Quercetin hydrate

别名: Quercetin hydrate; 849061-97-8; 2-(3,4-dihydroxyphenyl)-3,5,7-trihydroxy-4H-chromen-4-one hydrate; 1001001-36-0; Quercetin hydrate; Quercetin (hydrate); 2-(3,4-dihydroxyphenyl)-3,5,7-trihydroxychromen-4-one;hydrate; Quercetin monohydrate; 槲皮素水合物;Quercetin Hydrate 槲皮素水合物;槲皮素二水合物;槲皮素;槲皮素一水合物;一水合槲皮素;3,3',4',5,7-五羟基黄酮 水合物;槲皮素 水合物
目录号: V69228 纯度: ≥98%
槲皮素水合物是一种天然存在的黄酮类化合物,可激活或抑制许多蛋白质的活性。
Quercetin hydrate CAS号: 849061-97-8
产品类别: Reactive Oxygen Species
产品仅用于科学研究,不针对患者销售
规格 价格
500mg
1g
Other Sizes

Other Forms of Quercetin hydrate:

  • Quercetin 3,3'-dimethyl ether
  • Quercetin 3-O-(6''-O-galloyl)-β-D-glucoside (Tellimoside)
  • Quercetin-3,4-di-O-glucoside
  • Quercetin 3-O-sophoroside-7-O-rhamnoside
  • 槲皮素
  • Quercetin-d3 (槲皮素 d3)
  • 二水槲皮素
  • Quercetin-d5 (槲皮素 d5)
  • Quercetin-13C3 (quercetin 13C3)
  • (±)-Taxifolin-13C3 ((±)-Dihydroquercetin-13C3)
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InvivoChem产品被CNS等顶刊论文引用
产品描述
槲皮素水合物是一种天然存在的黄酮类化合物,可激活或抑制许多蛋白质的活性。 Quercetin Hydro 可激活 SIRT1,抑制 PI3K,并抑制 PI3Kγ、PI3Kδ 和 PI3Kβ,IC50 分别为 2.4 μM、3.0 μM 和 5.4 μM。
生物活性&实验参考方法
靶点
IC50: 2.4±0.6 μM (PI3K γ), 3.0±0.0 μM (PI3K δ), 5.4±0.3 μM (PI3K β)[1]
体外研究 (In Vitro)
水合槲皮素是一种植物化学物质或植物性物质,添加到食品、饮料和补充剂中。多项研究表明它具有抗氧化和抗炎功效,并且正在研究许多其他可能的健康优势。 PI3K 抑制剂槲皮素水合物的 IC50 范围为 2.4 至 5.4 μM。槲皮素水合物可强烈抑制 PI3K 和 Src 激酶,中度抑制 Akt1/2,并对 PKC、p38 和 ERK1/2 产生轻微影响[1]。槲皮素水合物可降低 TNF 反应中 LDH% 的产生、依赖于 EC 的中性粒细胞对牛肺动脉内皮细胞 (BPAEC) 的粘附以及 BPAEC DNA 的合成和增殖 [2]。
体内研究 (In Vivo)
当水合槲皮素(75 mg/kg)和2-甲氧基雌二醇联合使用时,PC-3细胞异种移植肿瘤和人前列腺癌LNCaP的生长得到更有效的抑制[3]。
在本研究中,研究人员确定了它们的组合是否可以在体内抑制LNCaP和PC-3异种移植物肿瘤的生长,并探讨了其潜在机制。在雄性BALB/c裸鼠体内皮下接种人前列腺癌症LNCaP和PC-3细胞。当异种移植物肿瘤达到约100mm3时,将小鼠随机分配到载体对照组、槲皮素或2-甲氧基雌二醇单独治疗组和联合治疗组。在治疗干预4周后,与载体对照组相比,槲皮素和2-ME i)的联合治疗显著抑制了前列腺癌症异种移植物肿瘤生长,LNCaP和PC-3分别抑制了46.8%和51.3%,比单独的槲皮素(LNCaP为28.4%,PC3为24.8%)或2-ME(LNCaP为32.1%,PC3的28.9%)更有效;ii)BALB/c小鼠耐受良好,未观察到明显的毒性反应;iii)导致更高的Bax/Bcl-2比值、切割的caspase-3蛋白表达和凋亡率;iv)导致磷酸化AKT(pAKT)蛋白水平、血管内皮生长因子蛋白和mRNA表达、微血管密度和增殖率低于单药治疗。与车辆组相比,这些效果更为显著。因此,槲皮素和2-ME的组合可以作为一种新的临床治疗方案,具有在体内增强对前列腺癌症的抗肿瘤作用并减轻单独使用槲皮素或2-ME的剂量和副作用的潜力。这些体内研究结果将为后续研究这种新型的人类前列腺癌症治疗方案奠定进一步的坚实基础。
酶活实验
分别支持血小板粘附胶原和纤维蛋白原的α(2)β(1)和α(IIb)β(3)整合素共享共同的信号分子。评估槲皮素对血小板与胶原蛋白和纤维蛋白原静态粘附的影响,并将其与激酶抑制活性相关联。槲皮素强烈抑制PI3K和Src激酶,轻度抑制Akt1/2,轻度影响PKC、p38和ERK1/2。槲皮素或二磷酸腺苷和血栓素A(2)抑制剂的联合使用在类似程度上消除了血小板在这些表面上的扩散。我们认为槲皮素对血小板激酶的抑制作用阻断了阻止血小板完全扩散的早期信号事件
细胞实验
本研究旨在评估quercetin/槲皮素对RTEC衰老和肾纤维化的抑制作用,并探讨其潜在机制。我们发现槲皮素在体外减轻了血管紧张素II(AngII)诱导的RTEC衰老,在体内减轻了单侧输尿管梗阻。此外,我们证明了AngII治疗的RTEC中发生了线粒体异常,如活性氧物种升高、膜电位降低以及线粒体质量的断裂和积累。槲皮素治疗逆转了这些影响。此外,槲皮素增强了AngII处理的RTEC中的丝裂吞噬作用,而用丝裂吞噬特异性抑制剂处理后,这种作用显著降低。去乙酰化酶-1(SIRT1)参与槲皮素介导的PTEN诱导的激酶1(PINK1)/Parkin相关的自噬激活。AngII处理的RTEC中SIRT1的药理学拮抗作用阻断了槲皮素对有丝分裂和细胞衰老的影响。最后,槲皮素通过线粒体吞噬减少RTEC衰老,从而缓解肾纤维化。总的来说,槲皮素的抗纤维化作用涉及抑制RTEC衰老,可能是通过激活SIRT1/PINK1/Parkin介导的自噬。这些发现表明,通过药物消除衰老细胞和刺激自噬是预防肾纤维化的有效治疗策略[4]。
