BuChE-IN-20

BuChE-IN-20 (Compound 4d-13) (5 μM, 10 min) shows selectivity for BuChE through enzymatic activity assays of hAChE and hBuChE^[1].
BuChE-IN-20 (20 μM, 48 h) prevents the aggregation and deposition of Aβ_1-42, thereby exerting neuroprotective effects by inhibiting the formation of toxic amyloid plaques, and mitigate the neurotoxicity induced by Aβ_1-42 through ROS generation^[1].
BuChE-IN-20 (1 mM, 30 min) exerts scavenging capacities for hydroxyl radicals 775 times that of vitamin C^[1].
BuChE-IN-20 (5-10 μM, 4 h pretreatment and 8 h cotreatment with LPS) decreases intracellular reactive oxygen species (ROS) concentration-dependently in LPS (1.5 μg/mL) (HY-D1056)-induced RAW264.7 cells^[1].
BuChE-IN-20 (6.25-12.5 μM, 4 h pretreatment and 24 h cotreatment with LPS) demonstrates potent inhibitory activity on LPS (2 μg/mL)-induced NO production in RAW264.7 cells^[1].
BuChE-IN-20 (1-100 μM, 24 h) exerts inhibitory effects and free radical scavenging at sub-micromolar concentrations in mouse BV-2 cell line, with a safety margin of nearly 150-fold regarding cytotoxicity^[1].
BuChE-IN-20 (1-10 μM, 24 h pretreatment and 24 h cotreatment with LPS) decreases IL-1β levels in LPS (100 ng/mL)-induced BV-2 cells^[1].
BuChE-IN-20 (1-20 μM, 6 h pretreatment and 24 h cotreatment with NMDA/Sodium L-Glutamate) mitigates the cytotoxic effects dose-dependently in NMDA (20 mM)/Sodium L-Glutamate(Glu) (HY-N0455B)-induced SH-SY5Y cell injury model^[1].

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