Publications

Explore the Evidence

Publications & Presentations

BBO-10203 inhibits tumor growth without inducing hyperglycemia by blocking RAS-PI3Kα interaction

June 12, 2025/in 2025, BBO-10203, Publications/by eallison

June 2025 • Science

BBO-11818, an orally bioavailable, highly potent and non-covalent pan-KRAS inhibitor demonstrates robust anti-tumor activity in KRAS-mutant preclinical models

May 16, 2025/in 2025, BBO-11818, Publications/by eallison

April 2025 • AACR 2025

BBO-8520, a first-in-class direct dual inhibitor of GTP-bound (ON) and GDP-bound (OFF) KRAS^G12C, exhibits robust efficacy in non-small cell lung cancer preclinical models

May 16, 2025/in 2025, BBO-8520, Publications/by eallison

April 2025 • AACR 2025

Beyond First-Generation KRAS Inhibitors: BBO-8520 Tests the Dual Mechanism Hypothesis

March 11, 2025/in 2025, BBO-8520, Publications/by Jake Robison

March 2025 • AACR Cancer Discovery

BBO-10203, a first-in-class, orally bioavailable, selective blocker of the PI3Kα:RAS interaction inhibits tumor growth alone and in combination with standard of care therapies in breast cancer models without inducing hyperglycemia

December 16, 2024/in 2024, BBO-10203, Publications/by eallison

December 2024 • San Antonio Breast Cancer Symposium

Discovery of BBO-8520, a first-in-class direct and covalent dual inhibitor of GTP-bound (ON) and GDP-bound (OFF) KRAS^G12C

December 9, 2024/in 2024, BBO-8520, Publications/by Jake Robison

December 2024 • AACR Cancer Discovery

BBO-10203, an orally bioavailable small molecule that disrupts the RAS:PI3Kα interaction leading to pAKT and tumor growth inhibition in models of breast, lung and colorectal cancer

October 28, 2024/in 2024, BBO-10203, Publications/by Robert Conor

October 2024 • EORTC-NCI-AACR Symposium on Molecular Targets and Cancer Therapeutics

BBO-11818, an orally bioavailable, highly potent and non covalent pan-KRAS inhibitor demonstrates robust anti-tumor activity in KRAS^G12D and KRAS^G12V preclinical models

October 28, 2024/in 2024, BBO-11818, Publications/by Robert Conor

October 2024 • The Fifth RAS Initiative Symposium

BBO-10203, a first-in-class breaker of the PI3Kα:RAS interaction, demonstrates in vitro and in vivo efficacy alone or in combination with standard-of-care therapies in solid tumor models

October 28, 2024/in 2024, BBO-10203, Publications/by Robert Conor

October 2024 • The Fifth RAS Initiative Symposium

BBO-8520, a first-in-class, direct, and covalent small molecule inhibitor of GTP-bound (ON) and GDP-bound (OFF) KRAS^G12C, demonstrates robust efficacy and compares favorably to GDP-bound KRAS^G12C (OFF) only inhibitors in preclinical models

October 24, 2024/in 2024, BBO-8520, Publications/by Robert Conor

October 2024 • The Fifth RAS Initiative Symposium

BBO-8520, a First-in-Class, Direct Inhibitor of KRAS^G12C (ON), Locks GTP-Bound KRAS^G12C in the State 1 Conformation Resulting in Rapid and Complete Blockade of Effector Binding

August 11, 2024/in 2024, BBO-8520, Publications/by eallison

April 2024 • AACR 2024

Revealing the Mechanism of Action of a First-in-Class Covalent Inhibitor of KRAS^G12C (ON) and Other Functional Properties of Oncogenic KRAS by ³¹P NMR

August 11, 2024/in 2024, Publications/by eallison

January 2024 • Journal of Biological Chemistry

Targeting RAS-Driven PI3Kα Activation in Human Tumors

August 11, 2024/in 2023, Publications/by eallison

December 2023 • SABCS 2023

Use of the Natural Nucleotide, GTP, is Essential for the Identification of Potent, Active-State KRAS^G12C Inhibitors That Bind in the Switch II Pocket

August 11, 2024/in 2023, Publications/by eallison

October 2023 • AACR-NCI-EORTC 2023

Targeting RAS-Driven PI3Kα Activation in Human Tumors

August 11, 2024/in 2023, Publications/by eallison

September 2023 • Targeting RAS Symposium 2023

BBO-8520, a First-in-Class, Direct Inhibitor of KRAS^G12C (ON)

