Mollugin

CAS# 55481-88-4

Mollugin

Catalog No. BCN5742----Order now to get a substantial discount!

Product Name & Size Price Stock
Mollugin: 5mg $12 In Stock
Mollugin: 10mg Please Inquire In Stock
Mollugin: 20mg Please Inquire Please Inquire
Mollugin: 50mg Please Inquire Please Inquire
Mollugin: 100mg Please Inquire Please Inquire
Mollugin: 200mg Please Inquire Please Inquire
Mollugin: 500mg Please Inquire Please Inquire
Mollugin: 1000mg Please Inquire Please Inquire

Quality Control of Mollugin

Number of papers citing our products

Chemical structure

Mollugin

3D structure

Chemical Properties of Mollugin

Cas No. 55481-88-4 SDF Download SDF
PubChem ID 124219 Appearance Yellow powder
Formula C17H16O4 M.Wt 284.3
Type of Compound Sesquiterpenoids Storage Desiccate at -20°C
Synonyms Rubimaillin
Solubility DMSO : 33.33 mg/mL (117.23 mM; Need ultrasonic)
Chemical Name methyl 6-hydroxy-2,2-dimethylbenzo[h]chromene-5-carboxylate
SMILES CC1(C=CC2=C(O1)C3=CC=CC=C3C(=C2C(=O)OC)O)C
Standard InChIKey VLGATXOTCNBWIT-UHFFFAOYSA-N
Standard InChI InChI=1S/C17H16O4/c1-17(2)9-8-12-13(16(19)20-3)14(18)10-6-4-5-7-11(10)15(12)21-17/h4-9,18H,1-3H3
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Source of Mollugin

The roots of Rubia cordifolia L.

Biological Activity of Mollugin

DescriptionMollugin is a JAK2 inhibitor and inhibits LPS-induced inflammatory responses by blocking the activation of the JAK-STAT pathway. Mollugin may be a novel therapeutic candidate for bone loss-associated disorders including osteoporosis, rheumatoid arthritis, and periodontitis. Mollugin has anticancer efficacy, can modulate the HER2, HO-1, Nrf2 , and NF- κB pathways.
TargetsJAK | STAT | HO-1 | Nrf2 | NF-kB | PI3K | p38MAPK | mTOR | Akt | ERK | Autophagy | GSK-3 | MEK | NO | NOS | IL Receptor | TNF-α | IkB | JNK | Bcl-2/Bax | MMP(e.g.TIMP) | VEGFR | EGFR | IKK
In vitro

Mollugin induces tumor cell apoptosis and autophagy via the PI3K/AKT/mTOR/p70S6K and ERK signaling pathways.[Pubmed: 24887566]

Biochem Biophys Res Commun. 2014 Jul 18;450(1):247-54.

Mollugin, a bioactive phytochemical isolated from Rubia cordifolia L., has shown preclinical anticancer efficacy in various cancer models. However the effects of Mollugin in regulating cancer cell survival and death remains undefined.
METHODS AND RESULTS:
In the present study we found that Mollugin exhibited cytotoxicity on various cancer models. The suppression of cell viability was due to the induction of mitochondria apoptosis. In addition, the presence of autophagic hallmarks was observed in Mollugin-treated cells. Notably, blockade of autophagy by a chemical inhibitor or RNA interference enhanced the cytotoxicity of Mollugin. Further experiments demonstrated that phosphatidylinositide 3-kinases/protein kinase B/mammalian target of rapamycin/p70S6 kinase (PI3K/AKT/mTOR/p70S6K) and extracellular regulated protein kinases (ERK) signaling pathways participated in Mollugin-induced autophagy and apoptosis.
CONCLUSIONS:
Together, these findings support further studies of Mollugin as candidate for treatment of human cancer cells.

Mollugin from Rubea cordifolia suppresses receptor activator of nuclear factor-κB ligand-induced osteoclastogenesis and bone resorbing activity in vitro and prevents lipopolysaccharide-induced bone loss in vivo.[Pubmed: 25636867]

Phytomedicine. 2015 Jan 15;22(1):27-35.

