1. BBO-10203 inhibits RAS-PI3Kα signaling without hyperglycemia risks. 2. Strong anti-tumor activity shown in PIK3CA breast cancer models. 3. Initial Phase 1 data for BREAKER-101 expected in H1 2026. 4. BBO-10203 offers a differentiated mechanism compared to previous inhibitors. 5. Combination therapies could enhance treatment responses for patients.
FAQ
Why Bullish?
BBO-10203's promising preclinical results can drive investor interest, similar to successful biotech launches.
How important is it?
Preclinical data indicates potential breakthroughs, positioning BBOT competitively in oncology markets.
Why Long Term?
Initial clinical data in 2026 may set momentum for longer-term growth and partnerships.
BBOT Unveils Late-Breaking Preclinical Data on BBO-10203 at SABCS
BridgeBio Oncology Therapeutics, Inc. (Nasdaq: BBOT), a clinical-stage biopharmaceutical company focusing on RAS-pathway malignancies, has announced significant preclinical findings on its innovative treatment BBO-10203. The new data, which reveals how BBO-10203 effectively blocks RAS-mediated activation of PI3Kα without inducing hyperglycemia, was presented at the San Antonio Breast Cancer Symposium (SABCS) on December 10, 2025. This breakthrough underscores the potential of BBO-10203 as a first-in-class covalent small molecule RAS:PI3Kα breaker.
Understanding BBO-10203's Mechanism and Efficacy
BBO-10203 demonstrates a unique mechanism that selectively inhibits the interaction between RAS and PI3Kα, thereby disrupting RAS-mediated PI3Kα-AKT signaling. This has shown to result in robust anti-tumor activity in both monotherapy and combination treatments for various breast cancer models, including those with mutant or wild-type PIK3CA.
“Although current PI3Kα inhibitors have had limited success due to side effects like hyperglycemia, BBO-10203 presents a differentiated approach,” stated Pedro Beltran, PhD, Chief Scientific Officer of BBOT. “By blocking the interaction rather than inhibiting kinase activity, we can achieve tumor growth suppression without the risks associated with glucose regulation.”
Key Findings from Preclinical Trials
- BBO-10203 binds covalently to PI3Kα at cysteine 242, obstructing its interaction with RAS.
- Orally administered BBO-10203 displays dose-dependent inhibition of pAKT, confirming its efficacy.
- The treatment does not induce hyperglycemia or hyperinsulinemia during oral glucose tolerance tests.
- It shows promising activity both alone and in combination with standard treatments like fulvestrant and ribociclib in ER+ HER2- breast cancer models.
Upcoming Clinical Trials: BREAKER-101
In addition to the impactful preclinical data, BBOT will present a trial-in-progress poster for BREAKER-101, a Phase 1 clinical trial aimed at evaluating BBO-10203 in patients with locally advanced or metastatic HER2+ breast cancer, HR+/HER2- breast cancer, and KRAS mutant cancers. This study seeks to assess the drug's safety, tolerability, and preliminary anti-tumor activity, with initial data expected in the first half of 2026.
“We anticipate that BBO-10203 could significantly enhance treatment options for patients, especially those with limited responses to existing therapies,” noted Andreas Varkaris, MD, PhD, an investigator in the BREAKER-101 trial.
About BridgeBio Oncology
BBOT is committed to developing next-generation small molecule therapeutics targeting vital oncogenes like RAS and PI3Kα. Their goal is to improve treatment outcomes for patients afflicted with some of the most prevalent cancers.
For further details on BBO-10203 and ongoing research, visit www.bbotx.com or follow BBOT on LinkedIn.