The Kras G12C mutation occurs in about 7.9 % of colon Cancer patients tumors. So granted this isn't perhaps a great therapeutic discovery for colon cancer. However it seems that a good (150nM IC50) inhibitor - ARS-1620 is an atropisomeric one selective for KRASG12C a mutant form of the guanosine triphosphatase (GTPase) KRAS. Seems it may have some synergy with EGFr FGFr and other inhibitors.
See: https://stke.sciencemag.org/content/12/ ... id=2836996
From the abstract I think this was probably a cellular assay and not a mouse or clinical model at this time but it seems to indicate that at least this mutation could be targeted with ARS-1620 and an EGFr Inhibitor or FGFR inhibitor to overcome the tendency of KRAS Mutations not being sensitive to these reagents. The study was done with Pancreatic and Lung Cancer cell lines mostly. Also note this targets only the mutant form which is good such that it doesn't effect the wild type and may be much less prone to systemic side effects on normal tissues!
Other work I have recently read about seems to indicate a similar small molecule synthesis approach to creating inhibitors for KRas G12D which is much more prevalent in Colon Cancers (34%) might also be able to follow a similar type of Therapeutic method as developed for this G12C mutation.
Regards,
GrouseMan