Osteopenic diseases, such as osteoporosis, are characterized by progressive and excessive bone resorption mediated by enhanced receptor activator of nuclear factor-κB ligand (RANKL) signaling. Therefore, downregulation of RANKL downstream signals may be a valuable approach for the treatment of bone loss-associated disorders.
METHODS AND RESULTS:
In this study, we investigated the effects of the naphthohydroquinone Mollugin on osteoclastogenesis and its function in vitro and in vivo. Mollugin efficiently suppressed RANKL-induced osteoclast differentiation of bone marrow macrophages (BMMs) and bone resorbing activity of mature osteoclasts by inhibiting RANKL-induced c-Fos and NFATc1 expression. Mollugin reduced the phosphorylation of signaling pathways activated in the early stages of osteoclast differentiation, including the MAP kinase, Akt, and GSK3β and inhibited the expression of different genes associated with osteoclastogenesis, such as OSCAR, TRAP, DC-STAMP, OC-STAMP, integrin αν, integrin β3, cathepsin K, and ICAM-1. Furthermore, mice treated with Mollugin showed significant restoration of lipopolysaccharide (LPS)-induced bone loss as indicated by micro-CT and histological analysis of femurs.
CONCLUSIONS:
Consequently, these results suggested that Mollugin could be a novel therapeutic candidate for bone loss-associated disorders including osteoporosis, rheumatoid arthritis, and periodontitis.

Protocol of Mollugin

Kinase Assay

Mollugin inhibits the inflammatory response in lipopolysaccharide-stimulated RAW264.7 macrophages by blocking the Janus kinase-signal transducers and activators of transcription signaling pathway.[Pubmed: 23318249]

Biol Pharm Bull. 2013;36(3):399-406. Epub 2013 Jan 11.

Mollugin, a kind of naphthohydroquinone, is a major constituent isolated from Rubia cordifolia L. and demonstrated to possess anti-inflammatory activity in recent reports. However, the effects and mechanism of action of Mollugin in inflammation have not been fully defined. The present study was therefore designed to investigate whether Mollugin suppresses the inflammatory response in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages.
METHODS AND RESULTS:
Mollugin attenuated the LPS-induced expression of nitric oxide (NO), inducible nitric oxide synthase (iNOS), interleukin (IL)-1β and IL-6 but augmented the expression of tumor necrosis factor (TNF)-α. Mollugin did not inhibit the degradation of inhibitory kappa B (IκB)-α or the nuclear translocation of p65 nuclear factor-kappa B (NF-κB) but rather enhanced the phosphorylation of p65 subunits evoked by LPS. Mollugin did not inhibit the phosphorylation of extracellular-signal-related kinase (ERK) 1/2, p38, and c-Jun N-terminal kinase (JNK) 1/2 either. Mollugin significantly reduced the LPS-mediated phosphorylation of Janus kinase (JAK) 2, signal transducers and activators of transcription (STAT) 1 and STAT3. Molecular docking analysis showed that Mollugin binds to JAK2 in a manner similar to that of AG490, a specific JAK2 inhibitor.
CONCLUSIONS:
We conclude that Mollugin may be a JAK2 inhibitor and inhibits LPS-induced inflammatory responses by blocking the activation of the JAK-STAT pathway.

Cell Research

Involvement of Nrf2-mediated upregulation of heme oxygenase-1 in mollugin-induced growth inhibition and apoptosis in human oral cancer cells.[Pubmed: 23738323]

Mollugin inhibits proliferation and induces apoptosis by suppressing fatty acid synthase in HER2-overexpressing cancer cells.[Pubmed: 23065756]

J Cell Physiol. 2013 May;228(5):1087-97.

Mollugin is a naphthohydroquine found in the roots of Rubia cordifolia, and has been reported to have a variety of biological activities, including anti-inflammatory and apoptotic effects. In the present study, we investigated the molecular mechanisms by which Mollugin exerts anti-tumor effect in HER2-overexpressing cancer cells.
METHODS AND RESULTS:
Our results showed that Mollugin exhibited potent inhibitory effects on cancer cell proliferation, especially in HER2-overexpressing SK-BR-3 human breast cancer cells and SK-OV-3 human ovarian cancer cells in a dose- and time-dependent manner without affecting immortalized normal mammary epithelial cell line MCF-10A. Furthermore, we found that a blockade of Akt/SREBP-1c signaling through Mollugin treatment significantly reduced FAS expression and subsequently suppressed cell proliferation and induced apoptosis in HER2-overexpressing cancer cells. Mollugin treatment caused a dose-dependent inhibition of HER2 gene expression at the transcriptional level, potentially in part through suppression of NF-κB activation. The combination of Mollugin with a MEK1/2 inhibitor may be required in order to achieve optimal efficacy in HER2-overexpressing cancers. These data provide evidence that Mollugin inhibits proliferation and induces apoptosis in HER2-overexpressing cancer cells by blocking expression of the FAS gene through modulation of a HER2/Akt/SREBP-1c signaling pathway.
CONCLUSIONS:
Our findings suggest that Mollugin is a novel modulator of the HER2 pathway in HER2-overexpressing cancer cells with a potential role in the treatment and prevention of human breast and ovarian cancer with HER2 overexpression.

