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Neobaicalein

$1,280

  • Brand : BIOFRON

  • Catalogue Number : BD-H0075

  • Specification : 98%

  • CAS number : 55084-08-7

  • Formula : C19H18O8

  • Molecular Weight : 374.35

  • PUBCHEM ID : 124211

  • Volume : 20mg

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Catalogue Number

BD-H0075

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

374.35

Appearance

Yellow powder

Botanical Source

Scutellariae radix

Structure Type

Flavonoids

Category

Standards;Natural Pytochemical;API

SMILES

COC1=CC=CC(=C1C2=CC(=O)C3=C(C(=C(C(=C3O2)OC)OC)OC)O)O

Synonyms

5-Hydroxy-2-(2-hydroxy-6-methoxyphenyl)-6,7,8-trimethoxy-4H-chromen-4-one/Neobaicalein/Skullcapflavone II/5-hydroxy-2-(2-hydroxy-6-methoxyphenyl)-6,7,8-trimethoxychromen-4-one/5,2'-Dihydroxy-6,7,8,6'-tetramethoxyflavone/4H-1-Benzopyran-4-one, 5-hydroxy-2-(2-hydroxy-6-methoxyphenyl)-6,7,8-trimethoxy-/Scullcapflavone II

IUPAC Name

5-hydroxy-2-(2-hydroxy-6-methoxyphenyl)-6,7,8-trimethoxychromen-4-one

Density

1.4±0.1 g/cm3

Solubility

Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.

Flash Point

230.9±25.0 °C

Boiling Point

636.9±55.0 °C at 760 mmHg

Melting Point

InChl

InChI=1S/C15H30O4/c1-2-3-4-5-6-7-8-9-10-11-15(18)19-13-14(17)12-16/h14,16-17H,2-13H2,1H3

InChl Key

GMQFOKBGMKVUQZ-UHFFFAOYSA-N

WGK Germany

RID/ADR

HS Code Reference

2914500000

Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:55084-08-7) 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.

PMID

31167359

Abstract

Skullcapflavone II is a flavonoid derived from the root of Scutellaria baicalensis, a herbal medicine used for anti-inflammatory and anti-cancer therapies. We analyzed the effect of skullcapflavone II on the expression of matrix metalloproteinase-1 (MMP-1) and integrity of type I collagen in foreskin fibroblasts. Skullcapflavone II did not affect the secretion of type I collagen but reduced the secretion of MMP-1 in a dose- and time-dependent manner. Real-time reverse transcription-PCR and reporter gene assays showed that skullcapflavone II reduced MMP-1 expression at the transcriptional level. Skullcapflavone II inhibited the serum-induced activation of the extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) signaling pathways required for MMP-1 transactivation. Skullcapflavone II also reduced tumor necrosis factor (TNF)-α-induced nuclear factor kappa light chain enhancer of activated B cells (NF-κB) activation and subsequent MMP-1 expression. In three-dimensional culture of fibroblasts, skullcapflavone II down-regulated TNF-α-induced MMP-1 secretion and reduced breakdown of type I collagen. These results indicate that skullcapflavone II is a novel biomolecule that down-regulates MMP-1 expression in foreskin fibroblasts and therefore could be useful in therapies for maintaining the integrity of extracellular matrix.

KEYWORDS

MMP-1; extracellular matrix; fibroblast; inflammation; skullcapflavone II; type I collagen

Title

Skullcapflavone II Inhibits Degradation of Type I Collagen by Suppressing MMP-1 Transcription in Human Skin Fibroblasts.

Author

Lee YH1, Seo EK2, Lee ST3.

