The most active compounds were compounds 31a (IC50 = 5.2 nM) and 31b (IC50 = 4.9 nM) (Figure 9) that inhibited BTK auto-phosphorylation, blocked the cell cycle in the G0/G1 phase, induced apoptosis in the TMD8 cells, and suppressed the tumor growth in a TMD8 cell xenograft model. Here, BTK is linked to neoplasm.