Biomed Res Int. 2013;2013:210604.

Although previous studies have shown that Mollugin, a bioactive phytochemical isolated from Rubia cordifolia L. (Rubiaceae), exhibits antitumor effects, its biological activity in oral cancer has not been reported.
METHODS AND RESULTS:
We thus investigated the effects and putative mechanism of apoptosis induced by Mollugin in human oral squamous cell carcinoma cells (OSCCs). Results show that Mollugin induces cell death in a dose-dependent manner in primary and metastatic OSCCs. Mollugin-induced cell death involved apoptosis, characterized by the appearance of nuclear shrinkage, flow cytometric analysis of sub-G1 phase arrest, and annexin V-FITC and propidium iodide staining. Western blot analysis and RT-PCR revealed that Mollugin suppressed activation of NF- κ B and NF- κ B-dependent gene products involved in antiapoptosis (Bcl-2 and Bcl-xl), invasion (MMP-9 and ICAM-1), and angiogenesis (FGF-2 and VEGF). Furthermore, Mollugin induced the activation of p38, ERK, and JNK and the expression of heme oxygenase-1 (HO-1) and nuclear factor E2-related factor 2 (Nrf2). Mollugin-induced growth inhibition and apoptosis of HO-1 were reversed by an HO-1 inhibitor and Nrf2 siRNA.
CONCLUSIONS:
Collectively, this is the first report to demonstrate the effectiveness of Mollugin as a candidate for a chemotherapeutic agent in OSCCs via the upregulation of the HO-1 and Nrf2 pathways and the downregulation of NF- κ B.

Mollugin Dilution Calculator

Concentration (start)
x
Volume (start)
=
Concentration (final)
x
Volume (final)
 
 
 
C1
V1
C2
V2

calculate

Mollugin Molarity Calculator

Mass
=
Concentration
x
Volume
x
MW*
 
 
 
g/mol

calculate

Preparing Stock Solutions of Mollugin

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 3.5174 mL 17.5871 mL 35.1741 mL 70.3482 mL 87.9353 mL
5 mM 0.7035 mL 3.5174 mL 7.0348 mL 14.0696 mL 17.5871 mL
10 mM 0.3517 mL 1.7587 mL 3.5174 mL 7.0348 mL 8.7935 mL
50 mM 0.0703 mL 0.3517 mL 0.7035 mL 1.407 mL 1.7587 mL
100 mM 0.0352 mL 0.1759 mL 0.3517 mL 0.7035 mL 0.8794 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

Organizitions Citing Our Products recently

 
 
 

Calcutta University

University of Minnesota

University of Maryland School of Medicine

University of Illinois at Chicago

The Ohio State University

University of Zurich

Harvard University

Colorado State University

Auburn University

Yale University

Worcester Polytechnic Institute

Washington State University

Stanford University

University of Leipzig

Universidade da Beira Interior

The Institute of Cancer Research

Heidelberg University

University of Amsterdam

University of Auckland
TsingHua University
TsingHua University
The University of Michigan
The University of Michigan
Miami University
Miami University
DRURY University
DRURY University
Jilin University
Jilin University
Fudan University
Fudan University
Wuhan University
Wuhan University
Sun Yat-sen University
Sun Yat-sen University
Universite de Paris
Universite de Paris
Deemed University
Deemed University
Auckland University
Auckland University
The University of Tokyo
The University of Tokyo
Korea University
Korea University
Featured Products
New Products
 

References on Mollugin

Involvement of Nrf2-mediated upregulation of heme oxygenase-1 in mollugin-induced growth inhibition and apoptosis in human oral cancer cells.[Pubmed:23738323]

Biomed Res Int. 2013;2013:210604.

