Two hit compounds, D-G09(58) and D-103 (59) (Figure 22), showed the expected phenotype for RAD52inhibition in these cell lines, while another three compounds D-105(60), D-K17 (61), and D-G23 (62) (Figure 22) showedactivity against two of the cells lines but were of a structurallydiverse scaffold, giving more opportunity for chemical space exploration.The best-performing compound of these, 59 (inhibits RAD52ssDNA annealing at IC50 = 5 μM), was also testedin BRCA1/2-positive and -negative chronic myeloid leukemia cells,showing preferential inhibition of growth of the BRCA1/2-negativecells. This evidence concerns the gene BRCA1 and chronic myelogenous leukemia, BCR-ABL1 positive.