CK2 0.13 μM (IC 50 , Human CK2) PIM1 0.148 μM (IC 50 ) PIM2 1.6 μM (IC 50 ) PIM3 0.097 μM (IC 50 ) HIPK2 0.37 μM (IC 50 ) HIPK3 0.59 μM (IC 50 ) DYRK1a 0.41 μM (IC 50 ) DYRK2 0.35 μM (IC 50 ) DYRK3 1.7 μM (IC 50 ) PKD1 0.18 μM (IC 50 ) CDK2 0.64 μM (IC 50 )

DMAT application in vivo reduces tumor growth in a xenotransplant model by interference with tumor cell proliferation. Biochemical parameters and histology following DMAT administration revealed no alterations in liver tissue.

DMAT (1 μM-2.5 μM) DMAT is more efficient in killing antiestrogen resistant cells than parental antiestrogen sensitive MCF-7 cells. DMAT-induced cell death of antiestrogen resistant cells is mediated by caspases. DMAT inhibits CK2 activity but the inhibition is similar in the three cell lines, MCF-7, TAMR-1 and 182R-6. DMAT has effects on H295R cell proliferation at concentrations of 10 -4 and 10 -5 mol/Las compared with the control. DMAT (100 μM) significantly increases apoptosis of H295R cells. DMAT (1 nM-1 μM) significantly decreases aldosterone release into supernatants of 72-h H295R cell cultures as compared with the control. DMAT also inhibits PIM1 by a mechanism which is competitive with respect to ATP, and it is a powerful inhibitor of kinases other than CK2.

DMAT 是一种有效的，特异性的 CK2 抑制剂，IC50 值为 130 nM。