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Gomisin G

$572

  • Brand : BIOFRON

  • Catalogue Number : BD-P0032

  • Specification : 98.0%(HPLC)

  • CAS number : 62956-48-3

  • Formula : C30H32O9

  • Molecular Weight : 536.6

  • PUBCHEM ID : 14992067

  • Volume : 25mg

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Catalogue Number

BD-P0032

Analysis Method

Specification

98.0%(HPLC)

Storage

-20℃

Molecular Weight

536.6

Appearance

Powder

Botanical Source

This product is isolated and purified from the fruits of Schizandra chinensis

Structure Type

Category

SMILES

CC1CC2=CC(=C(C(=C2C3=C(C4=C(C=C3C(C1(C)O)OC(=O)C5=CC=CC=C5)OCO4)OC)OC)OC)OC

Synonyms

(6S,7S,8S)-7-Hydroxy-1,2,3,13-tetramethoxy-6,7-dimethyl-5,6,7,8-tetrahydrobenzo[3',4']cycloocta[1',2':4,5]benzo[1,2-d][1,3]dioxol-8-yl benzoate/Benzo[3',4']cycloocta[1',2':4,5]benzo[1,2-d][1,3]dioxole-7,8-diol, 5,6,7,8-tetrahydro-1,2,3,13-tetramethoxy-6,7-dimethyl-, 8-benzoate, (6S,7S,8S)-/The dried fruit of Schisandra chinensis

IUPAC Name

Density

1.3±0.1 g/cm3

Solubility

Methanol

Flash Point

217.2±25.0 °C

Boiling Point

670.9±55.0 °C at 760 mmHg

Melting Point

InChl

InChl Key

OFDWKHIQKPKRKY-DSASHONVSA-N

WGK Germany

RID/ADR

HS Code Reference

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:62956-48-3) 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

29587339

Abstract

A type of breast cancer with a defect in three molecular markers such as the estrogen receptor, progesterone receptor, and human epidermal growth factor receptor is called triple-negative breast cancer (TNBC). Many patients with TNBC have a lower survival rate than patients with other types due to a poor prognosis. In this study, we confirmed the anti-cancer effect of a natural compound, Gomisin G, in TNBC cancer cells. Treatment with Gomisin G suppressed the viability of two TNBC cell lines, MDA-MB-231 and MDA-MB-468 but not non-TNBC cell lines such as MCF-7, T47D, and ZR75-1. To investigate the molecular mechanism of this activity, we examined the signal transduction pathways after treatment with Gomisin G in MDA-MB-231 cells. Gomisin G did not induce apoptosis but drastically inhibited AKT phosphorylation and reduced the amount of retinoblastoma tumor suppressor protein (Rb) and phosphorylated Rb. Gomisin G induced in a proteasome-dependent manner a decrease in Cyclin D1. Consequently, Gomisin G causes cell cycle arrest in the G1 phase. In contrast, there was no significant change in T47D cells except for a mild decrease in AKT phosphorylation. These results show that Gomisin G has an anti-cancer activity by suppressing proliferation rather than inducing apoptosis in TNBC cells. Our study suggests that Gomisin G could be used as a therapeutic agent in the treatment of TNBC patients.

KEYWORDS

AKT; Cell cycle; Cell proliferation; Cyclin D1; Gomisin G; Triple negative breast cancer

Title

Gomisin G Inhibits the Growth of Triple-Negative Breast Cancer Cells by Suppressing AKT Phosphorylation and Decreasing Cyclin D1.

Author

Maharjan S1, Park BK1, Lee SI1, Lim Y2, Lee K3, Kwon HJ1,4.

