[Triterpenoids] Euscaphic acid; 1,2,4-trimethoxy-5-prop-1-enylbenzene [CFN98888] [Cas No. 53155-25-2] - 코아사이언스

Euscaphic acid

=(1R,2R,4aS,6aR,6aS,6bR,8aR,10S,11R,12aR,14bS)-1,10,11-trihydroxy-1,2,6a,6b,9,9,12
a-heptamethyl-2,3,4,5,6,6a,7,8,8a,10,11,12,13,14b-tetradecahydropicene-4a-carboxylic
acid

Cat.# CFN98888 / Size: 5mg, 10mg, 20mg    

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Cas No.: 53155-25-2

Purity: ≥ 95%

C₃₀H₄₈O₅ = 488.7      
Physical Description: Powder 

Certification | Grade: NMR | HPLC

 

[ Intended Use ]
1. Reference standards;
2. Pharmacological research;
3. Synthetic precursor compounds;
4. Intermediates & Fine Chemicals;
5. Others.

 

[ Source ]

The dried fruit of Ziziphus jujuba.

 

[ Applications ]
The plasma glucose levels were significantly lowered in normoglycemic mice treated with
euscaphic acid compared to mice treated with 0.5% CMC-Na solution only. Moreover, the
dosage of 50 mg/kg exerted a significant (P<0.05) hypoglycemic effect in alloxan-diabetic
mice after orally administration.
Euscaphic acid (EA) concentration-dependently reduced the production of nitric oxide
(NO), prostaglandin E2 (PGE2), tumor necrosis factor-α (TNF-α), and interleukin-1β
(IL-1β) induced by LPS in RAW 264.7 macgophages. Consistent with these data,
ｅxpression levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2)
protein and iNOS, COX-2, TNF-α, and IL-1β mRNA were inhibited by EA in a
concentration-dependent manner. In addition, EA attenuated LPS-induced DNA binding
and transcriptional activity of nuclear factor-kappa B (NF-κB), which was accompanied by
a parallel reduction of degradation and phosphorylation of inhibitory kappa Bα (IκBα) and
consequently by decreased nuclear translocation of p65 subunit of NF-κB. Pretreatment
with EA significantly inhibited the LPS-induced phosphorylation of IκB kinase β (IKKβ),
p38, and JNK, whereas the phosphorylation of ERK1/2 was unaffected. Furthermore, EA
interfered with the LPS-induced clustering of TNF receptor-associated factor 6 (TRAF6)
with interleukin receptor associated kinase 1 (IRAK1) and transforming growth
factor-β-activated kinase 1 (TAK1). Taken together, these results suggest that EA inhibits
LPS-induced inflammatory responses by interference with the clustering of TRAF6 with
IRAK1 and TAK1, resulting in blocking the activation of IKK and MAPKs signal
transduction to downregulate NF-κB activations.
EA induces death by activation of caspase-3, dependent apoptotic pathway.

[ Solvent ]
Pyridine, DMSO, Chloroform, Dichloromethane, Acetone, etc.

[ HPLC Method ]
Mobile phase: Methanol : 0.2% Phosphoric acid H2O=87:13;
Flow rate: 1.0 ml/min;
The wave length of determination: 205 nm.

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[ Storage ]
2-8℃, Protected from air and light, refrigerate or freeze.

[ References ]
1. J. Cell. Biochem., 2012, 113(6), 1936-1946.
2. PHARMAZIE, 2008, 63(10), 765.
3. Bioorganic & Medicinal Chemistry, 2007, 15(23), 7355-7360.

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