How does binding affinity as well as an absorption, distribution, metabolism, and excretion (ADME) test help us to interpret how effective failed medical trials of certain ligands (Axitinib, Devimistat, Ibrutinib) were in interacting with pancreatic oncoproteins (KRAS, S100, A1BG) in comparison to available pancreatic ductal adenocarcinoma (PDAC) drugs (Gemcitabine, Paclitaxel, Capecitabine) in Homo Sapiens?
