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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
Applications
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.
28933726
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.
NF-κB; NF-κB target genes; cancer; mollugin
Mollugin Has an Anti-Cancer Therapeutic Effect by Inhibiting TNF-α-Induced NF-κB Activation.
Wang Z1, Li MY2, Mi C3, Wang KS4, Ma J5, Jin X6.
2017 Jul 26
29027119
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.
BMP-2; Bone formation; Mollugin; Osteoblast; Smad; p38
Mollugin enhances the osteogenic action of BMP-2 via the p38-Smad signaling pathway.
Moon SH1,2,3, Kim I4, Kim SH5.
2017 Nov
31880521
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.
Mitochondria-dependent apoptosis.; Ovarian cancer; Rubimaillin
Rubimaillin decreases the viability of human ovarian cancer cells via mitochondria-dependent apoptosis.
Siwei Z1, Zhen W2, Zhi Z3, Xuguang H2, Yousheng L1.
2019 Sep 30