DRAK2-IN-2

DRAK2-IN-2 (Compound I14) potently inhibits the kinase activity of DRAK2, with an IC₅₀ value of 198.5 nM^[1].
DRAK2-IN-2 (5-10 μM) increases glucose-stimulated insulin secretion in mouse primary islet cells by 1.86-fold at 5 μM and 1.72-fold at 10 μM^[1].
DRAK2-IN-2 (5-10 μM; 1 h) increases the mitochondrial membrane potential of INS-1E pancreatic β cells. After 1 hour of treatment, the potential in the 5 μM group reaches 108.4% of that in the control group, while that in the 10 μM group reaches 110.7% of the control level^[1].
DRAK2-IN-2 (5 μM; 24 h) attenuates Palmitic acid (HY-N0830)-induced apoptosis of INS-1E pancreatic β cells^[1].
DRAK2-IN-2 exhibits excellent selectivity, with no significant inhibitory effect on CHK1, FLT3, AKT1, JAK3, CDK2, ERK5 and IRAK4 (IC₅₀ > 10 μM)^[1].
DRAK2-IN-2 regulates the DRAK2-ULK1 signaling axis in INS-1E pancreatic β cells by inhibiting ULK1 phosphorylation at Ser56, thereby promoting autophagy and reducing apoptotic signals^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.