动物实验
Before the formal in vivo experiment, we evaluated the toxicity of two combined drugs and vehicle that would be administrated simultaneously using two groups of male BALB/c nude mice (n = 5 each). Solvent for quercetin was 25% hydroxypropyl-β-cyclodextrin (HPβCD, w/v in ddH2O) and for 2-Methoxyestradiol was 25% HPβCD containing 0.5% carboxymethyl cellulose (CMC, w/v in ddH2O). Drug group were given the two drugs, namely dissolved quercetin and 2-ME, and vehicle control group were given two drug-free vehicles, namely 25% HPβCD containing or not containing 0.5% CMC. After operation, toxic reaction was observed in the mice of both groups represented as poor mental state, lightly twisting the body, convulsion and occasional moderate haematuria that were in consistent with the description of Ehteda A and may be attributed to high concentration of HPβCD. For this reason, in the subsequent experiment, combination of quercetin and 2-ME was carried out in this way: quercetin was given on day 1, followed by 2-ME given on day 2.[3]
Mice were inoculated subcutaneously with 5×105 PC-3 cells suspended in 100μL PBS and 2×108 LNCaP cells suspended in 100μL of matrigel and PBS mixture (1:1) on the right back. When xenograft tumors reached a volume of approximately 100mm3, mice were randomly assigned to four groups (n = 8 each group) and treated intraperitoneally. Therapeutic schedule based on our in vitro results, preliminary experiments and many other researchers' studies was as follows: (1) Vehicle control group: vehicle of quercetin on day 1, vehicle of 2-ME on day 2, (2) Quercetin treated group: quercetin 75mg/kg on day 1, vehicle of 2-ME on day 2, (3) 2-ME treated group: vehicle of quercetin on day 1, 2-ME 150mg/kg on day 2, (4) Combination treatment group: quercetin 75mg/kg on day 1, 2-ME 150mg/kg on day 2. Two days was a treatment cycle and the whole treatment process lasted for 4 weeks. Tumor sizes were monitored every 2 days using caliper and tumor volume were calculated according to the formula: L×S2×0.5, in which L represents the longest diameter and S represents the shortest diameter of tumor. Mice were weighed as well. At the end of treatment procedure, on day 29, mice were anesthetized with chloral hydrate and sacrificed by cervical dislocation. Xenograft tumors were taken out quickly and weighed. One part of it was put into liquid nitrogen immediately for future biomarker analysis and the other part was fixed in 10% neutral buffered formalin for immunohistochemical analysis. Serum biochemical parameters such as ALT, AST, creatinine and urea nitrogen that reflected drug toxicity were also detected.[3]
参考文献

