BBOT Reports Third Quarter 2026 Financial Results and Update on Corporate Progress
Key Highlights
- ➤BBO-8520 plus pembrolizumab achieved 75% ORR at 500 mg QD in experienced NSCLC
- ➤BBO-8520 monotherapy delivered 63% ORR and 100% DCR in inhibitor-naïve NSCLC
- ➤BBOT held $315.3 million cash, equivalents and securities, funding operations into 2029
- ➤Q3 net loss narrowed to $34.2 million from $44.8 million year over year
- ➤BBO-11818 and BBO-10203 combination cohorts are enrolling in CRC and PDAC
Expert Statements
Pedro J. Beltran, Chief Executive Officer of BBOT
“The third quarter was an important period for BBOT as we reported updated clinical data for BBO-8520 and delineated our strategic focus. Driven by encouraging clinical data across all three programs we are executing on multiple combinations with the potential for significant patient benefit”
Pedro J. Beltran, Chief Executive Officer of BBOT
“With a strong balance sheet, multiple data catalysts expected through mid-2027, and cash runway into 2029, we believe BBOT is well positioned to advance differentiated therapies for patients with KRAS-driven cancers.”
* BBO-8520 plus pembrolizumab demonstrated a 75% ORR at 500 mg QD and 53% ORR across dose levels in 2L+ KRAS(G12C )inhibitor-experienced NSCLC patients * BBO-11818 and BBO-10203 combination cohorts enrolling in KRAS-mutant colorectal cancer (CRC) and pancreatic ductal adenocarcinoma (PDAC); BBO-11818 and BBO-10203 monotherapy data update expected in the fourth quarter of 2026 * Cash runway expected to fund operations into 2029 SOUTH SAN FRANCISCO, Calif., Nov. 10, 2026 (GLOBE NEWSWIRE) -- BridgeBio Oncology Therapeutics, Inc. (“BBOT”) (Nasdaq: BBOT), a clinical-stage biopharmaceutical company focused on RAS-pathway malignancies, today reported financial results for the quarter ended September 30, 2026, and provided a business update.
BBOT’s portfolio of RAS-pathway inhibitors is designed to enable direct dual inhibition of KRAS(G12C) (BBO-8520), or KRAS(G12D/V) (BBO-11818) in both their ON and OFF states as well as disruption of RAS-driven PI3Kα activation (BBO-10203) to achieve optimal target coverage of the most mutated driver oncogene in human cancer. Together, these assets uniquely position BBOT to achieve concurrent, high-level suppression of both the MAPK and PI3Kα pathways through a wholly-owned internal combination strategy.
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