BBOT Presents Preclinical Data Demonstrating pan-KRAS Inhibitor BBO-11818 Has Robust Anti-Tumor Activity in KRAS-Mutant Preclinical Models at the AACR Annual Meeting 2026
BBO-11818 targets KRAS in both its ON (active GTP-bound) and OFF (inactive GDP-bound) states, potently suppressing MAPK signaling and inhibiting cell proliferation in KRAS-mutant cell lines
BBO-11818 demonstrates robust anti-tumor activity as monotherapy and in combination across KRAS-mutant tumor models
Updated Phase 1 clinical data are expected in the second half of 2026
SOUTH SAN FRANCISCO, Calif., April 22, 2026 (GLOBE NEWSWIRE) -- BridgeBio Oncology Therapeutics, Inc. ("BBOT") (NASDAQ:BBOT), a clinical-stage biopharmaceutical company focused on RAS-pathway malignancies, today presented new preclinical data for BBO-11818, a selective, orally bioavailable non-covalent inhibitor that targets mutant KRAS in both the ON (active GTP-bound) and OFF (inactive GDP-bound) states with robust anti-tumor activity in KRAS-mutant preclinical models. The data underscore BBO-11818's differentiated activity across multiple KRAS-mutant cancer types. The data were presented at the American Association for Cancer Research (AACR) Annual Meeting 2026.
"BBO-11818 addresses a significant unmet need by targeting multiple KRAS variants for which no approved therapies exist, including KRASG12D and KRASG12V," said Pedro J. Beltran, PhD, Chief Scientific Officer of BBOT. "Its ability to inhibit KRAS in both its inactive and active states drives potent tumor regressions in pancreatic, lung, and colorectal cancer models — and its efficacy is meaningfully amplified in combination with BBO-10203, cetuximab, and anti-PD-1, underscoring its potential as a combination backbone in KRAS-mutant cancers."
Highlights from the poster include:
- BBO-11818 potently inhibits ERK phosphorylation and proliferation in KRAS-dependent cell lines in vitro.
- BBO-11818 demonstrates robust efficacy in KRASG12D and KRASG12V CDX models.
- BBO-11818 exhibits in vivo combination effect with BBO-10203, a RAS:PI3K⍺ breaker, and cetuximab in KRAS-mutant CDX and PDX models.
- BBO-11818 also shows combination benefit with anti-PD-1 treatment, resulting in complete tumor regressions and the induction of an adaptive immune response in the CT26 syngeneic model.
The presentation is titled "BBO-11818: an orally bioavailable, highly potent and selective non-covalent pan-KRAS (ON) and (OFF) inhibitor with robust anti-tumor activity in KRAS-mutant preclinical models." A copy of the poster will be available on the "Publications" page of the BBOT website following the conference.
About BBO-11818
BBO-11818 is a selective, orally bioavailable non-covalent inhibitor that targets KRAS in both the ON and OFF states, has high selectivity over HRAS and NRAS, and displays strong activity in KRAS-mutant preclinical models, including KRASG12D and KRASG12V. In addition, it potently suppresses MAPK signaling and inhibits cell proliferation in KRAS-mutant cell lines. BBO-11818 is currently being evaluated in the Phase 1 KONQUER-101 trial in subjects with locally advanced unresectable or metastatic KRAS-mutant solid tumors.
About BBOT
BBOT is a clinical-stage biopharmaceutical company advancing a next-generation pipeline of novel small molecule therapeutics targeting RAS and PI3Kα malignancies. BBOT has the goal of improving outcomes for patients with cancers driven by the two most prevalent oncogenes in human tumors. For more information, please visit www.bbotx.com and follow us on LinkedIn.
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