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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

Rhea-AI Impact
(High)
Rhea-AI Sentiment
(Positive)
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BridgeBio Oncology Therapeutics (Nasdaq: BBOT) presented preclinical data on BBO-11818 at AACR 2026 showing an orally bioavailable, non-covalent pan-KRAS inhibitor that targets mutant KRAS in both ON (GTP-bound) and OFF (GDP-bound) states. The poster reports potent MAPK/ERK suppression, anti-proliferative activity, monotherapy tumor regressions, and enhanced efficacy in combinations across KRASG12D and KRASG12V models. Combination partners included BBO-10203, cetuximab, and anti-PD-1; complete regressions and an adaptive immune response were reported in the CT26 syngeneic model. Updated Phase 1 clinical data are expected in the second half of 2026.

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AI-generated analysis. Not financial advice.

Positive

  • BBO-11818 targets KRAS in both ON and OFF states
  • Potent suppression of ERK phosphorylation in vitro
  • Robust efficacy in KRASG12D and KRASG12V CDX models
  • Combination benefit with BBO-10203, cetuximab, and anti-PD-1
  • Complete tumor regressions and adaptive immune response in CT26 model

Negative

  • Data are preclinical; no human efficacy demonstrated yet
  • Updated Phase 1 clinical data not available until H2 2026

News Market Reaction – BBOT

+1.13%
18 alerts
+1.13% News Effect
+4.8% Peak Tracked
-5.7% Trough Tracked
+$8M Valuation Impact
$726.55M Market Cap
0.5x Rel. Volume

On the day this news was published, BBOT gained 1.13%, reflecting a mild positive market reaction. Argus tracked a peak move of +4.8% during that session. Argus tracked a trough of -5.7% from its starting point during tracking. Our momentum scanner triggered 18 alerts that day, indicating notable trading interest and price volatility. This price movement added approximately $8M to the company's valuation, bringing the market cap to $726.55M at that time.

Data tracked by StockTitan Argus on the day of publication.

Market Reality Check

Price: $8.37 Vol: Volume 373,405 is slightl...
normal vol
$8.37 Last Close
Volume Volume 373,405 is slightly below the 20-day average of 406,337 (relative volume 0.92). normal
Technical Shares trade below the 200-day MA of 11.02 with the current price at 9.46, about 36.38% under the 52-week high.

Peers on Argus

BBOT is down 4.6% while several biotech peers also show modest declines (e.g., A...

BBOT is down 4.6% while several biotech peers also show modest declines (e.g., AVXL, GERN, IMNM, PRAX), but one peer (IVA) is up, and no peers appear on the momentum scanner. This mix indicates stock-specific trading rather than a coordinated sector move.

Historical Context

5 past events · Latest: Apr 22 (Neutral)
Pattern 5 events
Date Event Sentiment Move Catalyst
Apr 22 Leadership changes Neutral -4.6% New CEO, COO, and Executive Chairman appointments effective April 20, 2026.
Apr 21 Preclinical data Positive -4.6% AACR data showing BBO-10203 inhibits PI3Kα/AKT signaling with tumor regressions.
Apr 20 Regulatory designation Positive +2.2% U.S. FDA Fast Track designation for BBO-11818 in KRAS-mutant pancreatic cancer.
Apr 13 Equity inducement grant Neutral +2.6% Inducement stock options for 32,675 shares at $8.40 to a new hire.
Mar 18 Conference preview Positive +1.9% Announcement of multiple AACR 2026 presentations for BBO-10203 and BBO-11818.
Pattern Detected

Recent BBOT news often elicits modest moves, with several positive or neutral RAS-pathway updates and corporate actions showing mixed alignment between news tone and price reaction, including multiple divergences on scientific or governance items.

