JHB-17

JHB-17 potently inhibits IKKβ kinase activity in a cell-free system with an IC₅₀ of 1.1 μM, which is approximately 70 times more potent than EF24; it has a K_D of 1.293 μM for binding to wild-type IKKβ, and its binding affinity to IKKβ_K428A and IKKβ_Q432A mutant proteins is reduced^[1].
JHB-17 (0.625-5 μM; 1 h or 18 h) increases the survival rate of H₂O₂-damaged SH-SY5Y cells in a concentration-dependent manner^[1].
JHB-17 (5 μM; 1 h or 18 h) significantly reduces lipid peroxidation levels (MDA levels) and ROS accumulation in SH-SY5Y cells damaged by H₂O₂ after 1 h or 18 h of pretreatment^[1].
JHB-17 (5 μM; 6 h) promotes Nrf2 nuclear translocation^[1].
JHB-17 (1.25-5 μM; 18 h) upregulates the expression of HO-1 protein in SH-SY5Y cells in a dose-dependent manner^[1].
JHB-17 (5 μM; 18 h pretreatment, 6 h H₂O₂ exposure) inhibits H₂O₂-induced phosphorylation of IKKβ and upregulates the expression of HO-1 protein in SH-SY5Y cells after 18 h of pretreatment followed by 6 h of H₂O₂ exposure^[1].
JHB-17 (5 μM; 18 h pretreatment, followed by 24 h H₂O₂ exposure) loses its cytoprotective effect against H₂O₂-induced damage in SH-SY5Y cells when IKKβ is overexpressed, which confirms that IKKβ is its key target^[1].
JHB-17 acts in a dose-dependent manner, and this effect occurs after 18 h of pretreatment followed by 2 h of exposure to H₂O₂^[1].
JHB-17 (1.25-5 μM; 18 h pretreatment, 24 h H₂O₂ exposure) upregulates the expression of SLC7A11, increases intracellular GSH levels and reduces lipid ROS, and inhibits H₂O₂-induced ferroptosis in SH-SY5Y cells in a dose-dependent manner^[1].

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