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Moringin
Moringin
ChemFaces products have been cited in many studies from excellent and top scientific journals
Product Name Moringin
Price:
CAS No.: 73255-40-0
Catalog No.: CFN89445
Molecular Formula: C14H17NO5S
Molecular Weight: 311.35 g/mol
Purity: >=98%
Type of Compound: Phenols
Physical Desc.: Powder
Source: The seeds of Moringa oleifera.
Solvent: DMSO, Pyridine, Methanol, Ethanol, etc.
Download: COA    MSDS
Similar structural: Comparison (Web)  (SDF)
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According to end customer requirements, ChemFaces provide solvent format. This solvent format of product intended use: Signaling Inhibitors, Biological activities or Pharmacological activities.
Size /Price /Stock 10 mM * 1 mL in DMSO / Inquiry
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Related Screening Libraries
Size /Price /Stock 10 mM * 100 uL in DMSO / Inquiry / In-stock
10 mM * 1 mL in DMSO / Inquiry / In-stock
Related Libraries
Biological Activity
Description: Moringin is a modulator of neuroinflammation via the β-catenin-PPARγ axis, it can activate Wnt canonical pathway by inhibiting GSK3β in a mouse model of experimental autoimmune encephalomyelitis. Moringin is effective in inducing apoptosis through p53 and Bax activation and Bcl-2 inhibition, it demonstrates the antitumor efficacy in human malignant astrocytoma cells. The combination of cannabidiol and moringin has anti-inflammatory, antioxidative, and anti-apoptotic effects.
Targets: PPAR | GSK-3 | COX | IL Receptor | gp120/CD4 | Nrf2 | Wnt/β-catenin | TNF-α | Bcl-2/Bax | Caspase | p53
In vitro:
Fitoterapia. 2016 Jul;112:104-15.
Anti-inflammatory and antioxidant effects of a combination of cannabidiol and moringin in LPS-stimulated macrophages.[Pubmed: 27215129 ]
Inflammatory response plays an important role in the activation and progress of many debilitating diseases. Natural products, like cannabidiol, a constituent of Cannabis sativa, and Moringin, an isothiocyanate obtained from myrosinase-mediated hydrolysis of the glucosinolate precursor glucoMoringin present in Moringa oleifera seeds, are well known antioxidants also endowed with anti-inflammatory activity.
METHODS AND RESULTS:
This is due to a covalent-based mechanism for ITC, while non-covalent interactions underlie the activity of CBD. Since these two mechanisms are distinct, and the molecular endpoints are potentially complementary, we investigated in a comparative way the protective effect of these compounds alone or in combination on lipopolysaccharide-stimulated murine macrophages. Our results show that the cannabidiol (5μM) and Moringin (5μM) combination outperformed the single constituents that, at this dosage had only a moderate efficacy on inflammatory (Tumor necrosis factor-α, Interleukin-10) and oxidative markers (inducible nitric oxide synthase, nuclear factor erythroid 2-related factor 2, nitrotyrosine). Significant upregulation of Bcl-2 and downregulation of Bax and cleaved caspase-3 was observed in cells treated with cannabidiol-Moringin combination. Treatment with the transient receptor potential vanilloid receptor 1 antagonist was detrimental for the efficacy of cannabidiol, while no effect was elicited by cannabinoid receptor 1 and cannabinoid receptor 2 antagonists. None of these receptors was involved in the activity of Moringin.
CONCLUSIONS:
Taken together, our in vitro results testify the anti-inflammatory, antioxidative, and anti-apoptotic effects of the combination of cannabidiol and Moringin.
Fitoterapia. 2016 Apr;110:1-7.
Anticancer activity of glucomoringin isothiocyanate in human malignant astrocytoma cells.[Pubmed: 26882972]
Isothiocyanates (ITCs) released from their glucosinolate precursors have been shown to inhibit tumorigenesis and they have received significant attention as potential chemotherapeutic agents against cancer. Astrocytoma grade IV is the most frequent and most malignant primary brain tumor in adults without any curative treatment. New therapeutic drugs are therefore urgently required.
METHODS AND RESULTS:
In the present study, we investigated the in vitro antitumor activity of the glycosylated isothiocyanate Moringin [4-(α-l-rhamnopyranosyloxy)benzyl isothiocyanate] produced from quantitative myrosinase-induced hydrolysis of glucoMoringin (GMG) under neutral pH value. We have evaluated the potency of Moringin on apoptosis induction and cell death in human astrocytoma grade IV CCF-STTG1 cells. Moringin showed to be effective in inducing apoptosis through p53 and Bax activation and Bcl-2 inhibition. In addition, oxidative stress related Nrf2 transcription factor and its upstream regulator CK2 alpha expressions were modulated at higher doses, which indicated the involvement of oxidative stress-mediated apoptosis induced by Moringin. Moreover, significant reduction in 5S rRNA was noticed with Moringin treatment.
CONCLUSIONS:
Our in vitro results demonstrated the antitumor efficacy of Moringin derived from myrosinase-hydrolysis of GMG in human malignant astrocytoma cells.
Moringin Description
Source: The seeds of Moringa oleifera.
Solvent: DMSO, Pyridine, Methanol, Ethanol, etc.
Storage: Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com

