H3R antagonist 4

H3R antagonist 4 (compound 11l) inhibited eeAChE, eqBuChE and hAChE with IC₅₀ values of 7.04 μM, 13.40 μM and 9.73 μM, respectively^[1].
H3R antagonist 4 combines with AChE and occupies CAS, midgorge site and PAS. It interacts with the active site and peripheral anion site of hAChE, and can bind both CAS and PAS sites as two-site AChE inhibitors^[1].
H3R antagonist 4 inhibited the aggregation of Aβ_1-42 induced by itself and Cu²⁺ (95.48% and 88.63%, respectively)(ThT fluorescence assay) , and degraded the Aβ_1-42 fibrils induced by itself and Cu²⁺ (80.16% and 89.30% , respectively)(TEM) ^[1].
The IC₅₀ of H3R antagonist 4 (TRFRET) was 1.09 nM^[1].
H3R antagonist 4 (5 μM, 10 μM and 20 μM)(WB) inhibited abnormal tau phosphorylation in PC12 cells^[1].
H3R antagonist 4 (11 μM) increased the survival rate of PC12 (800 μM H₂O₂) to 75.66%, and decreased the level of ROS. PC12 cells were protected from H₂O₂ by decreasing ROS accumulation, and the percentage of apoptotic cells was significantly increased to 22.9% ± 0.36%^[1].
H3R antagonist 4 (5, 10, 20 μM) inhibited RSL3-induced iron death in PC12 cells and significantly increased cell viability. The induced injury increased the permeability of blood-brain barrier in vitro^[1].
H3R antagonist 4 (UV-vis spectrometry) can sequester Cu ²⁺, Zn ²⁺, Al ³⁺ and Fe ^{2+ [1]}.
H3R antagonist 4 increased PEPT1 protein expression in hPepT1-MDCK cells^[1].
H3R antagonist 4 (0-80 μM, 1h) showed anti-inflammatory effect in BV-2 cells and did not affect proliferation^[1] .

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