Recent Company History

Over the past months, BBOT has highlighted progress across its RAS-pathway pipeline and corporate structure. In March 2026, it flagged multiple AACR 2026 presentations (BBO-10203 and BBO-11818) and later reported Fast Track designation for BBO-11818 on April 20, 2026, which aligned with a positive price move. Inducement grants and governance updates, including leadership changes effective April 20, 2026, have produced mixed share reactions. Today’s AACR preclinical data for BBO-11818 fit this ongoing cadence of RAS-focused scientific updates.

Market Pulse Summary

This announcement details robust preclinical activity for BBO-11818, a dual ON/OFF pan-KRAS inhibito...
Analysis

This announcement details robust preclinical activity for BBO-11818, a dual ON/OFF pan-KRAS inhibitor, including combination benefits across KRAS-mutant models. It follows prior Fast Track designation and early clinical signals for the same program, reinforcing BBOT’s RAS-pathway focus. Investors may track how these data translate into updated Phase 1 results expected in the second half of 2026, along with future regulatory interactions and combination strategies across pancreatic, lung, and colorectal cancers.

Key Terms

pan-kras, kras, gtp-bound, mapk signaling, +3 more
7 terms
pan-kras medical
"an orally bioavailable, highly potent and selective non-covalent pan-KRAS (ON) and (OFF) inhibitor"
Pan-KRAS describes a drug or therapeutic approach designed to work against many different mutations of the KRAS gene rather than a single specific variant. For investors, a pan-KRAS treatment is important because it can address a larger group of patients—like a universal key that fits many locks—potentially increasing the market opportunity and clinical value, while also carrying development and regulatory risks tied to demonstrating safety and broad effectiveness.
kras medical
"BBO-11818 targets KRAS in both its ON (active GTP-bound) and OFF (inactive GDP-bound) states"
KRAS is a gene that makes a protein acting like a switch to control cell growth; certain changes (mutations) can lock that switch on and drive uncontrolled cell multiplication, which is a common cause of many cancers. Investors care because drugs or tests targeting KRAS mutations can create large markets or avoidable risks depending on trial results and regulatory decisions, much like a key product feature deciding a gadget’s commercial success.
gtp-bound medical
"ON (active GTP-bound) and OFF (inactive GDP-bound) states"
GTP-bound describes a protein that has the small molecule GTP attached, which usually switches that protein into its active or “on” state. For investors, seeing that a drug or diagnostic influences the GTP-bound state is important because it provides a direct readout of whether a treatment changes a key cellular switch tied to disease processes, much like checking whether a light turns on when you flip a circuit breaker.
mapk signaling medical
"potently suppressing MAPK signaling and inhibiting cell proliferation in KRAS-mutant cell lines"
MAPK signaling is a chain of molecular interactions inside cells that carries growth and stress messages from the cell surface to the nucleus, like a relay race that tells the cell to divide, adapt, or die. Investors care because drugs or tests that target this pathway can change how diseases like cancer or inflammatory disorders are treated, affecting the commercial value and regulatory risk of therapies and diagnostics tied to those mechanisms.
erk phosphorylation medical
"BBO-11818 potently inhibits ERK phosphorylation and proliferation in KRAS-dependent cell lines"
ERK phosphorylation is the chemical activation of the ERK enzyme, a protein that passes growth and survival signals inside cells by having a small chemical tag (a phosphate) attached. Investors care because changes in ERK phosphorylation are commonly used as a measurable sign that a drug or biological effect is hitting its target or altering cell behavior—like a circuit breaker flipping on—which can indicate potential efficacy, safety issues, or a useful biomarker for trials.
cdx models medical
"robust efficacy in KRASG12D and KRASG12V CDX models."
CDx models are laboratory tests or computer algorithms designed to identify which patients are likely to benefit from a particular drug or therapy, effectively pairing a treatment with the right people. For investors, they matter because regulatory approval, clinical uptake, and pricing of a therapy can depend on a reliable companion test—think of the test as a key that lets the right patients access a drug, which can shrink risk and shape the size and timing of future revenue.
pdx models medical
"combination effect with BBO-10203, a RAS:PI3K⍺ breaker, and cetuximab in KRAS-mutant CDX and PDX models."
PDX models are preclinical research tools created by implanting a small sample of a patient’s tumor into a lab animal, usually a mouse, so scientists can watch how the human cancer responds to treatments in a living system. For investors, PDX data matter because they can make a drug’s early testing more realistic than cell dishes alone—like taking a prototype car on a similar road before full production—helping to gauge clinical promise and reduce development risk.

