Methyl-β-cyclodextrin  (Synonyms: 甲基-β-環(huán)糊精; Methyl-beta-cyclodextrin)

Methyl-β-cyclodextrin (Methyl-beta-cyclodextrin) 是一種環(huán)庚糖，對(duì)非極性物質(zhì)有增溶作用，廣應(yīng)用于疏水性的藥物的釋放。Methyl-β-cyclodextrin (Methyl-beta-cyclodextrin) 也廣用作降膽gu醇劑。Methyl-β-cyclodextrin 可有效降低網(wǎng)格蛋白依賴性內(nèi)吞作用。Methyl-β-cyclodextrin 可阻斷細(xì)胞遷移體的形成。

生物活性

Methyl-β-cyclodextrin (Methyl-beta-cyclodextrin) is a cyclic heptasaccharide used to deliver hydrophobic drugs based on its property of solubilizing non-polar substances. Methyl-β-cyclodextrin is also extensively used as a cholesterol-depleting reagent^[1]. Methyl-β-cyclodextrin strongly reduces clathrin-dependent endocytosis^[2]. Methyl-β-cyclodextrin blocks cell migrasome formation^[3].

體外研究(In Vitro)

Methyl-β-cyclodextrin is extensively used to increase the permeability of cells, and thereby increase the uptake of small molecules such as glucose and nano-particles^[4].
Cyclodextrins are a family of cyclic oligosaccharides with a hydrophilic outer surface and a lipophilic central cavity. Cyclodextrins molecules are relatively large with a number of hydrogen donors and acceptors and, thus in general, they do not permeate lipophilic membranes. In the pharmaceutical industry, cyclodextrins have mainly been used as complexing agents to increase aqueous solubility of poorly soluble drugs and to increase their bioavailability and stability. Cyclodextrins are used in pharmaceutical applications for numerous purposes, including improving the bioavailability of drugs^[4].
Methyl-β-cyclodextrin quickly induces caspase-dependent apoptosis in PEL cells via cholesterol depletion from the plasma membrane. Methyl-β-cyclodextrin inhibits the growth of all PEL cell lines in a dose-dependent manner. The IC₅₀ is 3.33-4.23 mM in each cell line^[5].
Methyl-β-cyclodextrin is a highly water soluble cyclic heptasaccharide consisting of a β-glucopyranose unit, has been reported as the most effective agent for the depletion of cholesterol from cells among the various cholesterol-depleting agents^[5].

體內(nèi)研究(In Vivo)

In a PEL xenograft mouse model, Methyl-β-cyclodextrin significantly inhibits the growth and invasion of PEL cells without apparent adverse effects. Methyl-β-cyclodextrin-treated mice appears to be healthy, whereas non-treated mice has a distended abdominal region. The body weights of control are significantly higher than those of Methyl-β-cyclodextrin treated mice. Methyl-β-cyclodextrin-treated mice has a significantly lower volume of ascites than that of non-treated mice^[4].
Studies in both humans and animals have shown that cyclodextrins can be used to improve drug delivery from almost any type of drug formulation. Currently, there are approximately 30 different pharmaceutical products worldwide containing drug/cyclodextrins complexes in the market^[6].

分子量：1310 (Average)

性狀：Solid

CAS 號(hào)：128446-36-6

中文名稱：甲基-β-環(huán)糊精

運(yùn)輸條件：Room temperature in continental US; may vary elsewhere.

儲(chǔ)存方式

溶解性數(shù)據(jù)

參考文獻(xiàn)

[1]. Mundhara N, et al. Methyl-β-cyclodextrin, an actin depolymerizer augments the antiproliferative potential of microtubule-targeting agents. Sci Rep. 2019 May 21;9(1):7638.  [Content Brief]

[2]. Rodal SK, et al. Extraction of cholesterol with methyl-beta-cyclodextrin perturbs formation of clathrin-coated endocytic vesicles. Mol Biol Cell. 1999;10(4):961-974.  [Content Brief]

[3]. Yuwei Huang, et al. Migrasome formation is mediated by assembly of micron-scale tetraspanin macrodomains. Nat Cell Biol. 2019 Aug;21(8):991-1002.  [Content Brief]

[4]. Chen X, et al. Cholesterol depletion from the plasma membrane triggers ligand-independent activation of the epidermal growth factor receptor. J Biol Chem. 2002 Dec 20;277(51):49631-7.  [Content Brief]

[5]. Gotoh K, et al. The antitumor effects of methyl-β-cyclodextrin against primary effusion lymphoma via the depletion of cholesterol from lipid rafts. Biochem Biophys Res Commun. 2014 Dec 12;455(3-4):285-9.  [Content Brief]

[6]. Tiwari G, et al. Cyclodextrins in delivery systems: Applications. J Pharm Bioallied Sci. 2010 Apr;2(2):72-9.  [Content Brief]