August 11, 2024/in 2023, BBO-8520, Publications/by eallison

September 2023 • Hanson Wade RAS-Targeted Drug Development Summit

June 2025 • Science

BBO-10203 inhibits tumor growth without inducing hyperglycemia by blocking RAS-PI3Kα interaction

April 2025 • AACR 2025

BBO-11818, an orally bioavailable, highly potent and non-covalent pan-KRAS inhibitor demonstrates robust anti-tumor activity in KRAS-mutant preclinical models

April 2025 • AACR 2025

BBO-8520, a first-in-class direct dual inhibitor of GTP-bound (ON) and GDP-bound (OFF) KRAS^G12C, exhibits robust efficacy in non-small cell lung cancer preclinical models

March 2025 • AACR Cancer Discovery

Beyond First-Generation KRAS Inhibitors: BBO-8520 Tests the Dual Mechanism Hypothesis

December 2024 • San Antonio Breast Cancer Symposium

BBO-10203, a first-in-class, orally bioavailable, selective blocker of the PI3Kα:RAS interaction inhibits tumor growth alone and in combination with standard of care therapies in breast cancer models without inducing hyperglycemia

December 2024 • AACR Cancer Discovery

Discovery of BBO-8520, a first-in-class direct and covalent dual inhibitor of GTP-bound (ON) and GDP-bound (OFF) KRAS^G12C

October 2024 • EORTC-NCI-AACR Symposium on Molecular Targets and Cancer Therapeutics

BBO-10203, an orally bioavailable small molecule that disrupts the RAS:PI3Kα interaction leading to pAKT and tumor growth inhibition in models of breast, lung and colorectal cancer

October 2024 • The Fifth RAS Initiative Symposium

BBO-11818, an orally bioavailable, highly potent and non covalent pan-KRAS inhibitor demonstrates robust anti-tumor activity in KRAS^G12D and KRAS^G12V preclinical models

October 2024 • The Fifth RAS Initiative Symposium

BBO-10203, a first-in-class breaker of the PI3Kα:RAS interaction, demonstrates in vitro and in vivo efficacy alone or in combination with standard-of-care therapies in solid tumor models

October 2024 • The Fifth RAS Initiative Symposium

BBO-8520, a first-in-class, direct, and covalent small molecule inhibitor of GTP-bound (ON) and GDP-bound (OFF) KRAS^G12C, demonstrates robust efficacy and compares favorably to GDP-bound KRAS^G12C (OFF) only inhibitors in preclinical models

April 2024 • AACR 2024

BBO-8520, a First-in-Class, Direct Inhibitor of KRAS^G12C (ON), Locks GTP-Bound KRAS^G12C in the State 1 Conformation Resulting in Rapid and Complete Blockade of Effector Binding

January 2024 • Journal of Biological Chemistry

Revealing the Mechanism of Action of a First-in-Class Covalent Inhibitor of KRAS^G12C (ON) and Other Functional Properties of Oncogenic KRAS by ³¹P NMR

December 2023 • SABCS 2023

Targeting RAS-Driven PI3Kα Activation in Human Tumors

October 2023 • AACR-NCI-EORTC 2023

Use of the Natural Nucleotide, GTP, is Essential for the Identification of Potent, Active-State KRAS^G12C Inhibitors That Bind in the Switch II Pocket

September 2023 • Targeting RAS Symposium 2023

Targeting RAS-Driven PI3Kα Activation in Human Tumors

September 2023 • Hanson Wade RAS-Targeted Drug Development Summit

BBO-8520, a First-in-Class, Direct Inhibitor of KRAS^G12C (ON)

Publications

Publications & Presentations

BBO-10203 inhibits tumor growth without inducing hyperglycemia by blocking RAS-PI3Kα interaction

BBO-11818, an orally bioavailable, highly potent and non-covalent pan-KRAS inhibitor demonstrates robust anti-tumor activity in KRAS-mutant preclinical models

BBO-8520, a first-in-class direct dual inhibitor of GTP-bound (ON) and GDP-bound (OFF) KRAS^G12C, exhibits robust efficacy in non-small cell lung cancer preclinical models

Beyond First-Generation KRAS Inhibitors: BBO-8520 Tests the Dual Mechanism Hypothesis

