Hexadecanedioic acid
(Synonyms: 十六碳二酸) 目录号 : GC30677
A dicarboxylic fatty acid
Cas No.:505-54-4
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
Hexadecanedioic acid is a dicarboxylic fatty acid that has been found in the suberin component of silver birch (B. pendula) outer bark and soil.1,2 It stimulates mitochondrial respiration and decreases the production of reactive oxygen species (ROS) induced by rotenone in isolated rat liver mitochondria when used at concentrations of 100 and 40 ?M, respectively.3
1.Karnaouri, A., Lange, H., Crestini, C., et al.Chemoenzymatic fractionation and characterization of pretreated birch outer barkACS Sustainable Chem. Eng.4(10)5289-5302(2016) 2.Hamer, U., Rumpel, C., and Dignac, M.-F.Cutin and suberin biomarkers as tracers for the turnover of shoot and root derived organic matter along a chronosequence of Ecuadorian pasture soilsEur. J. Soil Sci.63(6)808-819(2012) 3.Sememova, A.A., V.N., S., Pavlova, S.I., et al.ω-Hydroxypalmitic and α,ω-hexadecanedioic acids as activators of free respiration and inhibitors of H2O2 generation in liver mitochondriaBiochem. Moscow Suppl. Ser. A14(1)24-33(2020)
| Cas No. | 505-54-4 | SDF | |
| 别名 | 十六碳二酸 | ||
| Canonical SMILES | O=C(O)CCCCCCCCCCCCCCC(O)=O | ||
| 分子式 | C16H30O4 | 分子量 | 286.41 |
| 溶解度 | DMSO: 100 mg/mL (349.15 mM) | 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 | 3.4915 mL | 17.4575 mL | 34.915 mL |
| 5 mM | 0.6983 mL | 3.4915 mL | 6.983 mL |
| 10 mM | 0.3491 mL | 1.7457 mL | 3.4915 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。
Metabolomic Profiling Identified Serum Metabolite Biomarkers and Related Metabolic Pathways of Colorectal Cancer
Background: The screening and early detection of colorectal cancer (CRC) still remain a challenge due to the lack of reliable and effective serum biomarkers. Thus, this study is aimed at identifying serum biomarkers of CRC that could be used to distinguish CRC from healthy controls. Methods: A prospective 1 : 2 individual matching case-control study was performed which included 50 healthy control subjects and 98 CRC patients. Untargeted metabolomic profiling was conducted with liquid chromatography tandem mass spectrometry (LC-MS/MS) to identify CRC-related metabolites and metabolic pathways. Results: In total, 178 metabolites were detected, and an orthogonal partial least-squares-discriminant analysis (OPLS-DA) model was useful to distinguish CRC patients from healthy controls. Nine metabolites showed significantly differential serum levels in CRC patients under the conditions of variable importance in projection (VIP) > 1, p < 0.05 using Student's t-test, and fold change (FC) ≥ 1.2 or ≤0.5. The above nine metabolites were 3-hydroxybutyric acid, hexadecanedioic acid, succinic acid semialdehyde, 4-dodecylbenzenesulfonic acid, prostaglandin B2, 2-pyrocatechuic acid, xanthoxylin, 12-hydroxydodecanoic acid, and formylanthranilic acid. Four potential biomarkers were identified to diagnose CRC through ROC curves: hexadecanedioic acid, 4-dodecylbenzenesulfonic acid, 2-pyrocatechuic acid, and formylanthranilic acid. All AUC values of these four serum biomarkers were above 0.70. In addition, the exploratory analysis of metabolic pathways revealed the activated states for the vitamin B metabolic pathway and the alanine, aspartate, and glutamate metabolic pathways associated with CRC. Conclusion: The 4 identified potential metabolic biomarkers could discriminate CRC patients from healthy controls, and the 2 metabolic pathways may be activated in the CRC tissues.
Subcellular localization of hexadecanedioic acid activation in human liver
The activation of hexadecanedioic acid has been studied in subcellular fractions of human liver. The activation capacity in a total homogenate of human liver was found to be 0.5 micro mole/min/g wet wt of tissue, about 10% of that for palmitic acid. Hexadecanedioic acid was activated by the mitochondrial and microsomal fractions. The mitochondrial enzyme is probably localized outside the inner mitochondrial compartment. The subcellular distribution of the hexadecanedioic acid activation was almost identical with the distribution of palmitic acid activation. Hexadecanedioic and palmitic acids seemed to compete for the same enzyme.
