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Mollugin

$60

  • Brand : BIOFRON

  • Catalogue Number : AV-P10622

  • Specification : 98%

  • CAS number : 55481-88-4

  • Formula : C17H16O4

  • Molecular Weight : 284.31

  • PUBCHEM ID : 124219

  • Volume : 20mg

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Catalogue Number

AV-P10622

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

284.31

Appearance

Yellow crystal

Botanical Source

Rubia cordifolia L.

Structure Type

Other Phenolic Compounds

Category

Standards;Natural Pytochemical;API

SMILES

CC1(C=CC2=C(O1)C3=CC=CC=C3C(=C2C(=O)OC)O)C

Synonyms

Methyl 6-hydroxy-2,2-dimethyl-2H-benzo[h]chromene-5-carboxylate/5-Carbomethoxy-6-hydroxy-2,2-dimethyl-2H-naphtho-pyran/2H-Naphtho[1,2-b]pyran-5-carboxylic acid, 6-hydroxy-2,2-dimethyl-, methyl ester/Rubimaillin/Mollugin/rubiMaillin/6-hydroxy-2,2-dimethyl-,methylester/mollugin

IUPAC Name

methyl 6-hydroxy-2,2-dimethylbenzo[h]chromene-5-carboxylate

Density

1.2±0.1 g/cm3

Solubility

DMSO; Acetone; Methanol

Flash Point

167.5±22.2 °C

Boiling Point

453.2±45.0 °C at 760 mmHg

Melting Point

132-134ºC

InChl

InChl Key

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#:55481-88-4) 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

28933726

Abstract

The NF-κB signaling pathway plays a pivotal role in regulating the immune response and inflammation. However, it has been shown that NF-κB also has a major role in oncogenesis. Therefore, NF-κB inhibitors have been considered as potential drugs against cancer. Herein, we searched for NF-κB inhibitors from natural sources and identified mollugin from the roots of Rubia cordifolia L. as an inhibitor of NF-κB activation. We found that mollugin significantly inhibited the expression of an NF-κB reporter gene induced by tumor necrosis factor (TNF)-α in a dose-dependent manner. Moreover, mollugin inhibited TNF-α-induced phosphorylation and nuclear translocation of p65, phosphorylation and degradation of inhibitor of κB (IκBα), and IκB kinase (IKK) phosphorylation. Furthermore, we discovered that pretreatment of cells with mollugin prevented the TNF-α-induced expression of NF-κB target genes, such as genes related to proliferation (COX-2, Cyclin D1 and c-Myc), anti-apoptosis (Bcl-2, cIAP-1 and survivin), invasion (MMP-9 and ICAM-1), and angiogenesis (VEGF). We also demonstrated that mollugin potentiated TNF-α-induced apoptosis and inhibited proliferation of HeLa cells. We further demonstrated in vivo that mollugin suppressed the growth of tumor xenografts derived from HeLa cells. Taken together, mollugin may be a valuable candidate for cancer treatment by targeting NF-κB.

KEYWORDS

NF-κB; NF-κB target genes; cancer; mollugin

Title

Mollugin Has an Anti-Cancer Therapeutic Effect by Inhibiting TNF-α-Induced NF-κB Activation.

Author

Wang Z1, Li MY2, Mi C3, Wang KS4, Ma J5, Jin X6.

Publish date

2017 Jul 26

PMID

29027119

Abstract

Bone morphogenetic protein 2 (BMP-2) has been used clinically to encourage bone regeneration; although, there can be major side effects with larger doses. Therefore, there is a need to identify new small molecules to potentiate the osteogenic action of BMP-2. In this study, we investigated the effect of mollugin on bone formation in murine bi-potential mesenchymal progenitor C2C12 cells by combination with BMP-2. We found mollugin could enhance the BMP-2-mediated osteoblast differentiation of C2C12 cells. This was accompanied by the induction of other osteogenic BMPs. We also found the enhancing potential of mollugin may involve activation of the p38-Smad1/5/8 signaling axis. Furthermore, mollugin promoted skeletal development in zebrafish. The combination of BMP-2 with small molecules, including mollugin, could minimize its clinical limitations, and these molecules might lead to the development of effective stem cell stimulants for bone regeneration and fracture healing.

KEYWORDS

BMP-2; Bone formation; Mollugin; Osteoblast; Smad; p38

Title

Mollugin enhances the osteogenic action of BMP-2 via the p38-Smad signaling pathway.

Author

Moon SH1,2,3, Kim I4, Kim SH5.

Publish date

2017 Nov

PMID

31880521

Abstract

This study was aimed to investigate the anti-tumor activity of rubimaillin in vitro, and the mechanism involved. The inhibitory effect of rubimaillin on cell proliferation was determined with MTT assay. Apoptosis was assayed using AV/PI double staining, while the mitochondrial membrane potential of SKOV-3 cells was determined with Rhodamine 123 (Rh123) staining. Western blot assay was used to determine the effect of rubimaillin on the expressions of Bcl-2, Bax, PARP, cleaved PARP, caspase3, cleaved caspase3, and other apoptosis-related proteins in SKOV-3 cells. Rubimaillin inhibited the growth of SKOV-3 cells in a concentration-dependent manner and induced apoptosis of tumor cells through the mitochondrial apoptosis pathway. These results indicate that rubimaillin is a potential anti-ovarian cancer drug.

KEYWORDS

Mitochondria-dependent apoptosis.; Ovarian cancer; Rubimaillin

Title

Rubimaillin decreases the viability of human ovarian cancer cells via mitochondria-dependent apoptosis.

Author

Siwei Z1, Zhen W2, Zhi Z3, Xuguang H2, Yousheng L1.

Publish date

2019 Sep 30


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