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Sinomenine hydrochloride

$43

  • Brand : BIOFRON

  • Catalogue Number : BF-S2010

  • Specification : 98%

  • CAS number : 6080-33-7

  • Formula : C19H23NO4.HCl

  • Molecular Weight : 365.85

  • PUBCHEM ID : 5464452

  • Volume : 20mg

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Catalogue Number

BF-S2010

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

365.85

Appearance

Yellow needle crystal

Botanical Source

Han Fangji

Structure Type

Alkaloids

Category

Standards;Natural Pytochemical;API

SMILES

CN1CCC23CC(=O)C(=CC2C1CC4=C3C(=C(C=C4)OC)O)OC.Cl

Synonyms

Morphinan-6-one, 7,8-didehydro-4-hydroxy-3,7-dimethoxy-17-methyl-, (9α,13α,14α)-, hydrochloride (1:1)/Cucoline, hydrochloride/(14α)-4-Hydroxy-3,7-dimethoxy-17-methyl-7,8-didehydromorphinan-6-one hydrochloride (1:1)/(9α,13α,14α)-4-Hydroxy-3,7-dimethoxy-17-methyl-7,8-didehydromorphinan-6-one hydrochloride (1:1)/Morphinan-6-one, 7,8-didehydro-4-hydroxy-3,7-dimethoxy-17-methyl-, (14α)-, hydrochloride (1:1)

IUPAC Name

(1R,9S,10S)-3-hydroxy-4,12-dimethoxy-17-methyl-17-azatetracyclo[7.5.3.01,10.02,7]heptadeca-2(7),3,5,11-tetraen-13-one;hydrochloride

Density

Solubility

Flash Point

264.4ºC

Boiling Point

513.6ºC at 760 mmHg

Melting Point

231.0 to 235.0 °C

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#:6080-33-7) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

31556312

Abstract

Sinomenine (Sino) is diffusely applied in heal rheumatoid arthritis and neuralgia. Howbeit, the activities of Sino in breast cancer cells remain confused. The research attempted to probe the anti-tumor function of Sino in breast cancer cells and divulge the feasible molecular mechanism. Sion at the 1-16 μM concentrations was exploited for the exposure of MDA-MB-231 or MCF7 cells, and cell growth, migration, invasion, cell cycle-relevant and apoptosis-correlative factors were estimated. Micro RNA (miR)-29 expression was evaluated via enforcing qRT-PCR, and the actions of miR-29 in MDA-MB-231 cells growth, migration and invasion were appraised after the overexpressed or suppressed vectors transfection. The functions of PDCD-4 in JNK and MEK/ERK pathways were estimated by employing western blot. We found that, Sino exposure impeded cell proliferation, provoked cell apoptosis and barricaded cell migration and invasion in MDA-MB-231 and MCF7 cells. Enhancement of miR-29 was observed in Sino-managed cells, and miR-29 overexpression further potentiated the activities of Sino in MDA-MB-231 cells. Additionally, Sino remarkably enhanced PCDC-4 expression via adjusting miR-29 in MDA-MB-231 cells. Beyond that, overexpressed PCDC-4 obstructed JNK and MEK/ERK pathways in MDA-MB-231 cells. Taken together, the explorations unveiled that Sino restrained MDA-MB-231 cells proliferation, migration, invasion, and provoked apoptosis through modulation of miR-29/PDCD-4 axis. Highlight Sino inhibits MDA-MB-231 and MCF7 cells proliferation and provokes apoptosis; Sino restrains MDA-MB-231 and MCF7 cells migration and invasion; Sino ascends miR-29 expression in MDA-MB-231 and MCF7 cells; Sino adjusts cell growth, migration and invasion via modulating miR-29; Sino up-regulates PDCD-4 expression through mediating miR-29; PDCD-4 obstructs JNK and MEK/ERK pathways in MDA-MB-231 cells.

KEYWORDS

JNK; MEK/ERK; PDCD-4; Sinomenine; breast cancer; microRNA-29

Title

Sinomenine restrains breast cancer cells proliferation, migration and invasion via modulation of miR-29/PDCD-4 axis.

Author

Gao G1, Liang X2, Ma W3.