[1]. Effect of quercetin on platelet spreading on collagen and fibrinogen and on multiple platelet kinases. Fitoterapia. 2010 Mar;81(2):75-80.

[2]. Inhibitory effects of protein kinase C inhibitors on tumor necrosis factor induced bovine pulmonary artery endothelial cell injuries. Yao Xue Xue Bao. 1996;31(3):176-81.

[3]. Combination of Quercetin and 2-Methoxyestradiol Enhances Inhibition of Human Prostate Cancer LNCaP and PC-3 Cells Xenograft Tumor Growth. PLoS One. 2015 May 26;10(5):e0128277.

[4]. Quercetin alleviates kidney fibrosis by reducing renal tubular epithelial cell senescence through the SIRT1/PINK1/mitophagy axis. Life Sci. 2020 Jul 20;118116.

其他信息
Quercetin appears as yellow needles or yellow powder. Converts to anhydrous form at 203-207 °F. Alcoholic solutions taste very bitter. (NTP, 1992) National Toxicology Program, Institute of Environmental Health Sciences, National Institutes of Health (NTP). 1992. National Toxicology Program Chemical Repository Database. Research Triangle Park, North Carolina.
Quercetin is a pentahydroxyflavone having the five hydroxy groups placed at the 3-, 3'-, 4'-, 5- and 7-positions. It is one of the most abundant flavonoids in edible vegetables, fruit and wine. It has a role as an antibacterial agent, an antioxidant, a protein kinase inhibitor, an antineoplastic agent, an EC 1.10.99.2 [ribosyldihydronicotinamide dehydrogenase (quinone)] inhibitor, a plant metabolite, a phytoestrogen, a radical scavenger, a chelator, an Aurora kinase inhibitor and a geroprotector. It is a pentahydroxyflavone and a 7-hydroxyflavonol. It is a conjugate acid of a quercetin-7-olate.
Quercetin is a flavonol widely distributed in plants. It is an antioxidant, like many other phenolic heterocyclic compounds. Glycosylated forms include RUTIN and quercetrin. Quercetin is a metabolite found in or produced by Escherichia coli (strain K12, MG1655).
Quercetin is a flavonoid found in many foods and herbs and is a regular component of a normal diet. Extracts of quercetin have been used to treat or prevent diverse conditions including cardiovascular disease, hypercholesterolemia, rheumatic diseases, infections and cancer but have not been shown to be effective in clinical trials for any medical condition. Quercetin as a nutritional supplement is well tolerated and has not been linked to serum enzyme elevations or to episodes of clinically apparent liver injury.
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Quercetin has been reported in Salvia miltiorrhiza, Hydrangea serrata, and other organisms with data available. Quercetin is a polyphenolic flavonoid with potential chemopreventive activity. Quercetin, ubiquitous in plant food sources and a major bioflavonoid in the human diet, may produce antiproliferative effects resulting from the modulation of either EGFR or estrogen-receptor mediated signal transduction pathways. Although the mechanism of action of action is not fully known, the following effects have been described with this agent in vitro: decreased expression of mutant p53 protein and p21-ras oncogene, induction of cell cycle arrest at the G1 phase and inhibition of heat shock protein synthesis. This compound also demonstrates synergy and reversal of the multidrug resistance phenotype, when combined with chemotherapeutic drugs, in vitro. Quercetin also produces anti-inflammatory and anti-allergy effects mediated through the inhibition of the lipoxygenase and cyclooxygenase pathways, thereby preventing the production of pro-inflammatory mediators.


