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Tectoridin

$113

  • Brand : BIOFRON

  • Catalogue Number : BF-T3004

  • Specification : 98%

  • CAS number : 611-40-5

  • Formula : C22H22O11

  • Molecular Weight : 462.405

  • PUBCHEM ID : 5281810

  • Volume : 20mg

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Catalogue Number

BF-T3004

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

462.405

Appearance

White crystalline powder

Botanical Source

Belamcanda chinensis,Iris tectorum,Iris dichotoma

Structure Type

Flavonoids

Category

Standards;Natural Pytochemical;API

SMILES

COC1=C(C=C2C(=C1O)C(=O)C(=CO2)C3=CC=C(C=C3)O)OC4C(C(C(C(O4)CO)O)O)O

Synonyms

4H-1-Benzopyran-4-one, 7-(β-D-glucopyranosyloxy)-5-hydroxy-3-(4-hydroxyphenyl)-6-methoxy-/Tectorigenin 7-glucoside/4',5-Dihydro-6-methoxy-7-(o-glucoside)isoflavone/5-Hydroxy-3-(4-hydroxyphenyl)-6-methoxy-4-oxo-4H-chromen-7-yl β-D-glucopyranoside/Shekanin/tectoridin/Tectoridin (7CI,8CI)/5-hydroxy-3-(4-hydroxyphenyl)-6-methoxy-7-[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxychromen-4-one

IUPAC Name

5-hydroxy-3-(4-hydroxyphenyl)-6-methoxy-7-[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxychromen-4-one

Density

1.6±0.1 g/cm3

Solubility

Methanol; Ethanol

Flash Point

279.7±26.4 °C

Boiling Point

798.1±60.0 °C at 760 mmHg

Melting Point

261.8-263.2ºC

InChl

InChl Key

WGK Germany

RID/ADR

HS Code Reference

2938900000

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:611-40-5) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

26452883

Abstract

A simple, inexpensive and highly sensitive voltammetric method for the determination of tectoridin was developed using a poly(L-Arginine) modified electrode. The redox character of tectoridin at proposed electrode was studied systematically and some dynamic parameters were calculated for the first time. A reasonable reaction mechanism of tectoridin on the poly(L-Arginine)/GCE was also dicussed and proposed, which could be a reference for the pharmacological action of tectoridin in clinical study. And the electroanalytical method for determination of tectoridin was established by differential pulse voltammograms (DPV). Under optimum conditions, the response peak currents were linear relationship with tectoridin concentrations in the range of 5.0×10(-8)-2.0×10(-6) mol L(-1) with a detection limit of 4.0×10(-8) mol L(-1). Therefore, the high sensitivity for tectoridin sensing at the proposed electrode was achieved, and the proposed method could also be used to detect tectoridin in the Chinese medicinal herb Blackberrylily with satisfactory results.

Copyright © 2015 Elsevier B.V. All rights reserved.

KEYWORDS

Electrochemical sensor; Electropolymerization; L-Arginine; Tectoridin

Title

Electrochemical behavior of tectoridin and its sensitive determination based on L-arginine modified electrode.

Author

Qiao W1, Wang L2, Li H1, Li G1, Li J1, Ye B3.

Publish date

2015 Nov 1

PMID

24252334

Abstract

AIM:
The stem bark of Maackia amurensis has been used as folk medicine for the treatment of cancer, cholecystitis, arthritis, and hyperthyroidism in females. In this study we examined the effects of the ethyl acetate fraction obtained from the 70% ethanol extract of M. amurensis and tectoridin, an active constituent isolated from the ethyl acetate fraction on thyroid and estrogen hormone activity.

METHODS:
The effect of the ethanolic extract of M. amurensis stem bark on thyroid hormone activity was evaluated using thyroid hormone responsive-luciferase assay. We isolated tectoridin from the ethyl acetate fraction using a recrystallization method. T-screen assays were used to confirm thyroid hormone activity. The estrogenic activity of the ethyl acetate fraction of M. amurensis and tectoridin was evaluated by estrogen responsive-luciferase assay and estrogen receptor alpha regulation as compared to 17β-estradiol.

RESULTS:
Both the ethyl acetate fraction and tectoridin activated thyroid-responsive reporters and increased thyroid hormone-dependent proliferation of rat pituitary GH3 cells, indicating modulation of thyroid hormone receptors. In parallel, the estrogenic activity of the fraction and tectoridin were characterized in a transient transfection system using estrogen-responsive luciferase plasmids in MCF-7 cells. The ethyl acetate fraction and tectoridin activated reporter gene expression and decreased the estrogen receptor protein level.

