Dehydroevodiamine (hydrochloride)

Dehydroevodiamine hydrochloride is a blood-brain barrier-permeable, orally effective AChE and BACE1 inhibitor (IC₅₀ = 40.96 μM). Dehydroevodiamine hydrochloride is isolated and extracted from Evodia rutaecarpa. Dehydroevodiamine hydrochloride attenuates neurotoxicity through multiple targets by inhibiting BACE1 to block Aβ production, inhibiting AChE activity, scavenging ROS, and suppressing calcium influx. Dehydroevodiamine hydrochloride can be used for research on Alzheimer's disease, cerebral ischemia, vascular dementia, and other cognitive disorder-related diseases^[1][2][3][4]. In Vitro:Dehydroevodiamine hydrochloride (0.5-4 μM; 4 h) attenuates Aβ_1-42 (HY-P1362)-induced neurotoxicity and reduces ROS production in primary cortical neurons in a dose-dependent manner^[3].
Dehydroevodiamine (hydrochloride) (10 μM; 5 min) reduces the KCl-dependent increase in intracellular calcium levels in primary cortical neurons^[3].
Dehydroevodiamine hydrochloride (25-100 µM; 1 h) acts as a competitive inhibitor of BACE1 in mouse brain homogenates, with an IC₅₀ of 40.96 µM^[2]. In Vivo:Dehydroevodiamine hydrochloride (0.5 mg/kg; i.p.; once daily; for 4 consecutive months) ameliorates memory impairment and reduces soluble Aβ and amyloid plaques in the cortex of Tg2576 transgenic AD mice and wild-type mice^[2].
Dehydroevodiamine hydrochloride (10 mg/kg; p.o.; single administration) ameliorates spatial memory impairment in the Scopolamine (HY-N0296)-induced amnesia model in Wistar rats^[3].
Dehydroevodiamine hydrochloride (10 mg/kg; p.o.; once daily; 21 days) ameliorates learning and spatial memory impairment in an Aβ_1-42 intracerebroventricular infusion-induced Wistar rat model^[3].
Dehydroevodiamine hydrochloride (10-20 mg/kg (p.o.) or 6.25 mg/kg (i.p.); single dose or once daily for 7 consecutive days) reverses memory acquisition and spatial working memory deficits in Scopolamine-induced Sprague-Dawley rat models^[4].
Dehydroevodiamine hydrochloride (6.25 mg/kg; i.p.; single administration 30 min before ischemia or once daily for 7 consecutive days after ischemia) reduces cerebral infarct size and attenuates neuronal damage in the hippocampus and cognitive deficits in a middle cerebral artery occlusion (MCA)-induced focal cerebral ischemia model in Sprague-Dawley rats^[4].
Dehydroevodiamine hydrochloride (6.25 mg/kg; i.p.; once daily; for 7 consecutive days) significantly reduces neuronal death in the hippocampus and dentate gyrus and ameliorates memory impairment in a Sprague-Dawley rat model of electrolytic lesion of the entorhinal cortex (EC)^[4].
Dehydroevodiamine hydrochloride (0.03-0.3 mg/kg; i.v.; single administration; observation for 1-10 min) selectively increases cerebral cortical blood flow without affecting other cardiopulmonary functions in anesthetized adult cats^[1].