MAO-B-IN-21 is an MAO-B inhibitor characterized by superior antioxidant and anti-Aβ aggregation activities, metal-ion chelating capabilities, and mitigation of neuroinflammation (NO, TNF-α). It demonstrates neuroprotective effects with notable BBB permeability and, in an Aβ1-42 induced Alzheimer's disease mouse model, significantly enhances memory and cognitive functions [1].

MAO-B-IN-21 at a concentration of 37.5 μM in a methanol solution (甲醇溶液) inhibits Cu2+-induced ROS production due to its metal chelating properties and/or its antioxidant capacity, capable of scavenging free radicals from the Cu2+-ascorbic acid redox system [1]. Additionally, MAO-B-IN-21 at 25 μM for 24 hours at 37℃ suppresses the self-induced aggregation of Aβ1-42 and disassembles preformed Aβ1-42 fibrils [1]. Furthermore, MAO-B-IN-21 in a range of 2.5-25 μM over 24 hours inhibits the production of ROS in LPS-stimulated BV-2 microglial cells [1].

MAO-B-IN-21 (30 mg/kg; ig; single dose) readily crosses the blood-brain barrier in Balb/C mice [1]. At 8 mg/kg and 32 mg/kg doses administered intragastrically, it reduces escape latency time (ELT) and decreases Aβ 1-42 levels, indicating potential improvements in learning and memory in an Aβ-induced Alzheimer's disease (AD) mouse model [1]. Pharmacokinetic analysis in Balb/C mice [1] shows the following parameters: Tissue T 1/2, T max, C max, AUC 0-t, and AUC brain/plasma ratio with plasma at 1.15 h, 0.5 h, 1539 ng/mL, 2941 ng·h/mL, 0.69, and brain at 2.07 h, 1.0 h, 922.7 ng/g, and 2032.5 ng·h/g, respectively.