The KRAS G12D mutation is extremely frequent in lots of cancers, for example pancreatic, colon and lung, and it has continued to be undruggable within the last 30 years, because of its fine surface and insufficient appropriate pockets. Recent small bits of evidence claim that individuals switch I/II of KRAS G12D mutant happens to be an efficient strategy. Therefore, in our study, we targeted the switch I (residues 25-40) and switch II (residues 57-76) parts of KRAS G12D with nutritional bioflavonoids in comparison to the reference KRAS SI/II inhibitor BI-2852. Initially, we screened 925 bioflavonoids according to drug-likeness qualities, and ADME qualities and selected 514 bioflavonoids for more studies. Molecular docking led to four lead bioflavonoids, namely 5-Dehydroxyparatocarpin K (L1), Carpachromene (L2), Sanggenone H (L3), and Kuwanol C (L4) with binding affinities of 8.8 Kcal/mol, 8.64 Kcal/mol, 8.62 Kcal/mol, and eight.58 Kcal/mol, correspondingly, in comparison to BI-2852 (-8.59 Kcal/mol). Further steered-molecular dynamics, molecular-dynamics simulation, toxicity, as well as in silico cancer-cell-line cytotoxicity predictions considerably support these four lead bioflavonoids as potential inhibitors of KRAS G12D SI/SII inhibitors. We finally conclude these four bioflavonoids have potential inhibitory activity from the KRAS G12D mutant, and therefore are further to become studied in vitro as well as in vivo, to judge their therapeutic potential and also the utility of those compounds against KRAS G12D mutated cancers.