Multitarget AD-IN-7

Multitarget AD-IN-7 (Compound 3c) exhibits excellent selectivity for GSK-3β/α in a screening panel consisting of 24 kinases, with an IC₅₀ of 0.83 nM against GSK-3α and an IC₅₀ of 928 nM against CDK5/p35^[1].
Multitarget AD-IN-7 (1-10 μM; 2.5 h) upregulates the level of p-GSK-3β-Ser9, thereby inactivating GSK-3β in SH-SY5Y cells, and upregulates the level of β-catenin in SH-SY5Y cells^[1].
Multitarget AD-IN-7 (1-10 μM; 1 h pre-incubation prior to 6 h Aβ_25-35 stimulation) inhibits Aβ_25-35 (HY-P0128)-induced tau-Ser396 phosphorylation in SH-SY5Y cells in a concentration-dependent manner in vitro^[1].
Multitarget AD-IN-7 (10 μM; 24 h) upregulates the mRNA expression levels of neurogenesis-related biomarkers GAP-43 and MAP-2 in SH-SY5Y cells^[1].
Multitarget AD-IN-7 (1 μM; 72 h) promotes axonal growth in SH-SY5Y cells, increasing the proportion of cells with axons to 44.11%^[1].
Multitarget AD-IN-7 (20 μM mixed with 40 μM metal ions; 30 min at ambient temperature) exhibits strong chelation with Alzheimer's disease (AD)-related metal ions Fe²⁺, Zn²⁺, Cu²⁺ and Al³⁺ (but does not chelate Na⁺, K⁺, Mg²⁺ or Ca²⁺)^[1].
Multitarget AD-IN-7 (20 μM mixed with 20 μM Aβ_1-42; 24 h at 37 °C) inhibits the self-aggregation of Aβ_1-42 with an inhibition rate of 33.35% and disaggregates preformed Aβ_1-42 aggregates by 46.48%, as detected by ThT fluorescence assay and transmission electron microscopy (TEM)^[1].
Multitarget AD-IN-7 (20 μM mixed with 20 μM Aβ_1-42 and 20 μM Cu²⁺; 24 h at 37 °C) exhibits 52.18% inhibition of Cu²⁺-mediated Aβ_1-42 aggregation and achieves a 56.12% disaggregation rate of preformed Cu²⁺-Aβ_1-42 aggregates, as determined by ThT fluorescence assay^[1].
Multitarget AD-IN-7 exhibits an IC₅₀ of 7.04 μM for scavenging ABTS•+^[1].

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