BBO-10203, a first-in-class, orally bioavailable, selective blocker of the PI3Kα:RAS interaction inhibits tumor growth alone and in combination with standard of care therapies in breast cancer models without inducing hyperglycemia

Discovery of BBO-8520, a first-in-class direct and covalent dual inhibitor of GTP-bound (ON) and GDP-bound (OFF) KRAS^G12C

BBO-10203, an orally bioavailable small molecule that disrupts the RAS:PI3Kα interaction leading to pAKT and tumor growth inhibition in models of breast, lung and colorectal cancer

BBO-11818, an orally bioavailable, highly potent and non covalent pan-KRAS inhibitor demonstrates robust anti-tumor activity in KRAS^G12D and KRAS^G12V preclinical models

BBO-10203, a first-in-class breaker of the PI3Kα:RAS interaction, demonstrates in vitro and in vivo efficacy alone or in combination with standard-of-care therapies in solid tumor models

BBO-8520, a first-in-class, direct, and covalent small molecule inhibitor of GTP-bound (ON) and GDP-bound (OFF) KRAS^G12C, demonstrates robust efficacy and compares favorably to GDP-bound KRAS^G12C (OFF) only inhibitors in preclinical models

BBO-8520, a First-in-Class, Direct Inhibitor of KRAS^G12C (ON), Locks GTP-Bound KRAS^G12C in the State 1 Conformation Resulting in Rapid and Complete Blockade of Effector Binding

Revealing the Mechanism of Action of a First-in-Class Covalent Inhibitor of KRAS^G12C (ON) and Other Functional Properties of Oncogenic KRAS by ³¹P NMR

Targeting RAS-Driven PI3Kα Activation in Human Tumors

Use of the Natural Nucleotide, GTP, is Essential for the Identification of Potent, Active-State KRAS^G12C Inhibitors That Bind in the Switch II Pocket

Targeting RAS-Driven PI3Kα Activation in Human Tumors

BBO-8520, a First-in-Class, Direct Inhibitor of KRAS^G12C (ON)

Year:

Program:

BBO-10203 inhibits tumor growth without inducing hyperglycemia by blocking RAS-PI3Kα interaction

BBO-11818, an orally bioavailable, highly potent and non-covalent pan-KRAS inhibitor demonstrates robust anti-tumor activity in KRAS-mutant preclinical models

BBO-8520, a first-in-class direct dual inhibitor of GTP-bound (ON) and GDP-bound (OFF) KRAS^G12C, exhibits robust efficacy in non-small cell lung cancer preclinical models

Beyond First-Generation KRAS Inhibitors: BBO-8520 Tests the Dual Mechanism Hypothesis

BBO-10203, a first-in-class, orally bioavailable, selective blocker of the PI3Kα:RAS interaction inhibits tumor growth alone and in combination with standard of care therapies in breast cancer models without inducing hyperglycemia

Discovery of BBO-8520, a first-in-class direct and covalent dual inhibitor of GTP-bound (ON) and GDP-bound (OFF) KRAS^G12C

BBO-10203, an orally bioavailable small molecule that disrupts the RAS:PI3Kα interaction leading to pAKT and tumor growth inhibition in models of breast, lung and colorectal cancer

BBO-11818, an orally bioavailable, highly potent and non covalent pan-KRAS inhibitor demonstrates robust anti-tumor activity in KRAS^G12D and KRAS^G12V preclinical models

BBO-10203, a first-in-class breaker of the PI3Kα:RAS interaction, demonstrates in vitro and in vivo efficacy alone or in combination with standard-of-care therapies in solid tumor models

BBO-8520, a first-in-class, direct, and covalent small molecule inhibitor of GTP-bound (ON) and GDP-bound (OFF) KRAS^G12C, demonstrates robust efficacy and compares favorably to GDP-bound KRAS^G12C (OFF) only inhibitors in preclinical models

BBO-8520, a First-in-Class, Direct Inhibitor of KRAS^G12C (ON), Locks GTP-Bound KRAS^G12C in the State 1 Conformation Resulting in Rapid and Complete Blockade of Effector Binding

Revealing the Mechanism of Action of a First-in-Class Covalent Inhibitor of KRAS^G12C (ON) and Other Functional Properties of Oncogenic KRAS by ³¹P NMR

Targeting RAS-Driven PI3Kα Activation in Human Tumors

Use of the Natural Nucleotide, GTP, is Essential for the Identification of Potent, Active-State KRAS^G12C Inhibitors That Bind in the Switch II Pocket