Quercetin is a flavonoid widely distributed in many plants and fruits including red grapes, citrus fruit, tomato, broccoli and other leafy green vegetables, and a number of berries, including raspberries and cranberries. Quercetin itself (aglycone quercetin), as opposed to quercetin glycosides, is not a normal dietary component. Quercitin glycosides are converted to phenolic acids as they pass through the gastrointestinal tract. Quercetin has neither been confirmed scientifically as a specific therapeutic for any condition nor been approved by any regulatory agency. The U.S. Food and Drug Administration has not approved any health claims for quercetin. Nevertheless, the interest in dietary flavonoids has grown after the publication of several epidemiological studies showing an inverse correlation between dietary consumption of flavonols and flavones and reduced incidence and mortality from cardiovascular disease and cancer. In recent years, a large amount of experimental and some clinical data have accumulated regarding the effects of flavonoids on the endothelium under physiological and pathological conditions. The meta-analysis of seven prospective cohort studies concluded that the individuals in the top third of dietary flavonol intake are associated with a reduced risk of mortality from coronary heart disease as compared with those in the bottom third, after adjustment for known risk factors and other dietary components. A limited number of intervention studies with flavonoids and flavonoid containing foods and extracts has been performed in several pathological conditions. (A7896) A7896: Perez-Vizcaino F, Duarte J, Andriantsitohaina R: Endothelial function and cardiovascular disease: effects of quercetin and wine polyphenols. Free Radic Res. 2006 Oct;40(10):1054-65. PMID:17015250
Quercetin is a metabolite found in or produced by Saccharomyces cerevisiae. A flavonol widely distributed in plants. It is an antioxidant, like many other phenolic heterocyclic compounds. Glycosylated forms include RUTIN and quercetrin.
Therapeutic Uses
Quercetin has been used in medicine to decrease capillary fragility. IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V73 P498 (1999)

/EXPL THER/ ... In a randomized, double-blind, placebo-controlled trial ... /among patients with category III chronic prostatitis syndromes (nonbacterial chronic prostatitis and prostatodynia)/ ... Significant improvement was achieved in the treated group, as measured by the NIH chronic prostatitis score. Some 67% of the treated subjects had at least 25% improvement in symptoms, compared with 20% of the placebo group achieving this same level of improvement. In a follow up, unblind, open-label study ... quercetin was combined with bromelain and papain, which may enhance its absorption. In this study, 82% achieved a minimum 25% improvement score.
Drug Warnings
Although quercetin seems to have potential as an anticancer agent, future studies are needed, because most studies are based on in vitro experiments using high concn of quercetin unachievable by dietary ingestion, and because its beneficial effects on cancer are still inconclusive in animal and/or human studies. Coates, P.M., Blackman, M.R., Cragg, G.M., Levine, M., Moss, J., White, J.D. (Ed), Encyclopedia of Dietary Supplements. Marcel Dekker, New York, NY, p. 580 (2005)

... Quercetin has been shown to protect low density lipoprotein (LDL) from oxidation and prevent platelet aggregation. It was also reported to inhibit the proliferation and migration of smooth muscle cells ... Quercetin was reported to significantly lower the plasma lipid, lipoprotein and hepatic cholesterol levels, inhibit the production of oxLDL produced by oxidative stress, and protect an enzyme, which can hydrolyzed specific lipid peroxides in oxidized lipoproteins and in atherosclerotic lesions ... /It/ induced endothelium-dependent vasorelaxation in rat aorta via incr nitric oxide production ... Quercetin and its glycosides were also reported to inhibit the angiotensin-converting enzyme activity, and ANG II-induced JNK activation inducing vascular smooth muscle cell (VSMC) hypertrophy ... However, some effects may not be feasible or negligible in physiological conditions, because concn of quercetin in most studies are too high to be achieved by dietary ingestion ... and beneficial effects of quercetin on cardiovascular diseases are still inconclusive in human studies
After oral administration of a single dose of 4 g quercetin to four male and two female volunteers, neither quercetin nor its conjugates was detected in the blood or urine during the first 24 hr; 53% of the dose was recovered in the feces within 72 hr. After a single intravenous injection of 100 mg quercetin to six volunteers, the blood plasma levels declined biphasically, with half-lives of 8.8 min and 2.4 hr; protein binding exceeded 98%. In the urine, 0.65% of the intravenous dose was excreted as unchanged quercetin and 7.4% as a conjugate within 9 hr; no further excretion occurred up to 24 hr ... IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V73 P501 (1999)

