146698-96-6

Basic information

• Product Name: 7-O-Ethyldaidzein
• Synonyms: 4H-1-benzopyran-4-one, 7-ethoxy-3-(4-hydroxyphenyl)-; 7-ethoxy-3-(4-hydroxyphenyl)-4H-chromen-4-one
• CAS NO: 146698-96-6
• Molecular Formula: C₁₇H₁₄O₄
• Molecular Weight: 282.294
• Product Categories: All Inhibitors;Inhibitors
• Mol File: 146698-96-6.mol
• Article Data: 5

Chemical Properties

• Melting Point: 210-212°C
• Boiling Point: 484.8°C at 760 mmHg
• Flash Point: 182.1°C
• Appearance: /
• Density: 1.293g/cm³
• Vapor Pressure: 5.03E-10mmHg at 25°C
• Refractive Index: 1.627
• Storage Temp.: -20?C Freezer
• CAS DataBase Reference: 7-O-Ethyldaidzein(CAS DataBase Reference)
• NIST Chemistry Reference: 7-O-Ethyldaidzein(146698-96-6)
• EPA Substance Registry System: 7-O-Ethyldaidzein(146698-96-6)

Safety Data

• Hazardous Substances Data: 146698-96-6(Hazardous Substances Data)

Usage

Chemical Properties

Off-White Solid

Uses

Different sources of media describe the Uses of 146698-96-6 differently. You can refer to the following data:
1. A potent inhibitor of MOA and aldehyde dehydrogenase isozyme (ALDH2)
2. A potent inhibitor of MOA and aldehyde dehydrogenase isozyme (ALDH2).This compound is suitable for aldehyde dehydrogenase (ALDH) related research.

InChI:InChI=1/C17H14O4/c1-2-20-13-7-8-14-16(9-13)21-10-15(17(14)19)11-3-5-12(18)6-4-11/h3-10,18H,2H2,1H3

Upstream product

• 486-66-8 daidzein 
• 75-03-6 ethyl iodide 
• 64-67-5 diethyl sulfate 
• 156-38-7 4-hydroxyphenylacetate 
• 108-46-3 recorcinol 
• 74-96-4 ethyl bromide 

Relevant articles and documents

Synthesis and crystal structure of 7-ethoxyl-4′-hydroxyisoflavone

7-Ethoxyl-4′-hydroxyisoflavone was prepared and its crystal structure was examined by X-ray diffraction. Crystallization of the title compound occurs in the monoclinic, space group P2(1)/c with a = 11.144(2) A, b = 10.209(1) A, c = 13.191(2) A, β = 113.43

Effects of 7-O substitutions on estrogenic and anti-estrogenic activities of daidzein analogues in MCF-7 breast cancer cells

Daidzein (1) is a natural estrogenic isoflavone. We report here that 1 can be transformed into anti-estrogenic ligands by simple alkyl substitutions of the 7-hydroxyl hydrogen. To test the effect of such structural modifications on the hormonal activities of the resulting compounds, a series of daidzein analogues have been designed and synthesized. When MCF-7 cells were treated with the analogues, those resulting from hydrogen substitution by isopropyl (3d), isobutyl (3f), cyclopentyl (3g), and pyrano- (2) inhibited cell proliferation, estrogen-induced transcriptional activity, and estrogen receptor (ER) regulated progesterone receptor (PgR) gene expression. However, methyl (3a) and ethyl (3b) substitutions of the hydroxyl proton only led to moderate reduction of the estrogenic activities. These results demonstrated the structural requirements for the transformation of daidzein from an ER agonist to an antagonist. The most effective analogue, 2, was found to reduce in vivo estrogen stimulated MCF-7 cell tumorigenesis using a xenograft mouse model.

The mitochondrial monoamine oxidase - Aldehyde dehydrogenase pathway: A potential site of action of daidzin

Recent studies showed that daidzin suppresses ethanol intake in ethanol-preferring laboratory animals. In vitro, it potently and selectively inhibits the mitochondrial aldehyde dehydrogenase (ALDH-2). Further, it inhibits the conversion of monoamines such as serotonin (5-HT) and dopamine (DA) into their respective acid metabolites, 5-hydroxyindole-3-acetic acid (5-HIAA) and 3,4-dihydroxyphenylacetic acid (DOPAC) in isolated hamster or rat liver mitochondria. Studies on the suppression of ethanol intake and inhibition of 5-HIAA (or DOPAC) formation by six structural analogues of daidzin suggested a potential link between these two activities. This, together with the finding that daidzin does not affect the rates of mitochondria-catalyzed oxidative deamination of these monoamines, raised the possibility that the ethanol intake-suppressive (antidipsotropic) action of daidzin is not mediated by the monoamines but rather by their reactive biogenic aldehyde intermediates such as 5-hydroxyindole-3-acetaldehyde (5-HIAL) and/or 3,4-dihydroxyphenylacetaldehyde (DOPAL) which accumulate in the presence of daidzin. To further evaluate this possibility, we synthesized more structural analogues of daidzin and tested and compared their antidipsotropic activities in Syrian golden hamsters with their effects on monoamine metabolism in isolated hamster liver mitochondria using 5-HT as the substrate. Effects of daidzin and its structural analogues on the activities of monoamine oxidase (MAO) and ALDH-2, the key enzymes involved in 5-HT metabolism in the mitochondria, were also examined. Results from these studies reveal a positive correlation between the antidipsotropic activities of these analogues and their abilities to increase 5-HIAL accumulation during 5-HT metabolism in isolated hamster liver mitochondria. Daidzin analogues that potently inhibit ALDH-2 but have no or little effect on MAO are most antidipsotropic, whereas those that also potently inhibit MAO exhibit little, if any, antidipsotropic activity. These results, although inconclusive, are consistent with the hypothesis that daidzin may act via the mitochondrial MAO/ALDH pathway and that a biogenic aldehyde such as 5-HIAL may be important in mediating its antidipsotropic action.