Subsequent optimization to improve the Rad51–BRCA2 PPI disruption resulted in a compound 35d (Fig. 5B), which exhibited an EC50 of 19 μM in the ELISA assay, had a binding affinity for Rad51 of 80 nM, inhibited HR by 54% in pancreatic cancer cells with a 20 μM concentration, and displayed synergy with PARPi in pancreatic cells with a concentration of 15 μM.232. This evidence concerns the gene RAD51 and pancreatic neoplasm.