When 14C-quercetin was administered orally to ACI rats, about 20% of the administered dose was absorbed from the digestive tract, more than 30% was decomposed to yield 14-CO2 & about 30% was excreted unchanged in feces..
Metabolism / Metabolites
The glycosides are hydrolyzed in the body to corresponding aglycones, which are then further metabolized by scission of the heterocyclic ring to give 3,4-dihydroxy-phenyl-substituted acids ... The site of ring scission depends on structure ... with flavonols (quercetin) scission occurs at the 1,2 & 3,4 bonds to yield homoprotocatechuic acid ... These acids are further metabolized by beta-oxidation of acyl side-chain, o-methylation & demethylation, & aromatic dehydroxylation. Parke, D. V. The Biochemistry of Foreign Compounds. Oxford: Pergamon Press, 1968., p. 151

o-Beta-hydroxyethylated derivatives of quercetin were isolated from urine samples & separated by HPLC. The 5,7,3',4'-tetra compd was separated from 3,7,3',4'-tetra derivative. The 7,3',4'-tri & 7'-mono compounds gave 1 common peak, separated from the peak for the 7,4'-di compd.
Biological Half-Life
One male and one female volunteer were given a diet containing quercetin glucosides (64.2 mg expressed as the aglycone) ... Half-lives /were/ 3.8 hr for the distribution phase and 16.8 hr for the elimination phase ... /Quercetin glucosides/ IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V73 P501 (1999)

...The elimination half-life of quercetin is approx 25 hr.
Mechanism of Action
Quercetin is a specific quinone reductase 2 (QR2) inhibitor, an enzyme (along with the human QR1 homolog) which catalyzes metabolism of toxic quinolines. Inhibition of QR2 in plasmodium may potentially cause lethal oxidative stress. The inhibition of antioxidant activity in plasmodium may contribute to killing the malaria causing parasites.

... The 5, 7, 3', 4'-hydroxyl groups on quercetin are capable of donating electrons to quench various radical oxygen species (ROS) and other radical species ... Oxygen radicals (superoxide, hydrogen peroxide, hydroxyl radicals, and other related radicals) ... are quenched by ... antioxidant systems, including antioxidant cmpd, which balance cellular redox status involved in cellular processes for cell homeostasis ... Generally, 3 criteria are considered to assess the antioxidant activity of flavonoids in vitro: first, B ring with 2 hydroxyl groups (adjacent), second, C ring with 2,3-double bond, 4-oxo, and 3-hydroxyl group, and third, A ring with 5,7-dihydroxyl groups. Quercetin meets all 3 criteria, indicating stronger antioxidant activity ... The flavonol was reported to prevent radicals from damaging carbohydrates, proteins, nucleotides, and lipids ... The glucuronide conjugates found in the plasma were also reported to have potent antioxidant activity, indicating that the activity may be retained depending on conjugation positions ... Coates, P.M., Blackman, M.R., Cragg, G.M., Levine, M., Moss, J., White, J.D. (Ed), Encyclopedia of Dietary Supplements. Marcel Dekker, New York, NY, p. 579 (2005)