The stimulation of succinate-fueled respiration of rat liver mitochondria in state 4 by α,ω-hexadecanedioic acid without induction of proton conductivity of the inner membrane. Intrinsic uncoupling of the bc1 complex
The paper shows that natural α,ω-dioic acid, α,ω-hexadecanedioic acid (HDA), is able to stimulate the respiration of succinate-fueled rat liver mitochondria in state 4 without induction of proton conductivity of the inner membrane. This effect of HDA is less pronounced in glutamate/malate-fueled mitochondria, as well as in the case of ascorbate/TMPD or ascorbate/ferrocyanide substrate systems, which transfer electrons directly to cytochrome c. It is noted that HDA-induced stimulation of respiration is not associated with damage to the inner membrane in a part of mitochondria and with shunting of electrons through the bc1 complex. Therefore, HDA can be considered as a natural decoupling agent. Specific inhibitors of the bc1 complex (antimycin A and myxothiazole) as well as malonate and dithionitrobenzoate were used in the inhibitory analysis. These and other experiments have shown that during the oxidation of succinate in liver mitochondria, the decoupling effect of HDA is mainly carried out at the level of the bc1 complex. We hypothesized that HDA is capable of promoting the cyclic transport of protons within the bc1 complex and thus switch this complex to the idle mode of operation (intrinsic uncoupling of the bc1 complex). Induction of free respiration in liver mitochondria by HDA at the level of the bc1 complex is considered as one of the "rescue pathways" of hepatocytes in various pathological conditions, accompanied by disorders of carbohydrate and lipid metabolism and increased oxidative stress.
LC-MS/MS bioanalysis of plasma 1, 14-tetradecanedioic acid and 1, 16-hexadecanedioic acid as candidate biomarkers for organic anion-transporting polypeptide mediated drug-drug interactions
Aim: A robust LC-MS/MS assay was developed to quantify endogenous 1, 14-tetradecanedioic acid (TDA) and 1, 16-hexadecanedioic acid (HDA) in human plasma as potential biomarkers for evaluating drug-drug interactions mediated by the hepatic drug transporters, organic anion-transporting polypeptides.
Results: This assay was validated using fit-for-purpose approach over standard curve range of 2.5-1000 nM for TDA and HDA using analyte-free charcoal-stripped human plasma as the surrogate matrix. Chromatographic separation condition was successfully optimized to separate TDA from an interference peak while maintaining both analytes in neutral forms to minimize carryover issue.
Conclusion: The described assay is currently applied to a clinical study for evaluating TDA/HDA as potential substitute biomarkers for drug-drug interaction studies.
Adipose reduction by beta,beta'-tetramethyl-substituted hexadecanedioic acid (MEDICA 16)
Treatment of normal rats kept on a balanced laboratory chow diet with beta,beta'-tetramethyl-substituted hexadecanedioic acid (MEDICA 16) (Bar-Tana et al., 1985, J. Biol. Chem, 260, 8404-8410) resulted in an acute reduction in adiposity, which was already established during the first week of treatment and was sustained as long as the drug was administered. Adipose reduction consisted of 30-80 percent decrease in the perirenal, omental, epididymal, parametrial and subcutaneous fat with a concomitant 50 percent decrease in total body neutral lipid mass. The reduction in adiposity was accounted for by a respective decrease in the lipid content of individual adipocytes together with a transient or sustained decrease in the number of adipocytes of selected adipose tissues. The decrease in the lipid content resulted from (a) an extensive hypotriglyceridemia in MEDICA 16-treated rats; (b) inhibition of adipose lipogenesis by MEDICA 16; (c) increased sensitivity to catecholamines-. ACTH- and forskolin-induced lipolysis in MEDICA 16 adipocytes. Adipose reduction by MEDICA 16 was not compromised by a decrease in overall net caloric intake but was accompanied by a 40 percent increase in resting metabolic rate.