Cholesteryl Myristate
(Synonyms: 胆固醇肉豆蔻酸; Cholesteryl myristate; Cholesteryl tetradecanoate) 目录号 : GC43261
A cholesterol ester
Cas No.:1989-52-2
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Cell experiment: | MSCs are cultured with or without serum in 96-well plates and treated with cholesterol myristate in various concentrations (0, 30 and 300 μg/mL) for 3 days. Each sample is repeated in five independent wells and is incubated for 72 h. After incubation, 20 μL MTT (5 mg/mL) is added and the culture is incubated for a further 4 h. The culture medium is discarded and replaced with 150 μL DMSO. The absorbance at 490nm is measured[1]. |
References: [1]. Chen DF, et al. Cholesterol myristate suppresses the apoptosis of mesenchymal stem cells via upregulation of inhibitor of differentiation. Steroids. 2010 Dec 12;75(13-14):1119-26. | |
Cholesterol myristate is a natural steroid present in traditional Chinese medicine. Cholesterol myristate binds to several ion channels such as the nicotinic acetylcholine receptor, GABAA receptor, and the inward-rectifier potassium ion channel.
Mesenchymal stem cells (MSCs) transfected by the Id1 promoter reporter construct, cholesterol myristate increases the activity of Id1 promoter. Cholesterol myristate inhibits the apoptosis of MSCs induced by serum-free. Cholesterol myristate increases the expression of Id1 and its target gene bcl-x/l in MSCs treated with serum-free. Moreover, noggin, a BMP antagonist, reduces the anti-apoptotic effects of cholesterol myristate[1]. Cholesterol myristate inhibits the apoptosis of PC12 cells induced in serum-free condition. Cholesterol myristate significantly increases the expression of BMP4, BMPRIA, p-Smad1/5/8, Id1 and its antiapoptotic target gene Bcl-xL in PC12 cells treated in serum-free condition[1].
References:
[1]. Chen DF, et al. Cholesterol myristate suppresses the apoptosis of mesenchymal stem cells via upregulation of inhibitor of differentiation. Steroids. 2010 Dec 12;75(13-14):1119-26.
[2]. Chen DF, et al. BMP-Id pathway targeted by cholesterol myristate suppresses the apoptosis of PC12 cells. Brain Res. 2011 Jan 7;1367:33-42.
[3]. Levitan I, et al. Cholesterol binding to ion channels. Front Physiol. 2014 Feb 26;5:65.
| Cas No. | 1989-52-2 | SDF | |
| 别名 | 胆固醇肉豆蔻酸; Cholesteryl myristate; Cholesteryl tetradecanoate | ||
| Canonical SMILES | C[C@]12C(C[C@@H](OC(CCCCCCCCCCCCC)=O)CC2)=CC[C@]3([H])[C@]1([H])CC[C@@]4(C)[C@@]3([H])CC[C@@]4([C@@H](CCCC(C)C)C)[H] | ||
| 分子式 | C41H72O2 | 分子量 | 597 |
| 溶解度 | Chloroform: 10 mg/mL | 储存条件 | Store at -20°C |
| 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 | 1.675 mL | 8.3752 mL | 16.7504 mL |
| 5 mM | 0.335 mL | 1.675 mL | 3.3501 mL |
| 10 mM | 0.1675 mL | 0.8375 mL | 1.675 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。
Self-assembly and molecular packing in cholesteryl esters at interfaces
J Chem Phys 2017 Jun 7;146(21):214702.PMID:28576087DOI:10.1063/1.4984119.
To understand the self-assembly and molecular packing in cholesteryl esters relevant to biological processes, we have studied them at the air-water and air-solid interfaces. Our phase and thickness studies employing imaging ellipsometry and atomic force microscopy along with surface manometry show that the molecular packing of cholesteryl esters at interfaces can be related to Craven's model of packing, given for bulk. At the air-water interface, following Craven's model, cholesteryl nonanoate and cholesteryl laurate exhibit a fluidic bilayer phase. Interestingly, we find the fluidic bilayer phase of cholesteryl laurate to be unstable and it switches to a crystalline bilayer phase. However, according to Craven, only cholesteryl esters with longer chain lengths starting from cholesteryl tridecanoate should show the crystalline bilayer phase. The thickness behavior of different phases was also studied by transferring the films onto a silicon substrate by using the Langmuir-Blodgett technique. Texture studies show that cholesterol, cholesteryl acetate, cholesteryl nonanoate, cholesteryl laurate, and Cholesteryl Myristate exhibit homogeneous films with large size domains, whereas cholesteryl palmitate and cholesteryl stearate exhibit less homogeneous films with smaller size domains. We suggest that such an assembly of molecules can be related to their molecular structures. Simulation studies may confirm such a relation.
