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Target Overview
KRAS is a small GTPase that functions as a molecular switch, cycling between GDP-bound and GTP-bound states to regulate downstream effector pathways controlling cellular proliferation and survival1.
KRAS is a major oncogenic driver and the most frequently mutated member of the RAS family in human cancers. Mutations in KRAS are particularly prevalent in pancreatic, colorectal and lung cancers, making it an important therapeutic target2.
A pan-KRAS inhibitor capable of targeting multiple oncogenic KRAS mutant variants could address a broad range of KRAS-driven tumours. Selectivity for KRAS over NRAS and HRAS may enhance the therapeutic window, support broader combination treatment strategies and expand the number of patients who could benefit from therapy3.
Compound Overview
JAB-23E73 is an allosteric pan-KRAS inhibitor designed to target both the GDP-bound “OFF” state and the GTP-bound “ON” state of KRAS. The compound inhibits multiple oncogenic KRAS mutations as well as wild type KRAS, while maintaining selectivity over NRAS and HRAS.4 It is currently being investigated as a potential treatment for KRAS-driven cancers.
Mechanism of Action
References
1. Simanshu DK, Nissley DV, McCormick F. RAS proteins and their regulators in human disease. Cell. 2017;170:17–33. 2.Prior IA , Hood FE , Hartley JL . The frequency of Ras mutations in cancer. Cancer Res 2020;80:2969–74. 3. Riedl JM et al. Emerging landscape of KRAS inhibitors in cancer treatment. Cancer Cell 2026; 44, 471-497 4. Wang P et al. Preclinical investigation of orally bioavailable, potent pan-KRAS (ON/OFF) inhibitor JAB-23E73 [abstract] In: Proceedings of the AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics; 2025 Oct 22-26; Boston, MA. Philadelphia (PA): AACR; Mol Cancer Ther 2025;24(10 Suppl):Abstract nr A068.
Target Overview
KRAS is a small GTPase that functions as a molecular switch, cycling between GDP-bound and GTP-bound states to regulate downstream effector pathways controlling cellular proliferation and survival1.
KRAS is a major oncogenic driver and the most frequently mutated member of the RAS family in human cancers. Mutations in KRAS are particularly prevalent in pancreatic, colorectal and lung cancers, making it an important therapeutic target2.
A pan-KRAS inhibitor capable of targeting multiple oncogenic KRAS mutant variants could address a broad range of KRAS-driven tumours. Selectivity for KRAS over NRAS and HRAS may enhance the therapeutic window, support broader combination treatment strategies and expand the number of patients who could benefit from therapy3.
Compound Overview
JAB-23E73 is an allosteric pan-KRAS inhibitor designed to target both the GDP-bound “OFF” state and the GTP-bound “ON” state of KRAS. The compound inhibits multiple oncogenic KRAS mutations as well as wild type KRAS, while maintaining selectivity over NRAS and HRAS.4 It is currently being investigated as a potential treatment for KRAS-driven cancers.
Mechanism of Action
References
1. Simanshu DK, Nissley DV, McCormick F. RAS proteins and their regulators in human disease. Cell. 2017;170:17–33. 2.Prior IA , Hood FE , Hartley JL . The frequency of Ras mutations in cancer. Cancer Res 2020;80:2969–74. 3. Riedl JM et al. Emerging landscape of KRAS inhibitors in cancer treatment. Cancer Cell 2026; 44, 471-497 4. Wang P et al. Preclinical investigation of orally bioavailable, potent pan-KRAS (ON/OFF) inhibitor JAB-23E73 [abstract] In: Proceedings of the AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics; 2025 Oct 22-26; Boston, MA. Philadelphia (PA): AACR; Mol Cancer Ther 2025;24(10 Suppl):Abstract nr A068.
Clinical trial information
Select trial for more information
NCT07640295 trial overview
NCT06973564 trial overview
NCT06959615 trial overview
Abbreviations
AEs
Adverse events
AUC
Area under the curve
Cmax
Maximum plasma concentration
CTCAE
Common Terminology Criteria for Adverse Events
Ctrough
Trough plasma concentration
CRC
Colorectal cancer
DCR
Disease control rate
DLT
Dose-limiting toxicity
DOR
Duration of response
ECOG PS
Eastern Cooperative Oncology Group performance status
KRAS
Kirsten rat sarcoma viral oncogene homolog
nab
Nanoparticle albumin-bound
NCT
National Clinical Trial
NSCLC
Non-small cell lung cancer
ORR
Objective response rate
OS
Overall survival
PDAC
Pancreatic ductal adenocarcinoma
PFS
Progression-free survival
PK
Pharmacokinetics
RP3D
Recommended Phase 3 dose
TTR
Time to response