Boundless Bio (BOLD) Corporate presentation summary

Unmet medical need and scientific foundation

• Oncogene amplified cancers represent a significant unmet need, with poor survival and limited response to current targeted or immunotherapies.

• Approximately 1.3 million new patients per year in major markets are affected by oncogene amplified cancers.

• ecDNA, cancer-specific circular DNA, is a root cause of oncogene amplification and resistance to therapies.

• ecDNA is present in 14–17% of cancer specimens at diagnosis and is rarely found in normal tissue.

• Amplifications on ecDNA are associated with worse survival and frequent clinical resistance to multiple therapies.

Platform and pipeline overview

• The Spyglass platform leverages ecDNA biology to identify synthetic lethal targets in oncogene amplified cancers.

• Pipeline includes BBI-940 (Kinesin degrader, Phase 1), BBI-355 (CHK1 inhibitor), and BBI-825 (RNR inhibitor), targeting distinct ecDNA lifecycle nodes.

• BBI-940 is a novel, oral, selective degrader of Kinesin, essential for ecDNA segregation but non-essential for normal chromosomes.

• Additional discovery efforts target epigenetic regulators, ubiquitin enzymes, and ATPases relevant to ecDNA biology.

BBI-940 preclinical and clinical development

• BBI-940 demonstrated potent, selective Kinesin degradation, anti-tumor activity, and tumor regressions in ecDNA+ breast cancer models.

• Well-tolerated in 28-day GLP toxicity studies in rats and dogs, with no dose-related adverse findings.

• Phase 1 KOMODO-1 trial is enrolling patients with advanced ER+/HER2- or TNBC-LAR breast cancer, with biomarker-driven expansion cohorts.

• Initial clinical proof-of-concept data is expected within the current cash runway, which extends into the second half of 2028.