ASM-IN-2

ASM-IN-2 (1 or 10 MG/KG, iv or ip) is rapidly absorbed (Tmax = 0.25 h) in male ICR mice with a high maximum concentration (Cmax = 4204.13 NG/ML) and moderate bioavailability (F=39.59%), which possesses an acceptable profile for antidepressant studies^[1].
ASM-IN-2 (6, 12, 24 MG/KG, i.p., 10 days) significantly reduces the immobility time of mice better than fluoxetine(12 mg/kg) (HY-W011235) in the forced swim test (FST) and tail suspension test (TST). ASM-IN-2 results in a significant increase in the expression of BDNF and increases the level of ceramide in the hippocampal and cerebral cortex. ASM-IN-2 improves the levels of oxidative stress in the brains of depressed mice through inhibiting ASM activity^[1].
ASM-IN-2 (6, 12, 24 MG/KG, i.p.) reduces the levels of TNF-α, IL-1β and IL-6 in a dose-dependent manner in CUMS model mice, attenuating the inflammatory response in the serum of mice^[1].
ASM-IN-2 (6, 12, 24 MG/KG, i.p.) significantly increases the levels of 5-HT in the hippocampus of mice, thereby promoting more effective antidepressant activity by inhibiting ASM^[1].