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ミリセチン

Myricetin

HCID 5281672
ノート反応
基本情報概要名称と識別子物性安全と法規制化学と産業関連反応化合物ノート
部分構造検索類似構造を探す

基本情報

CAS
529-44-2
標準SMILES
O=c1c(O)c(-c2cc(O)c(O)c(O)c2)oc2cc(O)cc(O)c12
InChIKey
IKMDFBPHZNJCSN-UHFFFAOYSA-N
分子式
C15H10O8
平均分子量
318.23 g/mol
単同位体質量
318.03756727

概要

Myricetin is a hexahydroxyflavone that is flavone substituted by hydroxy groups at positions 3, 3', 4', 5, 5' and 7. It has been isolated from the leaves of Myrica rubra and other plants. It has a role as a geroprotector, an antioxidant, a hypoglycemic agent, an antineoplastic agent, a cyclooxygenase 1 inhibitor, a plant metabolite and a food component. It is a hexahydroxyflavone and a 7-hydroxyflavonol. It is a conjugate acid of a myricetin(1-).

名称と識別子

優先名称
Myricetin
IUPAC
3,5,7-trihydroxy-2-(3,4,5-trihydroxyphenyl)chromen-4-one
現地名
ミリセチン
英語名
Myricetin
分子式
C15H10O8
分子量
318.24

名称と別名

myricetin529-44-2CannabiscetinMyricetol3,5,7-Trihydroxy-2-(3,4,5-trihydroxyphenyl)-4H-chromen-4-oneMyricitin3,3',4',5,5',7-Hexahydroxyflavone3,5,7,3',4',5'-Hexahydroxyflavone3,5,7-Trihydroxy-2-(3,4,5-trihydroxyphenyl)-4H-1-benzopyran-4-one3,5,7-trihydroxy-2-(3,4,5-trihydroxyphenyl)chromen-4-onedelphidenolon 15753,3',4,4',5',7-Hexahydro-2-phenyl-4H-chromen-4-one
名称をさらに表示
3,5,7,3',4',5'-ヘキサヒドロキシフラボン2-(3,4,5-トリヒドロキシフェニル)-3,5,7-トリヒドロキシ-4H-1-ベンゾピラン-4-オンカンナビスセチンミリセトール3,3',4',5,5',7-ヘキサヒドロキシフラボン3,5,7-トリヒドロキシ-2-(3,4,5-トリヒドロキシフェニル)-4H-クロメン-4-オンカナビセチンミリセチン3,5,7-トリヒドロキシ-2-(3,4,5-トリヒドロキシフェニル)-4H-1-ベンゾピラン-4-オン3,5,7,3′,4′,5′-ヘキサヒドロキシフラボン3,3′,4′,5,5′,7-ヘキサヒドロキシフラボンbayberry bark extractMYRICETIN 95%MYRISETINNSC 407290LDN 0014058Myricetin>
DTXSID80224004H-1-Benzopyran-4-one, 3,5,7-trihydroxy-2-(3,4,5-trihydroxyphenyl)-76XC01FTOJNSC-407290FLAVONE, 3,3',4',5,5',7-HEXAHYDROXY-CHEBI:18152RefChem:6547DTXCID002400

物性

構造計算による物性

XLogP
1.2
極性表面積
148 Ų
水素結合供与体数
6
水素結合受容体数
8
回転可能結合数
1
重原子数
23
形式電荷
0
複雑度
506

実験および物理化学的性質

DrugsPharmaceuticals -> Listed in ZINC15
LipidsPolyketides [PK] -> Flavonoids [PK12] -> Flavones and Flavonols [PK1211]
LogP0.72
Color/FormYellow needles from dilute alcohol
SolubilitySparingly soluble in boiling water; soluble in alcohol. Practically insoluble in chloroform, acetic acid
Endocrine DisruptorsPotential endocrine disrupting compound
DecompositionWhen heated to decomposition it emits acrid smoke and irritating vapors.
Melting Point · 2 件

357 °C

357 °C

Physical DescriptionSolid
Collision Cross Section · 4 件

174.4 Ų [M+H]+ [CCS Type: DT; Method: stepped-field]

166.12 Ų [M+H]+ [CCS Type: TW; Method: calibrated with polyalanine and drug standards]

167.3 Ų [M+H]+ [CCS Type: TW; Method: calibrated with polyalanine and drug standards]

192.7 Ų [M+H]+

安全と法規制

安全情報は参考情報です。供給元の安全データシート（SDS）、適用法令、専門家による評価に代わるものではありません。

GHS分類

GHS Classification · 5 件

This chemical does not meet GHS hazard criteria for 50% (3 of 6) of reports.

