Blossomhill Therapeutics, Inc. · NASDAQ:BLSM
Blossomhill Therapeutics — Investor Presentation (September 2026)
37 slides from Blossomhill Therapeutics's investor presentation, September 2026
Slide 1: BlossomHill Therapeutics Corporate Presentation
BlossomHill Therapeutics, Inc. Corporate Presentation September 2026 San Diego, CA
Slide 2: Disclaimer
2 Disclaimer This presentation regarding BlossomHill Therapeutics, Inc. (the “Company,” “BlossomHill,” “we,” “us,” or “our”) contains forward-looking statements. All statements other than statements of historical facts contained in this presentation, including statements regarding the Company’s stra
Slide 3: Intentionally designing novel medicines to address significant unmet medical needs in cancer treatment
Intentionally designing novel medicines to address significant unmet medical needs in cancer treatment Strong leadership team Differentiated wholly- Early launch opportunity Broad EGFR development with proven track record of owned pipeline spanning targeting EGFR C797S ongoing including TKI designin
Slide 4: Seasoned Management Team and Board
4 Seasoned Management Team and Board Executive Team Experience Board of Directors J. Jean Cui, Ph.D. Bihua Chen, M.B.A. Scientific Founder, President & CEO Board of Directors Y. Peter Li, Ph.D., M.B.A. Carl L. Gordon, Ph.D. Co-Founder, Executive Chairman Board of Directors Geoffrey Oxnard, M.D. John
Slide 5: Designing Cancer Medicines the BlossomHill Way
5 Designing Cancer Medicines the BlossomHill Way Identify unmet medical need for patients Structural analysis of existing molecules and their limitations Precision drug design based on deep understanding of target biology and protein structure dynamics Iterate and optimize toward specified performan
Slide 6: BlossomHill Product Candidate Pipeline
6 BlossomHill Product Candidate Pipeline Indication / Design/ IND Target Candidate Therapeutic Area Discovery Enabling Phase 1 Phase 2 Phase 3 EGFR-mutant EGFR BH-30643 NSCLC BH-30236 R/R AML and CLK +/- venetoclax HR-MDS Pan-KRAS BH-501284 Solid Tumors Our goal is to develop orally available, poten
Slide 7: BH-30643: OMNI-EGFR Inhibitor
BH-30643: OMNI-EGFRTM Inhibitor I N V E S T I G AT I O N A L , M A C R O C Y C L I C , N O N - C O VA L E N T, B R A I N A C T I V E I N H I B I T O R TA RG E T I N G M U TA N T EG F R ACT I V E CO N FO R M AT I O N
Slide 8: Targeting EGFR-Mutant NSCLC: C797S Resistance And Beyond
8 Targeting EGFR-Mutant NSCLC: C797S Resistance And Beyond Total EGFR-mutant NSCLC incidence in 2025 Substantial Market Opportunity in USA, Europe, Japan, China EGFR Mutant NSCLC 316,000 1 (2025 Tagrisso sales: ~$7.3B)4 Early launch opportunity: 209,000 • ~5,4005 C797S patients annually across plann
Slide 9: Why a Leap in EGFR-mutant NSCLC Is Attainable
9 Why a Leap in EGFR-mutant NSCLC Is Attainable AC H I E V I N G LO N G E R P F S A N D P R E - E M P T I O N O F R E S I S TA N C E W I T H H I G H - P OT E N CY EML4-ALK Inhibitors in ALK+ NSCLC ROS1 Inhibitor in ROS1+ NSCLC 3rd Gen: 2nd Gen: Macrocyclic Lorlatinib Macrocyclic Repotrectinib Cell P
Slide 10: Existing EGFR Tyrosine Kinase Inhibitors Share Structural Families and Design Liabilities
Existing EGFR Tyrosine Kinase Inhibitors Share Structural 10 Families and Design Liabilities Many TKI designs use a back-pocket motif for BH-30643 Other TKI designs use a covalent bond for potency, potency, vulnerable to T790M resistance vulnerable to C797S resistance Gefitinib Afatinib Osimertinib
Slide 11: BH-30643: An Intentionally Designed Macrocyclic, Mutant-Selective OMNI-EGFR Inhibitor
BH-30643: An Intentionally Designed Macrocyclic, Mutant- 11 Selective OMNI-EGFRTM Inhibitor • High cell potency against EGFR classical, • ~ 10 times more potent than osimertinib for atypical, and exon20ins L858R / 19del • Equipotent in the setting of on-target • Avoided potency limitations of recent
Slide 12: BH-30643 SOLARA Phase 1/2 Trial
BH-30643 SOLARA Phase 1/2 Trial P R E L I M I N A RY D O S E E S C A L AT I O N & E X PA N S I O N E X P E R I E N C E
Slide 13: SOLARA: Study Design and Patient Characteristics for Dose Escalation
