2-hydroxy Palmitic Acid
(Synonyms: 2-羟基十六烷酸) 目录号 : GC42168An intermediate in the metabolism of phytosphingosine
Cas No.:764-67-0
Sample solution is provided at 25 µL, 10mM.
Quality Control & SDS
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- Purity: >97.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
2-hydroxy Palmitic acid is a form of the 16:0 long-chain saturated palmitic acid . It is an intermediate in the metabolism of phytosphingosine to odd-numbered fatty acids. 2-hydroxy Palmitic acid levels in yeast fermentations increase following treatment with fumonisin B1 .
Cas No. | 764-67-0 | SDF | |
别名 | 2-羟基十六烷酸 | ||
Canonical SMILES | OC(C(O)CCCCCCCCCCCCCC)=O | ||
分子式 | C16H32O3 | 分子量 | 272.4 |
溶解度 | DMF: 20 mg/ml,DMSO: 20 mg/ml,DMSO:PBS (pH 7.2) (1:2): 0.33 mg/mL,Ethanol: 2.5 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 | |||
1 mg | 5 mg | 10 mg | |
1 mM | 3.6711 mL | 18.3554 mL | 36.7107 mL |
5 mM | 0.7342 mL | 3.6711 mL | 7.3421 mL |
10 mM | 0.3671 mL | 1.8355 mL | 3.6711 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 | ||||||||||
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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。
Fatty acid 2-hydroxylase mediates diffusional mobility of Raft-associated lipids, GLUT4 level, and lipogenesis in 3T3-L1 adipocytes
J Biol Chem 2010 Aug 13;285(33):25438-47.PMID:20519515DOI:10.1074/jbc.M110.119933.
Straight chain fatty acid alpha-oxidation increases during differentiation of 3T3-L1 adipocytes, leading to a marked accumulation of odd chain length fatty acyl moieties. Potential roles of this pathway in adipocyte differentiation and lipogenesis are unknown. Mammalian fatty acid 2-hydroxylase (FA2H) was recently identified and suggested to catalyze the initial step of straight chain fatty acid alpha-oxidation. Accordingly, we examined whether FA2H modulates adipocyte differentiation and lipogenesis in mature adipocytes. FA2H level markedly increases during differentiation of 3T3-L1 adipocytes, and small interfering RNAs against FA2H inhibit the differentiation process. In mature adipocytes, depletion of FA2H inhibits basal and insulin-stimulated glucose uptake and lipogenesis, which are partially rescued by the enzymatic product of FA2H, 2-hydroxy Palmitic Acid. Expression of fatty-acid synthase and SCD1 was decreased in FA2H-depleted cells, and levels of GLUT4 and insulin receptor proteins were reduced. 2-Hydroxy fatty acids are enriched in cellular sphingolipids, which are components of membrane rafts. Accelerated diffusional mobility of raft-associated lipids was shown to enhance degradation of GLUT4 and insulin receptor in adipocytes. Consistent with this, depletion of FA2H appeared to increase raft lipid mobility as it significantly accelerated the rates of fluorescence recovery after photobleaching measurements of lipid rafts labeled with Alexa 488-conjugated cholera toxin subunit B. Moreover, the enhanced recovery rates were partially reversed by treatment with 2-hydroxy Palmitic Acid. In conclusion, our findings document the novel role of FA2H in adipocyte lipogenesis possibly by modulation of raft fluidity and level of GLUT4.
Levels of SCS7/FA2H-mediated fatty acid 2-hydroxylation determine the sensitivity of cells to antitumor PM02734
Cancer Res 2008 Dec 1;68(23):9779-87.PMID:19047157DOI:10.1158/0008-5472.CAN-08-1981.
PM02734 is a novel synthetic antitumor drug that is currently in phase I clinical trials. To gain some insight into its mode of action, we used the yeast Saccharomyces cerevisiae as a model system. Treatment of S. cerevisiae with PM02734 rapidly induced necrosis-like cell death, as also found for mammalian cells treated with its close analogue kahalalide F. We have screened the complete set of 4,848 viable S. cerevisiae haploid deletion mutants to identify genes involved in sensitivity or resistance to PM02734. Forty-five percent of the 40 most sensitive strains identified had a role in intracellular vesicle trafficking, indicating that the drug severely affects this process. A mutant strain lacking the sphingolipid fatty acyl 2-hydroxylase Scs7 was found to be the most resistant to PM02734, whereas overexpression of Scs7 rendered the cells hypersensitive to PM02734. To validate these findings in human cells, we did small interfering RNA experiments and also overexpressed the Scs7 human homologue FA2H in human cancer cell lines. As in yeast, FA2H silencing turned the cells resistant to the drug, whereas FA2H overexpression led to an increased sensitivity. Moreover, exogenous addition of the 2-hydroxylated fatty acid 2-hydroxy Palmitic Acid to different human cell lines increased their sensitivity to the cytotoxic compound. Taken together, these results suggest that the cell membrane and, in particular, 2-hydroxy fatty acid-containing ceramides are important for PM02734 activity. These findings may have important implications in the development of PM02734 because tumor cells with high FA2H expression are expected to be particularly sensitive to this drug.