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Actein

$400

  • Brand : BIOFRON

  • Catalogue Number : BD-R0122

  • Specification : 98%

  • CAS number : 18642-44-9

  • Formula : C37H56O11

  • Molecular Weight : 676.9

  • PUBCHEM ID : 10032468

  • Volume : 5mg

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Catalogue Number

BD-R0122

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

676.9

Appearance

Powder

Botanical Source

Actaea racemosa (Cimicifuga racemosa) and Cimicifuga spicata

Structure Type

Triterpenoids

Category

SMILES

CC1CC2(C3C(O3)(C(O2)O)C)OC4C1C5(C(CC67CC68CCC(C(C8CCC7C5(C4)C)(C)C)OC9C(C(C(CO9)O)O)O)OC(=O)C)C

Synonyms

[(1S,1'R,2S,3'R,4R,4'R,5R,5'R,6'R,10'S,12'S,13'S,16'R,18'S,21'R)-2-hydroxy-1,4',6',12',17',17'-hexamethyl-18'-[(2S,3R,4S,5R)-3,4,5-trihydroxyoxan-2-yl]oxyspiro[3,6-dioxabicyclo[3.1.0]hexane-4,8'-9-oxahexacyclo[11.9.0.01,21.04,12.05,10.016,21]docosane]-3'-yl] acetate

IUPAC Name

[(1S,1'R,2S,3'R,4R,4'R,5R,5'R,6'R,10'S,12'S,13'S,16'R,18'S,21'R)-2-hydroxy-1,4',6',12',17',17'-hexamethyl-18'-[(2S,3R,4S,5R)-3,4,5-trihydroxyoxan-2-yl]oxyspiro[3,6-dioxabicyclo[3.1.0]hexane-4,8'-9-oxahexacyclo[11.9.0.01,21.04,12.05,10.016,21]docosane]-3'-yl] acetate

Density

1.4±0.1 g/cm3

Solubility

Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.

Flash Point

Boiling Point

Melting Point

246-250ºC

InChl

InChI=1S/C37H56O11/c1-17-12-37(29-34(7,47-29)30(42)48-37)46-20-13-32(5)22-9-8-21-31(3,4)23(45-28-27(41)26(40)19(39)15-43-28)10-11-35(21)16-36(22,35)14-24(44-18(2)38)33(32,6)25(17)20/h17,19-30,39-42H,8-16H2,1-7H3/t17-,19-,20+,21+,22+,23+,24-,25+,26+,27-,28+,29-,30+,32+,33-,34+,35-,36+,37-/m1/s1

InChl Key

NEWMWGLPJQHSSQ-PSDKAYTQSA-N

WGK Germany

RID/ADR

HS Code Reference

2933990000

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:18642-44-9) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

No Technical Documents Available For This Product.

PMID

29969672

Abstract

Previous studies indicate that the herb black cohosh (Actaea racemosa L.) and the triterpene glycoside actein inhibit the growth of human breast cancer cells and activate stress-associated responses. This study assessed the transcriptomic effects of black cohosh and actein on rat liver tissue, using Ingenuity and ToxFX analyses. Sprague-Dawley rats were treated with an extract of black cohosh enriched in triterpene glycosides (27%) for 24 h or actein for 6 and 24 h, at 35.7 mg/kg, and liver tissue collected for gene expression analysis. Ingenuity analysis indicates the top canonical pathways are, for black cohosh, RAR Activation, and, for actein, Superpathway of Cholesterol Biosynthesis, at 24 h. Actein alters the expression of cholesterol biosynthetic genes, but does not inhibit HMG-CoA reductase activity. Black cohosh and actein inhibited the growth of human breast and colon cancer cells and synergized with the statin simvastatin. Combinations of black cohosh with certain classes of statins could enhance their activity, as well as toxic, such as inflammatory liver, side effects. Transcriptomic analysis indicates black cohosh and actein warrant further study to prevent and treat cancer and lipid disorders. This study lays the basis for an approach to characterize the mode of action and toxicity of herbal medicines.

KEYWORDS

Actein; Actein (PubChem CID: 24764419); Black cohosh; Microarrays; Ranunculaceae; Simvastatin; Simvastatin (PubChem CID: 54454); Triterpene glycoside.