13 SOLARA (NCT06706076): Study Design and Patient Characteristics for Dose Escalation Phase 1 escalation / backfill enrolled a heavily pretreated and heterogeneous patient population, with a median of 3 prior lines of therapy, 66% with history of brain metastases, and 71% ECOG=1 Phase 1 Part 1A (Esc
Slide 14: High PK Exposures Observed in Escalation / Backfill Experience
14 High PK Exposures Observed in Escalation / Backfill Experience Median preliminary steady state plasma exposures at High exposure and high potency combined with ≥40mg BID achieved high coverage over target EC90 Kp,uu of 27% (CSF, primate) supports the observed and exceeded reported exposures of ma
Slide 15: Responses in Diverse EGFR-mutant Subtypes May Support Multiple Paths for Future Clinical Development
Responses in Diverse EGFR-mutant Subtypes May Support 15 Multiple Paths for Future Clinical Development • 44 yo female, enrolled at 40mg BID • 68 yo female enrolled at 80mg QD • 51 yo male enrolled at 80mg BID • EGFR exon 19 deletion & C797S • EGFR L861Q previously treated with • EGFR exon 20 insert
Slide 16: BH-30643 Experience in C797S +/- T790M Resistance
BH-30643 Experience in C797S +/- T790M Resistance P R E L I M I N A RY D O S E E S C A L AT I O N / B A C K F I L L A N D E A R LY E X PA N S I O N E X P E R I E N C E
Slide 17: C797S Efficacy Results: Confirmed Responses Observed Across Dose Levels
17 C797S Efficacy Results: Confirmed Responses Observed Across Dose Levels in Patients with C797S • 40 patients from the target C797S population (19 chemo naïve and 21 chemo treated) were response evaluable across escalation and expansion cohorts • Responses (45% ORR with 17 confirmed and 1 unconfir
Slide 18: C797S Efficacy Results: Preliminary Durability
18 C797S Efficacy Results: Preliminary Durability • Studied 40 patients in the target C797S population enrolled as of the data cutoff ➢ Excludes patients with concurrent driver alterations or who previously received EGFR TKI specifically targeting a known C797S • Median follow-up was 6.9 months • 25
Slide 19: Maturing Safety Data Supports RP2D Selection
19 Maturing Safety Data Supports RP2D Selection Treatment-related adverse events (TRAE) i ≥1 %p i 1 Preferred Term, 40 mg, 50mg, 60 mg BID • Dose reduction (9%) and treatment discontinuation N=174 N (%) (3%) due to TRAE are uncommon All Grade Grade 1 Grade 2 Grade 3/43 • EGFR-wildtype associated TRA
Slide 20: BH-30643 Experience in EGFR TKI Naive Classical Mutation
BH-30643 Experience in EGFR TKI Naive Classical Mutation P R E L I M I N A RY E A R LY E X PA N S I O N E X P E R I E N C E
Slide 21: Compelling Early Activity Observed in the Classical TKI-naive Setting
21 Compelling Early Activity Observed in the Classical TKI-naive Setting • Response (confirmed or 10 unconfirmed and ongoing) in 21 Best Change in SoD of Target Lesions (%) * * * * 0 of 27 patients (78%) with on- -10 NE treatment imaging; all had SD SD -20 tumor reduction SD SD -30 SD uPR cPR uPR -4
Slide 22: First-line Activity Against Challenging EGFR Mutations
22 First-line Activity Against Challenging EGFR Mutations L858R Exon19del & H870R • Treatment naive, treated at 40mg BID, with • TKI naive, presented with multiple brain mets treatment ongoing • Treated at 40mg BID with systemic and CNS PR, in the • Partial response confirmed on second scan (-86%) a
Slide 23: Early Clinical Activity of BH-30643 in Classical TKI-naive Cohort
23 Early Clinical Activity of BH-30643 in Classical TKI-naive Cohort BH-30643 TKI-naive Osimertinib Phase 1 Treatment-naive Total (40mg+50mg BID) Total 80 mg 160 mg # Patients 27 # Patients 60 30 30 Brain mets n (%) 13 (48%) Brain mets n (%) 15 (25%) 7 (23%) 8 (27%) ORR 78% ORR 77% 67% 87% DCR% 96%
Slide 24: SOLARA Expansion Cohorts Now Enrolling Globally
24 SOLARA Expansion Cohorts Now Enrolling Globally Expansion cohorts to inform Phase 2/3 development TKI resistance • C797S detected after most recent therapy • Atypical resistance mutations (L718X, G724X, etc.) Potentially Escalation Targeted therapy naive • Classical mutations registrational and b
Slide 25: BH-30643 Key Takeaways
