ChemicalBook--->CAS DataBase List--->2284-31-3

2284-31-3

2284-31-3 Structure

2284-31-3 Structure
IdentificationBack Directory
[Name]

PRATENSEIN
[CAS]

2284-31-3
[Synonyms]

PRATENSEIN
PRALENREIN
OROBOL 4'-METHYL ETHER
PATCHOULI ALCOHOL (RG)
4'-METHOXY-3',5,7-TRIHYDROXYISOFLAVONE
5,7,3'-Trihydroxy-4'-methoxyisoflavone
5,7-Dihydroxy-3-(3-hydroxy-4-methoxyphenyl)-4H-1-benzopyran-4-one
[Molecular Formula]

C16H12O6
[MDL Number]

MFCD00210594
[MOL File]

2284-31-3.mol
[Molecular Weight]

300.26
Chemical PropertiesBack Directory
[Melting point ]

272-273°
[Boiling point ]

576.7±50.0 °C(Predicted)
[density ]

1.512±0.06 g/cm3(Predicted)
[form ]

Solid
[pka]

6.45±0.20(Predicted)
[color ]

White to off-white
Hazard InformationBack Directory
[Uses]

Pratensein, a flavonoid, ameliorates β-amyloid-induced cognitive impairment in rats via reducing oxidative damage and restoring synapse and BDNF levels[1].
[Definition]

ChEBI: A member of the class of 7-hydroxyisoflavones in which isoflavone is substituted by hydroxy groups at the 5, 7, and 3' positions, and by a methoxy group at the 4' position.
[in vivo]

Pratensein significantly attenuates neuronal degeneration and apoptosis in hippocampus. The over-expression in IL-1β and TNF-α as well as the extensive astrogliosis and microgliosis in hippocampus induced by Aβ1-42 are significantly reduced following administration of Pratensein. Pratensein treatment significantly suppresses the activation of NF-κB in hippocampus. Pratensein is able to increase the levels of synaptophysin and brain-derived neurotrophic factor (BDNF)[1].
Pratensein (20 mg/kg; p.o.; once daily for 3 weeks) ameliorates learning and memory deficits in Aβ1-42 rat model of Alzheimer’s disease[1].

Animal Model:Male 10-week old Wistar rats[1]
Dosage:20 mg/kg
Administration:P.o.; once daily for 3 weeks
Result:The spatial learning and memory ability of rats was improved.
[References]

[1] Liang C, et al. Pratensein ameliorates β-amyloid-induced cognitive impairment in rats via reducing oxidative damage and restoring synapse and BDNF levels. Neurosci Lett. 2015;592:48-53. DOI:10.1016/j.neulet.2015.03.003
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