Dehydroevodiamine hydrochloride
(Synonyms: 盐酸去氢吴茱萸碱) 目录号 : GC38435An alkaloid with diverse biological activities
Cas No.:111664-82-5
Sample solution is provided at 25 µL, 10mM.
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Dehydroevodiamine is an alkaloid that has been isolated from E. rutaecarpa and has anti-inflammatory, antiarrhythmic, hypotensive, and anti-amnesic biological activities.1,2,3,4 It inhibits LPS-induced secretion of prostaglandin E2 in RAW 264.7 mouse macrophages when used at a concentration of 30 μM.1 Dehydroevodiamine (0.1-0.3 μM) reduces the upstroke velocity, action potential amplitude, and contractile force of electrically-stimulated primary human atrial trabeculae.2 In vivo, dehydroevodiamine (10 mg/kg) decreases mean arterial blood pressure (MAP) by approximately 30% in rats.3 Dehydroevodiamine (1.5 mg/kg) also inhibits amnesia induced by amyloid-β (25-35) and increases latency to step-through in a passive avoidance test in mice.4
1.Noh, E.J., Ahn, K.S., Shin, E.M., et al.Inhibition of lipopolysaccharide-induced iNOS and COX-2 expression by dehydroevodiamine through suppression of NF-κB activation in RAW 264.7 macrophagesLife Sci.79(7)695-701(2006) 2.Loh, S.-H., Tsai, Y.-T., Lee, C.-Y., et al.Antiarrhythmic effects of dehydroevodiamine in isolated human myocardium and cardiomyocytesJ. Ethnopharmacol.153(3)753-762(2014) 3.Yang, M.C.M., Wu, S.-L., Kuo, J.-S., et al.The hypotensive and negative chronotropic effects of dehydroevodiamineEur. J. Pharmacol.182(3)537-542(1990) 4.Wang, H.-H., Chou, C.-J., Liao, J.-F., et al.Dehydroevodiamine attenuates β-amyloid peptide-induced amnesia in miceEur. J. Pharmacol.413(2-3)221-225(2001)
Cas No. | 111664-82-5 | SDF | |
别名 | 盐酸去氢吴茱萸碱 | ||
Canonical SMILES | O=C1N2C(N(C)C3=C1C=CC=C3)=C4C(CC2)=C5C=CC=CC5=N4.[H]Cl | ||
分子式 | C19H16ClN3O | 分子量 | 337.8 |
溶解度 | DMF: 2.5 mg/ml,DMSO: 12.5 mg/ml,Ethanol: 2.5 mg/ml | 储存条件 | 4°C, protect from light |
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1 mM | 2.9603 mL | 14.8017 mL | 29.6033 mL |
5 mM | 0.5921 mL | 2.9603 mL | 5.9207 mL |
10 mM | 0.296 mL | 1.4802 mL | 2.9603 mL |
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Increased feline cerebral blood flow induced by Dehydroevodiamine hydrochloride from Evodia rutaecarpa
J Nat Prod 1994 Mar;57(3):387-9.PMID:8201313DOI:10.1021/np50105a009.
Dehydroevodiamine hydrochloride (0.1-0.3 mg/kg iv), which was isolated from the leaves of Evodia rutaecarpa, increased the cerebral blood flow recorded from the surface of the supra-sylvian gyrus in anesthetized cats. This action reached a maximum 1-4 min after injection and continued for 10 min. However, the compound had negligible effects on other cardiorespiratory functions at the doses examined. These results suggest that the compound selectively increases cerebral blood flow.
Novel anticholinesterase and antiamnesic activities of dehydroevodiamine, a constituent of Evodia rutaecarpa
Planta Med 1996 Oct;62(5):405-9.PMID:8923803DOI:10.1055/s-2006-957926.
To find a new compound with antiamnesic activity, we screened 29 natural products for their abilities to inhibit acetylcholinesterase and reverse scopolamine-induced amnesia. Among the plants tested Evodia rutaecarpa Bentham showed a strong inhibitory effect on acetylcholinesterase in vitro and an anti-amnesic effect in vivo. By sequential fractionation of E. rutaecarpa, the active component was finally identified as Dehydroevodiamine hydrochloride (DHED). DHED inhibited acetylcholinesterase activity in a dose-dependent and non-competitive manner. The IC50 value of DHED is 37.8 microM. A single administration of DHED to rats (6.25 mg/kg) significantly reversed the scopolamine-induced memory impairment in a passive avoidance test. The antiamnesic effect of DHED was more potent than that of tacrine which is the only drug for Alzheimer's disease approved by FDA. This potent antiamnesic effect of DHED was thought to be due to the combined effects of acetylcholinesterase inhibition and the known cerebral blood flow enhancement. These results indicate that DHED has novel anti-cholinesterase and antiamnesic activities and might have therapeutic potential in various disorders including Alzheimer's disease.