Higenamine (hydrochloride)

Higenamine hydrochloride is a selective LSD1 inhibitor (IC₅₀=1.47 μM) that can be isolated from aconite. Higenamine hydrochloride has anti-inflammatory and antibacterial activity. Higenamine (Norcoclaurine) can attenuate IL-1β-induced Apoptosis through ROS-mediated PI3K/Akt signaling pathway. Higenamine hydrochloride protects brain cells from oxygen deprivation. Higenamine can promote bone formation in osteoporosis through the SMAD2/3 pathway. Higenamine hydrochloride can be used to study cancer, inflammation, cardiorenal syndrome and other diseases^{[1][2][3][4][5][6]}. IC50 & Target:IC50: 1.47 μM (LSD1)^[1]. In Vitro:Higenamine hydrochloride (3-100 μM; 72 h) can inhibit the differentiation of MV4-11 and MOLM-13 cells by inhibiting the activity of LSD1^[1].
Higenamine hydrochloride (1-100μM; 8 h) can enhance the activity of HO-1 in C6 cells and protect brain cells from cell hypoxia damage ^[2].
Higenamine hydrochloride (10-50 μM; 8 h) can inhibit apoptosis in C6 cells^[2].
Higenamine hydrochloride (10-40 μM; 24 h) can inhibit the production of IL-1β-induced ROS and activate the ROS-mediated PI3K/Akt signaling pathway, which has anti-apoptotic activity in HNPCs^[3].
Higenamine hydrochloride (0.08-250 μM; 0.5-24 h) promotes phosphorylation of SMAD2/3 in a time- and dose-dependent manner in BMSCs^[6].
In Vivo:Higenamine hydrochloride (10 mg/kg; Intraperitoneal injection; Single dose) can significantly reduce the inflammation and infarct size of cerebral ischemic injury caused by middle cerebral artery occlusion (MCAO) in Sprague-Dawley rats^[2].
Higenamine hydrochloride (0.5-4.5 mg/kg; Single dose) improves cardiac and renal function in rats with cardio-renal syndrome (CRS) and alleviates cardiac and renal fibrosis by targeting ASK1/MAPK (ERK, P38)/NF-kB signaling pathway in Sprague-Dawley rats^[4].
Higenamine hydrochloride (20 mg/kg-30 mg/kg; Intraperitoneal injection; Once daily for 60 days) promotes bone formation and prevents accelerated bone loss in SAMP6 mice^[6].