Publish date

2019 Jun 4

PMID

30216110

Abstract

Many bone diseases, such as osteoporosis and rheumatoid arthritis, are attributed to an increase in osteoclast number or activity; therefore, control of osteoclasts has significant clinical implications. This study shows how skullcapflavone II (SFII), a flavonoid with anti-inflammatory activity, regulates osteoclast differentiation, survival, and function. SFII inhibited osteoclastogenesis with decreased activation of MAPKs, Src, and cAMP response element-binding protein (CREB), which have been known to be redox sensitive. SFII decreased reactive oxygen species by scavenging them or activating nuclear factor-erythroid 2-related factor 2 (Nrf2), and its effects were partially reversed by hydrogen peroxide cotreatment or Nrf2 deficiency. In addition, SFII attenuated survival, migration, and bone resorption, with a decrease in the expression of integrin β3, Src, and p130 Crk-associated substrate, and the activation of RhoA and Rac1 in differentiated osteoclasts. Furthermore, SFII inhibited osteoclast formation and bone loss in an inflammation- or ovariectomy-induced osteolytic mouse model. These findings suggest that SFII inhibits osteoclastogenesis through redox regulation of MAPKs, Src, and CREB and attenuates the survival and resorption function by modulating the integrin pathway in osteoclasts. SFII has therapeutic potential in the treatment and prevention of bone diseases caused by excessive osteoclast activity.-Lee, J., Son, H. S., Lee, H. I., Lee, G.-R., Jo, Y.-J., Hong, S.-E., Kim, N., Kwon, M., Kim, N. Y., Kim, H. J., Lee, Y. J., Seo, E. K., Jeong, W. Skullcapflavone II inhibits osteoclastogenesis by regulating reactive oxygen species and attenuates the survival and resorption function of osteoclasts by modulating integrin signaling.

KEYWORDS

Nrf2; Rho GTPase; bone resorption

Title

Skullcapflavone II inhibits osteoclastogenesis by regulating reactive oxygen species and attenuates the survival and resorption function of osteoclasts by modulating integrin signaling.

Author

Lee J1, Son HS1, Lee HI1, Lee GR1, Jo YJ1, Hong SE1, Kim N1, Kwon M1, Kim NY1, Kim HJ1, Lee YJ2, Seo EK2, Jeong W1.

Publish date

2019 Feb

PMID

28886581

Abstract

Allergic rhinitis is a common heterogeneous chronic upper airway disorder and is an IgE-mediated inflammation characterized by one or more nasal symptoms such as sneezing, itching, nasal discharge, rhinorrhea, post nasal drainage and nasal blockage. In the present study, the effects of skullcapflavone II (SCFII) on upper airway inflammation, Th2 cytokines, and NF-κB signaling in an ovalbumin (OVA)-induced allergic rhinitis (AR) murine model in vivo were investigated. OVA-induced AR mice increased nasal symptoms, eosinophils and mast cells infiltration into nasal cavity, OVA-specific IgE/IgG1 and histamine in serum, Th2 cytokines including IL-13 and GATA3, and NF-κB signaling in NALF and lung homogenate. Interestingly, treatment of SCFII reduced the levels of OVA-specific IgE/IgG1 and histamine in serum, of Th2 cytokines and of NF-κB signaling in the NALF and the lung homogenate, and histopathological changes in the nasal tissue and the lung. Also, dexamethasone suppressed such increases. The results of this study suggested that SCFII may ameliorate allergic inflammation of upper airway in AR mice model by blocking the Th2 cytokine production, the NF-κB signal pathway and the mast cell histamine release. Taken together, we suggest that SCFII may be used as a therapeutic agent for patients with Th2-mediated or mast cell-mediated allergic diseases.

Copyright © 2017 Elsevier B.V. All rights reserved.

KEYWORDS

Allergic rhinitis; Histamine; Mast cells; OVA-specific IgE/IgG1; Skullcapflavone II; Th2 cytokine

Title

Skullcapflavone II attenuates ovalbumin-induced allergic rhinitis through the blocking of Th2 cytokine production and mast cell histamine release.

Author

Bui TT1, Piao CH1, Song CH2, Chai OH3.

Publish date

2017 Nov 14


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