25 BH-30643 Key Takeaways Compelling activity in patients with C797S with potential path to accelerated approval Early activity in TKI naive patients with potential to expand 1L development Differentiated safety profile mitigating many of the idiopathic toxicities seen with osimertinib EOP1 meeting
Slide 26: BH-30236: CLK Inhibitor
BH-30236: CLK Inhibitor I N V E ST I GAT I O N A L , M AC RO CYC L I C, N O N- COVA L E N T I N H I B I TO R TA R G E T I N G A B E R R A N T A LT E R N AT I V E S P L I C I N G
Slide 27: BH-30236: Potent CLK inhibitor Modulating Aberrant Alternative Splicing
27 BH-30236: Potent CLK inhibitor Modulating Aberrant Alternative Splicing • Upregulation and mutations of serine/arginine rich splicing factors (SRSFs) have been reported in hematological malignancies and solid tumors • CDC-like kinases (CLKs) can modulate aberrant splicing via phosphorylation of S
Slide 28: BH-30236 Monotherapy Anti-leukemic Activity at ≥ 30mg QD
28 BH-30236 Monotherapy Anti-leukemic Activity at ≥ 30mg QD • 6/21 (28.6%) patients with post-baseline marrow assessment had ≥50% blast count reduction on therapy • Of 6 evaluable patients with previously treated HR-MDS, 2 (33%) had a CR on monotherapy Best Change in Baseline Marrow Blast % Anti-Leu
Slide 29: Venetoclax Combo: Anti-leukemic Activity Observed in Ven Pre-treated Patients
Venetoclax Combo: Anti-leukemic Activity Observed 29 in Ven Pre-treated Patients Across Dose Levels • 13/15 patients with prior venetoclax exposure • ≥ 50% blast count reduction in 8/15 (53%) patients with post-baseline marrow assessments • In 11 evaluable patients with R/R AML, overall response rat
Slide 30: BH-30236 Key Takeaways
30 BH-30236 Key Takeaways Novel approach to target aberrant alternative splicing, an emergent driver of cancer progression and resistance Tolerable with once daily dosing, both as monotherapy and in combination with venetoclax Preliminary anti-leukemic effect motivating additional investigation in m
Slide 31: BH-501284: pan-KRAS Inhibitor
BH-501284: pan-KRAS Inhibitor D UA L - STAT E , P S E U D O - I R R E V E R S I B L E , PA N - K R A S I N H I B I TO R
Slide 32: A Fresh Approach to Pan-KRAS Inhibition
32 A Fresh Approach to Pan-KRAS Inhibition Recent progress against KRAS comes with limitations: • Covalent KRAS inhibition is limited to G12C alleles • Tricomplex pan-RAS inhibitors have burdensome toxicity that challenges combinations Non-covalent Switch-II KRAS inhibitors offer the potential for t
Slide 33: Cell Potency of BH-501284 Versus Clinical Stage KRAS Inhibitors
33 Cell Potency of BH-501284 Versus Clinical Stage KRAS Inhibitors • Cellular potency mirrored divarasib in G12C with a non-covalent inhibitor and provided potency against diverse KRAS driver mutations and amplification that exceeded the potency of AMG-410 • Cellular potency matched daraxonrasib, bu
Slide 34: BH-501284 Demonstrated Long Residence Time and Sustained Tumor Regression
34 BH-501284 Demonstrated Long Residence Time, Deep Blocking of RAS (GTP)-cRAF Interaction and Sustained Tumor Regression • BH-501284 showed pseudo-irreversible characteristics with long residence time • BH-501284 showed greater max % KRAS inhibition than daraxonrasib, suggesting more complete elimi
Slide 35: BH-501284 Achieved Sustained Blocking of KRAS Signaling & Marked Efficacy
BH-501284 Achieved Sustained Blocking of KRAS Signaling 35 & Marked Efficacy, Comparable to Covalent KRAS G12Ci Divarasib • In wash-off experiment, BH-501284 sustained pERK inhibition as effectively as divarasib, while AMG410 lost pERK inhibition • In H358 KRAS G12C tumor model, BH-501284 induced tu
Slide 36: BH-501284 Key Takeaways
36 BH-501284 Key Takeaways Designed for potent pan-KRAS inhibition while sparing HRAS/NRAS, to reduce toxicity seen with tricomplex inhibitors Unique pseudo-irreversible binding (>54-hour residence time) through use of a novel non-covalent Switch–II chemical scaffold, can lead to prolonged blocking
Slide 37: Thank you
Thank you THE NEXT LEAP FORWARD IN PRECISION MEDICINE
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