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Anhydroicaritin

$143

  • Brand : BIOFRON

  • Catalogue Number : BF-A2004

  • Specification : 98%

  • CAS number : 38226-86-7

  • Formula : C21H20O6

  • Molecular Weight : 368.38

  • PUBCHEM ID : 14583584

  • Volume : 20mg

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Catalogue Number

BF-A2004

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

368.38

Appearance

Yellow crystalline powder/Yellow powder

Botanical Source

Epimedium koreanum

Structure Type

Flavonoids

Category

Standards;Natural Pytochemical;API

SMILES

CC1(CCC2=C(O1)C=C(C3=C2OC(=C(C3=O)O)C4=CC=C(C=C4)OC)O)C

Synonyms

3,5-Dihydroxy-2-(4-methoxyphenyl)-8,8-dimethyl-9,10-dihydro-4H,8H-pyrano[2,3-f]chromen-4-one/Anhydroicaritin/Cycloicaritin/4H,8H-Benzo[1,2-b:3,4-b']dipyran-4-one, 9,10-dihydro-3,5-dihydroxy-2-(4-methoxyphenyl)-8,8-dimethyl-/Anhydroicaritin, Beta-/Anhydroicaritin, β-

IUPAC Name

3,5-dihydroxy-2-(4-methoxyphenyl)-8,8-dimethyl-9,10-dihydropyrano[2,3-h]chromen-4-one

Applications

β-Anhydroicaritin is isolated from Boswellia carterii Birdware, has important biological and pharmacological effects, such as antiosteoporosis, estrogen regulation and antitumor properties[1][2]. β-Anhydroicaritin decreases the overproduction of NO, IL-10, TNF-α, MCP-1 and IL-6 in inperitonitis mice. β-Anhydroicaritin inhibits the elevation of intracellular Ca2+, and markedly decreases iNOS protein expression[3].

Density

1.4±0.1 g/cm3

Solubility

Methanol; Dichloromethane

Flash Point

205.5±23.6 °C

Boiling Point

575.3±50.0 °C at 760 mmHg

Melting Point

InChl

InChl Key

WGK Germany

RID/ADR

HS Code Reference

2932990000

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:38226-86-7) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

30237061

Abstract

Cycloicaritin is a bioactive natural phenolic compound from Epimedium species. However, the glucuronidation and excretion which would influence oral bioavailability and pharmacokinetics of cycloicaritin still remain unknown. Here we aimed to establish UGT1A1 stably transfected HeLa cells, and to determine the contributions of BCRP and MRPs transporters to excretion of cycloicaritin-3-O-glucuronide. First, β-estradiol was used to validate the expression of active UGT1A1 protein in engineered HeLa1A1 cells. Furthermore, Ko143 (5 and 20 μM) led to a significant decrease (42.4%-63.8%, p < 0.01) in CICT-3-G excretion and obvious accumulation (19.7%-54.2%, p < 0.05) of intracellular CICT-3-G, while MK571 (5 and 20 μM) caused a significant reduction (46.8%-64.8%, p < 0.05) in the excretion and obvious elevation (50.7%-85.2%, p < 0.01) of intracellular level of CICT-3-G. Furthermore, BCRP knocked-down brought marked reduction in excretion rates of CICT-3-G (26.0%-42.2%, p < 0.01), whereas MRP1 and MRP4-mediated silencing led to significant decrease in the excretion of CICT-3-G (23.8%-35.4%, p < 0.05 for MRP1 and 11.9%-16.0%, p < 0.05 for MRP4). By contrast, neither CICT-3-G excretion nor CICT-3-G accumulation altered in MRP3 knocked-down cells as compared to scramble cells. Taken together, BCRP, MRP1 and MRP4 were identified as the most important contributors for CICT-3-G excretion. Meanwhile, the UGT1A1 modified HeLa cells were a simple and practical tool to study UGT1A1-mediated glucuronidation and to characterize BCRP and MRPs-mediated glucuronide transport at a cellular level.

KEYWORDS

Cycloicaritin, UGT1A1, Glucuronidation, HeLa cells, Efflux transporters

Title

The roles of breast cancer resistance protein (BCRP/ABCG2) and multidrug resistance-associated proteins (MRPs/ABCCs) in the excretion of cycloicaritin-3-O-glucoronide in UGT1A1-overexpressing HeLa cells

Author

Shishi Li,a,1 Jinjin Xu,a,1 Zhihong Yao,a,b,* Liufang Hu,a Zifei Qin,a,c,** Hao Gao,a,b Kristopher W. Krausz,d Frank J. Gonzalez,d and Xinsheng Yaoa,b

Publish date

2018 Sep 17

PMID

28501578

Abstract

Nowadays, more and more attention has been paid to osteoporosis caused by diabetes mellitus. Elevated levels of pro-inflammatory cytokines in diabetic patients activate the activity of osteoclasts through the RANKL/OPG pathway. The nuclear transcription factor SREBP2, a master regulator of cholesterol metabolism, has been found involved in osteoclastogenesis. In our previous study, we have identified anhydroicaritin as a potent inhibitor of transcription factor SREBPs, which improves dyslipidemia and insulin resistance. In this study, we demonstrated that anhydroicaritin could also decrease the level of SREBP2 and its target genes in osteoclasts induced by RANKL without significant cytotoxicity. Moreover, anhydroicaritin suppressed RANKL-induced osteoclasts differentiation. In STZ-induced diabetic mice model, we found that the osteoclasts were largely increased accompanied with deterioration of bone structure. Anhydroicaritin decreased the level of blood glucose and alleviated insulin resistance. More importantly, anhydroicaritin inhibited osteoclast differentiation and rescued diabetes-induced bone loss in vivo. In conclusion, anhydroicaritin, a potent SREBP2 inhibitor, inhibits the osteoclasts formation and improves diabetes-induced bone loss.

Copyright © 2017 Elsevier B.V. All rights reserved.

KEYWORDS

Anhydroicaritin; Diabetic osteoporosis; Osteoclastic differentiation; SREBP2

Title

Anhydroicaritin, a SREBPs inhibitor, inhibits RANKL-induced osteoclastic differentiation and improves diabetic osteoporosis in STZ-induced mice.

Author

Zheng ZG1, Zhang X1, Zhou YP1, Lu C1, Thu PM1, Qian C1, Zhang M1, Li P1, Li HJ2, Xu X3.

Publish date

2017 Aug 15