We are a clinical-stage oncology company dedicated to unlocking a new paradigm in cancer therapeutics that addresses the significant unmet need in patients with oncogene amplified tumors by targeting extrachromosomal DNA (ecDNA), a root cause of oncogene amplification observed in more than 14% of cancer patients. (Incorporated in Delaware)

Our mission is to be the foremost biopharma company interrogating ecDNA biology to deliver transformative therapies that improve and extend the lives of patients with previously intractable oncogene amplified cancers.

ecDNA are large circular units of nuclear DNA that are a primary mechanism of gene amplification and, like oncogene amplifications, are detected only in cancer cells, not in healthy cells. Despite tremendous advancements in treating cancer broadly, patients with oncogene amplified cancers generally derive little benefit from existing therapies, such as molecular targeted therapies or immunotherapies, and have worse survival rates than patients with other types of cancer. Using our proprietary Spyglass platform, we identify targets essential for ecDNA functionality in oncogene amplified cancer cells, then design and develop small molecule drugs called ecDNA-directed therapeutic candidates (ecDTx) to inhibit those targets, with the aim to prevent cancer cells from using ecDNA to express amplified oncogenes and grow, adapt, and become resistant to existing therapies. Instead of directly targeting the proteins produced by amplified oncogenes, which is the approach of traditional targeted therapies, our ecDTx are intended to be synthetic lethal in tumor cells reliant on ecDNA. In the context of drug development, synthetic lethality is a therapeutic approach wherein using a drug to pharmacologically inhibit one target is lethal to cancer cells harboring a specific genetic alteration to a second target, but not lethal to healthy cells that lack the genetic alteration to the second target. Accordingly, our ecDTx are designed to preferentially kill ecDNA-bearing cancer cells, but not healthy cells without ecDNA. They are engineered to disrupt the underlying cellular machinery that enables ecDNA to function properly, such as proteins essential for ecDNA replication, transcription, assembly, repair, and segregation.

Our lead ecDTx, BBI-355, is a novel, oral, selective inhibitor of checkpoint kinase 1 (CHK1), which manages ecDNA replication and transcription in cancer cells. BBI-355 demonstrated CHK1 inhibition and tumor regressions in ecDNA-enabled preclinical cancer models and is currently being studied in a first-in-human, Phase 1/2 clinical trial in patients with oncogene amplified cancers. We refer to this trial as POTENTIATE (Precision Oncology Trial Evaluating Novel Therapeutic Interrupting Amplifications Tied to ecDNA). We expect to have preliminary clinical proof of concept safety and antitumor activity data of BBI-355 as a single agent and in combination with targeted therapies from the POTENTIATE trial in the second half of 2024 from approximately 50 to 90 total enrolled patients (single agent cohorts N=~30 to 40, combination cohorts N=~20 to 50).

Our second ecDTx, BBI-825, is a novel, oral, selective inhibitor of ribonucleotide reductase (RNR), which is essential for ecDNA assembly and repair in cancer cells. BBI-825 demonstrated RNR inhibition and tumor regressions in amplification-enabled preclinical cancer models. In February 2024, we initiated a first-in-human, Phase 1/2 clinical trial of BBI-825 in patients with resistance gene amplifications. We refer to this trial as STARMAP (Study Treating Acquired Resistance: MAPK Amplifications). We expect to have preliminary clinical proof of concept safety and antitumor activity data of BBI-825 in combination with targeted therapies from the STARMAP trial in the second half of 2025.

Our third ecDTx program is directed at a previously undrugged kinesin target essential for ecDNA segregation and inheritance during cell division. We are advancing our third ecDTx program through drug discovery to candidate identification and expect to submit an investigational new drug application (IND) as early as the first half of 2026.

(Note: Boundless Bio, Inc. priced its IPO on March 27, 2024, at $16.00 – the mid-point of its $15.00-to-$17.00 range – on 6.25 million shares – to raise $100.0 million.)

(Note: Boundless Bio, Inc. set the terms for its IPO – 6.25 million shares at a price range of $15.00 to $17.00 to raise $100.0 million – in its S-1/A filing dated March 21, 2024. The Phase 1/Phase 2 biotech also set its IPO pricing date for the following week. Background: Boundless Bio, Inc. filed its S-1 on March 6, 2024, without disclosing terms, and with estimated proceeds at $100 million. Background: The Phase 1 clinical biotech company submitted a confidential IPO filing to the SEC on Sept. 1, 2023.)