Methysticin

CAS# 20697-20-5

Methysticin

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Quality Control of Methysticin

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Chemical structure

Methysticin

3D structure

Chemical Properties of Methysticin

Cas No. 20697-20-5 SDF Download SDF
PubChem ID 16760121 Appearance Cryst.
Formula C15H14O5 M.Wt 274.27
Type of Compound Phenols Storage Desiccate at -20°C
Synonyms DL-Methysticin; (±)-Methystici
Solubility Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.
Chemical Name (2S)-2-[(E)-2-(1,3-benzodioxol-5-yl)ethenyl]-4-methoxy-2,3-dihydropyran-6-one
SMILES COC1=CC(=O)OC(C1)C=CC2=CC3=C(C=C2)OCO3
Standard InChIKey GTEXBOVBADJOQH-JRBALWBOSA-N
Standard InChI InChI=1S/C15H14O5/c1-17-12-7-11(20-15(16)8-12)4-2-10-3-5-13-14(6-10)19-9-18-13/h2-6,8,11H,7,9H2,1H3/b4-2+/t11-/m1/s1
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 Methysticin

The herbs of Piper methysticum

Biological Activity of Methysticin

Description1. Methysticin and yangonin show in vitro hepatotoxicity on human hepatocytes (HepG2) . 2. Methysticin and 7,8-dihydroMethysticin contribute to CYP1A1 induction. 3. Methysticin is a potent NF-kappaB inhibitor in kava with minimum toxicity. 4. Methysticin possesses anticonvulsant and neuroprotective properties, possibly by interfering with frequency potentiation.
TargetsP450 (e.g. CYP17) | NF-kB | Calcium Channel | Potassium Channel

Methysticin Dilution Calculator

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Methysticin Molarity Calculator

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Preparing Stock Solutions of Methysticin

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 3.646 mL 18.2302 mL 36.4604 mL 72.9208 mL 91.1511 mL
5 mM 0.7292 mL 3.646 mL 7.2921 mL 14.5842 mL 18.2302 mL
10 mM 0.3646 mL 1.823 mL 3.646 mL 7.2921 mL 9.1151 mL
50 mM 0.0729 mL 0.3646 mL 0.7292 mL 1.4584 mL 1.823 mL
100 mM 0.0365 mL 0.1823 mL 0.3646 mL 0.7292 mL 0.9115 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.

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Background on Methysticin

Methysticin is a major kavalactone in kava extract to induce CYP1A1.

In Vitro:Methysticin triggers the most profound inducing effect on CYP1A1. Consistent with the experimental results, in silico molecular docking studies based on the aryl hydrocarbon receptor (AhR)-ligand binding domain homology model also reveals favorable binding to AhR for Methysticin compared with the remaining kavalactones. Additionally, results from a luciferase gene reporter assay suggested that kava extract, Methysticin is able to activate the AhR signaling pathway. Kava extract induces the expression of CYP1A1 via an AhR-dependent mechanism and that Methysticin contributes to CYP1A1 induction. The induction of CYP1A1 indicates a potential interaction between kava or kavalactones and CYP1A1-mediated chemical carcinogenesis. The MTS cell viability assay is used to determine the effects of kava extract and kavalactones on cell viability in mouse hepatic cells. Hepa1c1c7 cells are treated with various concentrations of kava extract (0-50 µg/mL) and six kavalactones (0-100 µM) for 24 h. The results indicate that kava extract at concentrations up to 50 µg/mL and kavalactones up to 100 µM do not induce cell death. For the following studies, kava extract at 0.78-6.25 µg/mL and kavalactones at 0.78-25 µM, concentrations that cause no damage to cells, are used[1].

In Vivo:The kavalactone Methysticin (6 mg/kg) is administered once a week for a period of 6 months to 6 month old transgenic APP/Psen1 mice by oral gavage. Methysticin treatment activates the Nrf2 pathway in the hippocampus and cortex of mice. The Aβ deposition in brains of Methysticin-treated APP/Psen1 mice is not altered compared to untreated mice. However, Methysticin treatment significantly reduces microgliosis, astrogliosis and secretion of the pro-inflammatory cytokines TNF-α and IL-17A. Methysticin treatment results in a significant activation of the Nrf2/ARE pathway in hippocampus and the cortex but not in the midbrain and cerebellum of ARE-luciferase reporter gene mice. Methysticin treatment significantly increases the expression of both genes compared to untreated animals[2].

References:
[1]. Li Y, et al. Methysticin and 7,8-dihydromethysticin are two major kavalactones in kava extract to induce CYP1A1. Toxicol Sci. 2011 Dec;124(2):388-99. [2]. Fragoulis A, et al. Oral administration of Methysticin improves cognitive deficits in a mouse model of Alzheimer's disease. Redox Biol. 2017 Aug;12:843-853.

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References on Methysticin

Methysticin and 7,8-dihydromethysticin are two major kavalactones in kava extract to induce CYP1A1.[Pubmed:21908763]

Toxicol Sci. 2011 Dec;124(2):388-99.

