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Target Overview
KRAS, a small GTPase, acts as a molecular switch, regulating cellular signaling, proliferation and survival. In its wild-type form, KRAS transitions between an inactive, GDP-bound state and an active, GTP-bound state in response to growth factor signaling at the cell membrane, such as RTK activation.1-4
KRAS is one of the most frequently mutated genes in cancer, with the KRASG12D mutation being the most common.1-4 This mutation is highly prevalent in pancreatic ductal adenocarcinoma (34%), colorectal cancer (12%), and non-small cell lung cancer (4%).2 KRASG12D mutations promote binding to GTP, resulting in constitutive pathway activation.1,4
KRASG12D is a well-established oncogenic driver and an important therapeutic target.1,4 KRASG12D inhibition has the potential to provide therapeutic benefit to patients with KRASG12D mutant cancer.
Compound Overview
AZD0022 is a potent KRASG12D-selective oral small molecule inhibitor that is being evaluated in advanced solid tumors (Colorectal, Pancreatic Ductal Adenocarcinoma and Non-Small Cell Lung cancers) harboring a KRASG12D mutation.
Mechanism of Action
References
1. Isermann T, Sers C, Der CJ, Papke B. Trends Cancer. 2025;11(2):91-116. 2. Li S, Balmain A, Counter CM. Nat Rev Cancer. 2018;18(12):767-777. 3. Prior IA, Hood FE, Hartley JL. Cancer Res. 2020;80(14):2969-2974. 4. Singhal A, Li BT, O'Reilly EM. Nat Med. 2024;30(4):969-983.
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Abbreviations
GDP
guanosine diphosphate
GTP
guanosine triphosphate
GTPase
guanosine triphosphatase
KRAS
Kirsten rat sarcoma viral oncogene homolog
NSCLC
non-small cell lung cancer
RTK
receptor tyrosine kinase
Target Overview
KRAS, a small GTPase, acts as a molecular switch, regulating cellular signaling, proliferation and survival. In its wild-type form, KRAS transitions between an inactive, GDP-bound state and an active, GTP-bound state in response to growth factor signaling at the cell membrane, such as RTK activation.1-4
KRAS is one of the most frequently mutated genes in cancer, with the KRASG12D mutation being the most common.1-4 This mutation is highly prevalent in pancreatic ductal adenocarcinoma (34%), colorectal cancer (12%), and non-small cell lung cancer (4%).2 KRASG12D mutations promote binding to GTP, resulting in constitutive pathway activation.1,4
KRASG12D is a well-established oncogenic driver and an important therapeutic target.1,4 KRASG12D inhibition has the potential to provide therapeutic benefit to patients with KRASG12D mutant cancer.
Compound Overview
AZD0022 is a potent KRASG12D-selective oral small molecule inhibitor that is being evaluated in advanced solid tumors (Colorectal, Pancreatic Ductal Adenocarcinoma and Non-Small Cell Lung cancers) harboring a KRASG12D mutation.
Mechanism of Action
References
1. Isermann T, Sers C, Der CJ, Papke B. Trends Cancer. 2025;11(2):91-116. 2. Li S, Balmain A, Counter CM. Nat Rev Cancer. 2018;18(12):767-777. 3. Prior IA, Hood FE, Hartley JL. Cancer Res. 2020;80(14):2969-2974. 4. Singhal A, Li BT, O'Reilly EM. Nat Med. 2024;30(4):969-983.
Abbreviations
GDP
guanosine diphosphate
GTP
guanosine triphosphate
GTPase
guanosine triphosphatase
KRAS
Kirsten rat sarcoma viral oncogene homolog
NSCLC
non-small cell lung cancer
RTK
receptor tyrosine kinase