Warning

H315 (50%): Causes skin irritation [Warning Skin corrosion/irritation]

P261, P264, P264+P265, P271, P280, P302+P352, P304+P340, P305+P351+P338, P319, P321, P332+P317, P337+P317, P362+P364, P403+P233, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 6 reports by companies from 3 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

危険有害性情報

Hazard Classes and CategoriesSkin Irrit. 2 (50%)

安全と保護具

Disposal Methods · 1 件

SRP: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.

毒性情報

Interactions · 5 件

... Addition of apigenin, chrysin, fisetin, flavonone, galangin, hesperitin, kaempferol, morin, myricetin, haringenin, or quercetin to human liver microsomes inhibited the hydroxylation of benzo(a)pyrene. In contrast to these results, the addition of flavone, nobiletin, tangeretin, or 7,8-benzoflavone to human liver microsomes caused a many-fold stimulation in the hydroxylation of benzo(a)pyrene, the metabolism of aflatoxin B1 to 2,3-dihydro-2,3-dihydroxyaflatoxin B1, and the metabolic activation of aflatoxin B1 to mutagenic products. ... An examination of the structural features required for the inhibition and stimulation of benzo(a)pyrene hydroxylation indicated that all of the 12 flavonoid inhibitors that were studied possessed hydroxyl groups whereas the flavonoid activators were less polar molecules that lacked hydroxyl groups.

化学と産業

薬理情報

Mechanism of Action · 5 件

Dietary polyphenols are a diverse and complex group of compounds that are linked to human health. Many of their effects have been attributed to the ability to poison (i.e., enhance DNA cleavage by) topoisomerase II. Polyphenols act against the enzyme by at least two different mechanisms. Some compounds are traditional, redox-independent topoisomerase II poisons, interacting with the enzyme in a noncovalent manner. Conversely, others enhance DNA cleavage in a redox-dependent manner that requires covalent adduction to topoisomerase II. Unfortunately, the structural elements that dictate the mechanism by which polyphenols poison topoisomerase II have not been identified. To resolve this issue, the activities of two classes of polyphenols against human topoisomerase IIalpha were examined. The first class was a catechin series, including (-)-epigallocatechin gallate (EGCG), (-)-epigallocatechin (EGC), (-)-epicatechin gallate (ECG), and (-)-epicatechin (EC). The second was a flavonol series, including myricetin, quercetin, and kaempferol. Compounds were categorized into four distinct groups: EGCG and EGC were redox-dependent topoisomerase II poisons, kaempferol and quercetin were traditional poisons, myricetin utilized both mechanisms, and ECG and EC displayed no significant activity. On the basis of these findings, a set of rules is proposed that predicts the mechanism of bioflavonoid action against topoisomerase II. The first rule centers on the B ring. While the C4'-OH is critical for the compound to act as a traditional poison, the addition of -OH groups at C3' and C5' increases the redox activity of the B ring and allows the compound to act as a redox-dependent poison. The second rule centers on the C ring. The structure of the C ring in the flavonols is aromatic and planar and includes a C4-keto group that allows the formation of a proposed pseudo ring with the C5-OH. Disruption of these elements abrogates enzyme binding and precludes the ability to function as a traditional topoisomerase II poison.

Selected flavonoids were tested for their ability to inhibit the catalytic activity of DNA topoisomerase (topo) I and II. Myricetin, quercetin, fisetin, and morin were found to inhibit both enzymes, while phloretin, kaempferol, and 4',6,7-trihydroxyisoflavone inhibited topo II without inhibiting topo I. Flavonoids demonstrating potent topo I and II inhibition required hydroxyl group substitution at the C-3, C-7, C-3', and C-4' positions and also required a keto group at C-4. Additional B-ring hydroxylation enhanced flavonoid topo I inhibitory action. A C-2, C-3 double bond was also required, but when the A ring is opened, the requirement for the double bond was eliminated. Genistein has been previously reported to stabilize the covalent topo II-DNA cleavage complex and thus function as a topo II poison. All flavonoids were tested for their ability to stabilize the cleavage complex between topo I or topo II and DNA. None of the agents stabilized the topo I-DNA cleavage complex, but prunetin, quercetin, kaempferol, and apigenin stabilized the topo II DNA-complex. Competition experiments have shown that genistein-induced topo II-mediated DNA cleavage can be inhibited by myricetin, suggesting that both types of inhibitors (antagonists and poisons) interact with the same functional domain of their target enzyme...

