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.
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
BH-30236
CLK inhibitor
Acute myeloid leukemia (AML)
Phase 1
Candidate Selection
Reversible mutant-selective ALK/CLK dual inhibitor
Research
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. An Investigational New Drug application (IND) submission is planned for mid-2024, with the Phase 1 proof-of-concept clinical trial slated for late 2024.
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).
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.