Publish date

2019 Dec

PMID

31356903

Abstract

AIMS:
The initiation of pressure ulcers is accompanied by inflammation. Sinomenine emerges as a potential anti-inflammation agent. The aim of this study was to corroborate its anti-inflammatory property in skin keratinocyte HaCaT cells. Long non-coding RNA colon cancer associated transcript-1 (CCAT1)-associated mechanisms were also investigated.

MAIN METHODS:
HaCaT cells were stimulated with lipopolysaccharide (LPS) for 6 h after sinomenine pre-administration. Transfection was carried out to induce CCAT1 overexpression or silence it in HaCaT cells. Viability and apoptosis of HaCaT cells were determined by MMT and observed using flow cytometry, respectively. Protein expression was quantified using Western blot or ELISA. CCAT1 was measured by qRT-PCR.

KEY FINDINGS:
LPS notably decreased cell viability and exaggerated apoptosis with the cleavage of caspase-3/-9. The secretion of inflammatory factors was promoted. Sinomenine pre-administration maintained cell viability, blocked apoptosis and relieved inflammation with the decrease in cleaved caspase-3/-9 and inflammatory factors. LPS-induced phosphorylation of p65, IκBα and p38MAPK and overexpression of CCAT1 were precluded by sinomenine. CCAT1 overexpression, which per se induced inflammatory lesions, negated the positive effects of sinomenine with the restored phosphorylation of p65, IκBα, and p38MAPK.

SIGNIFICANCE:
Sinomenine played a protective role against LPS-induced inflammation. The anti-inflammatory activity of sinomenine might be mediated by CCAT1 down-regulation.

Copyright © 2019. Published by Elsevier Inc.

KEYWORDS

CCAT1; Inflammation; NF-κB/MAPK; Sinomenine

Title

Sinomenine retards LPS-elicited inflammation via down-regulating CCAT1 in HaCaT cells.

Author

Liu Y1, Zhao C1, Ma Q2, Li Y3.

Publish date

2019 Sep 15;

PMID

31228805

Abstract

The aim of this study was to investigate the release behaviors of sinomenine hydrochloride loaded via in situ hexagonal liquid crystal (ISH), and its potential to improve the local bioavailability in knee joints of sinomenine hydrochloride (SMH) after intra-articular administration. The ISH was prepared by a liquid precursor mixture containing phytantriol (PT), Vitamin E acetate (VEA), ethanol (ET), and water. The in vitro release profiles revealed a sustained release of SMH from the optimized ISH formula (PT/VEA/ET/water, 60.8:3.2:16.0:20.0, w/w/w/w), which was selected for the in vivo pharmacokinetics and preliminary pharmacodynamics studies. In both healthy and adjuvant-induced arthritis (AA) rats, the SMH loaded ISH showed significantly smaller SMH AUC0-∞ in plasma (P < 0.01), and higher SMH concentration in synoviums (2˜168 h) than that of SMH solution, indicating that the ISH significantly reduced the leakage of SMH into systemic circulation. The t1/2α of SMH loaded ISH in the knee joints of AA rats, was longer (13.42 h) than that of healthy rats (1.34 h) (P < 0.05), most likely that in vivo drug release behavior of SMH loaded ISH was affected by the physiological environment of the joint. It was found that the SMH loaded ISH could benefit AA-rats by suppressing the level of IL-1β in comparison to SMH solutions. The results of the histopathology of knee joints in AA rats displayed that the SMH loaded ISH might be suitable for the development of treatment strategies for rheumatoid arthritis diseases.

Copyright © 2019 The Authors. Published by Elsevier Masson SAS.. All rights reserved.

KEYWORDS

In Situ hexagonal liquid crystal; Intra-articular administration; Rheumatoid arthritis; Sinomenine hydrochloride; Sustained release

Title

In situ hexagonal liquid crystal for intra-articular delivery of sinomenine hydrochloride.

Author

Liang X1, Chen Y1, Wu L2, Maharjan A2, Regmi B3, Zhang J2, Gui S4.

Publish date

2019 Sep


Description :

Sinomenine hydrochloride is a blocker of the NF-κB activation and also an activator of μ-opioid receptor.