Although previous studies have shown that Mollugin, a bioactive phytochemical isolated from Rubia cordifolia L. (Rubiaceae), exhibits antitumor effects, its biological activity in oral cancer has not been reported. We thus investigated the effects and putative mechanism of apoptosis induced by Mollugin in human oral squamous cell carcinoma cells (OSCCs). Results show that Mollugin induces cell death in a dose-dependent manner in primary and metastatic OSCCs. Mollugin-induced cell death involved apoptosis, characterized by the appearance of nuclear shrinkage, flow cytometric analysis of sub-G1 phase arrest, and annexin V-FITC and propidium iodide staining. Western blot analysis and RT-PCR revealed that Mollugin suppressed activation of NF- kappa B and NF- kappa B-dependent gene products involved in antiapoptosis (Bcl-2 and Bcl-xl), invasion (MMP-9 and ICAM-1), and angiogenesis (FGF-2 and VEGF). Furthermore, Mollugin induced the activation of p38, ERK, and JNK and the expression of heme oxygenase-1 (HO-1) and nuclear factor E2-related factor 2 (Nrf2). Mollugin-induced growth inhibition and apoptosis of HO-1 were reversed by an HO-1 inhibitor and Nrf2 siRNA. Collectively, this is the first report to demonstrate the effectiveness of Mollugin as a candidate for a chemotherapeutic agent in OSCCs via the upregulation of the HO-1 and Nrf2 pathways and the downregulation of NF- kappa B.

Mollugin inhibits the inflammatory response in lipopolysaccharide-stimulated RAW264.7 macrophages by blocking the Janus kinase-signal transducers and activators of transcription signaling pathway.[Pubmed:23318249]

Biol Pharm Bull. 2013;36(3):399-406. Epub 2013 Jan 11.

Mollugin, a kind of naphthohydroquinone, is a major constituent isolated from Rubia cordifolia L. and demonstrated to possess anti-inflammatory activity in recent reports. However, the effects and mechanism of action of Mollugin in inflammation have not been fully defined. The present study was therefore designed to investigate whether Mollugin suppresses the inflammatory response in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages. Mollugin attenuated the LPS-induced expression of nitric oxide (NO), inducible nitric oxide synthase (iNOS), interleukin (IL)-1beta and IL-6 but augmented the expression of tumor necrosis factor (TNF)-alpha. Mollugin did not inhibit the degradation of inhibitory kappa B (IkappaB)-alpha or the nuclear translocation of p65 nuclear factor-kappa B (NF-kappaB) but rather enhanced the phosphorylation of p65 subunits evoked by LPS. Mollugin did not inhibit the phosphorylation of extracellular-signal-related kinase (ERK) 1/2, p38, and c-Jun N-terminal kinase (JNK) 1/2 either. Mollugin significantly reduced the LPS-mediated phosphorylation of Janus kinase (JAK) 2, signal transducers and activators of transcription (STAT) 1 and STAT3. Molecular docking analysis showed that Mollugin binds to JAK2 in a manner similar to that of AG490, a specific JAK2 inhibitor. We conclude that Mollugin may be a JAK2 inhibitor and inhibits LPS-induced inflammatory responses by blocking the activation of the JAK-STAT pathway.

Mollugin inhibits proliferation and induces apoptosis by suppressing fatty acid synthase in HER2-overexpressing cancer cells.[Pubmed:23065756]

J Cell Physiol. 2013 May;228(5):1087-97.