関連反応

0 件
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化合物ノート

読み込み中…

このページの内容基本情報概要名称と識別子物性安全と法規制化学と産業関連反応化合物ノート

データベース識別子

CAS
529-44-2
PubChem CID
5281672
DTXSID
DTXSID8022400
ChEMBL
CHEMBL164
ChEBI
CHEBI:18152
UNII
76XC01FTOJ
EC Number
208-463-2
Nikkaji
J1.585G
Other Experimental Properties · 2 件

Crystals, mp 213 °C /Hexaacetate/

Needles from alcohol, mp 149-151 °C /Hexaethyl ether/

物理化学的性質

融点
300 °C · >300 °C(lit.)
沸点
377.41 °C · 377.41°C (rough estimate)
比重(密度)
1.4222 · 1.4222 (rough estimate)
屈折率
1.4395 · 1.4395 (estimate)
貯蔵温度
2 · 2-8°C
溶解性
10 mg/mL、透明～微濁、黄色～非常に濃い緑黄色 · エタノール：可溶10mg/mL、透明～微濁、黄色～非常に濃い緑黄色
酸解離定数(Pka)
6.3 · 6.30±0.40(Predicted)
外見
結晶性
色
黄褐色
水溶解度
ジメチルスルホキシド、ジメチルホルムアミド、エタノールに可溶。水に不溶。
Merck
14 · 14,6332
BRN
332331 · 332331
安定性
吸湿性
化粧品成分の機能
抗酸化物質スキンコンディショニング
InChI
1S/C15H10O8/c16-6-3-7(17)11-10(4-6)23-15(14(22)13(11)21)5-1-8(18)12(20)9(19)2-5/h1-4,16-20,22H
InChIKey
IKMDFBPHZNJCSN-UHFFFAOYSA-N
SMILES
Oc1cc(O)c2C(=O)C(O)=C(Oc2c1)c3cc(O)c(O)c(O)c3
LogP
1.206 · 1.206 (est)
CAS データベース
529 · 529-44-2(CAS DataBase Reference)
化学的性質 · 1 件

化学的特性The substance is a brown-yellow to brown-green crystalline powder. It can dissolve in methanol, ethanol, acetone, and ethyl acetate, and has a low solubility in water. It is not soluble in chloroform and petroleum ether. This compound is derived from the fruit of Myrica rubra (Lour.) Sieb. et Zucc. and belongs to the Populus family.

... Myricetin suppresses UVB-induced cyclooxygenase-2 (COX-2) expression in mouse skin epidermal JB6 P+ cells. The activation of activator protein-1 and nuclear factor-kappaB induced by UVB was dose-dependently inhibited by myricetin treatment. Western blot and kinase assay data revealed that myricetin inhibited Fyn kinase activity and subsequently attenuated UVB-induced phosphorylation of mitogen-activated protein kinases. Pull-down assays revealed that myricetin competitively bound with ATP to suppress Fyn kinase activity. Importantly, myricetin exerted similar inhibitory effects compared with 4-amino-5-(4-chloro-phenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine, a well-known pharmacologic inhibitor of Fyn. In vivo mouse skin data also revealed that myricetin inhibited Fyn kinase activity directly and subsequently attenuated UVB-induced COX-2 expression. Mouse skin tumorigenesis data clearly showed that pretreatment with myricetin significantly suppressed UVB-induced skin tumor incidence in a dose-dependent manner. Docking data suggest that myricetin is easily docked to the ATP-binding site of Fyn, which is located between the N and C lobes of the kinase domain. Overall, these results indicated that myricetin exerts potent chemopreventive activity mainly by targeting Fyn in skin carcinogenesis.

