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Isoliquiritigenin

$93

  • Brand : BIOFRON

  • Catalogue Number : BF-I2002

  • Specification : 98%

  • CAS number : 961-29-5

  • Formula : C15H12O4

  • Molecular Weight : 256.25

  • PUBCHEM ID : 638278

  • Volume : 20mg

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Catalogue Number

BF-I2002

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

256.25

Appearance

Yellow crystalline powder

Botanical Source

Albizia julibrissin,Myristica fragrans,Periploca forrestii,Polygonatum kingianum,Gleditsia sinensis

Structure Type

Flavonoids

Category

Standards;Natural Pytochemical;API

SMILES

C1=CC(=CC=C1C=CC(=O)C2=C(C=C(C=C2)O)O)O

Synonyms

iso-Liquiritigenin/Isoliquiritigenin/QR CQ DV1U1R DQ &&E Form/ISL/(2E)-1-(2,4-dihydroxyphenyl)-3-(4-hydroxyphenyl)prop-2-en-1-one/1914296/gu17/2-Propen-1-one, 1-(2,4-dihydroxyphenyl)-3-(4-hydroxyphenyl)-, (2E)-/(2E)-1-(2,4-Dihydroxyphenyl)-3-(4-hydroxyphenyl)-2-propen-1-one/(E)-1-(2,4-Dihydroxyphenyl)-3-(4-hydroxyphenyl)-2-propen-1-one/ISOLIQUIRTIGENIN/4,2',4'-TRIHYDROXYCHALCONE/Isqliquiritigenin/2',4',4-TRIHYDROXYCHALCONE/(E)-1-(2,4-Dihydroxyphenyl)-3-(4-hydroxyphenyl)prop-2-en-1-one/2',4,4'-Trihydroxychalcone

IUPAC Name

(E)-1-(2,4-dihydroxyphenyl)-3-(4-hydroxyphenyl)prop-2-en-1-one

Density

1.4±0.1 g/cm3

Solubility

Methanol

Flash Point

272.7±24.4 °C

Boiling Point

504.0±42.0 °C at 760 mmHg

Melting Point

206-210°C

InChl

InChl Key

WGK Germany

RID/ADR

HS Code Reference

2914500000

Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:961-29-5) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

31623144

Abstract

The epithelial-to-mesenchymal transition (EMT) plays a prominent role in cancer metastasis. Isoliquiritigenin (ISL), one of the flavonoids in licorice, has been shown to exhibit anticancer activities in many cancer types through various mechanisms. However, it is unknown whether ISL impacts the EMT process. Here, we show that ISL is able to suppress mesenchymal features of ovarian cancer SKOV3 and OVCAR5 cells, evidenced by an apparent morphological change from a mesenchymal to an epithelial phenotype and reduced levels of mesenchymal markers accompanied by the gain of E-cadherin expression. The suppression of EMT is also supported by the observed decrease in cell migration and in vitro invasion upon ISL treatment. Moreover, we show that ISL effectively blocks the intraperitoneal xenograft development of the SKOV3 cell line and prolonged the survival of tumor-bearing mice. These data suggest that ISL inhibits intraperitoneal ovary tumor development through the suppression of EMT, indicating that ISL may be an effective therapeutic agent against ovarian cancer.

KEYWORDS

epithelial-to-mesenchymal transition; isoliquiritigenin; metastasis; ovarian cancer

Title

Isoliquiritigenin Inhibits Ovarian Cancer Metastasis by Reversing Epithelial-to-Mesenchymal Transition.

Author

Chen C1, Huang S2, Chen CL3, Su SB4, Fang DD5.

Publish date

2019 Oct 16

PMID

31444000

Abstract

Secretory diarrhea is one of the most common causes of death world-wide especially in children under 5 years old. Isoliquiritigenin (ISLQ), a plant-derived chalcone, has previously been shown to exert anti-secretory action in vitro and in vivo by inhibiting CFTR Cl- channels. However, its CFTR inhibition potency is considerably low (IC50 > 10 μM) with unknown mechanism of action. This study aimed to identify novel chalcone derivatives with improved potency and explore their mechanism of action. Screening of 27 chalcone derivatives identified CHAL-025 as the most potent chalcone analog that reversibly inhibited CFTR-mediated Cl- secretion in T84 cells with an IC50 of ∼1.5 μM. As analyzed by electrophysiological and biochemical analyses, the mechanism of CFTR inhibition by CHAL-025 is through AMP-activated protein kinase (AMPK), a negative regulator of CFTR activity. Furthermore, Western blot analyses and molecular dynamics (MD) results suggest that CHAL-025 activates AMPK by binding at the allosteric site of an upstream kinase calcium/calmodulin-dependent protein kinase kinase β (CaMKKβ). Interestingly, CHAL-025 inhibited both cholera toxin (CT) and bile acid-induced Cl- secretion in T84 cells and prevented CT-induced intestinal fluid secretion in mice. Therefore, CHAL-025 represents a promising anti-diarrheal agent that inhibits CFTR Cl- channel activity via CaMKKβ-AMPK pathways.

