Genentech Oncology
This compound and its uses are investigational and have not been approved by the US Food and Drug Administration. Efficacy and safety have not been established. The information presented should be not construed as a recommendation for use. The relevance of findings in preclinical studies to humans is currently being evaluated.
Divarasib is an orally available small molecule, and in preclinical models showed potent and selective inhibition of the KRAS G12C protein.1
By locking the mutant KRAS G12C into its inactive GDP-bound state, divarasib turns off oncogenic signaling in preclinical models.
Divarasib is designed to selectively bind to the switch II pocket of KRAS G12C protein through a specific interaction with the cysteine residue at position 12, and irreversibly lock it in the inactive GDP-bound state.1
In preclinical models, the combination of KRAS G12C inhibitors with other agents demonstrated synergistic anti-tumor activity.2,3
Purkey H. ND11 - discovery of GDC-6036, a clinical stage treatment for KRAS G12C-positive cancers. Abstract presented at: Proceedings of the 113th Annual Meeting of the American Association for Cancer Research; April 8-13, 2022; New Orleans, LA. Abstract nr ND11.
Purkey H. ND11 - discovery of GDC-6036, a clinical stage treatment for KRAS G12C-positive cancers. Abstract presented at: Proceedings of the 113th Annual Meeting of the American Association for Cancer Research; April 8-13, 2022; New Orleans, LA. Abstract nr ND11.
Huang L, Guo Z, Wang F, Fu L. KRAS mutation: from undruggable to druggable in cancer. Signal Transduct Target Ther. 2021;6(1):386. PMID: 34776511
Huang L, Guo Z, Wang F, Fu L. KRAS mutation: from undruggable to druggable in cancer. Signal Transduct Target Ther. 2021;6(1):386. PMID: 34776511
Williams B, Taylor A, Orozco O, et al. Discovery and characterization of the potent, allosteric SHP2 inhibitor GDC-1971 for the treatment of RTK/RAS driven tumors. Abstract presented at: Proceedings of the 113th Annual Meeting of the American Association for Cancer Research; April 8-13, 2022; New Orleans, LA. Abstract nr 3327.
Williams B, Taylor A, Orozco O, et al. Discovery and characterization of the potent, allosteric SHP2 inhibitor GDC-1971 for the treatment of RTK/RAS driven tumors. Abstract presented at: Proceedings of the 113th Annual Meeting of the American Association for Cancer Research; April 8-13, 2022; New Orleans, LA. Abstract nr 3327.
The compounds and their uses mentioned on this website are investigational and have not been approved by the US Food and Drug Administration. Efficacy and safety have not been established. The information presented should not be construed as a recommendation for use. Do you wish to proceed?
The link you have selected will take you away from this site to one that is not owned or controlled by Genentech, Inc. Genentech, Inc. makes no representation as to the accuracy of the information contained on sites we do not own or control. Genentech does not recommend and does not endorse the content on any third-party websites. Your use of third-party websites is at your own risk and subject to the terms and conditions of use for such sites.