MasterKey EGFR Inhibitor Targeting Classical, Non-Classical and C797S Resistance Mutation

    BDTX-1535 – A MasterKey EGFR Inhibitor Targeting Classical, Non-Classical and the C797S Resistance Mutation to Address the Evolved Landscape of EGFR Mutant NSCLC E. Dardenne1, M. O'Connor1, M. Nilsson2, J. He2, X. Yu2, J. V. Heymach2, X. Le2, E. Buck1; 1Black Diamond Therapeutics, Cambridge, MA, 2MD

  2. Slide 2: Financial relationships disclosure

    Etienne Dardenne I have the following financial relationships to disclose: Stockholder in: Black Diamond Therapeutics Employee of: Black Diamond Therapeutics I will not discuss off-label use and/or investigational use in my presentation. 2

  3. Slide 3: Key takeaways on EGFR landscape and BDTX-1535

    v Small molecules directed against oncogenic EGFR mutations expressed in NSCLC is a 20-year success story. BDTX-1535 clinical data from 2023 EORTC v The EGFR mutational landscape in NSCLC continues to evolve – today we present real world data that reveals new mutations and treatment opportunities. v

  4. Slide 4: Real World Data Describe a Broad EGFR Mutational Landscape in NSCLC

    Real World Data Describe a Broad EGFR Mutational Landscape in NSCLC & Reveal New Opportunities for EGFR Targeting 2004 Today Two classical EGFR oncogenic Real World Data reveals a broad landscape of classical & non-classical EGFR mutations first described1 oncogenic mutations in NSCLC Black Diamond

  5. Slide 5: 20-30% of Newly Diagnosed EGFRm NSCLC Patients Carry Non-Classical Mutations

    20-30% of Newly Diagnosed EGFRm NSCLC Patients Carry Non-Classical Mutations; Are Not Adequately Addressed by Current Therapies1 Classical and non-classical driver mutations 22-30% of newly diagnosed EGFRm NSCLC express non-classical mutations are distributed across EGFR structure Ectodomain- 50+ Ju

  6. Slide 6: C797S and Non-Classical Mutations are Major Mechanisms of Acquired On-Target EGFR Resistance

    C797S and Non-Classical Mutations are Major Mechanisms of Acquired On-Target EGFR Resistance On-target EGFR resistance mechanisms have shifted C797S & non-classical mutations are major mechanisms of since approval of 3G TKI osimertinib in 1L setting on-target EGFR resistance in patients post-osimert

  7. Slide 7: BDTX-1535 Potently Targets Non-Classical EGFR Mutations Co-Expressed with L858R

    BDTX-1535 Potently Targets Non-Classical EGFR Mutations Commonly Co-Expressed with L858R Which are Insensitive to Osimertinib EGFR-L858R tumors more frequently co- Patients with L858R do less well on Non-classical mutations co-expressed express non-classical EGFR mutations osimertinib therapy vs Ex1

  8. Slide 8: BDTX-1535 preclinical proliferation potency across EGFR mutations

    Proliferation (IC50) nM 0 20 40 60 80 100 120 L WT Ex 19 Ex 858 L8 de 19 R 5 l d L8 8R +S7 el 58 +A 68 Classical R 8 I​ L8 L85 +A2 59S 58 8R 8 9 EGFR-WT L8 R+E +L6 V 58 G 2R L8 R+ FRv 5 G I L8 8R 59 II​ 5 + 8 L8 8R S78 V 58 +S 4F L8 R 78 ​ 5 + 4 L8 8R E70 S 58 +E 9K L8 R+ 70 58 R1 9V R+ 08 L858R+ No

  9. Slide 9: BDTX-1535 preclinical potency against PACC mutations

    Proliferation (IC50) nM 0 20 40 60 80 100 120 L WT Ex 19 Ex 858 L8 de 19 R 5 l d L8 8R +S7 el 58 +A 68 Classical R 8 I​ L8 L85 +A2 59S 58 8R 8 9 EGFR-WT L8 R+E +L6 V 58 G 2R L8 R+ FRv 5 G I L8 8R 59 II​ 5 + 8 L8 8R S78 V 58 +S 4F L8 R 78 ​ 5 + 4 L8 8R E70 S 58 +E 9K L8 R+ 70 58 R1 9V R+ 08 L858R+ No

  10. Slide 10: BDTX-1535 potency and well-tolerated oral doses of 100-200mg QD

    Proliferation (IC50) nM 0 20 40 60 80 100 120 L WT Ex 19 Ex 858 d L8 e 19 R 5 l d L8 8R +S7 el 58 +A 68 Classical R 8 I​ L8 L85 +A2 59S 58 8R 8 9 EGFR-WT L8 R+E +L6 V 58 G 2R L8 R+ Rv F 5 G I L8 8R 59 II​ 5 + 8 L8 8R S78 V 58 +S 4F L8 R 78 ​ 5 + 4 L8 8R E70 S 58 +E 9K L8 R+ 70 58 R1 9V R+ 08 L858R+

  11. Slide 11: BDTX-1535 Drives Clearance of Mutant EGFR VAF and ctDNA in Phase 1 Trial

    BDTX-1535 Drives Clearance of Mutant EGFR VAF and ctDNA in Phase 1 Trial Clearance of plasma ctDNA Clearance classical mutations Clearance of C797S Clearance of non-classical mutations (9/9 patients) (7/7 patients) (6/6 patients) (4/4 patients) 100 100 100 100 L748Q ctDNA L858R %Change in total ctDN

  12. Slide 12: BDTX-1535 Achieves Radiographical Responses in Efficacy-Evaluable NSCLC Patients

    BDTX-1535 Achieves Radiographical Responses in Efficacy-Evaluable NSCLC Patients Across Relevant Mutations in Phase 1 Trial Best overall response PD SD SD SD SD SD SD PR PR** uPR* PR PR PR 20 Best % SoD change On treatment 0 PR = Partial response -20 SD = Stable disease -40 PD = Progressive disease

  13. Slide 13: BDTX-1535 Achieves Radiographical Responses Across Relevant Mutations in Phase 1

    BDTX-1535 Achieves Radiographical Responses in Efficacy-Evaluable NSCLC Patients Across Relevant Mutations in Phase 1 Trial BDTX-1535: potent inhibition of non-classical mutations that are insensitive to osimertinib Best overall response PD SD SD SD SD SD SD PR PR** uPR* PR PR PR 160 20 Osimertinib

  14. Slide 14: BDTX-1535: Potential First- and Best-in-Class Therapy for EGFRm NSCLC

    BDTX-1535: Potential First- and Best-in-Class Therapy to Address Major Unmet Medical Needs in EGFRm NSCLC (Classical, Non-Classical, and C797S Resistance Mutation) Evolution of the EGFR mutation landscape over the past 20 years BDTX-1535 2005 2013 2015 2018 2024 Classical drivers L858R / Ex19del Non

  15. Slide 15: BDTX-1535: Currently in Phase 2 Trial for 1L/2L/3L EGFRm NSCLC

    BDTX-1535: Currently in Phase 2 Trial for 1L/2L/3L EGFRm NSCLC; Multiple Additional Opportunities BDTX-1535 clinical Classical Classical data from 2023 EORTC Non-Classical (L858R) (Ex19del) Ongoing P2 Ongoing P2 2/3L Ongoing P2 C797S C797S Non-classical Non-classical Potential Potential BDTX-1535 cl

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