Mollugin is a naphthohydroquine found in the roots of Rubia cordifolia, and has been reported to have a variety of biological activities, including anti-inflammatory and apoptotic effects. In the present study, we investigated the molecular mechanisms by which Mollugin exerts anti-tumor effect in HER2-overexpressing cancer cells. Our results showed that Mollugin exhibited potent inhibitory effects on cancer cell proliferation, especially in HER2-overexpressing SK-BR-3 human breast cancer cells and SK-OV-3 human ovarian cancer cells in a dose- and time-dependent manner without affecting immortalized normal mammary epithelial cell line MCF-10A. Furthermore, we found that a blockade of Akt/SREBP-1c signaling through Mollugin treatment significantly reduced FAS expression and subsequently suppressed cell proliferation and induced apoptosis in HER2-overexpressing cancer cells. Mollugin treatment caused a dose-dependent inhibition of HER2 gene expression at the transcriptional level, potentially in part through suppression of NF-kappaB activation. The combination of Mollugin with a MEK1/2 inhibitor may be required in order to achieve optimal efficacy in HER2-overexpressing cancers. These data provide evidence that Mollugin inhibits proliferation and induces apoptosis in HER2-overexpressing cancer cells by blocking expression of the FAS gene through modulation of a HER2/Akt/SREBP-1c signaling pathway. Our findings suggest that Mollugin is a novel modulator of the HER2 pathway in HER2-overexpressing cancer cells with a potential role in the treatment and prevention of human breast and ovarian cancer with HER2 overexpression.

Mollugin from Rubea cordifolia suppresses receptor activator of nuclear factor-kappaB ligand-induced osteoclastogenesis and bone resorbing activity in vitro and prevents lipopolysaccharide-induced bone loss in vivo.[Pubmed:25636867]

Phytomedicine. 2015 Jan 15;22(1):27-35.

Osteopenic diseases, such as osteoporosis, are characterized by progressive and excessive bone resorption mediated by enhanced receptor activator of nuclear factor-kappaB ligand (RANKL) signaling. Therefore, downregulation of RANKL downstream signals may be a valuable approach for the treatment of bone loss-associated disorders. In this study, we investigated the effects of the naphthohydroquinone Mollugin on osteoclastogenesis and its function in vitro and in vivo. Mollugin efficiently suppressed RANKL-induced osteoclast differentiation of bone marrow macrophages (BMMs) and bone resorbing activity of mature osteoclasts by inhibiting RANKL-induced c-Fos and NFATc1 expression. Mollugin reduced the phosphorylation of signaling pathways activated in the early stages of osteoclast differentiation, including the MAP kinase, Akt, and GSK3beta and inhibited the expression of different genes associated with osteoclastogenesis, such as OSCAR, TRAP, DC-STAMP, OC-STAMP, integrin alphanu, integrin beta3, cathepsin K, and ICAM-1. Furthermore, mice treated with Mollugin showed significant restoration of lipopolysaccharide (LPS)-induced bone loss as indicated by micro-CT and histological analysis of femurs. Consequently, these results suggested that Mollugin could be a novel therapeutic candidate for bone loss-associated disorders including osteoporosis, rheumatoid arthritis, and periodontitis.

Mollugin induces tumor cell apoptosis and autophagy via the PI3K/AKT/mTOR/p70S6K and ERK signaling pathways.[Pubmed:24887566]

Biochem Biophys Res Commun. 2014 Jul 18;450(1):247-54.

Mollugin, a bioactive phytochemical isolated from Rubia cordifolia L., has shown preclinical anticancer efficacy in various cancer models. However the effects of Mollugin in regulating cancer cell survival and death remains undefined. In the present study we found that Mollugin exhibited cytotoxicity on various cancer models. The suppression of cell viability was due to the induction of mitochondria apoptosis. In addition, the presence of autophagic hallmarks was observed in Mollugin-treated cells. Notably, blockade of autophagy by a chemical inhibitor or RNA interference enhanced the cytotoxicity of Mollugin. Further experiments demonstrated that phosphatidylinositide 3-kinases/protein kinase B/mammalian target of rapamycin/p70S6 kinase (PI3K/AKT/mTOR/p70S6K) and extracellular regulated protein kinases (ERK) signaling pathways participated in Mollugin-induced autophagy and apoptosis. Together, these findings support further studies of Mollugin as candidate for treatment of human cancer cells.

Description

Mollugin is a major bioactive component isolated from Rubia cordifolia L.. Mollugin has an anti-cancer therapeutic effect by inhibiting TNF-α-induced NF-κB activation. Mollugin enhances the osteogenic action of BMP-2 via the p38-Smad signaling pathway .

Keywords:

Mollugin,55481-88-4,Rubimaillin,Natural Products, buy Mollugin , Mollugin supplier , purchase Mollugin , Mollugin cost , Mollugin manufacturer , order Mollugin , high purity Mollugin

Online Inquiry for:

      Fill out the information below

      • Size:Qty: - +

      * Required Fields

                                      Result: