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Kukoamine B

$480

  • Brand : BIOFRON

  • Catalogue Number : BD-D1302

  • Specification : 98%(HPLC)

  • CAS number : 164991-67-7

  • Formula : C28H42N4O6

  • Molecular Weight : 530.666

  • PUBCHEM ID : 10346914

  • Volume : 20MG

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Catalogue Number

BD-D1302

Analysis Method

HPLC,NMR,MS

Specification

98%(HPLC)

Storage

2-8℃

Molecular Weight

530.666

Appearance

White crystalline powder

Botanical Source

Cortex Lycii

Structure Type

Alkaloids

Category

Standards;Natural Pytochemical;API

SMILES

C1=CC(=C(C=C1CCC(=O)NCCCNCCCCN(CCCN)C(=O)CCC2=CC(=C(C=C2)O)O)O)O

Synonyms

N-(3-Aminopropyl)-3-(3,4-dihydroxyphenyl)-N-{4-[(3-{[3-(3,4-dihydroxyphenyl)propanoyl]amino}propyl)amino]butyl}propanamide/Benzenepropanamide, N-[3-[[4-[(3-aminopropyl)[3-(3,4-dihydroxyphenyl)-1-oxopropyl]amino]butyl]amino]propyl]-3,4-dihydroxy-/Kukoamine B

IUPAC Name

N-[3-[4-[3-aminopropyl-[3-(3,4-dihydroxyphenyl)propanoyl]amino]butylamino]propyl]-3-(3,4-dihydroxyphenyl)propanamide

Applications

Kukoamine B is a component of Lycii Cortex, with anti-oxidant, anti-acute inflammatory and anti-diabetic properties[1].

Density

1.2±0.1 g/cm3

Solubility

Methanol

Flash Point

464.4±34.3 °C

Boiling Point

844.3±65.0 °C at 760 mmHg

Melting Point

InChl

InChI=1S/C28H42N4O6/c29-13-3-18-32(28(38)12-8-22-6-10-24(34)26(36)20-22)17-2-1-14-30-15-4-16-31-27(37)11-7-21-5-9-23(33)25(35)19-21/h5-6,9-10,19-20,30,33-36H,1-4,7-8,11-18,29H2,(H,31,37)

InChl Key

IWRAOCFRRTWUDF-UHFFFAOYSA-N

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#:164991-67-7) 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

25667619

Abstract

Kukoamine B (KB), derived from the traditional Chinese herb cortex Lycii, exerts anti-inflammatory effects due to its potent affinity with lipopolysaccharide (LPS) and CpG DNA; however, little is known regarding whether the in vivo administration of KB can effectively inhibit inflammation in septic mice. The present study thus aimed to investigate the inhibitory effects of KB on the inflammatory response in the livers of LPS-induced septic mice. KB treatment in the LPS-induced septic mice significantly decreased the plasma level of LPS. In addition, KB protected against liver injury, as confirmed by improved histology and decreased aminotransferase levels in the serum. Further experiments revealed that KB attenuated liver myeloperoxidase activity and reduced the expression of vascular cell adhesion molecule-1 and intercellular adhesion molecule-1. These effects were accompanied by decreases in the levels of tumor necrosis factor α and interleukin-1β in the liver tissue. In parallel, the activity of nuclear factor-κ-gene binding (NF-κB) in the livers of LPS-induced septic mice was markedly inhibited with KB treatment. In combination, these results demonstrate that KB inhibits inflammation in septic mice by reducing the concentrations of plasma LPS, decreasing leukocyte sequestration and interfering with NF-κB activation, and, therefore, suppressing the pro-adhesive phenotype of endothelial cells.

KEYWORDS

inflammatory response; kukoamine B; lipopolysaccharide; liver; nuclear factor κ-light-chain-enhancer of activated B cells.