Publish date

2018 May 1

PMID

29902863

Abstract

Colorectal cancer is one of the leading causes of cancer related death due to a poor prognosis. In this study, we investigated the effect of Gomisin G on colon cancer growth and examined the underlying mechanism of action. We found that Gomisin G significantly suppressed the viability and colony formation of LoVo cells. Gomisin G reduced the phosphorylation level of AKT implying that Gomisin G suppressed the PI3K-AKT signaling pathway. Gomisin G also induced apoptosis shown by Annexin V staining and an increased level of cleaved poly-ADP ribose polymerase (PARP) and Caspase-3 proteins. Furthermore, Gomisin G remarkably triggered the accumulation of cells at the sub-G1 phase which represents apoptotic cells. In addition, the level of cyclin D1 and phosphorylated retinoblastoma tumor suppressor protein (Rb) was also reduced by the treatment with Gomisin G thus curtailing cell cycle progression. These findings show the suppressive effect of Gomisin G by inhibiting proliferation and inducing apoptosis in LoVo cells. Taken together, these results suggest Gomisin G could be developed as a potential therapeutic compound against colon cancer.

KEYWORDS

AKT; Apoptosis; Cell cycle; Colon cancer; Gomisin G; PARP

Title

Gomisin G Suppresses the Growth of Colon Cancer Cells by Attenuation of AKT Phosphorylation and Arrest of Cell Cycle Progression.

Author

Maharjan S1, Park BK1, Lee SI1, Lim Y2, Lee K3, Lee Y4, Kwon HJ1,5.

Publish date

2019 Mar 1

PMID

28344076

Abstract

Gomisin C (GC) and gomisin G (GG) are two lignan analogs isolated from the Traditional Chinese Medicine Schisandra chinensis which possesses multiple pharmacological activities. However, the potential herb-drug interactions (HDI) between these lignans and other drugs through inhibiting human cytochrome P450 3A4 (CYP3A4) and CYP3A5 remains unclear. In the present study, the inhibitory action of GC and GG on CYP3A4 and CYP3A5 were investigated. The results demonstrated that both GC and GG strongly inhibited CYP3A-mediated midazolam 1′-hydroxylation, nifedipine oxidation and testosterone 6β-hydroxylation. Notably, the inhibitory intensity of GC towards CYP3A4 was stronger than CYP3A5 when using midazolam and nifedipine as substrates. While inhibition of GC towards CYP3A5 was weaker than CYP3A4 when using testosterone as substrate. In contrast, GG showed a stronger inhibitory activity on CYP3A5 than CYP3A4 without substrate-dependent behavior. In addition, docking simulations indicated that the π-π interaction between CYP3A4 and GC, and hydrogen-bond interaction between CYP3A5 and GG might result in their different inhibitory actions. Furthermore, the AUC of drugs metabolized by CYP3A was estimated to increase by 8%-321% and 2%-3190% in the presence of GC and GG, respectively. These findings strongly suggested that GC and GG showed high HDI potentials, and the position of methylenedioxy group determined their different inhibitory effect towards CYP3A4 and CYP3A5, which are of significance for the application of Schisandra chinensis-containing herbs.

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

KEYWORDS

CYP3A4; CYP3A5; Gomisin C; Gomisin G; Herb-drug interactions; Inhibition

Title

Inhibition of human CYP3A4 and CYP3A5 enzymes by gomisin C and gomisin G, two lignan analogs derived from Schisandra chinensis.

Author

Zhao J1, Sun T2, Wu JJ3, Cao YF4, Fang ZZ5, Sun HZ6, Zhu ZT6, Yang K7, Liu YZ7, Gonzalez FJ8, Yin J9.

Publish date

2017 Jun


Description :

Anti-AIDS agents--XXVI. Structure-activity correlations of gomisin-G-related anti-HIV lignans from Kadsura interior and of related synthetic analogues. PUMID/DOI:9313872 Bioorg Med Chem. 1997 Aug;5(8):1715-23. Gomisin G (11) exhibited the most potent anti-HIV activity with EC50 and therapeutic index (TI) values of 0.006 microgram/mL and 300, respectively. Drug-drug interation prediction between ketoconazole and anti-liver cancer drug Gomisin G PUMID/DOI:26124807 Afr Health Sci. 2015 Jun;15(2):590-3. Gomisin G, isolated from herb Schisandra chinensis, exhibits anti-tumor activities. Therefore, Gomisin G is a drug candidate for anti-liver cancer therapy.