... Bor-tezomib is a dipeptide boronate proteasome inhibitor that has activity in the treatment of multiple myeloma but is not effective in chronic lymphocytic leukemia (CLL). Although CLL cells are sensitive in vitro to bortezomib-induced apoptosis when cultured in medium, the killing activity was blocked when cultured in 50% fresh autologous plasma. Dietary flavonoids, quercetin and myricetin, which are abundant in plasma, inhibited bortezomib-induced apoptosis of primary CLL and malignant B-cell lines in a dose-dependent manner...

The purpose of this study was to investigate the potential neuroprotective effects of myricetin (flavonoid) and fraxetin (coumarin) on rotenone-induced apoptosis in SH-SY5Y cells, and the possible signal pathway involved in a neuronal cell model of Parkinson's disease. ... Rotenone caused a time- and dose-dependent decrease in cell viability and the degree of LDH release was proportionally to the effects on cell viability. Cells were pretreated with fraxetin, myricetin and N-acetylcysteine at different concentrations for 30 min before exposure to rotenone. Cytotoxicity of rotenone (5 uM) for 16 hr was significantly diminished as well as the release of LDH into the medium, by the effect of fraxetin, myricetin and N-acetylcysteine, with fraxetin (100 uM) and N-acetylcysteine (100 uM) being more effective than myricetin (50 uM)...

The effects of myricetin on either MRP1 or MRP2 mediated vincristine resistance in transfected MDCKII cells were examined. The results obtained show that myricetin can inhibit both MRP1 and MRP2 mediated vincristine efflux in a concentration dependent manner. The IC50 values for cellular vincristine transport inhibition by myricetin were 30.5+/-1.7 uM for MRP1 and 24.6+/-1.3 uM for MRP2 containing MDCKII cells. Cell proliferation analysis showed that the MDCKII control cells are very sensitive towards vincristine toxicity with an IC50 value of 1.1+/-0.1 uM. The MDCKII MRP1 and MRP2 cells are less sensitive towards vincristine toxicity with IC50 values of 33.1+/-1.9 and 22.2+/-1.4 uM, respectively. In both the MRP1 and MRP2 cells, exposure to 25 uM myricetin enhances the sensitivity of the cells towards vincristine toxicity to IC50 values of 7.6+/-0.5 and 5.8+/-0.5 uM, respectively. The increase of sensitivity represents a reversal of the resistance towards vincristine as a result of MRP1 and MRP2 inhibition...

Natural Pollution SourcesFrom the bark of Myrica nagi Thumb., Myriaceae ... Occurrence in Hamamelidaceae and Anacardiaceae
Human Toxicity Excerpts · 5 件

/EPIDEMIOLOGY STUDIES/ ... The flavonoids quercetin, kaempferol, myricetin, apigenin, and luteolin /were measured/ in foods and ... flavonoid intake in 1985 /was assessed. by dietary history in 738 men aged 65-84 years without a history of cancer, who were then followed for five years. Mean flavonoid intake was 25.9 mg/day. The major sources of flavonoid intake were tea at 61% and vegetables and fruits (mainly onions, kale, endive, and apples) at 38%. Between 1985 and 1990, 75 men developed cancer (all sites) and 34 men died from cancer. Flavonoid intake in 1985 was not associated with incidence of all-cause cancer (p for trend = 0.54) or with mortality from all-cause cancer (p for trend = 0.51). Flavonoid intake was also not associated with risk of cancers of the alimentary and respiratory tract (p for trend = 0.92). Adjustment for age, body mass index, smoking, physical activity, and vitamin C, vitamin E, beta-carotene, and dietary fiber intake did not change the relative risks. A high intake of flavonoids from vegetables and fruits only was inversely associated with risk of cancer of the alimentary and respiratory tract (relative risk of highest vs. lowest tertile = 0.51, 95% confidence interval 0.25-1.05); these results suggest the presence of other nonvitamin components with anticarcinogenic potential in these foods. We conclude that intake of flavonoids, mainly from tea, apples, and onions, does not predict a reduced risk of all-cause cancer or of cancer of the alimentary and respiratory tract in elderly men. The effect of flavonoids on risk of cancer at specific sites needs further investigation in prospective cohort studies.