Cytokines such as tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) can induce apoptosis in colon cancer cells through engagement of death receptors. Nevertheless, evading apoptosis induced by anticancer drugs characterizes many types of cancers. This results in the need for combination therapy. In this study ... whether the flavonoid quercetin could sensitize human colon adenocarcinoma cell lines to TRAIL-induced apoptosis /was investigated/ ... Quercetin enhanced TRAIL-induced apoptosis by causing the redistribution of DR4 and DR5 into lipid rafts. Nystatin, a cholesterol-sequestering agent, prevented quercetin-induced clustering of death receptors and sensitization to TRAIL-induced apoptosis in colon adenocarcinoma cells ... Qercetin, in combination with TRAIL, triggered the mitochondrial-dependent death pathway, as shown by Bid cleavage and the release of cytochrome c to the cytosol. Together /the/ findings propose that quercetin, through its ability to redistribute death receptors at the cell surface, facilitates death-inducing signaling complex formation and activation of caspases in response to death receptor stimulation. Based on these results, this study provides a challenging approach to enhance the efficiency of TRAIL-based therapies.
Methods of Manufacturing
Quercetin ... has been obtained for use as a natural coloring agent (Natural Yellow 10) by the rapid extraction of powdered quercitron bark with dilute ammonia and boiling of the extract with sulphuric acid ... The first successful synthesis of quercetin was reported in 1962 ... in which treatment of 2-methoxyacetyl phloroglucinol with O-benzylvanillic acid anhydride in triethylamine and then with potassium hydroxide produced 5,7-dihydroxy-4'-benzyloxy-3,3'- dimethexyflavone. The benzyl ether was cleaved with acetic acid-hydrochloric acid, and the methyl ethers were then cleaved with hydriodic acid to produce quercetin.
Hepatotoxicity
Quercetin supplements have not been linked serum aminotransferase elevations during therapy, although there have been few focused studies of its hepatic safety. Furthermore, there have been no published reports of clinically apparent liver injury attributable to quercetin. Indeed, many in vitro and in vivo studies have shown that quercetin protects against hepatic injury caused by drugs and toxins including acetaminophen and cancer chemotherapeutic agents. These hepatoprotective effects have not been demonstrated in prospective clinical trials in humans.
Likelihood score: E (unlikely cause of clinically apparent liver injury).
Other Names: Often a component in Bioflavonoid Extracts
Drug Class: Herbal and Dietary Supplements

*注: 文献方法仅供参考, InvivoChem并未独立验证这些方法的准确性
化学信息 & 存储运输条件
分子式
C15H10O7.XH2O
分子量
320.2510
精确质量
320.053
CAS号
849061-97-8
相关CAS号
Quercetin;117-39-5; Quercetin-d3;263711-79-1; 117-39-5; Quercetin dihydrate;6151-25-3;Quercetin hydrate;849061-97-8; Quercetin-d5;263711-78-0;Quercetin-13C3
PubChem CID
16212154
外观&性状
Light yellow to yellow solid powder
沸点
714.6ºC at 760 mmHg
熔点
>300ºC
闪点
386ºC
LogP
1.923
tPSA
140.59
氢键供体(HBD)数目
6
氢键受体(HBA)数目
8
可旋转键数目(RBC)
1
重原子数目
23
分子复杂度/Complexity
488
定义原子立体中心数目
0
SMILES
O=C1C2C(=CC(=CC=2O)O)OC(C2C=C(O)C(O)=CC=2)=C1O.O
InChi Key
OKXFBEYCJRMINR-UHFFFAOYSA-N
InChi Code
InChI=1S/C15H10O7.H2O/c16-7-4-10(19)12-11(5-7)22-15(14(21)13(12)20)6-1-2-8(17)9(18)3-6;/h1-5,16-19,21H;1H2
化学名
2-(3,4-dihydroxyphenyl)-3,5,7-trihydroxychromen-4-one;hydrate
别名
Quercetin hydrate; 849061-97-8; 2-(3,4-dihydroxyphenyl)-3,5,7-trihydroxy-4H-chromen-4-one hydrate; 1001001-36-0; Quercetin hydrate; Quercetin (hydrate); 2-(3,4-dihydroxyphenyl)-3,5,7-trihydroxychromen-4-one;hydrate; Quercetin monohydrate;
HS Tariff Code
2934.99.9001
存储方式

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

运输条件
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
溶解度数据
溶解度 (体外实验)
May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples
溶解度 (体内实验)
注意: 如下所列的是一些常用的体内动物实验溶解配方,主要用于溶解难溶或不溶于水的产品(水溶度<1 mg/mL)。 建议您先取少量样品进行尝试,如该配方可行,再根据实验需求增加样品量。

