We are a clinical-stage biopharmaceutical company applying our intentional, chemistry-based approach to develop innovative small molecule medicines that address significant unmet medical needs in cancer treatment. With each of our programs, we combine a deep understanding of disease and protein dynamics with our structure-based rational drug design expertise to identify the specific structural liabilities that limit existing therapies or approaches, and then design novel chemical scaffolds to directly address these limitations. Our scientific founder and the team we have assembled have a proven track record of developing innovative small molecule medicines that overcome the limitations of existing therapies, including multiple approved therapies that have delivered transformational patient outcomes. Our initial development efforts are focused on our two clinical-stage programs: BH-30643, an investigational, non-covalent, macrocyclic, brain active, mutant-selective OMNI-EGFR inhibitor for the treatment of epidermal growth factor receptor (EGFR)-mutant non-small cell lung cancer (NSCLC), and BH-30236, an investigational macrocyclic CDC-like kinase (CLK) inhibitor being evaluated first in relapsed or refractory acute myeloid leukemia (R/R AML) and higher-risk myelodysplastic syndromes (HR-MDS). We also have a preclinical-stage product candidate, BH-501284, that leverages a novel chemical scaffold to selectively target and modulate activated KRAS. Our most advanced product candidate, BH-30643, is an OMNI-EGFR inhibitor being evaluated in SOLARA, a global Phase 1/2 clinical trial in patients with EGFR-mutant NSCLC. While there are commercially available drugs targeting EGFR subtypes, there is a fragmentation of care in EGFR-mutant NSCLC because no drug is effective across all EGFR mutations. Moreover, the durability of response to prior-generation EGFR tyrosine kinase inhibitors (TKIs) has frequently been limited by the emergence of acquired on-target resistance mutations, notably the T790M gatekeeper mutation for first- and second-generation EGFR TKIs and C797S-mediated resistance for third-generation EGFR TKIs, such as osimertinib. BH-30643 is designed to address a broad spectrum of EGFR mutations, including classical mutations, on-target resistance mutations such as C797S and T790M, atypical mutations and exon 20 insertion mutations, with selectivity over wild-type EGFR. The SOLARA Phase 1/2 clinical trial is currently enrolling patients across dose expansion cohorts in both TKI-pretreated and TKI-naive settings, including a C797S resistance cohort, a population with no currently approved targeted therapy. To date, treatment with BH-30643 has been evaluated for safety, pharmacokinetics and preliminary efficacy in patients with EGFR-mutant NSCLC, including in patients with the C797S resistance mutation across diverse molecular contexts (with or without T790M) in the setting of classical or atypical mutations, and in TKI-naive patients with classical mutations. We believe the early clinical data observed in this trial support a near-term development path in C797S resistance and establish the foundation for BH-30643’s potential against a broad spectrum of EGFR activating mutations. We plan to seek an end-of-Phase 1 meeting with the U.S. Food and Drug Administration (FDA) regarding the recommended Phase 2 dose and a potential accelerated approval pathway for BH-30643 in patients with advanced or metastatic C797S-positive EGFR-mutant NSCLC in the fourth quarter of 2026. Our second clinical-stage product candidate, BH-30236, is a CLK inhibitor currently being evaluated in an ongoing Phase 1 clinical trial in patients with R/R AML and HR-MDS. BH-30236 represents a novel approach to cancer treatment through the inhibition of CLK to target aberrant alternative mRNA splicing (aberrant alternative splicing), a defining feature implicated in cancer progression and therapeutic resistance across both hematologic malignancies and solid tumors. Our Phase 1 clinical trial is currently enrolling patients in the dose escalation part of the trial and is evaluating BH-30236 as a monotherapy and in combination with the BCL-2 inhibitor venetoclax, the established standard of care therapy for acute myeloid leukemia (AML) patients. To date, BH-30236 has been evaluated for safety, pharmacokinetics and preliminary efficacy across multiple dose levels as a monotherapy and in combination with venetoclax. We expect to report updated safety and efficacy data from the BH-30236 Phase 1 trial in the first half of 2027. We are also advancing our pan-KRAS program, initially focusing on our preclinical product candidate, BH-501284, which is designed using a novel chemical scaffold to achieve prolonged, potent and selective inhibition of KRAS mutations, but sparing HRAS and NRAS. We believe this molecule, which leverages a newly designed non-covalent scaffold, is unique in its potential to achieve tight and durable binding, a feature described as “pseudo-irreversible” binding. BH-501284 has demonstrated potent cellular pan-KRAS activity, achieved tumor regression at low oral dose levels in multiple KRAS-mutant mouse tumor models and improved oral bioavailability across species. We are currently conducting Investigational New Drug Application (IND) enabling studies of BH-501284 and plan to submit an IND in the first quarter of 2027. Our principal executive offices are located in San Diego, California.