Figure 5.

Strategies to target KRAS mutations. Several therapies have been developed to target KRAS, namely, KRAS plasma membrane association inhibitors, KRAS synthetic lethal interactors, KRAS downstream signaling pathways blockade, KRAS-mediated inflammation, and immunotherapy. One of the most promising strategies is the novel KRAS synthetic lethal interactors that specifically target the cysteine in the mutated KRAS^G12C through covalent irreversible binding and favor KRAS-GDP state over GTP. These alterations impair RAF binding and the activation of the signaling pathway, decreasing cell viability and increasing apoptosis of those cells harboring KRAS^G12C mutations.