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Nitidine Chloride

$178

  • Brand : BIOFRON

  • Catalogue Number : BF-N3011

  • Specification : 98%

  • CAS number : 13063-04-2

  • Formula : C21H18ClNO4

  • Molecular Weight : 383.82

  • PUBCHEM ID : 25659

  • Volume : 20mg

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Catalogue Number

BF-N3011

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

383.82

Appearance

Light yellow crystalline powder

Botanical Source

roots of Zanthoxylum nitidum (Roxb.) DC.

Structure Type

Alkaloids

Category

Standards;Natural Pytochemical;API

SMILES

C[N+]1=CC2=CC(=C(C=C2C3=C1C4=CC5=C(C=C4C=C3)OCO5)OC)OC.[Cl-]

Synonyms

2,3-Dimethoxy-12-methyl-[1,3]benzodioxolo[5,6-c]phenanthridinium chloride/[1,3]Benzodioxolo[5,6-c]phenanthridinium, 2,3-dimethoxy-12-methyl-, chloride (1:1)/2,3-Dimethoxy-12-methyl[1,3]benzodioxolo[5,6-c]phenanthridin-12-ium chloride/Nitidine chloride/2,3-dimethoxy-12-methyl-[1,3]benzodioxolo[5,6-c]phenanthridin-12-ium,chloride

IUPAC Name

2,3-dimethoxy-12-methyl-[1,3]benzodioxolo[5,6-c]phenanthridin-12-ium;chloride

Applications

Density

1.35g/cm3

Solubility

DMSO

Flash Point

189.4ºC

Boiling Point

619ºC at 760 mmHg

Melting Point

281-282ºC

InChl

InChl Key

WGK Germany

RID/ADR

HS Code Reference

2934990000

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:13063-04-2) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

29516498

Abstract

Objectives: To explore the apoptotic effects and underlying mechanisms of nitidine chloride (NC) in epithelial ovarian cancer.
Methods: The MTT cell proliferation assay was used to detect the inhibitory effects of different concentrations of NC (0, 0.3125, 0.625, 1.25, 2.5, 5 and 10 μg/ml) in SKOV3 ovarian carcinoma cells. The number of apoptotic cells was observed by Hoechst staining and measured by flow cytometry. Quantitative PCR was used to measure the expression of Fas, Fas-associated death domain-containing protein (FADD), caspase-8 and caspase-3. RNA interference (RNAi) was used to determine whether caspase-8 played an important role in NC-induced apoptosis.
Key findings: Nitidine chloride inhibited the proliferation of SKOV3 cells (IC50 = 2.317 ± 0.155 μg/ml) after 24 h of treatment and induced apoptosis (15.9-64.3%). Compared with the control group, a significant increase in Fas, FADD, caspase-8 and caspase-3 gene expression was observed in the NC-treated groups (P < 0.05). After silencing caspase-8 by RNAi, the antiproliferative activity and pro-apoptotic activity of NC in SKOV3 cells decreased (P < 0.05).
Conclusions: Our study showed that NC induced apoptosis in SKOV3 cells by activating the Fas signalling pathway, and caspase-8 played an important role in this process.

KEYWORDS

Fas signalling pathway; apoptosis; nitidine chloride; ovarian cancer.

Title

Nitidine Chloride Inhibits Proliferation and Induces Apoptosis in Ovarian Cancer Cells by Activating the Fas Signalling Pathway

Author

Shipeng Chen 1 , Luo Yang 1 , Jie Feng 1

Publish date

2018 Jun

PMID

29924888

Abstract

Background: We have shown previously that nitidine chloride (NC) induces apoptosis via inhibition of signal transducer and activator of transcription 3 (STAT3). However, its downstream molecules are not fully understood yet. Here, we report that NC as STAT3 inhibitor downregulates myeloid cell leukemia-1 (Mcl-1) protein in HSC-3 and HSC-4 human oral squamous cell carcinoma (OSCC) cells and a nude mouse tumor xenograft model.
Methods: This study investigated the effects of NC on Mcl-1 expression in HSC-3 and HSC-4 cells using Western blotting, RT-PCR, and dual-luciferase assay. Immunohistochemistry was employed to evaluate Mcl-1 expression levels in mouse tumor tissues. Construction of Mcl-1 overexpression vector and transient transfection was done to test the apoptosis of HSC-3 cells.
Results: Nitidine chloride did not affect either mRNA level or promoter activity of Mcl-1, and the decrease in Mcl-1 protein by NC was caused by lysosome-dependent degradation, but not proteasome-dependent degradation. The overexpression of Mcl-1 protein in OSCC cell lines was sufficient to block the induction of apoptosis. In addition, NC strongly reduced the expression level of Mcl-1 protein compared with other STAT3 inhibitors such as cryptotanshione and S3I-201 in OSCCs.
Conclusions: Our findings suggest that NC triggers apoptosis via lysosome-dependent Mcl-1 protein degradation and could be chosen as a promising chemotherapeutic candidate against human OSCCs.

KEYWORDS

apoptosis; lysosome; myeloid cell leukemia-1; nitidine chloride; oral squamous cell carcinoma.

Title

Nitidine Chloride Represses Mcl-1 Protein via Lysosomal Degradation in Oral Squamous Cell Carcinoma

Author

In-Hyoung Yang 1 , Won Jung 2 , Lee-Han Kim 1 , Ji-Ae Shin 3 , Nam-Pyo Cho 1 , Seong Doo Hong 3 , Kyoung-Ok Hong 3 , Sung-Dae Cho 3

Publish date

2018 Oct

PMID

29773554

Abstract

Nitidine chloride (NC) is a benzophenanthridine alkaloid isolated from the roots of Zanthoxylum nitidum (Roxb.) DC, a widely used traditional herbal medicine. Several reports have revealed NC’s multiple pharmacologic properties. The inhibitory effects of NC on human cytochrome P450 enzymes were investigated in the present study. We found that NC caused time- and concentration-dependent inhibition of CYP2D6, and more than 50% of CYP2D6 activity was suppressed after a 15-minute incubation with NC at 100 μM in the primary incubation mixtures, with KI of 4.36 μM, kinact of 0.052 minute-1, and a partition ratio of approximately 290. Moreover, the loss of CYP2D6 activity required the presence of NADPH. Superoxide dismutase/catalase and glutathione showed minor protection against the NC-induced enzyme inhibition. Quinidine as a competitive inhibitor of CYP2D6 slowed down the inactivation by NC. Trapping experiments using N-acetylcysteine demonstrated that quinone and/or carbene intermediate(s) were/was generated in human liver microsomal incubations with NC. In addition, potassium ferricyanide prevented the enzyme from the inactivation mediated by NC, which provided evidence that inhibition of CYP2D6 resulted from heme destruction by the formation of a carbene-iron complex. CYP1A2 was found to be the major enzyme involved in the generation of NC quinone metabolites. In conclusion, NC is a mechanism-based inactivator of CYP2D6. The generation of a carbene intermediate might be mainly responsible for the enzyme inactivation.

Title

Nitidine Chloride Is a Mechanism-Based Inactivator of CYP2D6

Author

Xu Mao 1 , Zixia Hu 1 , Qian Wang 1 , Na Zhang 1 , Shenzhi Zhou 1 , Ying Peng 2 , Jiang Zheng 2

Publish date

2018 Aug