/GENOTOXICITY/ The flavonoids, silymarin, myricetin, quercitin, kaempferol, rutin and kaempferol-3-rutinoside have been examined in combination with the food mutagens, 3-amino-1-methyl-5H-pyrido (4,3-b)indole (Trp-P-2) and 2-amino-3-methylimidazo-(4,5-f) quinoline (IQ), in the Comet assay in human lymphocytes from donor A and human sperm from donor B. These compounds alone have been shown to produce positive responses in the Comet assay, as have the food mutagens. However, in combination with the food mutagens, the flavonoids produced antigenotoxic effects since DNA damage was reduced in the Comet assay in lymphocytes and sperm. The assays were performed in the absence of metabolic activation...

/GENOTOXICITY/ ... The protective effect of dietary polyphenols against N-nitrosodimethylamine (NDMA), N-nitrosopyrrolidine (NPYR) and benzo(a)pyrene (BaP)-induced DNA damage (strand breaks and oxidized purines/pyrimidines) in HepG2 cells /was investigated/. ... Human hepatocellular carcinoma (HepG2) cells, which retain many specialized liver functions and drug metabolizing enzyme activities, were used as in vitro model for human hepatocytes. NDMA, NPYR and BaP were employed to induce DNA damage. DNA damage (strand breaks, oxidized pyrimidines and oxidized purines) was evaluated by the alkaline single cell gel electrophoresis or comet assay. ... None of the polyphenols concentrations tested in presence or absence of Fpg (formamidopyrimidine-DNA glycosylase), or Endo III (Endonuclease III) caused DNA damage per se. Increasing concentrations of BaP (25-100 uM) induced a significant increase of DNA strand breaks, Fpg and Endo III sensitive sites in a dose dependent manner. Myricetin and quercetin decreased DNA strand breaks and oxidized pyrimidines induced by NDMA, but not oxidized purines. However, both flavonoids reduced oxidized pyrimidines and purines induced by NPYR. DNA strand breaks induced by NPYR were prevented by quercetin, but not by myricetin. BaP-induced DNA strand breaks and oxidized pyrimidines were strongly reduced by myricetin and quercetin, respectively. While oxidized purines induced by BaP were reduced by quercetin, myricetin had no protective effect. (+)-Catechin and (-)-epicatechin reduced DNA strand breaks, oxidized pyrimidines and oxidized purines induced by NDMA. DNA strand breaks, and oxidized purines induced by NPYR were also prevented by (+)-catechin and (-)-epicatechin, while the maximum reduction of oxidized pyrimidines was found by (+)-catechin and (-)-epicatechin at 10 uM. (+)-Catechin and (-)-epicatechin decreased also DNA strand breaks and oxidized pyrimidines but not oxidized purines induced by BaP...

/GENOTOXICITY/ The effects of the flavonoids quercetin and myricetin, and the antihepatotoxic agent silymarin, on hydrogen peroxide-mediated DNA damage in human lymphocytes were determined using alkaline single-cell gel electrophoresis (the comet assay). Treatment with hydrogen peroxide increased the levels of DNA strand breaks and oxidised pyrimidine bases in these cells. Quercetin was protective at concentrations above 10 uM and myricetin decreased oxidant-induced DNA strand breakage at concentrations of 100 uM. Cellular metabolism may alter the antioxidant efficacy of the flavonoids. Silymarin had no protective effect at any of the concentrations tested. None of these flavonoids was itself genotoxic. Neither alpha-tocopherol nor beta-carotene decreased hydrogen peroxide-induced DNA breakage. The differences in effectiveness of these dietary compounds against oxidative DNA damage may be explained by differences in their chemical structure or location within the cell.

For more Human Toxicity Excerpts (Complete) data for MYRICETIN (6 total), please visit the HSDB record page.

Non-Human Toxicity Excerpts · 5 件

/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ ... Treatment of preweanling mice with 1/7, 2/7 and 4/7 of the total dose of ellagic acid (300 nmol), robinetin (1400 nmol), myricetin (1400 nmol) or quercetin (1400 nmol) i.p. on their first, eighth and fifteenth day of life, respectively, did not cause the formation of tumors in animals that were killed 9-11 months later...

