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Cyclovirobuxine D

$45

  • Brand : BIOFRON

  • Catalogue Number : AV-P11540

  • Specification : 98%

  • CAS number : 860-79-7

  • Formula : C26H46N2O

  • Molecular Weight : 402.66

  • PUBCHEM ID : 260439

  • Volume : 50mg

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Catalogue Number

AV-P11540

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

402.66

Appearance

White crystalline powder

Botanical Source

Buxus sinica (Rehd. et Wils.) Cheng subsp. sinica var. parvifolia M. Cheng

Structure Type

Other Alkaloids

Category

Standards;Natural Pytochemical;API

SMILES

CC(C1C(CC2(C1(CCC34C2CCC5C3(C4)CCC(C5(C)C)NC)C)C)O)NC

Synonyms

9,19-Cyclopregnan-16-ol, 4,4,14-trimethyl-3,20-bis(methylamino)-, (3β,5α,9β,16α,20S)-/bebuxine/cyclovirobuxind/cyclovirobuxinum D/cyclobuxine D/(3β,5α,9β,16α,20S)-4,4,14-Trimethyl-3,20-bis(methylamino)-9,19-cyclopregnan-16-ol/cvb-d/Cyclovirobuxine-D/CYCLOVIROBUXINE

IUPAC Name

(1S,3R,6S,8R,11S,12S,14R,15S,16R)-7,7,12,16-tetramethyl-6-(methylamino)-15-[(1S)-1-(methylamino)ethyl]pentacyclo[9.7.0.01,3.03,8.012,16]octadecan-14-ol

Density

1.1±0.1 g/cm3

Solubility

Flash Point

34.1±9.6 °C

Boiling Point

495.7±10.0 °C at 760 mmHg

Melting Point

InChl

InChl Key

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#:860-79-7) 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

29458577

Abstract

The blood-brain barrier (BBB) restricts the delivery of most drugs to the brain. In our previous study, the feasibility of cyclovirobuxine D delivery to the brain by a non-invasive nasal route was evaluated. In this study, a suitable drug delivery system by way of intranasal administration was developed, which could improve brain targeting. First, a formulation of cyclovirobuxine D (CVB-D) based on chitosan nanoparticles (CS-CVB-D-NPs) was prepared by the modified ionotropic gelation method through single-factor screening experiment. The CS-CVB-D-NPs with a entrapment efficiency (EE) of (62.82±2.59)% were found to be of a narrow polydispersity index (PI) (0.19±0.01) and (235.37± 12.71) nm in size, with a zeta potential of (33.9 ± 1.7) mV. The NPs possessed a sustained release characterization with in vitro release of 88.03 ± 2.30% at 24 h. In vivo, the higher AUC0-t(brain) of CS-CVB-D-NPs by intranasal administration revealed the development of a novel brain-targeting delivery method of CVB-D.

Title

A Novel Delivery Method of Cyclovirobuxine D for Brain-Targeting: Chitosan Coated Nanoparticles Loading Cyclovirobuxine D by Intranasal Administration.

Author

Wei H1, Lai S1, Wei J1, Yang L2, Jiang N1, Wang Q1, Yu Y1.

Publish date

2018 Aug 1

PMID

26075032

Abstract

The clinical application of doxorubicin (DOX) is compromised by its cardiac toxic effect. Cyclovirobuxine D (CVB-D) is a steroid alkaloid extracted from a traditional Chinese medicine, Buxus microphylla. Our results showed that CVB-D pretreatment markedly attenuated DOX-induced cardiac contractile dysfunction and histological alterations. By using TUNEL assay and western blot analysis, we found that CVB-D pretreatment reduced DOX-induced apoptosis of myocardial cells and mitochondrial cytochrome c release to cytosol. CVB-D pretreatment ameliorated DOX-induced cardiac oxidative damage including lipid peroxidation and protein carbonylation and a decrease in the ratio of reduced glutathione (GSH) to oxidized glutathione (GSSG). Moreover, CVB-D was found to prevent DOX-induced mitochondrial biogenesis impairment as evidenced by preservation of peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) and nuclear respiratory factor 1 (NRF1), as well as mitochondrial DNA copy number. These findings demonstrate that CVB-D protects against DOX-induced cardiomyopathy, at least in part, by suppression of oxidative damage and mitochondrial biogenesis impairment.

Title

Cyclovirobuxine D Attenuates Doxorubicin-Induced Cardiomyopathy by Suppression of Oxidative Damage and Mitochondrial Biogenesis Impairment.

Author

Guo Q1, Guo J2, Yang R2, Peng H2, Zhao J2, Li L3, Peng S2.

Publish date

2015

PMID

32020219

Abstract

Gliomas are the most common neoplasm of the human central nervous system. Glioblastoma multiforme (GBM) is one of the most serious types of gliomas. Although considerable progress has been made in the development of cancer therapeutic agents, several antineoplastic drugs fail to penetrate the blood?brain barrier (BBB), resulting in a low survival rate of glioma patients. Recent studies have revealed that the traditional Chinese medicine Buxus microphylla contains the main active component Cyclovirobuxine D (CVB?D), which can cross the BBB with a novel delivery system. However, it remains unclear whether CVB?D exerts anticancer effects against GBM and low?grade glioma (LGG). The aim of the present study was to explore the feasibility of CVB?D as a new effective agent in the treatment of GBM and LGG. The ability of CVB?D to inhibit GBM and LGG cell proliferation was detected by CCK8 assay. Flow cytometry was used to detect cell cycle progression and apoptosis induction by Annexin V?FITC/PI assay. The expression levels of the apoptosis?associated proteins, namely cleaved caspase?3 and Bax/Bcl?2, were detected by western blot analysis. The mitochondrial membrane potential (ΔΨm) was detected by Rh123 dyed fluorescence micrograph. Hoechst staining was used to observe the morphological characteristics of the apoptotic cells. The scratch test was used to evaluate the migration of GBM and LGG cells. The results indicated that CVB?D reduced cell viability of T98G and Hs683 cells. Flow cytometry demonstrated that CVB?D?treated cells were arrested at the S phase of their cell cycle. The expression levels of the apoptosis?associated proteins were increased in CVB?D?treated cells. Rh123 and Hoechst staining indicated morphological changes and mitochondrial membrane potential changes of the cells undergoing apoptosis. The data confirmed that CVB?D inhibited cell proliferation by arresting the cell cycle of GBM and LLG cells and that it promoted the induction of cell apoptosis by altering the mitochondrial membrane potential. The findings of the present study indicate the potential value of CVB?D in the treatment of glioma.

Title

Cyclovirobuxine D inhibits cell proliferation and migration and induces apoptosis in human glioblastoma multiforme and low?grade glioma.

Author

Zhou L1, Tang H2, Wang F3, Ou S1, Wu T1, Fang Y1, Xu J1, Guo K1.

Publish date

2020 Mar


Description :

Cyclovirobuxine D (CVB-D) is the main active component of the traditional Chinese medicine Buxus microphylla. Cyclovirobuxine D induces autophagy and attenuates the phosphorylation of Akt and mTOR[1]. Cyclovirobuxine D inhibits cell proliferation of gastric cancer cells through suppression of cell cycle progression and inducement of mitochondria-mediated apoptosis[2]. Cyclovirobuxine D is beneficial for heart failure induced by myocardial infarction[3].