As it is not clear whether the GDP-bound inactive-state selective trapping mechanism afforded by covalent G12C inhibitors will work against non-G12C KRAS mutants, the covalent warhead was removed from a G12C inhibitor prototype, and further optimized to develop into BI-2865, a non-covalent pan-KRAS inhibitor that was able to dampen tumor growth in multiple KRAS mutation carrying cell lines with similar potency to sotorasib [102]. Here, KRAS is linked to neoplasm.