注射用配方
(IP/IV/IM/SC等)
注射用配方1: DMSO : Tween 80: Saline = 10 : 5 : 85 (如: 100 μL DMSO 50 μL Tween 80 850 μL Saline)
*生理盐水/Saline的制备:将0.9g氯化钠/NaCl溶解在100 mL ddH ₂ O中,得到澄清溶液。
注射用配方 2: DMSO : PEG300Tween 80 : Saline = 10 : 40 : 5 : 45 (如: 100 μL DMSO 400 μL PEG300 50 μL Tween 80 450 μL Saline)
注射用配方 3: DMSO : Corn oil = 10 : 90 (如: 100 μL DMSO 900 μL Corn oil)
示例: 注射用配方 3 (DMSO : Corn oil = 10 : 90) 为例说明, 如果要配制 1 mL 2.5 mg/mL的工作液, 您可以取 100 μL 25 mg/mL 澄清的 DMSO 储备液,加到 900 μL Corn oil/玉米油中, 混合均匀。
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注射用配方 4: DMSO : 20% SBE-β-CD in Saline = 10 : 90 [如:100 μL DMSO 900 μL (20% SBE-β-CD in Saline)]
*20% SBE-β-CD in Saline的制备(4°C,储存1周):将2g SBE-β-CD (磺丁基-β-环糊精) 溶解于10mL生理盐水中,得到澄清溶液。
注射用配方 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (如: 500 μL 2-Hydroxypropyl-β-cyclodextrin (羟丙基环胡精) 500 μL Saline)
注射用配方 6: DMSO : PEG300 : Castor oil : Saline = 5 : 10 : 20 : 65 (如: 50 μL DMSO 100 μL PEG300 200 μL Castor oil 650 μL Saline)
注射用配方 7: Ethanol : Cremophor : Saline = 10: 10 : 80 (如: 100 μL Ethanol 100 μL Cremophor 800 μL Saline)
注射用配方 8: 溶解于Cremophor/Ethanol (50 : 50), 然后用生理盐水稀释。
注射用配方 9: EtOH : Corn oil = 10 : 90 (如: 100 μL EtOH 900 μL Corn oil)
注射用配方 10: EtOH : PEG300Tween 80 : Saline = 10 : 40 : 5 : 45 (如: 100 μL EtOH 400 μL PEG300 50 μL Tween 80 450 μL Saline)


口服配方
口服配方 1: 悬浮于0.5% CMC Na (羧甲基纤维素钠)
口服配方 2: 悬浮于0.5% Carboxymethyl cellulose (羧甲基纤维素)
示例: 口服配方 1 (悬浮于 0.5% CMC Na)为例说明, 如果要配制 100 mL 2.5 mg/mL 的工作液, 您可以先取0.5g CMC Na并将其溶解于100mL ddH2O中,得到0.5%CMC-Na澄清溶液;然后将250 mg待测化合物加到100 mL前述 0.5%CMC Na溶液中,得到悬浮液。
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口服配方 3: 溶解于 PEG400 (聚乙二醇400)
口服配方 4: 悬浮于0.2% Carboxymethyl cellulose (羧甲基纤维素)
口服配方 5: 溶解于0.25% Tween 80 and 0.5% Carboxymethyl cellulose (羧甲基纤维素)
口服配方 6: 做成粉末与食物混合


注意: 以上为较为常见方法,仅供参考, InvivoChem并未独立验证这些配方的准确性。具体溶剂的选择首先应参照文献已报道溶解方法、配方或剂型,对于某些尚未有文献报道溶解方法的化合物,需通过前期实验来确定(建议先取少量样品进行尝试),包括产品的溶解情况、梯度设置、动物的耐受性等。

请根据您的实验动物和给药方式选择适当的溶解配方/方案:
1、请先配制澄清的储备液(如:用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液,按从左到右的顺序依次添加助溶剂,澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明,并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中,混合均匀/澄清;向上述体系中加入50 μL Tween-80,混合均匀/澄清;然后继续加入450 μL ddH2O (或 saline)定容至 1 mL;

3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出,可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果,工作液请现配现用!
6、如不确定怎么将母液配置成体内动物实验的工作液,请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。
制备储备液 1 mg 5 mg 10 mg
1 mM 3.1226 mL 15.6128 mL 31.2256 mL
5 mM 0.6245 mL 3.1226 mL 6.2451 mL
10 mM 0.3123 mL 1.5613 mL 3.1226 mL

1、根据实验需要选择合适的溶剂配制储备液 (母液):对于大多数产品,InvivoChem推荐用DMSO配置母液 (比如:5、10、20mM或者10、20、50 mg/mL浓度),个别水溶性高的产品可直接溶于水。产品在DMSO 、水或其他溶剂中的具体溶解度详见上”溶解度 (体外)”部分;