Targeting RAS-Driven PI3Kα Activation in Human Tumors

BBO-8520, a First-in-Class, Direct Inhibitor of KRAS^G12C (ON)

Publications

Publications & Presentations

Year:

Program:

BBO-10203 inhibits tumor growth without inducing hyperglycemia by blocking RAS-PI3Kα interaction

BBO-11818, an orally bioavailable, highly potent and non-covalent pan-KRAS inhibitor demonstrates robust anti-tumor activity in KRAS-mutant preclinical models

BBO-8520, a first-in-class direct dual inhibitor of GTP-bound (ON) and GDP-bound (OFF) KRASG12C, exhibits robust efficacy in non-small cell lung cancer preclinical models

Beyond First-Generation KRAS Inhibitors: BBO-8520 Tests the Dual Mechanism Hypothesis

BBO-10203, a first-in-class, orally bioavailable, selective blocker of the PI3Kα:RAS interaction inhibits tumor growth alone and in combination with standard of care therapies in breast cancer models without inducing hyperglycemia

Discovery of BBO-8520, a first-in-class direct and covalent dual inhibitor of GTP-bound (ON) and GDP-bound (OFF) KRASG12C

BBO-10203, an orally bioavailable small molecule that disrupts the RAS:PI3Kα interaction leading to pAKT and tumor growth inhibition in models of breast, lung and colorectal cancer

BBO-11818, an orally bioavailable, highly potent and non covalent pan-KRAS inhibitor demonstrates robust anti-tumor activity in KRASG12D and KRASG12V preclinical models

BBO-10203, a first-in-class breaker of the PI3Kα:RAS interaction, demonstrates in vitro and in vivo efficacy alone or in combination with standard-of-care therapies in solid tumor models

BBO-8520, a first-in-class, direct, and covalent small molecule inhibitor of GTP-bound (ON) and GDP-bound (OFF) KRASG12C, demonstrates robust efficacy and compares favorably to GDP-bound KRASG12C (OFF) only inhibitors in preclinical models

BBO-8520, a First-in-Class, Direct Inhibitor of KRASG12C (ON), Locks GTP-Bound KRASG12C in the State 1 Conformation Resulting in Rapid and Complete Blockade of Effector Binding

Revealing the Mechanism of Action of a First-in-Class Covalent Inhibitor of KRASG12C (ON) and Other Functional Properties of Oncogenic KRAS by 31P NMR

Targeting RAS-Driven PI3Kα Activation in Human Tumors

Use of the Natural Nucleotide, GTP, is Essential for the Identification of Potent, Active-State KRASG12C Inhibitors That Bind in the Switch II Pocket

Targeting RAS-Driven PI3Kα Activation in Human Tumors

BBO-8520, a First-in-Class, Direct Inhibitor of KRASG12C (ON)

BBO-8520, a first-in-class direct dual inhibitor of GTP-bound (ON) and GDP-bound (OFF) KRAS^G12C, exhibits robust efficacy in non-small cell lung cancer preclinical models

Discovery of BBO-8520, a first-in-class direct and covalent dual inhibitor of GTP-bound (ON) and GDP-bound (OFF) KRAS^G12C

BBO-11818, an orally bioavailable, highly potent and non covalent pan-KRAS inhibitor demonstrates robust anti-tumor activity in KRAS^G12D and KRAS^G12V preclinical models

BBO-8520, a first-in-class, direct, and covalent small molecule inhibitor of GTP-bound (ON) and GDP-bound (OFF) KRAS^G12C, demonstrates robust efficacy and compares favorably to GDP-bound KRAS^G12C (OFF) only inhibitors in preclinical models

BBO-8520, a First-in-Class, Direct Inhibitor of KRAS^G12C (ON), Locks GTP-Bound KRAS^G12C in the State 1 Conformation Resulting in Rapid and Complete Blockade of Effector Binding

Revealing the Mechanism of Action of a First-in-Class Covalent Inhibitor of KRAS^G12C (ON) and Other Functional Properties of Oncogenic KRAS by ³¹P NMR

Use of the Natural Nucleotide, GTP, is Essential for the Identification of Potent, Active-State KRAS^G12C Inhibitors That Bind in the Switch II Pocket

BBO-8520, a First-in-Class, Direct Inhibitor of KRAS^G12C (ON)