/GENOTOXICITY/ Over 70 naturally occurring and synthetic flavonoids were screened for mutagenicity with 5 tester strains in the Salmonella/mammalian microsome assay: TA1535, TA100, TA1537, TA1538 and TA98. Frameshift mutagenicity was confined to the flavonols (flavon-3-ols) in strain TA98, TA1537 and TA100. The two most mutagenic falvonols, namely, quercetin (3,3',4',5,7-pentahydroxyflavone) and kaempferol (3,4',5,7-tetrahydroxyflavone), exhibiting 12 and 7 revertants/nmol in TA98 respectively, are also the most common flavonols occurring in plants. Other flavonols exhibited less activity (revertants/nmol): galangin (2.0), rhamnetin (0.45), kaempferide (0.24), fisetin (0.14), myricetin (0.12), robinetin (0.06) and morin (0.05). All of these flavonols apparently exhibited significant activation by Aroclor 1254 induced rat-liver microsome preparations (S9). However, subsequent study revealed that only those flavonols either lacking or possessing one B ring hydroxyl group had an absolute requirement for microsomal activation...

/GENOTOXICITY/ Naturally occurring plant phenols such as tannic acid, quercetin, myricetin, and anthraflavic acid are known to inhibit the mutagenicity of several bay-region diol-epoxides of polycyclic aromatic hydrocarbons (PAHs). The binding of bay-region diol-epoxides of PAHs to target tissue DNA is thought to be essential for the initiation of cancer by these compounds. ...This study ... investigated the effect of these plant phenols on PAH-DNA adduct formation in the epidermis and lung of SENCAR mice. In vitro addition of tannic acid, quercetin, myricetin, and anthraflavic acid (25 uM) to an incubation system containing epidermal microsomes prepared from either control or 3-methylcholanthrene-pretreated mice inhibited benzo(a)pyrene binding to calf thymus DNA by 63-64, 38-43, 36-37, and 27-33%, respectively. A single topical application of tannic acid, quercetin, myricetin, and anthraflavic acid at a dose of 400 umol/kg body weight resulted in the inhibition of [3H]benzo(a)pyrene binding to epidermal DNA (48-73%) and protein (51-63%). The same dose of these plant phenols (400 umol/kg) caused even greater inhibition of (+/-)-[3H]-7 beta,8 alpha-dihydroxy-7,8-dihydrobenzo(a)pyrene and [3H]-7,12-dimethybenz(a)anthracene binding to epidermal DNA and protein. The formation of (+)-7 beta,8 alpha-dihydroxy-9 alpha,10 alpha-epoxy-7,8,9,10-tetrahydrobenzo(a)pyrene-deoxyguanosine adducts was substantially diminished in both epidermis (62-86%) and lungs (38-84%). These results indicate that tannic acid, quercetin, myricetin, and anthraflavic acid are potent inhibitors of carcinogen binding to epidermal and lung DNA and suggest that these plant phenols could prove useful in modifying the risk of tumor induction by PAHs such as benzo(a)pyrene and 7,12-dimethylbenz(a)anthracene in these two tissues.

/GENOTOXICITY/ The plant flavonoids quercetin (3,5,7,3',4'-pentahydroxyflavone), morin (3,5,7,2',4'-pentahydroxyflavone), kaempferol (3,5,7,4'-tetrahydroxyflavone), chrysin (5,7-dihydroxyflavone), fisetin (3,7,3',4'-tetrahydroxyflavone), myricetin (3,5,7,3',4',5'-hexahydroxyflavone), myricitrin (myricetin-3-rhamnoside), hesperetin (3',5,7-trihydroxy-4'-methoxyflavanone), quercitrin (quercetin-3-L-rhamnoside), rutin (quercetin-3-rhamnosylglucoside or quercetin-3-rutinoside), and hesperidin (hesperetin-7-rutinoside) have been assayed for mutagenicity in the Salmonella/microsomal activation system. Quercetin, morin, kaempferol, fisetin, myricetin, quercitrin and rutin were mutagenic in the histidine reversion system with the frameshift strain TA98. The flavonols quercetin and myricetin are mutagenic without metabolic activation, although more effective when a rat liver microsomal preparation (S-9) is included; all others require metabolic activation...

For more Non-Human Toxicity Excerpts (Complete) data for MYRICETIN (16 total), please visit the HSDB record page.

