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Home > Product Catalog > Compound Types > Alkaloids

Kukoamine B

CAS No.:164991-67-7

Kukoamine B
Catalogue No.: BP0834
Formula: C28H42N4O6
Mol Weight: 530.666
Contacts
+86-28-82633860  +86-18080483897
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Kukoamine B

CAS No.:164991-67-7

Kukoamine B
Catalogue No.: BP0834
Formula: C28H42N4O6
Mol Weight: 530.666
Contacts
+86-28-82633860  +86-18080483897
skype skype
Email: sales@biopurify.com biopurify@gmail.com
Over 15 years of industry experience in phytochemicals from R&D(reference substances) to Industrialization, please feel free to contact us!

Product name: Kukoamine B
Synonym name:
Catalogue No.: BP0834
Cas No.: 164991-67-7
Formula: C28H42N4O6
Mol Weight: 530.666
Botanical Source: Lycii Cortex
Physical Description:
Type of Compound: Alkaloids

Purity: 95%~99%
Analysis Method: HPLC-DAD or/and HPLC-ELSD
Identification Method: Mass, NMR
Packing: Brown vial or HDPE plastic bottle

Storage: Store in a well closed container, protected from air and light. Put into refrigerate or freeze for long term storage.

The product could be supplied from milligrams to grams
Inquire for bulk scale.




Description:

Kukoamine B is a potent dual inhibitor for both Lipopolysaccharides (LPS) and oligodeoxynucleotides containing CpG motifs (CpG DNA), LPS and CpG DNA are important pathogenic molecules for the induction of sepsis,are drug targets for sepsis treatment, thus kukoamine B is worthy of further investigation as a potential candidate to treat sepsis. Kukoamine B may potentially serve as an agent for prevention of several human neurodegenerative and other disorders caused by oxidative stress, it has protective effects against hydrogen peroxide (H2O2) induced cell injury and potential mechanisms in SH-SY5Y cells.

 

References:

Exp. Ther. Med. ,2015, 9(3):725-32.    

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    

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. 

METHODS AND RESULTS:

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. 

CONCLUSIONS:

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.   

 

HPLC of Kukoamine B

 

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