Title

A transcriptomic analysis of black cohosh: Actein alters cholesterol biosynthesis pathways and synergizes with simvastatin

Author

Linda Saxe Einbond 1, Morando Soffritti 2, Davide Degli Esposti 3, Hsan-Au Wu 4, Michael Balick 5, Hongbao Ma 4, Stephen Redenti 6, Alan Roter 7

Publish date

2018 Oct;

PMID

29156528

Abstract

Insulin and leptin resistance are highly involved in metabolic syndrome and non-alcoholic fatty liver disease (NAFLD). Presently, no approved treatment is available. Actein is isolated from the rthizomes of Cimicifuga foetida, a triterpene glycoside, exhibiting important biological properties, such as anti-inflammatory, anti-cancer, and anti-oxidant activity. However, its effects on metabolic syndrome are poorly understood. The aims of the study were mainly to investigate the molecular mechanisms regulating insulin and leptin resistance, and lipogenic action of actein in high fat diet-fed mice. Our data indicated that actein-treated mice displayed lower body weight, epididymal and subcutaneous fat mass, as well as serum lipid levels. Also, improved insulin and leptin resistance were observed in actein-treated groups. Liver inflammation and fibrosis triggered by high fat diet were decreased for actein administration. Moreover, hepatic lipid accumulation was also reduced by actein along with reductions of hepatic de novo lipogenesis-linked signals in actein-treated rodents with high fat diet. High fat diet-induced activation of insulin receptor substrate 1/Forkhead box protein O1 (IRS1/FOXO1), Janus kinase 2 gene/signal transducer and activator of transcription (JAK2/STAT3) and Protein Kinase B/Glycogen synthase kinase 3 beta (AKT/GSK3β) pathways in liver was inhibited by actein, a potential mechanism by which hyperinsulinemia, hyperleptindemia and dyslipidemia were attenuated. Thus, the findings above might be of nutritional and therapeutic importance for the treatment of NAFLD.

KEYWORDS

AKT/GSK3β; Actein; IRS1/FOXO1; Insulin and leptin resistance; JAK2/STAT3; NAFLD.

Title

Actein ameliorates hepatic steatosis and fibrosis in high fat diet-induced NAFLD by regulation of insulin and leptin resistant

Author

Hong-Jun Chen 1, Jin Liu 2

Publish date

2018 Jan;

PMID

29089760

Abstract

Actein (AT) is a triterpene glycoside isolated from the rhizomes of Cimicifuga foetida that has been investigated for its antitumor effects. AT treatment leads to apoptosis in various cell types, including breast cancer cells, by regulating different signaling pathways. Iron oxide (Fe3O4) magnetic nanoparticles (MNPs) are nanomaterials with biocompatible activity and low toxicity. In the present study, the possible benefits of AT in combination with MNPs on non-small-cell lung cancer (NSCLC) were explored in in vitro and in vivo studies. AT-MNP treatment contributed to apoptosis in NSCLC cells, as evidenced by activation of the caspase 3-signaling pathway, which was accompanied by downregulation of the antiapoptotic proteins Bcl2 and BclXL, and upregulation of the proapoptotic signals Bax and Bad. The death receptors of TRAIL were also elevated following AT-MNP treatment in a p53-dependent manner. Furthermore, a mouse xenograft model in vivo revealed that AT-MNP treatment exhibited no toxicity and suppressed NSCLC growth compared to either AT or MNP monotherapies. In conclusion, this study suggests a novel therapy to induce apoptosis in suppressing NSCLC growth in a p53-dependent manner by combining AT with Fe3O4 MNPs.

KEYWORDS

Fe3O4 magnetic nanoparticles; NSCLC; actein; apoptosis; p53.

Title

Iron oxide magnetic nanoparticles combined with actein suppress non-small-cell lung cancer growth in a p53-dependent manner

Author

Ming-Shan Wang 1, Liang Chen 2, Ya-Qiong Xiong 2, Jing Xu 2, Ji-Peng Wang 2, Zi-Li Meng 2

Publish date

2017 Oct 17;


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