Fig. 6: Compounds 18 and 22 repress PI3K-AKT signaling in tumor cells.
From: Leveraging molecular structure and bioactivity with chemical language models for de novo drug design
a Representative immunoblot analysis p-AKT (S473), AKT, and GAPDH (loading control) using total lysates of human HD-MB03 tumor cells stimulated with 10 ng ml−1 EGF for 15 min in the absence or presence of compounds 18 or 22, or copanlisib (Cop.). Compounds and copanlisib were used at 100 nM concentration. DMSO was used as solvent control. b Quantification of p-AKT levels relative to EGF-stimulated DMSO control. N = 2 from two independent experiments. c CellTiter-Glo assay to monitor the viability of cells after 72 h of exposure to increasing concentrations of 18, 22, or copanlisib in a medium supplemented with FBS. A nonlinear fit of inhibitor versus normalized response is shown. Means (dots) and SD (error bars) of N = 4 (copanlisib) or N = 7 (compounds 18 or 22) measurements combined from two independent experiments are shown.