CONCLUSIONS:
These data indicate that tectoridin acts as a weak phytoestrogen as well as a thyroid hormone-like agent by activating both estrogen and thyroid hormone receptors.

Copyright © 2013 Elsevier GmbH. All rights reserved.

KEYWORDS

Estrogen receptor; Maackia amurensis; Tectoridin; Thyroid receptor

Title

Tectoridin from Maackia amurensis modulates both estrogen and thyroid receptors.

Author

Shim M1, Bae JY2, Lee YJ3, Ahn MJ4.

Publish date

2014 Apr 15

PMID

25256063

Abstract

This study investigated the urinary and biliary excretion of tectoridin, a major active isoflavonoid found in the flowers of Pueraria thomsonii Benth. and the rhizomes of Belamcanda chinensis (L.) DC. Using UHPLC/Q-TOFMS, seven glucuronides and/or sulfated metabolites and four Phase I metabolites were simultaneously quantified in rat urine after oral administration of tectoridin at 100 and 200 mg/kg. Over a 72-h period, 14.2% and 14.7% of the tectoridin were excreted as eleven metabolites in urine, among which, two major metabolites tectorigenin-7-O-β-D-glucuronide (Te-7G) and tectorigenin accounted for 5.5-5.5% and 4.3-4.4%. Furthermore, the cumulative excretion of four glucuronides and sulfated metabolites in bile accounted for 7.3% and 3.9% of the dose within 60 h, among which, Te-7G and tectorigenin-7-O-glucuronide-4′-O-sulfate (Te-7G-4’S) accounted for 2.3-3.0% and 1.4-3.9%, respectively. The results indicate that the urine was the primary elimination route, and glucuronidation after deglycosylation at C-7 position was the major metabolic pathway of tectoridin in vivo. Moreover, the inhibitory activities of tectoridin and its five metabolites on rat lens aldose reductase were confirmed (IC₅₀: 1.4-15.5 μM), whereas irisolidone-7-O-glucuronide (Ir-7G) and irisolidone showed little activity.

Copyright © 2014 Elsevier B.V. All rights reserved.

KEYWORDS

Aldose reductase inhibitory activity; Conjugate metabolites; Excretion; Tectoridin; UHPLC/Q-TOF MS

Title

Excretion of tectoridin metabolites in rat urine and bile orally administrated at different dosages and their inhibitory activity against aldose reductase.

Author

Qu J1, Wu Z2, Gao J1, Wen H1, Wang T3, Yuan D4.

Publish date

2014 Dec


Description :

