The third KRAS inhibitory compound tested here, BI-2852, that acts as a pan-KRAS inhibitor for the switch I/II pocket, showed moderate reduction of clonogenicity in KRAS G12C mutant MiaPaCa cells with additive reduction upon combined irradiation (Figure 4a,b), but there was no tangible efficacy in the KRAS G12D mutant Panc-1 or KRAS wt BxPC3 cells, respectively, suggesting this compound is a less promising drug candidate for pancreatic cancer therapy at least in this specific experimental setup applied here (Figure 4c–f). Here, KRAS is linked to familial pancreatic carcinoma.