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Pipeline

Our oncology programs aim to outmaneuver treatment resistance and significantly improve the patient’s quality of life. We design small molecules for improved selectivity, durability and safety.

BH-30643 | BH-30236 | POSTERS & PRESENTATIONS

Candidate
Indication
Research Ind-Enabling Phase 1 Phase 2 Phase 3

BH-30643

Mutant-selective OMNI-EGFR™ inhibitor

Non-small cell lung cancer (NSCLC)

Phase 1

Phase 1

BH-30236

CLK inhibitor

Acute myeloid leukemia (AML)

Phase 1

Phase 1

Candidate Selection

Reversible mutant-selective ALK/CLK dual inhibitor

Research

Phase 1

Our Programs

BH-30643

A mutant-selective OMNI-EGFR™ inhibitor

We are evaluating a potentially better way to treat EGFR-positive NSCLC. BH-30643 is a mutant-selective OMNI-EGFR™ inhibitor with an aim to provide greater benefit to patients by:

  • Super-high potency against common, atypical and compound EGFR mutations, including those induced by treatment with other EGFR inhibitors.
  • Low potency against wild-type EGFR to decrease the risk of toxicities associated with wild-type EGFR activity, including skin rash.
  • Concurrently targeting active EGFR and HER2 to reduce the chances of resistance.

BH-30643 has demonstrated a promising PK and safety profile, including good preclinical cardio-safety. The company is actively enrolling the Phase 1/2 SOLARA clinical trial.

Learn More
Older woman in a yellow sweater
woman holding a pill bottle

BH-30236

A Multi-Targeted CLK Inhibitor

Our orally available, multi-targeted CLK inhibitor BH-30236 is designed to selectively induce splicing alterations in cancerous tissue and shut down cancer’s ability to use off-target resistance mechanisms. We aim for BH-30236 to be applied to hematologic cancers and solid tumors. The first indications for its use are in treating adult AML and higher-risk myelodysplastic syndrome (HR-MDS).

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Candidate Selection

ALK/CLK Dual Inhibitor

ALK inhibitors have been successful in the treatment of ALK+ cancers, with four ALK inhibitors now approved. However, ALK mutations have emerged for all four approved treatments. In addition to these on-target mutations, it has been shown that aberrant splicing functions as an oncogenic driver and induces off-target treatment resistance in these cancers.

Targeting CLK kinases can be an effective strategy in modulating aberrant alternative splicing in cancer and cancer treatment resistance. Our approach addresses both on-target and off-target mutations driving treatment resistance via dual inhibition of ALK/CLK.

Our programs show promising activity against CLK1/2/4 to suppress survival signals and promote cell death in cancer cells, including those with TP53 mutations. Our approach could help minimize or prevent treatment resistance to approved medicines such as LORBRENA®, ALECENSA® and VENETOCLAX®.

With favorable pharmacokinetic profiles, we expect to select a candidate, initiate IND-enabling studies in 2024, and start clinical studies in early 2025.

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POSTERS AND PRESENTATIONS

BH-30643

  • Design and discovery of BH-30643: A novel, reversible, mutant-selective macrocyclic EGFR inhibitor invulnerable to common resistance mutations

    AACR 2025 Poster

BH-30236

  • Novel Multikinase CLK Inhibitor BH-30236 Targets Hematological Malignancies through Alternative Splicing Regulation

    AACR 2025 Poster

  • BH-30236, a Novel, Macrocyclic CLK Inhibitor Modulating RNA splicing, Demonstrates Potent Anti- Proliferation Activity in a Broad Panel of Cancer Cell Lines

    AACR 2024 Poster

  • Discovery of BH-30236: A Novel Macrocyclic CLK Inhibitor Targeting Alternative Splicing in Cancers

    AACR 2024 Poster

© 2025 BlossomHill Therapeutics, Inc. | Terms of Service | Privacy Notice
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