Methyl-Hesperidin
(Synonyms: 甲基橙皮甙) 目录号 : GC38439
A methylated form of hesperidin
Cas No.:11013-97-1
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Methylhesperidin is a methylated form of the flavanone rutinoside hesperidin .1
1.Li, J., and Wang, S.Molecular spectroscopic on interaction between Methyl hesperidin and Buman serum albuminSpectrochim. Acta A Mol. Biomol. Spectrosc.102200-204(2013)
| Cas No. | 11013-97-1 | SDF | |
| 别名 | 甲基橙皮甙 | ||
| Canonical SMILES | O=C1C[C@@H](C2=CC=C(OC)C(OC)=C2)OC3=CC(O[C@H]4[C@@H]([C@H]([C@@H]([C@@H](CO[C@H]5[C@@H]([C@@H]([C@H]([C@H](C)O5)O)O)O)O4)O)O)O)=CC(O)=C13 | ||
| 分子式 | C29H36O15 | 分子量 | 624.59 |
| 溶解度 | DMF: 3 mg/ml,DMSO: 5 mg/ml,DMSO:PBS (pH 7.2) (1:5): 0.1 mg/ml | 储存条件 | 4°C, protect from light |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 1.6011 mL | 8.0053 mL | 16.0105 mL |
| 5 mM | 0.3202 mL | 1.6011 mL | 3.2021 mL |
| 10 mM | 0.1601 mL | 0.8005 mL | 1.6011 mL |
| 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） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
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，
体内配方配制方法：取 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 saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Amentoflavone and Methyl Hesperidin, novel lead molecules targeting epitranscriptomic modulator in acute myeloid leukemia: in silico drug screening and molecular dynamics simulation approach
J Mol Model 2022 Dec 16;29(1):9.PMID:36522514DOI:10.1007/s00894-022-05407-1.
Introduction: M6A modification in transcriptome is critical in regulating different cellular processes, including cancer. In human beings, METTL3 is the major m6A writer that works in association with METTL14, an accessory protein. Extensive study revealed that cancer progression for acute myeloid leukemia, gastric cancer, colorectal cancer, hepatocellular carcinoma, and lung cancer is directly contributed by irregular expression of METTL3. Objective: Targeting METTL3 has opened a new window in the development of novel inhibitors/drugs. Methods: In this study, commercially available natural compounds were randomly screened to avoid the bias of screening small molecules on the basis of structural similarity. From 810 compounds that were screened, 80 commercially available compounds were showing better score when compared with the existing substrate/substrate-analogue and the inhibitor bound crystal structures in terms of docking score and binding energy calculation. Results and conclusion: Among this pool of compounds, the best seven small molecules have been selected and further validated by different computational tools like binding energy calculation, molecular dynamics simulation, ADME analysis, and toxicity prediction. The novel hits found in this study can function as lead compounds which can be developed into inhibitors as well as drugs, specific against METTL3.
Development of nobiletin-methyl hesperidin amorphous solid dispersion: Novel application of Methyl Hesperidin as an excipient for hot-melt extrusion
Int J Pharm 2019 Mar 10;558:215-224.PMID:30654059DOI:10.1016/j.ijpharm.2018.12.092.
A novel amorphous solid dispersion (ASD) of poorly water-soluble nobiletin (Nob) with highly water-soluble Methyl Hesperidin (MeHes) was developed. Mixtures of Nob and excipients (MeHes, cellulose derivatives, and synthetic polymers) were processed by hot-melt extrusion (HME). Powder X-ray diffraction analysis proved that most of the HME products were fully amorphized. In dissolution studies, Nob-MeHes ASD showed a prominently higher Nob concentration than other HME products with polymeric excipients. Nob concentration upon dissolution of Nob-MeHes ASD was 400 and 7.5 times higher than that upon dissolution of crystalline Nob and a Nob-MeHes physical mixture, respectively. In addition, Nob-MeHes ASD showed good preservation stability for 6 months under an accelerated condition of 40 °C and 80% relative humidity. Permeation studies using a Caco-2 cell monolayer showed that Nob-MeHes ASD markedly increased the amount of Nob transported. In mice, the plasma Nob concentration and accumulated amount of Nob in various tissues drastically increased after administration of Nob-MeHes ASD. This is the first successful application of MeHes, with a relatively low glass-transition temperature, as an excipient for an ASD formulation prepared by hot-melt extrusion. The drastic improvement in Nob concentration with a small-molecule excipient may be an important finding.
Carcinogenicity study of Methyl Hesperidin in B6C3F1 mice
Food Chem Toxicol 1990 Sep;28(9):613-8.PMID:2272558DOI:10.1016/0278-6915(90)90168-m.
A long-term carcinogenicity study of Methyl Hesperidin, a compound of the vitamin P group, was carried out in B6C3F1 mice receiving dietary concentrations of 0, 1.25 or 5%. Administration was continued for 96 wk and then the mice were maintained on basal diet for an additional 8 wk. Growth retardation during the experiment with final changes in organ weights were observed in females given the 1.25% dose of Methyl Hesperidin and in both sexes receiving the 5.0% treatment. However, no biologically significant effects were evident with respect to mortality or clinical signs. Furthermore, treatment with Methyl Hesperidin did not result in any changes in haematology, clinical chemistry and urinalysis data. On histological examination, no significant alteration of non-neoplastic and neoplastic lesion incidence was observed in treated mice. The results thus demonstrated that Methyl Hesperidin lacked any carcinogenicity for B6C3F1 mice in the 96-wk feeding regimen used in this study.
Molecular spectroscopic on interaction between Methyl Hesperidin and Buman serum albumin
Spectrochim Acta A Mol Biomol Spectrosc 2013 Feb;102:200-4.PMID:23220657DOI:10.1016/j.saa.2012.10.012.
The interaction of Methyl Hesperidin (MH) with Buman serum albumin was studied by spectroscopic methods including Fluorescence quenching technology, UV absorbance spectra and Fourier transform infrared (FT-IR) spectroscopy under simulative physiological conditions. The result of fluorescence titration revealed that Methyl Hesperidin could quench the intrinsic fluorescence of BSA and the quenching mechanism should be a combined quenching process. The binding constants at three temperatures (296, 303, and 310 K) were 1.82, 2.69, and 3.4 × 10(4)L mol(-1), respectively. The distance between donor (BSA) and acceptor (MH) was 5.54 nm according to the Förster theory of non-radiation energy transfer. In addition, FT-IR spectroscopy showed that the binding of MH to BSA changed the secondary structure of protein.
Subchronic toxicity study of Methyl Hesperidin in mice
Toxicol Lett 1993 Jul;69(1):37-44.PMID:8356566DOI:10.1016/0378-4274(93)90143-l.
A subchronic toxicity study of Methyl Hesperidin was performed using B6C3F1 mice. The flavonoid was administered to groups of ten males and ten females in dietary levels of 0, 0.3, 0.6, 1.25, 2.5 and 5.0% for 13 weeks. No significant treatment-related differences were found in data for body weights, food and water consumption, hematology, clinical chemistry and organ weights. Furthermore, no effects of treatment were observed on gross and histopathological examination of the major organs. The present experiment thus demonstrated that Methyl Hesperidin exerts no obvious toxic effects in mice of either sex when administered at a level as high as 5.0% in the diet.