2、如果您找不到您想要的溶解度信息,或者很难将产品溶解在溶液中,请联系我们;

3、建议使用下列计算器进行相关计算(摩尔浓度计算器、稀释计算器、分子量计算器、重组计算器等);

4、母液配好之后,将其分装到常规用量,并储存在-20°C或-80°C,尽量减少反复冻融循环。

计算器

摩尔浓度计算器可计算特定溶液所需的质量、体积/浓度,具体如下:

  • 计算制备已知体积和浓度的溶液所需的化合物的质量
  • 计算将已知质量的化合物溶解到所需浓度所需的溶液体积
  • 计算特定体积中已知质量的化合物产生的溶液的浓度
使用摩尔浓度计算器计算摩尔浓度的示例如下所示:
假如化合物的分子量为350.26 g/mol,在5mL DMSO中制备10mM储备液所需的化合物的质量是多少?
  • 在分子量(MW)框中输入350.26
  • 在“浓度”框中输入10,然后选择正确的单位(mM)
  • 在“体积”框中输入5,然后选择正确的单位(mL)
  • 单击“计算”按钮
  • 答案17.513 mg出现在“质量”框中。以类似的方式,您可以计算体积和浓度。

稀释计算器可计算如何稀释已知浓度的储备液。例如,可以输入C1、C2和V2来计算V1,具体如下:

制备25毫升25μM溶液需要多少体积的10 mM储备溶液?
使用方程式C1V1=C2V2,其中C1=10mM,C2=25μM,V2=25 ml,V1未知:
  • 在C1框中输入10,然后选择正确的单位(mM)
  • 在C2框中输入25,然后选择正确的单位(μM)
  • 在V2框中输入25,然后选择正确的单位(mL)
  • 单击“计算”按钮
  • 答案62.5μL(0.1 ml)出现在V1框中
g/mol

分子量计算器可计算化合物的分子量 (摩尔质量)和元素组成,具体如下:

注:化学分子式大小写敏感:C12H18N3O4  c12h18n3o4
计算化合物摩尔质量(分子量)的说明:
  • 要计算化合物的分子量 (摩尔质量),请输入化学/分子式,然后单击“计算”按钮。
分子质量、分子量、摩尔质量和摩尔量的定义:
  • 分子质量(或分子量)是一种物质的一个分子的质量,用统一的原子质量单位(u)表示。(1u等于碳-12中一个原子质量的1/12)
  • 摩尔质量(摩尔重量)是一摩尔物质的质量,以g/mol表示。
/

配液计算器可计算将特定质量的产品配成特定浓度所需的溶剂体积 (配液体积)

  • 输入试剂的质量、所需的配液浓度以及正确的单位
  • 单击“计算”按钮
  • 答案显示在体积框中
动物体内实验配方计算器(澄清溶液)
第一步:请输入基本实验信息(考虑到实验过程中的损耗,建议多配一只动物的药量)
第二步:请输入动物体内配方组成(配方适用于不溶/难溶于水的化合物),不同的产品和批次配方组成不同,如对配方有疑问,可先联系我们提供正确的体内实验配方。此外,请注意这只是一个配方计算器,而不是特定产品的确切配方。
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计算结果:

工作液浓度 mg/mL;

DMSO母液配制方法 mg 药物溶于 μL DMSO溶液(母液浓度 mg/mL)。如该浓度超过该批次药物DMSO溶解度,请首先与我们联系。

体内配方配制方法μL DMSO母液,加入 μL PEG300,混匀澄清后加入μL Tween 80,混匀澄清后加入 μL ddH2O,混匀澄清。

(1) 请确保溶液澄清之后,再加入下一种溶剂 (助溶剂) 。可利用涡旋、超声或水浴加热等方法助溶;
            (2) 一定要按顺序加入溶剂 (助溶剂) 。

临床试验信息
NCT Number Status Interventions Conditions Sponsor/Collaborators Start Date Phases
NCT01881919 Completed Dietary Supplement: Control
Dietary Supplement: Treatment
Gout
Diabetes
Hyperuricemia
University of Leeds February 2013 Early Phase 1
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