Most previous experimental and/or computational search for anticoronaviral molecules has been focused on approved drugs (drug repurposing) to other protein targets rather to the coronavirus inner-cavity. Most of those earlier works included the inhibition of the S2 coiled-coil bundle by complementary peptides , the blocking of the surface interphase of S1 with the ACE2 human receptor , and/or the active sites of viral proteases among others. In contrast, our previous efforts to use ligands rather than mutations , explored the inner-cavity. In the past we have used limited explorations of chemical spaces by combining computational strategies previously reported by others, including neural networks and large public libraries 39 , 40-43 , 44