Antidote and Emergency Treatment · 3 件

/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Poisons A and B/

/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/

/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/

Non-Human Toxicity ValuesLD50 Mouse intraperitoneal 1410 mg/kg

安全データ

F
10
wgk
3
rtecs
LK8646000
hs_code
29329990
safety_code
24/25
ストレージクラス
11 - Combustible Solids
有毒物質データの
529-44-2(Hazardous Substances Data)

... myricetin (3, 3', 4', 5, 5', 7-hexahydroxyflavone) ... could directly bind to JAK1/STAT3 molecules to inhibit cell transformation in epidermal growth factor (EGF)-activated mouse JB6 P(+) cells. Colony assay revealed that myricetin had the strongest inhibitory effect on cell transformation among three flavonols including myricetin, quercetin and kaempferol. Molecular data revealed that myricetin inhibited DNA- binding and transcriptional activity of STAT3. Furthermore, myricetin inhibited the phosphorylation of STAT3 at Tyr705 and Ser727. Cellular signaling analyses revealed that EGF could induce the phosphorylation of Janus Kinase (JAK) 1, but not JAK2. Myricetin inhibited the phosphorylation of JAK1 and increased the autophosphorylation of EGF receptor (EGFR). Moreover, ex vivo and in vitro pull-down assay revealed that myricetin bound to JAK1 and STAT3, but not EGFR. Affinity data further demonstrated that myricetin had a higher affinity for JAK1 than STAT3. Thus, ... myricetin might directly target JAK1 to block cell transformation in mouse JB6 cells.

Abnormal expression of cyclooxygenase-2 (COX-2) has been implicated in the development of cancer. ... Here /it is reported/ that 3,3',4',5,5',7-hexahydroxyflavone (myricetin), one of the major flavonols in red wine, inhibits 12-O-tetradecanoylphorbol-13-acetate (phorbol ester)-induced COX-2 expression in JB6 P+ mouse epidermal (JB6 P+) cells by suppressing activation of nuclear factor kappa B (NF-kappaB). Myricetin at 10 and 20 uM inhibited phorbol ester-induced upregulation of COX-2 protein, while resveratrol at the same concentration did not exert significant effects. The phorbol ester-induced production of prostaglandin E 2 was also attenuated by myricetin treatment. Myricetin inhibited both COX-2 and NF-kappaB transactivation in phorbol ester-treated JB6 P+ cells, as determined using a luciferase assay. Myricetin blocked the phorbol ester-stimulated DNA binding activity of NF-kappaB, as determined using an electrophoretic mobility shift assay. Moreover, TPCK (N-tosyl-l-phenylalanine chloromethyl ketone), a NF-kappaB inhibitor, significantly attenuated COX-2 expression and NF-kappaB promoter activity in phorbol ester-treated JB6 P+ cells. In addition, red wine extract inhibited phorbol ester-induced COX-2 expression and NF-kappaB transactivation in JB6 P+ cells. Collectively, these data suggest that myricetin contributes to the chemopreventive effects of red wine through inhibition of COX-2 expression by blocking the activation of NF-kappaB.

For more Mechanism of Action (Complete) data for MYRICETIN (6 total), please visit the HSDB record page.

Metabolism/MetabolitesMyricetin has known human metabolites that include (2S,3S,4S,5R)-6-[5,7-Dihydroxy-4-oxo-2-(3,4,5-trihydroxyphenyl)chromen-3-yl]oxy-3,4,5-trihydroxyoxane-2-carboxylic acid.
Absorption, Distribution and Excretion · 1 件

... Significant quantities of quercetin and possibly myricetin and kaempferol are absorbed in the gut. A larger fraction probably remains in the lumen, and thus a substantial proportion of the gastrointestinal mucosa is exposed to biologically significant concentrations of these compounds. ...

用途と製造

UsesExperimental drug ... lipid kinase activity
General Manufacturing Information · 1 件

Biological activities of myricetin: Allelochemic; AntiHIV; Antiallergenic; Antibacterial; Antifeedant; Antigastric; Antigingivitic; Antigonadotrophic; Antihistaminic; Antiinflammatory; Antimutagenic; Antioxidant; Antiperiodontic; Antiplaque; Antiseptic; Antiviral; Apoptotic; COMP-Inhibitor; Cancer-Preventive; Candidicide; Diuretic; Hypoglycemic; Larvistat; Lipoxygenase-Inhibitor; Mutagenic; Oxidase-Inhibitor; Pesticide; Quinone-Reductase-Inducer; Topoisomerase-I-Inhibitor; Topoisomerase-II-Inhibitor; Tyrosine-Kinase-Inhibitor; Vasodilator