Title

A Novel Role of Kukoamine B: Inhibition of the Inflammatory Response in the Livers of Lipopolysaccharide-Induced Septic Mice via Its Unique Property of Combining With Lipopolysaccharide

Author

Wei-Ting Qin 1 , Xu Wang 1 , Wei-Chang Shen 1 , Bing-Wei Sun 1

Publish date

2015 Mar

PMID

26065936

Abstract

A major cause of cerebral ischemia is overactivation of the N-methyl-D-aspartate receptors (NMDARs). Therefore, NMDAR antagonists are needed for the treatment of cerebral ischemia. In our research, KuB protected the SH-SY5Y cells against NMDA-induced injury, apoptosis, LDH release and MMP loss. In addition, KuB could decrease MDA levels while increasing SOD activity. Meanwhile, KuB decreased NADPH oxidase-mediated ROS production, inhibited Ca(2+) influx, and increased the Bcl-2/Bax ratio. Furthermore, KuB not only down-regulated expression of the NR2B subunit of NMDAR but also actively modulated expression of the signaling molecules downstream of NR2B, including p-ERK, p-CREB, p-AKT and SAPKs. Finally, docking results showed that KuB had a high affinity for NR2B-containing NMDARs. Therefore, we conclude that KuB protected the SH-SY5Y cells from NMDA-induced injury likely by antagonizing NMDARs and reducing oxidative stress.

KEYWORDS

inflammatory response; kukoamine B; lipopolysaccharide; liver; nuclear factor κ-light-chain-enhancer of activated B cells.

Title

Kukoamine B, an Amide Alkaloid, Protects Against NMDA-induced Neurotoxicity and Potential Mechanisms in Vitro

Author

Xiao-Long Hu 1 , Li-Ping Guo 2 , Qi Song 2 , Qiao Zhang 2 , Ying Chen 3 , Jian Wang 2 , Wei-Hong Meng 3 , Qing-Chun Zhao 4

Publish date

2015 Aug

PMID

27542278

Abstract

Free bacterial lipopolysaccharide (LPS) is generally removed from the bloodstream through hepatic uptake via TLR4, the LPS pattern recognition receptor, but mechanisms for internalization and clearance of conjugated LPS are less clear. Kukoamine B (KB) is a novel cationic alkaloid that interferes with LPS binding to TLR4. In this study, KB accelerated blood clearance of LPS. KB also enhanced LPS distribution in the hepatic tissues of C57 BL/6 mice, along with LPS uptake in primary hepatocytes and HepG2 cells. By contrast, KB inhibited LPS internalization in Kupffer and RAW 264.7 cells. Loss of TLR4 did not affect LPS uptake into KB-treated hepatocytes. We also detected selective upregulation of the asialoglycoprotein receptor (ASGPR) upon KB treatment, and ASGPR colocalized with KB in cultured hepatocytes. Molecular docking showed that KB bound to ASGPR in a manner similar to GalNAc, a known ASGPR agonist. GalNAc dose-dependently reduced KB internalization, suggesting it competes with KB for ASGPR binding, and ASGPR knockdown also impaired LPS uptake into hepatocytes. Finally, while KB enhanced LPS uptake, it was protective against LPS-induced inflammation and hepatocyte injury. Our study provides a new mechanism for conjugated LPS hepatic uptake induced by the LPS neutralizer KB and mediated by membrane ASGPR binding.

KEYWORDS

Immunology and Microbiology Section; asialoglycoprotein receptor; hepatocytes; kukoamine B; lipopolysaccharide; Immune response; Immunity.

Title

Kukoamine B Promotes TLR4-independent Lipopolysaccharide Uptake in Murine Hepatocytes

Author

Dong Yang 1 , Xinchuan Zheng 1 , Ning Wang 1 , Shijun Fan 1 , Yongjun Yang 1 , Yongling Lu 1 , Qian Chen 1 , Xin Liu 1 , Jiang Zheng 1

Publish date

2016 Sep 6