AI-generated analysis. Not financial advice.

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.

Forward-Looking Statements 
This press release contains forward-looking statements within the meaning of the U.S. Private Securities Litigation Reform Act of 1995, as amended, and other federal securities laws. Any statements in this press release that are not historical facts may be deemed forward-looking statements,  which generally are accompanied by words such as “believe,” “may,” “will,” “estimate,” “continue,” “anticipate,” “intend,” “expect,” “should,” “would,” “plan,” “predict,” “potential,” “seem,” “seek,” “future,” “outlook” and similar expressions that predict or indicate future events or trends. These statements are based on various assumptions, whether or not identified in this press release, and are the current expectations of BBOT’s management and are not predictions of actual performance. Many actual events and circumstances are beyond the control of BBOT. These forward-looking statements are subject to a number of risks and uncertainties, including changes in domestic and foreign business, market, financial, political, and legal conditions; risks related to the timing of expected regulatory and business milestones, including the progress of enrollment in clinical trials and availability of data from ongoing and planned clinical trials; and those factors discussed in documents BBOT has filed or will file with the U.S. Securities and Exchange Commission. 
  
In addition, forward-looking statements reflect BBOT’s expectations, plans, or forecasts of future events and views as of the date of this press release and are qualified in their entirety by reference to the cautionary statements herein. BBOT anticipates that subsequent events and developments will cause BBOT’s assessments to change. These forward-looking statements should not be relied upon as any guarantee, assurance, prediction or definitive statement of fact or probability or as representing BBOT’s assessments as of any date subsequent to the date of this press release. Neither BBOT, nor any of its affiliates undertake any obligation to update these forward-looking statements, except as required by law. 

BBOT Contacts:

Investor Contact:
Heather Armstrong, Head of Investor Relations
BBOT
Investors@BBOTx.com

Media Contact:
Jake Robison
Inizio Evoke Comms
Jake.robison@inizioevoke.com


FAQ

What is BBO-11818 and what does it target (BBOT)?

BBO-11818 is an orally bioavailable, non-covalent pan-KRAS inhibitor that targets mutant KRAS in both ON and OFF states. According to BridgeBio Oncology Therapeutics, it potently suppresses MAPK/ERK signaling and inhibits proliferation in KRAS-mutant cell lines.

Which KRAS mutations did BBO-11818 show efficacy against in preclinical models?

BBO-11818 demonstrated robust efficacy in models bearing KRASG12D and KRASG12V mutations. According to BridgeBio Oncology Therapeutics, efficacy was observed in CDX and PDX tumor models across pancreatic, lung, and colorectal cancer types.

How did BBO-11818 perform in combination therapy preclinical studies (BBOT)?

BBO-11818 enhanced anti-tumor activity when combined with BBO-10203, cetuximab, and anti-PD-1 in preclinical models. According to BridgeBio Oncology Therapeutics, combinations produced greater regressions and immune effects than monotherapy in several KRAS-mutant models.

Did BBO-11818 produce immune responses in any preclinical model?

Yes, BBO-11818 plus anti-PD-1 induced complete tumor regressions and an adaptive immune response in the CT26 syngeneic model. According to BridgeBio Oncology Therapeutics, this combination produced durable regressions in that immune-competent model.

When will BBOT provide updated clinical data for BBO-11818?

Updated Phase 1 clinical data for BBO-11818 are expected in the second half of 2026. According to BridgeBio Oncology Therapeutics, those interim updates will follow the presented preclinical AACR 2026 poster.