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Gomisin J

$225

  • Brand : BIOFRON

  • Catalogue Number : BF-G1023

  • Specification : 98%

  • CAS number : 66280-25-9

  • Formula : C22H28O6

  • Molecular Weight : 388.45

  • PUBCHEM ID : 3001686

  • Volume : 10mg

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Catalogue Number

BF-G1023

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

-20℃

Molecular Weight

388.45

Appearance

White crystalline powder

Botanical Source

Schisandra chinensis

Structure Type

Lignanoids

Category

Standards;Natural Pytochemical;API

SMILES

CC1CC2=CC(=C(C(=C2C3=C(C(=C(C=C3CC1C)O)OC)OC)OC)OC)O

Synonyms

Dibenzo[a,c]cyclooctene-3,10-diol, 5,6,7,8-tetrahydro-1,2,11,12-tetramethoxy-6,7-dimethyl-, (6R,7S)-/(-)-gomisin J/(6R,7S)-1,2,11,12-Tetramethoxy-6,7-dimethyl-5,6,7,8-tetrahydrodibenzo[a,c][8]annulene-3,10-diol/6(S),7(R)-Dibenzo(a,c)cyclooctene-3,10-diol,5,6,7,8-tetrahydro-1,2,11,12-tetramethoxy-6,7-dimethyl/Dibenzo(a,c)cyclooctene-3,10-diol,5,6,7,8-tetrahydro-1,2,11,12-tetramethoxy-6,7-dimethyl-,stereoisomer

IUPAC Name

(9S,10R)-3,4,15,16-tetramethoxy-9,10-dimethyltricyclo[10.4.0.02,7]hexadeca-1(16),2,4,6,12,14-hexaene-5,14-diol

Density

1.161

Solubility

Methanol; Acetone; Ethyl Acetate

Flash Point

309.1±30.1 °C

Boiling Point

587.5±50.0 °C at 760 mmHg

Melting Point

148-149 ºC

InChl

InChI=1S/C22H28O6/c1-11-7-13-9-15(23)19(25-3)21(27-5)17(13)18-14(8-12(11)2)10-16(24)20(26-4)22(18)28-6/h9-12,23-24H,7-8H2,1-6H3/t11-,12+

InChl Key

PICOUNAPKDEPCA-TXEJJXNPSA-N

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#:66280-25-9) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

26455261

Abstract

The aim of our study is to investigate the molecular mechanism of gomisin J from Schisandra chinensis on the oleic acid (OA)-induced lipid accumulation in HepG2 cells. Gomisin J attenuated lipid accumulation in OA-induced HepG2 cells. It also suppressed the expression of lipogenic enzymes and inflammatory mediators and increased the expression of lipolytic enzymes in OA-induced HepG2 cells. Furthermore, the use of specific inhibitors and fetuin-A siRNA and liver kinase B1 (LKB1) siRNA transfected cells demonstrated that gomisin J regulated lipogenesis and lipolysis via inhibition of fetuin-A and activation of an AMP-activated protein kinase (AMPK)-dependent pathway in HepG2 cells. Our results showed that gomisin J suppressed lipid accumulation by regulating the expression of lipogenic and lipolytic enzymes and inflammatory molecules through activation of AMPK, LKB1, and Ca(2+)/calmodulin-dependent protein kinase II and inhibition of fetuin-A in HepG2 cells. This suggested that gomisin J has potential benefits in treating nonalcoholic fatty liver disease.

KEYWORDS

AMPK; CaMKII; LKB1; fetuin-A; gomisin J

Title

Gomisin J Inhibits Oleic Acid-Induced Hepatic Lipogenesis by Activation of the AMPK-Dependent Pathway and Inhibition of the Hepatokine Fetuin-A in HepG2 Cells.

Author

Kim M1, Lim SJ1,2, Lee HJ1, Kim SY1, Nho CW1.

Publish date

2015 Nov 11

PMID

30542721

Abstract

In attempting to identify effective anticancer drugs from natural products that are harmless to humans, we found that the gomisin J from Schisandra chinensis fruit has anticancer activity. Schisandra chinensis fruits are used in traditional herbal medicine and gomisin J is one of their chemical constituents. In the present study, we examined the anticancer activity of gomisin J in MCF7 and MDA-MB-231 breast cancer cell lines and in MCF10A normal cell line, in a time- and concentration-dependent manner. Our data revealed that gomisin J exerted a much stronger cytotoxic effect on MCF7 and MDA-MB-231 cancer cells than on MCF10A normal cells. Gomisin J suppressed the proliferation and decreased the viability of MCF7 and MDA-MB-231 cells at relatively low (<10 µg/ml) and high (>30 µg/ml) concentrations, respectively. Our data also revealed that gomisin J induced necroptosis, a programmed form of necrosis, as well as apoptosis. Notably, gomisin J predominantly induced necroptosis in MCF7 cells that are known to have high resistance to many pro-apoptotic anticancer drugs, while MDA-MB-231 exhibited a much lower level of necroptosis but instead a higher level of apoptosis. This data indicated the possibility that it may be used as a more effective anticancer drug, especially in apoptosis-resistant malignant cancer cells. In an extended study, gomisin J exhibited a strong cytotoxic effect on all tested various types of 13 cancer cell lines, indicating its potential to be used against a wide range of different types of cancer cells.

Title

Anticancer activity of gomisin J from Schisandra chinensis fruit.

Author

Jung S1, Moon HI2, Kim S1, Quynh NTN1, Yu J2, Sandag Z1, Le DT1, Lee H1, Lee H1, Lee MS1.

Publish date

2019 Jan

PMID

9863151

Abstract

AIM:
To study the influences of gomisin J on lipid peroxidation and calcium paradox.

METHODS:
Using two in vitro models of rat liver mitochondria membrane lipid peroxidation (LPO) and cultured myocardial cells.

RESULTS:
Gomisin J inhibited Fe2+/ascorbic acid and ADP/NADPH-induced LPO with IC50 (95% confidence limits) 5.5 (4.5-6.7) and 4.7 (2.8-7.8) mumol.L-1, respectively, when cultured myocardial cells preincubated with Ca(2+)-free medium for 2 min were incubated with normal medium containing Ca2+, a marked increase of malondialdehyde (MDA) formation occurred and gomisin J 10 mumol.L-1 protected myocardial cells through decreasing MDA formation.

CONCLUSION:
Gomisin J inhibits LPO in rat liver mitochondria and protects cultured myocardial cells from being injured by calcium paradox.

Title

Anti-lipid peroxidation of gomisin J on liver mitochondria and cultured myocardial cells.

Author

Peng HL1, Chen DF, Lan HX, Zhang XM, Gu Z, Jiang MH.

Publish date

1996 Nov


Description :

Gomisin J is a small molecular weight lignan found in Schisandra chinensis and has been demonstrated to have vasodilatory activity[1]. Gomisin J suppresses lipid accumulation by regulating the expression of lipogenic and lipolytic enzymes and inflammatory molecules through activation of AMPK, LKB1 and Ca2+/calmodulin-dependent protein kinase II and inhibition of fetuin-A in HepG2 cells. gomisin J has potential benefits in treating nonalcoholic fatty liver disease[2].