After receiving: The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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Recently, ChemFaces products have been cited in many studies from excellent and top scientific journals

Cell. 2018 Jan 11;172(1-2):249-261.e12.
doi: 10.1016/j.cell.2017.12.019.
IF=36.216(2019)

PMID: 29328914

Cell Metab. 2020 Mar 3;31(3):534-548.e5.
doi: 10.1016/j.cmet.2020.01.002.
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PMID: 29149595

ACS Nano. 2018 Apr 24;12(4): 3385-3396.
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IF=13.903(2019)

PMID: 29553709

Nature Plants. 2016 Dec 22;3: 16206.
doi: 10.1038/nplants.2016.205.
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PMID: 28005066

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IF=12.804(2019)

PMID: 30417089
Calculate Dilution Ratios(Only for Reference)
1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 3.2118 mL 16.0591 mL 32.1182 mL 64.2364 mL 80.2955 mL
5 mM 0.6424 mL 3.2118 mL 6.4236 mL 12.8473 mL 16.0591 mL
10 mM 0.3212 mL 1.6059 mL 3.2118 mL 6.4236 mL 8.0295 mL
50 mM 0.0642 mL 0.3212 mL 0.6424 mL 1.2847 mL 1.6059 mL
100 mM 0.0321 mL 0.1606 mL 0.3212 mL 0.6424 mL 0.803 mL
* Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
Protocol
Animal Research:
Drug Des Devel Ther. 2016 Oct 4;10:3291-3304.
Moringin activates Wnt canonical pathway by inhibiting GSK3β in a mouse model of experimental autoimmune encephalomyelitis.[Pubmed: 27784989]
Aberrant canonical Wnt-β-catenin signaling has been reported in multiple sclerosis (MS), although the results are controversial.
METHODS AND RESULTS:
The present study aimed to examine the role of the Wnt-β-catenin pathway in experimental MS and also to test Moringin (4-[α-L-rhamnopyranosyloxy]-benzyl isothiocyanate), resulting from exogenous myrosinase hydrolysis of the natural phytochemical glucoMoringin 4(α-L-rhamnosyloxy)-benzyl glucosinolate as a modulator of neuroinflammation via the β-catenin-PPARγ axis. Experimental autoimmune encephalomyelitis (EAE), the most common model of MS, was induced in C57BL/6 mice by immunization with MOG35-55. Released Moringin (10 mg/kg glucoMoringin +5 μL myrosinase/mouse) was administered daily for 1 week before EAE induction and continued until mice were killed on day 28 after EAE induction. Our results clearly showed that the Wnt-β-catenin pathway was downregulated in the EAE model, whereas Moringin pretreatment was able to avert this. Moringin pretreatment normalizes the aberrant Wnt-β-catenin pathway, resulting in GSK3β inhibition and β-catenin upregulation, which regulates T-cell activation (CD4 and FoxP3), suppresses the main inflammatory mediators (IL-1β, IL-6, and COX2), through activation of PPARγ. In addition, Moringin attenuates apoptosis by reducing the expression of the Fas ligand and cleaved caspase 9, and in parallel increases antioxidant Nrf2 expression in EAE mice.
CONCLUSIONS:
Taken together, our results provide an interesting discovery in identifying Moringin as a modulator of the Wnt-β-catenin signaling cascade and as a new potential therapeutic target for MS treatment.
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