Kava is a plant traditionally used for making beverages in Pacific Basin countries and has been used for the treatment of nervous disorders in the United States. The pharmacological activity of kava is achieved through kavalactones in kava extract, which include kawain, 7,8-dihydrokawain, yangonin, 5,6-dehydrokawain, Methysticin, and 7,8-dihydroMethysticin. Recent studies have shown that kava extract induces hepatic CYP1A1 enzyme; however, the mechanisms of CYP1A1 induction have not been elucidated, and the kavalactones responsible for CYP1A1 induction have not yet been identified. Using a combination of biochemical assays and molecular docking tools, we determined the functions of kava extract and kavalactones and delineated the underlying mechanisms involved in CYP1A1 induction. The results showed that kava extract displayed a concentration-dependent effect on CYP1A1 induction. Among the six major kavalactones, Methysticin triggered the most profound inducing effect on CYP1A1 followed by 7,8-dihydroMethysticin. The other four kavalactones (yangonin, 5,6-dehydrokawain, kawain, and 7,8-dihydrokawain) did not show significant effects on CYP1A1. Consistent with the experimental results, in silico molecular docking studies based on the aryl hydrocarbon receptor (AhR)-ligand binding domain homology model also revealed favorable binding to AhR for Methysticin and 7,8-dihydroMethysticin compared with the remaining kavalactones. Additionally, results from a luciferase gene reporter assay suggested that kava extract, Methysticin, and 7,8-dihydroMethysticin were able to activate the AhR signaling pathway. Moreover, kava extract-, Methysticin-, and 7,8-dihydroMethysticin-mediated CYP1A1 induction was blocked by an AhR antagonist and abolished in AhR-deficient cells. These findings suggest that kava extract induces the expression of CYP1A1 via an AhR-dependent mechanism and that Methysticin and 7,8-dihydroMethysticin contribute to CYP1A1 induction. The induction of CYP1A1 indicates a potential interaction between kava or kavalactones and CYP1A1-mediated chemical carcinogenesis.

Effects of methysticin on three different models of seizure like events studied in rat hippocampal and entorhinal cortex slices.[Pubmed:7630425]

Naunyn Schmiedebergs Arch Pharmacol. 1995 Apr;351(4):348-55.

Methysticin is one of the constituents of Piper methysticum which possesses anticonvulsant and neuroprotective properties. Its effects on different in vitro seizure models were tested using extracellular recordings in rat temporal cortex slices containing the hippocampus and the entorhinal cortex. Elevating [K+]0 induced seizure-like events with tonic and clonic electrographic phases in area CA1. Lowering [Ca2+]0 caused recurrent seizure like episodes with large negative field potential shifts. Lowering Mg2+ induced short recurrent discharges in area CA3 and CA1 while ictaform events lasting for many seconds were induced in the subiculum, entorhinal and temporal neocortex. In the hippocampus the activity stayed stable over a number of hours. In contrast, the ictaform events in the subiculum, entorhinal and temporal cortex changed their characteristics after one to two hours to late recurrent discharges. In a concentration-range from 10 to 100 microM Methysticin reversibly blocked all these types of epileptiform activity. Decreases in [Ca2+]0 and associated slow field potentials evoked by repetitive stimulation of the stratum radiatum or the alveus remained almost unaffected by Methysticin. A paired pulse stimulus paradigm used to test for effects of Methysticin on synaptically evoked transient field potentials in normal medium revealed interference with mechanisms involved in frequency potentiation. While responses to alvear stimulation were largely unaffected, the responses to a paired pulse stimulus to stratum radiatum were depressed over the whole range of tested stimulus intervals. The findings suggest that Methysticin has effects on different patterns of epileptiform activity possibly by interfering with processes responsible for frequency potentiation.

Kavalactones Yangonin and Methysticin induce apoptosis in human hepatocytes (HepG2) in vitro.[Pubmed:20734326]

Phytother Res. 2011 Mar;25(3):417-23.

While cases of severe kava hepatotoxicity have been reported, studies examining the toxicity of individual kavalactones are limited. The present study examined the in vitro hepatotoxicity of kavain, Methysticin and yangonin on human hepatocytes (HepG2) and the possible mechanism(s) involved. Cytotoxicity was assessed using lactate dehydrogenase (LDH) and ethidium bromide (EB) assays. The mode of cell death was analysed with acridine orange/ethidium bromide dual staining with fluorescence microscopy. Glutathione oxidation was measured using the ortho-phthalaldehyde (OPT) fluorescence assay. Kavain had minimal cytotoxicity, Methysticin showed moderate concentration-dependent toxicity and yangonin displayed marked toxicity with ~ 40% reduction in viability in the EB assay. Acridine orange/ethidium bromide staining showed the predominant mode of cell death was apoptosis rather than necrosis. No significant changes were observed in glutathione levels, excluding this as the primary mechanism of cell death in this model. Further studies may elucidate the precise apoptotic pathways responsible and whether toxic kavalactone metabolites are involved.

Identification of methysticin as a potent and non-toxic NF-kappaB inhibitor from kava, potentially responsible for kava's chemopreventive activity.[Pubmed:19716299]

Bioorg Med Chem Lett. 2009 Oct 1;19(19):5732-6.

Nuclear factor-kappaB (NF-kappaB) is a transcription factor that plays an essential role in cancer development. The results of our recent chemopreventive study demonstrate that kava, a beverage in the South Pacific Islands, suppresses NF-kappaB activation in lung adenoma tissues, potentially a mechanism responsible for kava's chemopreventive activity. Methysticin is identified as a potent NF-kappaB inhibitor in kava with minimum toxicity. Other kava constituents, including four kavalactones of similar structures to Methysticin, demonstrate minimum activities in inhibiting NF-kappaB.

Description

Methysticin is a major kavalactone in kava extract to induce CYP1A1.

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