応用分野 · 4 件

解説3,5,7-trihydroxy-2-(3,4,5-trihydroxyphenyl)-4H-1-benzopyran-4-one．C15H10O8(318.24)．ミリセチンは，フラボノールの一種．配糖体ミリシトリン(3-ラムノシド)としてヤマモモMyrica rubraの樹皮，シナノガキDiospyros lotusの葉，アカショウマAstilbe thunbergii var.congestaの根茎などに含まれる．ヤマモモの樹皮から見出された。ミリシトリン (ミリセチンの3-ラムノース配糖体) とともに樹皮に含まれている。濃黄色の針状晶．3，3′，4′，5，5′，7-ヘキサヒドロキシフラボンに相当する。融点 357℃の黄色針状晶。λmax 254，374 nm(メタノール)．エタノールに易溶，熱水に難溶，クロロホルム，酢酸にはほとんど不溶．FeCl3によって黒褐色を呈し，酢酸鉛で橙赤色沈殿を生じる．ミリセチンはエチルアルコールに溶け，熱水にはわずかに溶けるが，クロロホルム，酢酸などには難溶である。ヤマモモの樹皮はこの色素とタンニンを含んでいるので，古くから黄色ないし褐色の染料として利用された。 森北出版「化学辞典（第2版）

説明Myricetin[529-44-2] is a flavonoid compound found in many fruits and vegetables, including red wine, that acts as a powerful antioxidant. Myricetin inhibits TBARS formation with an IC50 value of 6.34 and at 20 μM, blocks oxLDL uptake by U937-derived macrophages, reducing CD36 expression. Myricetin demonstrates potent chemopreventative potential by binding JAK1/STAT3 to inhibit the neoplastic transformation of murine JB6 P+ cells and inhibiting MEK1 kinase activity.

使用Myricetin is used as an antioxidant. It is a cell-permeable flavonoid used in inflammatory, diabetes, and cancer studies. It is effective in protecting neurons against oxidative stresses. Further, it inhibits yeast alfa-glucosidase,1 glyoxalase I in vitro and bovine milk xanthine oxidase.

一般的な説明Myricetin is a novel flavanoid compound useful as chemotherapeutic, chemopreventive, and antiangiogenic agent. It also acts as an antioxidant, anti-inflammatory, and anti-cancer agent, and can inhibit the activity of reverse transcriptase.

調製方法 · 1 件

純化方法Myricetin (Cannabiscetin, 3,3',4',5,5',7-hexahydroxyflavone) [529-44-2] M 318.2, m > 3 0 0o, 357o(dec) (polyphenolic pKEst~8-11). Recrystallise myricetin from aqueous EtOH (m 357o dec, as monohydrate) or Me2CO (m 350o dec, with one mol of Me2CO) as yellow crystals. It is almost insoluble in CHCl3 and AcOH. The hexaacetate has m 213o. [Hergert J Org Chem 21 534 1956, Spada & Cameroni Gazzetta 86 965, 975 1956, Kalff & Robinson J Chem Soc 127 181 1925, Beilstein 18/5 V 670.]

上流・下流製品情報

上流原料

3,5,7-trihydroxy-2-(3,4,5-trihydroxyphenyl)-2,3-dihydrochromen-4-one3-(α-L-ラムノピラノシルオキシ)-3',4',5,5',7-ペンタヒドロキシフラボン5,7-ジヒドロキシ-3,3',4',5'-テトラメトキシフラボンジヒドロミリセチン

下流製品

(2R,3S,4R,5S)-5-カルボキシ-2,3,4,5-テトラヒドロキシペンタナールD-キノボースD-ガラクトピラノースL-(+)-ラムノース一水和物D-(+)-ガラクトース (無水)

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補足説明 · 2 件

定義本品は、次の化学式で表される有機化合物である。

定義ChEBI: Myricetin is a hexahydroxyflavone that is flavone substituted by hydroxy groups at positions 3, 3', 4', 5, 5' and 7. It has been isolated from the leaves of Myrica rubra and other plants. It has a role as a cyclooxygenase 1 inhibitor, an antineoplastic agent, an antioxidant, a plant metabolite, a food component, a hypoglycemic agent and a geroprotector. It is a hexahydroxyflavone and a 7-hydroxyflavonol. It is a conjugate acid of a myricetin(1-).