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kaempferol 3-O-sophoroside

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kaempferol 3-O-sophoroside Basic information

Product Name:
kaempferol 3-O-sophoroside
Synonyms:
  • kaempferol 3-O-sophoroside
  • 3-(2-O-β-D-Glucopyranosyl-β-D-glucopyranosyloxy)-4',5,7-trihydroxyflavone
  • 3-[(2-O-β-D-Glucopyranosyl-β-D-glucopyranosyl)oxy]-4',5,7-trihydroxyflavone
  • 3-[[2-O-(β-D-Glucopyranosyl)-β-D-glucopyranosyl]oxy]-4',5,7-trihydroxyflavone
  • Kaempferol 3-sophoroside
  • Kaempferol 3-β-sophoroside
  • Sophoraflavanoloside
  • 3-[(2-O-beta-D-Glucopyranosyl-beta-D-glucopyranosyl)oxy]-5,7-dihydroxy-2-(4-hydroxyphenyl)-4H-1-benzopyran-4-one
CAS:
19895-95-5
MF:
C27H30O16
MW:
610.52
Mol File:
19895-95-5.mol
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kaempferol 3-O-sophoroside Chemical Properties

Melting point:
194-198℃
Boiling point:
995.0±65.0 °C(Predicted)
Density 
1.82
storage temp. 
Inert atmosphere,Room Temperature
solubility 
DMSO (Slightly), Ethanol (Slightly), Methanol (Slightly), Water (Slightly)
pka
6.20±0.40(Predicted)
form 
Solid
color 
Light Yellow
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Safety Information

Toxicity
LD50 intraperitoneal in mouse: > 1gm/kg
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kaempferol 3-O-sophoroside Usage And Synthesis

Uses

Kaempferol 3-β-Sophoroside is a derivative of Kaempferol (K100000), a plant flavonoid which play a beneficial role in human health promotion.

Definition

ChEBI: A kaempferol O-glucoside that is kaempferol attached to a beta-D-sophorosyl residue at position 3 via a glycosidic linkage.

in vivo

Kaempferol 3-O-sophoroside (10 and 20 mg/kg, p.o., once daily for 20 days) binds to AMP-activated protein kinase (AMPK) to promote brain-derived neurotrophic factor (BDNF) production and autophagy enhancement in corticosterone (HY-B1618)-induced mouse depression model and chronic unpredictable mild stress (CUMS) model, ultimately achieving antidepressant effects[3]. Kaempferol 3-O-sophoroside (100 and 200 mg/kg, p.o., 30-minute administration duration) exhibits analgesic effects in the acetic acid-induced writhing mice model[4].

Animal Model:Acetic acid-induced writhing mice model[4]
Dosage:50, 100, 200 mg/kg
Administration:Oral gavage (p.o.), administration duration of 30 minutes
Result:Caused dose-dependent inhibition of the writhing response induced by acetic acid.
Animal Model:Corticosterone (HY-B1618)-induced mouse depression model; Chronic unpredictable mild stress (CUMS) model[3]
Dosage:10 and 20 mg/kg
Administration:Oral gavage (p.o.), once per day for 20 consecutive days
Result:Ameliorated weight loss, dyskinesia, and hippocampal volume reduction induced by Corticosterone and CUMS.

IC 50

TLR2; TLR4

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