Excretion of tectoridin metabolites in rat urine and bile orally administrated at different dosages and their inhibitory activity against aldose reductase PUMID/DOI:25256063 Fitoterapia. 2014 Dec;99:99-108. This study investigated the urinary and biliary excretion of Tectoridin, a major active isoflavonoid found in the flowers of Pueraria thomsonii Benth. and the rhizomes of Belamcanda chinensis (L.) DC. Using UHPLC/Q-TOFMS, seven glucuronides and/or sulfated metabolites and four Phase I metabolites were simultaneously quantified in rat urine after oral administration of Tectoridin at 100 and 200 mg/kg. Over a 72-h period, 14.2% and 14.7% of the Tectoridin were excreted as eleven metabolites in urine, among which, two major metabolites tectorigenin-7-O-β-D-glucuronide (Te-7G) and tectorigenin accounted for 5.5-5.5% and 4.3-4.4%. Furthermore, the cumulative excretion of four glucuronides and sulfated metabolites in bile accounted for 7.3% and 3.9% of the dose within 60 h, among which, Te-7G and tectorigenin-7-O-glucuronide-4'-O-sulfate (Te-7G-4'S) accounted for 2.3-3.0% and 1.4-3.9%, respectively. The results indicate that the urine was the primary elimination route, and glucuronidation after deglycosylation at C-7 position was the major metabolic pathway of Tectoridin in vivo. Moreover, the inhibitory activities of Tectoridin and its five metabolites on rat lens aldose reductase were confirmed (IC50: 1.4-15.5 μM), whereas irisolidone-7-O-glucuronide (Ir-7G) and irisolidone showed little activity. Tectoridin from Maackia amurensis modulates both estrogen and thyroid receptors. PUMID/DOI:24252334 Phytomedicine. 2014 Apr 15;21(5):602-6. AIM:||The stem bark of Maackia amurensis has been used as folk medicine for the treatment of cancer, cholecystitis, arthritis, and hyperthyroidism in females. In this study we examined the effects of the ethyl acetate fraction obtained from the 70% ethanol extract of M. amurensis and Tectoridin, an active constituent isolated from the ethyl acetate fraction on thyroid and estrogen hormone activity.||METHODS:||The effect of the ethanolic extract of M. amurensis stem bark on thyroid hormone activity was evaluated using thyroid hormone responsive-luciferase assay. We isolated Tectoridin from the ethyl acetate fraction using a recrystallization method. T-screen assays were used to confirm thyroid hormone activity. The estrogenic activity of the ethyl acetate fraction of M. amurensis and Tectoridin was evaluated by estrogen responsive-luciferase assay and estrogen receptor alpha regulation as compared to 17β-estradiol.||RESULTS:||Both the ethyl acetate fraction and Tectoridin activated thyroid-responsive reporters and increased thyroid hormone-dependent proliferation of rat pituitary GH3 cells, indicating modulation of thyroid hormone receptors. In parallel, the estrogenic activity of the fraction and Tectoridin were characterized in a transient transfection system using estrogen-responsive luciferase plasmids in MCF-7 cells. The ethyl acetate fraction and Tectoridin activated reporter gene expression and decreased the estrogen receptor protein level.||CONCLUSIONS:||These data indicate that Tectoridin acts as a weak phytoestrogen as well as a thyroid hormone-like agent by activating both estrogen and thyroid hormone receptors. Inhibition by tectorigenin and tectoridin of prostaglandin E2 production and cyclooxygenase-2 induction in rat peritoneal macrophages. PUMID/DOI:10366782 Biochim Biophys Acta. 1999 Jun 10;1438(3):399-407. Tectorigenin and Tectoridin, isolated from the rhizomes of Korean Belamcanda chinensis (Iridaceae) which are used as Chinese traditional medicine for the treatment of inflammation, suppressed prostaglandin E2 production by rat peritoneal macrophages stimulated by the protein kinase C activator, 12-O-tetradecanoylphorbol 13-acetate (TPA), or the endomembrane Ca2+-ATPase inhibitor, thapsigargin. Tectorigenin inhibited prostaglandin E2 production more potently than Tectoridin. Neither compound inhibited the release of radioactivity from [3H]arachidonic acid-labeled macrophages stimulated by TPA or thapsigargin. In addition, activities of isolated cyclooxygenase (COX)-1 and COX-2 were not inhibited by the two compounds. Western blot analysis revealed that the induction of COX-2 by TPA or thapsigargin was inhibited by the two compounds in parallel with the inhibition of prostaglandin E2 production. These findings suggest that one of the mechanisms of the anti-inflammatory activities of the rhizomes of Belamcanda chinensis is the inhibition of prostaglandin E2 production by tectorigenin and Tectoridin due to the inhibition of the induction of COX-2 in the inflammatory cells. Metabolism of 6""-O-xylosyltectoridin and tectoridin by human intestinal bacteria and their hypoglycemic and in vitro cytotoxic activities PUMID/DOI:10746163 Biol Pharm Bull. 1999 Dec;22(12):1314-8. 6""-O-XylosylTectoridin and Tectoridin isolated from the flowers of Pueraria thunbergiana (Leguminosae), are metabolized to tectorigenin by human intestinal bacteria. Although Tectoridin is metabolized to tectorigenin by most intestinal bacteria, 6""-O-xylosylTectoridin is metabolized to tectorigenin via Tectoridin by only a few intestinal bacteria, such as Bifidobacterium breve K-110 and Eubacterium A-44. The metabolite, tectorigenin, had more potent hypoglycemic activity as well as in vitro cytotoxic activity against tumor cell lines than 6""-O-xylosylTectoridin and Tectoridin. These results suggest that 6""-O-xylosylTectoridin and Tectoridin are prodrugs which can be transformed to the active agents by human intestinal bacteria. Tectoridin, a poor ligand of estrogen receptor alpha, exerts its estrogenic effects via an ERK-dependent pathway. PUMID/DOI:19326083 Mol Cells. 2009 Mar 31;27(3):351-7. The Tectoridin-induced estrogenic effect was severely abrogated by treatment with U0126, a specific MEK1/2 inhibitor. Tectoridin promoted phosphorylation of ERK1/2, but did not affect phosphorylation of ER alpha at Ser(118). It also increased cellular accumulation of cAMP, a hallmark of GPR30-mediated estrogen signaling. These data imply that Tectoridin exerts its estrogenic effect mainly via the GPR30 and ERK-mediated rapid nongenomic estrogen signaling pathway. This property of Tectoridin sets it aside from genistein where it exerts the estrogenic effects via both an ER-dependent genomic pathway and a GPR30-dependent nongenomic pathway.