Chemical stability of phospholipid-stabilized supercooled smectic Cholesteryl Myristate nanoparticles
Eur J Pharm Biopharm 2012 Oct;82(2):262-71.PMID:22750438DOI:10.1016/j.ejpb.2012.06.009.
Supercooled smectic Cholesteryl Myristate nanoparticle dispersions, a potential carrier system for lipophilic drugs, can be stabilized with phospholipids and their mixtures with sodium glycocholate. Such dispersions are commonly prepared by high-pressure melt homogenization. As cholesterol esters and phospholipids are both susceptible to oxidation and hydrolysis, the chemical stability of the dispersions was studied directly after preparation and during storage. Despite the high temperatures occurring during processing, no hydrolysis was detected in the dispersions directly after preparation. During storage for 5-8 months, dispersions solely stabilized with phospholipids exhibited massive phospholipid hydrolysis as determined by HPTLC. Phospholipid hydrolysis resulted in distinct changes of the physicochemical properties such as pH, zeta potential, and phase behavior of the dispersions. In systems additionally containing sodium glycocholate as stabilizer, hydrolytic degradation occurred only to a minor extent. Phospholipid hydrolysis could also be reduced by adding TRIS- or phosphate-buffer (10mM, pH 7.4) to the aqueous phase before the preparation process. The addition of EDTA and α-tocopherol, which were mainly employed with the aim to suppress oxidation processes, also reduced the phospholipid hydrolysis to a certain extent. A partial oxidation of the Cholesteryl Myristate was observed in several dispersions by HPTLC, HPLC and mass spectrometry after long-term storage, but could be reduced by adding EDTA or α-tocopherol.
Analysis of adrenal cholesteryl esters by reversed phase high performance liquid chromatography
J Lipid Res 1994 Jun;35(6):1115-21.PMID:8077850doi
A reversed phase high performance liquid chromatographic (HPLC) method was developed for direct profiling and determination of adrenal cholesteryl ester composition. Cholesteryl adrenate and cholesteryl cervonate, which are not commercially available, were synthesized as markers. Lipid extracts of rat adrenal homogenates or lipid droplets were individually applied to a conditioned silica gel-60 column which separated cholesteryl esters from other native lipids. The eluted cholesteryl ester fraction was then analyzed by HPLC. With cholesteryl heptadecanoate as internal standard, seven adrenal cholesteryl esters were detected and quantified: cholesteryl cervonate, cholesteryl arachidonate, cholesteryl adrenate, Cholesteryl Myristate, cholesteryl oleate, cholesteryl palmitate, and cholesteryl stearate. Among them, cholesteryl adrenate appeared to be the major sterol ester stored in the rat adrenal.
Cholesteryl Myristate conformation in liquid crystalline mesophases determined by neutron scattering
Proc Natl Acad Sci U S A 1981 Nov;78(11):6863-7.PMID:6947261DOI:10.1073/pnas.78.11.6863.
The possible involvement of cholesteryl ester states in the development and persistence of atherosclerosis and the transport and storage of cholesteryl esters has led to questions concerning the organization and conformation of cholesteryl ester molecules in both pure phases and membranes. The experiments we report here were designed to measure the distance between the center of mass of the fatty acyl terminal methyl group and the center of mass of the three-carbon branched terminus of the cholesterol moiety at the opposite end of the molecule. The distance obtained is thus a gauge of cholesteryl ester conformation through the conformational range from a completely extended conformation to a U-shaped conformation. Neutron scattering experiments on partially deuterated samples of pure Cholesteryl Myristate in the crystalline, smectic, cholesteric, and isotropic phases indicate that the molecule is extended in each of these states. A discussion of specific molecular models consistent with these results and extension of these conclusions to other cholesteryl esters is included.
Interactions of cholesterol esters with phospholipids: Cholesteryl Myristate and dimyristoyl lecithin
J Lipid Res 1979 Feb;20(2):183-99.PMID:438660doi
The ternary phase diagram of cholesteryl myristate--dimyristoyl lecithin--water has been determined by polarizing light microscopy, scanning calorimetry, and x-ray diffraction. Hydrated dimyristoyl lecithin forms a lamellar liquid--crystalline phase (L alpha) at temperatures greater than 23 degrees C into which limited amounts of Cholesteryl Myristate (less than 5 wt. %) can be incorporated. The amount of cholesterol ester incorporated is dependent upon the degree of hydration of the L alpha phase. Below 23 degrees C dimyristoyl lecithin forms ordered hydrocarbon chain structures (L beta' and P beta') which do not incorporate cholesterol ester. Comparison with other phospholipid--cholesterol ester--water phase diagrams suggests the following general principles: i) the incorporation of cholesterol ester occurs only into liquid crystalling phospholipid bilayers, ii) the extent of incorporation is temperature-dependent, with increasing amounts of cholesterol ester being incorporated at higher temperatures, and iii) unsaturated cholesterol esters induce increased disordering of the phospholipid bilayers.