DIHYDROFISETIN
DIHYDROFISETIN Basic information
- Product Name:
- DIHYDROFISETIN
- Synonyms:
-
- DIHYDROFISETIN
- 3,3',4',7-TETRAHYDROXYFLAVANONE
- 3',4',7-TRIHYDROXYFLAVANONOL
- 2,3-DIHYDROFISETH
- 2,3-DIHYDROFISETIN
- 3,3,4,7-TETRAHYDROXYFLAVANONE 97%
- 3,7,3'',4''-TETRAHYDROXYFLAVANONE WITH HPLC
- 5-Deoxydihydrouercetin
- CAS:
- 20725-03-5
- MF:
- C15H12O6
- MW:
- 288.25
- EINECS:
- 243-989-6
- Product Categories:
-
- Dihydro-Flavanols
- Mol File:
- 20725-03-5.mol
DIHYDROFISETIN Chemical Properties
- Melting point:
- 216-217°C
- storage temp.
- -20°C
- solubility
- Acetone: soluble,Chloroform: soluble,Dichloromethane: soluble,DMSO: soluble,Ethyl Acetate: soluble
- form
- A solid
- Boiling point:
- 644.2±55.0 °C(Predicted)
- Density
- 1.599±0.06 g/cm3(Predicted)
- pka
- 7.59±0.60(Predicted)
- color
- White to off-white
- LogP
- 0.870
DIHYDROFISETIN Usage And Synthesis
Uses
Fustinis ((±)-Fustin; 3,7,3',4'-Tetrahydroxyflavanone) is a potent amyloid β (Aβ) inhibitor. Fustinis ((±)-Fustin; 3,7,3',4'-Tetrahydroxyflavanone) increases the expression of acetylcholine (ACh) levels, choline acetyltransferase (ChAT) activity, and ChAT gene induced by Aβ (1-42). Fustinis ((±)-Fustin; 3,7,3',4'-Tetrahydroxyflavanone) decreases in acetyl cholinesterase (AChE) activity and AChE gene expression induced by Aβ (1-42). Fustinis ((±)-Fustin; 3,7,3',4'-Tetrahydroxyflavanone) increases muscarinic M1 receptor gene expression and muscarinic M1 receptor binding activity. Fustinis ((±)-Fustin; 3,7,3',4'-Tetrahydroxyflavanone) can be used for Alzheimer's disease research[1].
Definition
ChEBI: A dihydroflavonol that is the 2,3-dihydro derivative of fisetin.
in vivo
Fustinis ((±)-Fustin; 3,7,3',4'-Tetrahydroxyflavanone) (50-100 mg/kg; p.o.; daily, for 11days; Aβ-treated C57BL/6 mice) attenuates Aβ (1-42)-induced impairments in conditioned fear learning and passive avoidance behavior[1].
Fustinis ((±)-Fustin; 3,7,3',4'-Tetrahydroxyflavanone) (50-100 mg/kg; p.o.; daily, for 11days; Aβ-treated C57BL/6 mice) alters Aβ (1-42)-induced changes in ACh level and AChE and ChAT activity and gene expression[1].
Fustinis ((±)-Fustin; 3,7,3',4'-Tetrahydroxyflavanone) (50-100 mg/kg; p.o.; daily, for 11days; Aβ-treated C57BL/6 mice) increases Aβ (1-42)-induced reduction in M1 receptor mRNA and protein expression in Aβ-treated C57BL/6 mice. Fustin increases p-ERK and p-CREB expression in Aβ-treated C57BL/6 mice[1].
| Animal Model: | Aβ-treated C57BL/6 mice[1] |
| Dosage: | 50 and 100 mg/kg |
| Administration: | Oral administration;daily, for 11days |
| Result: | Decreased freezing response in Aβ-treated C57BL/6 mice. |
| Animal Model: | Aβ-treated C57BL/6 mice[1] |
| Dosage: | 50 and 100 mg/kg |
| Administration: | Oral administration;daily, for 11days |
| Result: | Increased the expression of Ach, ChAT gene and ChAT activity. Decreased the expression of AChE gene and AChE activity. |
| Animal Model: | Aβ-treated C57BL/6 mice[1] |
| Dosage: | 50 and 100 mg/kg |
| Administration: | Oral administration;daily, for 11days |
| Result: | Increased gene expression of M2- , M3- ,M4-, M5-, α4β, α7-receptor, p-ERK and p-CREB. |
References
[1] Jin CH, et, al. Fustin flavonoid attenuates beta-amyloid (1-42)-induced learning impairment. J Neurosci Res. 2009 Dec;87(16):3658-70. DOI:10.1002/jnr.22159
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