Catalogue Number
BN-O1331
Analysis Method
Specification
94%(HPLC)
Storage
2-8°C
Molecular Weight
248.32
Appearance
Botanical Source
Structure Type
Category
SMILES
CC1=CC2=C(C(=C1CCO)C)C(=O)C(C2)(C)CO
Synonyms
(S)-6-(2-Hydroxy-ethyl)-2-hydroxymethyl-2,5,7-trimethyl-indan-1-one/(2S)-Pterosin-A/(2S)-Pterosin A/Pterosin A/pterosin A
IUPAC Name
(2S)-6-(2-hydroxyethyl)-2-(hydroxymethyl)-2,5,7-trimethyl-3H-inden-1-one
Density
Solubility
Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.
Flash Point
Boiling Point
Melting Point
InChl
InChl Key
BDZJLPDYMKPKGC-HNNXBMFYSA-N
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#:35910-16-8) 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.
23069626
The therapeutic effect of pterosin A, a small-molecular-weight natural product, on diabetes was investigated. Pterosin A, administered orally for 4 weeks, effectively improved hyperglycemia and glucose intolerance in streptozotocin, high-fat diet-fed, and db/db diabetic mice. There were no adverse effects in normal or diabetic mice treated with pterosin A for 4 weeks. Pterosin Asignificantly reversed the increased serum insulin and insulin resistance (IR) in dexamethasone-IR mice and in db/db mice. Pterosin A significantly reversed the reduced muscle GLUT-4 translocation and the increased liver phosphoenolpyruvate carboxyl kinase (PEPCK) expression in diabetic mice. Pterosin A also significantly reversed the decreased phosphorylations of AMP-activated protein kinase (AMPK) and Akt in muscles of diabetic mice. The decreased AMPK phosphorylation and increased p38 phosphorylation in livers of db/db mice were effectively reversed by pterosin A. Pterosin A enhanced glucose uptake and AMPK phosphorylation in cultured human muscle cells. In cultured liver cells, pterosin A inhibited inducer-enhanced PEPCK expression, triggered the phosphorylations of AMPK, acetyl CoA carboxylase, and glycogen synthase kinase-3, decreased glycogen synthase phosphorylation, and increased the intracellular glycogen level. These findings indicate that pterosin A may be a potential therapeutic option for diabetes.
Antidiabetic effects of pterosin A, a small-molecular-weight natural product, on diabetic mouse models.
Hsu FL1, Huang CF, Chen YW, Yen YP, Wu CT, Uang BJ, Yang RS, Liu SH.
2013 Feb
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