Copyright © 2019 The Authors. Production and hosting by Elsevier B.V. All rights reserved.

KEYWORDS

AMPK; CFTR; Chalcone; Chloride secretion; Diarrhea

Title

Discovery of a novel chalcone derivative inhibiting CFTR chloride channel via AMPK activation and its anti-diarrheal application.

Author

Yibcharoenporn C1, Chusuth P2, Jakakul C3, Rungrotmongkol T4, Chavasiri W5, Muanprasat C6.

Publish date

2019 Jul;

PMID

31438982

Abstract

BACKGROUND:
Arachidonic acid (AA) metabolic enzymes including cyclooxygenase-2 (COX-2), microsomal prostaglandin E synthase-1 (mPGES-1) and cytochrome P450 (CYP) 4A11 play important roles in glioma angiogenesis. Thus, there is an urgent need to identify the underlying mechanisms and develop strategies to overcome them.

METHODS:
A homology model of human CYP4A11 was constructed using SYBYL-X 2.0. Structure-based virtual screening against COX-2, mPGES-1 and CYP4A11was performed using the Surflex-Dock of the SYBYL suite. The candidates were further evaluated their antiangiogenic activities in a zebrafish embryo and rabbit corneal angiogenesis model. Laser doppler analysis was used to measure tumor perfusion. The expression of CD31 and α-SMA was measured by immunofluorescence. Western blot was used to measure the expression of HIF-1, Akt and p-Akt. The gene expression of FGF-2, G-CSF, PDGF, TGF-β, Tie-2, VEGF, lncRNA NEAT1 and miR-194-5p were determined using qPCR. The production of FGF-2, TGF-β and VEGF were analyzed using ELISA. Bioinformatic analysis and luciferase reporter assays confirmed the interaction between lncRNA NEAT1 and miR-194-5p.

RESULTS:
The nearly 36,043 compounds from the Traditional Chinese Medicine (TCM) database were screened against COX-2, mPGES-1 and CYP4A11 3D models, and the 17 top flavonoids were identified. In zebrafish screening, isoliquiritigenin (ISL) exhibited the most potent antiangiogenic activities with the EC50 values of 5.9 μM. Conversely, the antiangiogenic effects of ISL in the zebrafish and rabbit corneal models were partly reversed by 20-hydroxyeicosatetraenoic acid (20-HETE) or prostaglandin E2 (PGE2). ISL normalized glioma vasculature and improved the efficacy of temozolomide therapy in the rat C6 glioma model. Inhibition of COX-2, mPGES-1 and CYP4A by ISL decreased FGF-2, TGF-β and VEGF production in the C6 and U87 glioma cells with p-Akt downregulation, which was reversed by Akt overexpression. Furthermore, ISL downregulated lncRNA NEAT1 but upregulated miR-194-5p in the U87 glioma cell. Importantly, lncRNA NEAT1 overexpression reversed ISL-mediated increase in miR-194-5p expression, and thereby attenuated FGF-2, TGF-β and VEGF production.

CONCLUSIONS:
Reprogramming COX-2, mPGES-1 and CYP4A mediated-AA metabolism in glioma by flavonoid ISL inhibits the angiogenic Akt- FGF-2/TGF-β/VEGF signaling through ceRNA effect of miR-194-5p and lncRNA NEAT1, and may serve as a novel therapeutic strategy for human glioma.

KEYWORDS

Akt; Angiogenesis; Arachidonic acid; Flavonoids; Metabolism; ceRNA

Title

Inhibition of COX-2, mPGES-1 and CYP4A by isoliquiritigenin blocks the angiogenic Akt signaling in glioma through ceRNA effect of miR-194-5p and lncRNA NEAT1.

Author

Wang C1,2, Chen Y2, Wang Y2, Liu X2, Liu Y2, Li Y2, Chen H3, Fan C4, Wu D5, Yang J6.

Publish date

2019 Aug 22


Description :

Isoliquiritigenin is an anti-tumor flavonoid from the root of Glycyrrhiza glabra, which inhibits aldose reductase with an IC50 of 320 nM.