577-38-8
Chemical Structure
Flavanomarein
- CAS No.: 577-38-8
- Formula:C21H22O11
- Molecular Weight:450.39
IUPAC Name: (S)-2-(3,4-dihydroxyphenyl)-8-hydroxy-7-(((2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)tetrahydro-2H-pyran-2-yl)oxy)chroman-4-one
InChIKey: DGGOLFCPSUVVHX-RTHJTPBESA-N
SMILES: O=C1C[C@@H](C2=CC=C(O)C(O)=C2)OC3=C(O)C(O[C@H]4[C@@H]([C@H]([C@@H]([C@@H](CO)O4)O)O)O)=CC=C13
Biological Activity: Flavanomarein is a substance with cytoprotective, anti-inflammatory and antioxidant activities, with a Ka of 3.064e-5 M against human Syk. Flavanomarein enhances the phosphorylation level of AKT, regulates the expression of PKC-δ, P85α, PKC-β1, Sirt1, Bcl-2 and ICAD, and inhibits the nuclear translocation of NF-κB p65. Flavanomarein regulates EMT marker proteins, promotes the proliferation of HK-2 cells, and protects neuronal cells from 6-OHDA-induced neurotoxic damage. Flavanomarein can be used in studies related to Parkinson's disease and diabetic nephropathy.[1][2]
| Cat. No. | Product Name | Purity | Description | Pricing | |||||||||||||||||||
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Flavanomarein | 99.92% | Flavanomarein is a substance with cytoprotective, anti-inflammatory and antioxidant activities, with a Ka of 3.064e-5 M against human Syk. Flavanomarein enhances the phosphorylation level of AKT, regulates the expression of PKC-δ, P85α, PKC-β1, Sirt1, Bcl-2 and ICAD, and inhibits the nuclear translocation of NF-κB p65. Flavanomarein regulates EMT marker proteins, promotes the proliferation of HK-2 cells, and protects neuronal cells from 6-OHDA-induced neurotoxic damage. Flavanomarein can be used in studies related to Parkinson's disease and diabetic nephropathy. | ||||||||||||||||||||
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- [1]. Le L, et al. The protective effects of the native flavanone flavanomarein on neuronal cells damaged by 6-OHDA. Phytomedicine. 2019;53:193-204. [Content Brief]
- [2]. Zhang NN, et al. Flavanomarein inhibits high glucose-stimulated epithelial-mesenchymal transition in HK-2 cells via targeting spleen tyrosine kinase. Sci Rep. 2020;10(1):439. Published 2020 Jan 16. [Content Brief]
Keywords