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Catalogue Number : BF-G1021
Specification : 98%
CAS number : 40246-10-4
Formula : C22H22O10
Molecular Weight : 446.4
PUBCHEM ID : 187808
Volume : 20mg

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Glycitin (Synonyms: Glycitein 7-O-β-glucoside)

Glycitin is a natural isoflavone isolated from legumes; promotes the proliferation of bone marrow stromal cells and osteoblasts and suppresses bone turnover.Glycitin is antibacterial, antiviral and estrogenic.

Catalogue Number


Analysis Method






Molecular Weight



White crystalline powder

Botanical Source

Pueraria montana var. lobata,Astragalus membranaceus,Glycine max,Glycyrrhiza uralensis,Maackia amurensis

Structure Type



Standards;Natural Pytochemical;API




BIDD:ER0468/4',7-Dihydroxy-6-methoxyisoflavone-7-D-glucoside/3-(4-Hydroxyphenyl)-6-methoxy-4-oxo-4H-chromen-7-yl b-D-glucopyranoside/Glycitein 7-O-|A-glucoside/Glycitein-7-|A-O-glucoside/Glycitein 7-O-β-D-glucoside/3-(4-Hydroxyphenyl)-6-methoxy-4-oxo-4H-chromen-7-yl β-D-glucopyranoside/4H-1-Benzopyran-4-one/4H-1-Benzopyran-4-one, 7-(β-D-glucopyranosyloxy)-3-(4-hydroxyphenyl)-6-methoxy-/Glycitin/Glycitein 7-O-glucoside




1.5±0.1 g/cm3


Methanol; Ethanol; DMF

Flash Point

264.1±26.4 °C

Boiling Point

751.1±60.0 °C at 760 mmHg

Melting Point



InChl Key

WGK Germany


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#:40246-10-4) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Osteoarthritis (OA), a chronic joint disease, is characterized by cartilage surface erosion, subchondral bone rebuilding, and formation of osteophytes. To date, the nosogenesis and underlying mechanisms of OA have not yet been elucidated. However, it is widely accepted that TNF-α is a crucial cytokine in the development of OA. Glycitin, a natural isoflavone extracted from legumes, affects physiological reactions and pathological responses. Recently, the anti-inflammatory effect of glycitin has been reported. However, the function of glycitin in cartilage degeneration in OA remains to be investigated. In the current study, primary murine chondrocytes were isolated and stimulated by TNF-α to evaluate the anti-inflammatory effects and protective function of glycitin in chondrocytes. In vivo, the ACLT mouse model, a frequently-used OA model, was used to further examine the therapeutic role of glycitin in cartilage degeneration and inflammation in OA. Consequently, glycitin functions were examined both in vivo and in vitro. Moreover, the underlying mechanism of action of glycitin was investigated and was found to involve the NF-κB signaling pathway. Collectively, this study suggests that glycitin can be potentially used for the treatment of joint degenerative diseases, including OA.


NF-κB signaling pathway; glycitin; inflammation; osteoarthritis.


Glycitin Suppresses Cartilage Destruction of Osteoarthritis in Mice


Wenhan Wang 1 2 , Ruitong Yang 1 2 , Minfa Zhang 3 , Jiayi Li 2 , Jiangfan Peng 2 , Mingyang Xu 2 , Yunpeng Zhao 1 , Hao Li 4 , Xin Pan 5

Publish date

2020 Mar 28




The aim of the present study was to examine the effect of glycitin on the regulation of osteoblasts from bone marrow stem cells (BMSCs) through transforming growth factor (TGF)-β or protein kinase B (AKT) signaling pathways. BMSCs were extracted from New Zealand white rabbits and used to analyze the effect of glycitin on BMSCs. BMSCs were cleared using xylene and observed via light microscopy. BMSCs were subsequently induced with glycitin (0.01, 0.5, 1, 5 and 10 µM) for 7 days, and stained with Oil Red O. The mechanism of action of glycitin on BMSCs was investigated, in which contact with collagen type I (Col I), alkaline phosphatase (ALP), TGF-β and AKT was studied. Firstly, BMSCs appeared homogeneously mazarine blue, and which showed that BMSCs were successful extracted. Administration of glycitin increased cell proliferation and promoted osteoblast formation from BMSCs. Furthermore, glycitin activated the gene expression of Col I and ALP in BMSCs. Notably, glycitin suppressed protein expression of TGF-β and AKT in BMSCs. These results indicated that glycitin may regulate osteoblasts through TGF-β or AKT signaling pathways in BMSCs.


NF-κB signaling pathway; glycitin; inflammation; osteoarthritis.


Glycitin Regulates Osteoblasts Through TGF-β or AKT Signaling Pathways in Bone Marrow Stem Cells


Liyan Zhang 1 , Jiying Chen 2 , Wei Chai 2 , Min Ni 2 , Xin Sun 3 , Dan Tian 3

Publish date

2016 Nov




Acute lung injury (ALI) is a pulmonary diffuse dysfunction disease caused by immoderate inflammatory response breaking the coordination of physiological structures and functions, and there are very few effective treatments to reduce high morbidity of ALI in critical patients. Glycitin is a natural ingredient derived from the seeds of leguminous plants and may have potent anti-inflammation features. The purpose of this study was to investigate the anti-inflammation effect of glycitin on LPS-induced ALI in mice and elucidate its possible anti-inflammatory mechanisms. The results of histopathological changes, the wet/dry weight ratio as well as the myeloperoxidase (MPO) activity indicated that glycitin obviously alleviated the lung injury induced by LPS. In addition, qPCR and ELISA results found that glycitin could dose-dependently decrease the expressions of pro-inflammatory cytokines IL-1β, IL-6, and TNF-α. Western blotting was performed to revealed that glycitin inhibited the activation of NF-κB and MAPKs signaling pathways by suppressing the expression of TLR4 protein and the phosphorylation of IKKβ, IκBα, p65, p38, ERK, and JNK. All data indicated that glycitin could protect lung tissues from LPS-induced inflammation via inhibiting TLR4-mediated NF-κB and MAPKs signaling pathways.


ALI; Glycitin; Inflammation; MAPKs; NF-κB.


Glycitin Alleviates Lipopolysaccharide-Induced Acute Lung Injury via Inhibiting NF-κB and MAPKs Pathway Activation in Mice


Yu Chen 1 , Shuai Guo 1 , Kangfeng Jiang 1 , Ying Wang 1 , Mei Yang 1 , Mengyao Guo 2

Publish date

2019 Oct