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KRAS G12C

(RG6330)

Solid Tumor

Phase I

A Study to Evaluate the Safety, Pharmacokinetics, and Activity of GDC-6036 in Patients With Advanced or Metastatic Solid Tumors With a KRAS G12C Mutation

NCT04449874

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.

Designed to inhibit the KRAS G12C mutant protein and lock it in its inactive state

GDC-6036 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, GDC-6036 turns off oncogenic signaling in preclinical models.

GDC-6036 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

KRAS GDC-6036

In preclinical models, the combination of KRAS G12C inhibitors with other agents demonstrated synergistic anti-tumor activity.2,3

KRAS G12C inhibitors
    • 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.

      Huang L, Guo Z, Wang F, Fu L. KRAS mutation: from undruggable to druggable in cancer. Signal Transduct Target Ther. 2021;6(1):386.

    • 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.