Hexadecanamide
(Synonyms: 十六碳酰胺) 目录号 : GC43821
A primary fatty acid amide
Cas No.:629-54-9
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
Hexadecanamide is a primary fatty acid amide that is derived from palmitic acid (C16:0) and belongs to a class of important cell signaling lipids. While the physiological significance of this compound is not yet clear, it is reported to demonstrate weak anticonvulsant activity in a maximal electroshock seizure test in mice when compared with the endocannabinoid palmitoyl ethanolamide .
| Cas No. | 629-54-9 | SDF | |
| 别名 | 十六碳酰胺 | ||
| Canonical SMILES | NC(CCCCCCCCCCCCCCC)=O | ||
| 分子式 | C16H33NO | 分子量 | 255.4 |
| 溶解度 | DMF: 14 mg/ml,DMSO: 20 mg/ml,Ethanol: 22 mg/ml,PBS (pH 7.2): 50 µ g/ml | 储存条件 | Store at RT |
| 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 | 3.9154 mL | 19.5771 mL | 39.1543 mL |
| 5 mM | 0.7831 mL | 3.9154 mL | 7.8309 mL |
| 10 mM | 0.3915 mL | 1.9577 mL | 3.9154 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。
N-(4-Methoxy-2-nitrophenyl)Hexadecanamide, a palmitoylethanolamide analogue, reduces formalin-induced nociception
Life Sci 2012 Dec 17;91(25-26):1288-94.PMID:23069585DOI:10.1016/j.lfs.2012.09.024.
Aims: To investigate the local antinociceptive effect as well as the possible mechanisms of action of a novel analogue of palmitoylethanolamide (PEA) N-(4-methoxy-2-nitrophenyl)Hexadecanamide (HD) in the rat formalin test. Main methods: The formalin test was used to assess the antinociceptive activity of HD in vivo. The hydrolysis of anandamide catalyzed by fatty acid amide hydrolase (FAAH) was used to determine the action of HD on FAAH activity in vitro. Key findings: Local peripheral ipisilateral, but not contralateral, administration of HD (10-100μg/paw) produced a dose-dependent antinociceptive effect in rats. The CB(1) and CB(2) receptor antagonists AM281 (0.3-30μg/paw) and SR144528 (0.3-30μg/paw), respectively, reduced the antinociceptive effect of HD (100μg/paw). In addition, methiothepin (0.03-0.3μg/paw) and naloxone (5-50μg/paw) significantly reduced HD-induced antinociception (100μg/paw). In vitro, HD reduced only to a minor extent the hydrolysis of anandamide catalyzed by FAAH. Significance: HD local administration produces antinociception that probably results from an indirect activation of peripheral CB(1) and CB(2) cannabinoid receptors. Data suggest that 5-HT(1) and opioid receptors also participate in the antinociceptive effect of this compound. HD may have potential as analgesic drug.
N-(2-hydroxyethyl)Hexadecanamide is orally active in reducing edema formation and inflammatory hyperalgesia by down-modulating mast cell activation
Eur J Pharmacol 1996 Apr 11;300(3):227-36.PMID:8739213DOI:10.1016/0014-2999(96)00015-5.
Mast cells play a key role in inflammatory reactions triggered by tissue injury or immune perturbations. Little is known about endogenous molecules and mechanisms capable of modulating inappropriate mast cell activity. N-(2-Hydroxyethyl)Hexadecanamide (palmitoylethanolamide), found in peripheral tissues, has been proposed to act as a local autacoid capable of negatively regulating mast cell activation and inflammation-hence the acronym Autacoid Local Inflammation Antagonism (ALIA). Recently, N-(2-hydroxyethyl)Hexadecanamide (LG 2110/1) has been reported to down-modulate mast cell activation in vitro by behaving as an agonist at the peripheral cannabinoid CB2 receptor. Here, we have characterized and functionally correlated the anti-inflammatory actions of LG 2110/1 with its ability to control mast cell activation, when given orally in a battery of rodent models of inflammation. LG 2110/1 diminished, in a dose-dependent and correllated manner, the number of degranulated mast cells and plasma extravasation induced by substance P injection in the mouse ear pinna. In addition, LG 2110/1 reduced dose dependently plasma extravasation induced by passive cutaneous anaphylaxis reaction. In adult rats LG 2110/1 decreased, in a dose-dependent manner, carrageenan-induced hindpaw edema and hyperalgesia, but not phospholipase A2-induced hindpaw edema. Further, anti-edema effects were observed when utilizing dextran and formalin, known to also cause mast cell activation. Locally administered LG 2110/1 was likewise effective in minimizing dextran-induced hind paw edema. In contrast, equivalent amounts of palmitic acid plus ethanolamine were ineffective against plasma extravasation provoked by substance P. LG 2110/1 did not decrease plasma extravasation induced by the substance P fragment, substance P-(6-11), known to be inactive on mast cells. These results indicate that orally administered N-(2-hydroxyethyl)Hexadecanamide is effective in: (a) directly down-modulating mast cell activation in vivo; (b) suppressing pathological consequences initiated by mast cell activation independently of the activating stimuli; (c) exerting an anti-inflammatory action distinguishable from that of classical steroidal and non-steroidal anti-inflammatory agents. These findings raise the possibility that N-(2-hydroxyethyl)Hexadecanamide and related saturated N-acylamides ('ALIAmides') represent novel therapeutic agents useful in the management of inflammatory disease conditions.
Isolation and characterization of N-(2-Hydroxyethyl)Hexadecanamide from Colletotrichum gloeosporioides with apoptosis-inducing potential in breast cancer cells
Biofactors 2023 Feb 6.PMID:36744732DOI:10.1002/biof.1940.
Endophytic fungi are a well-established reservoir of bioactive compounds that are pharmaceutically valuable and therefore, contribute significantly to the biomedical field. The present study aims to identify the bioactive anticancer compound from ethyl acetate extract of fungal endophyte, Colletotrichum gloeosporioides associated with the leaf of the medicinal plant Oroxylum indicum. The fatty acid amide compound N-(2-Hydroxyethyl)Hexadecanamide (Palmitoylethanolamide; PEA) was identified using antioxidant activity-guided fractionation assisted with tandem liquid chromatography coupled with quadrupole time of flight mass spectrometry, Fourier transform-infrared spectroscopy, time-of-flight mass spectrometry, and nuclear magnetic resonance. In-Silico molecular docking analysis showed that PEA potentially docked to the active sites of apoptosis-inducing proteins including BAX, BCL-2, P21, and P53. Further validation was done using in vitro study that showed PEA inhibitsthe proliferation, alters nuclear morphology and attenuates the wound closure ability of MDA-MB-231 and MCF-7 cells. PEA induces apoptosis via upregulating cell-cycle arrest (P21), tumor suppression (P53), pro-apoptotic (BAX, CASPASE-8, and FADD) genes, and downregulating anti-apoptotic gene BCL-2. The upregulation of the active form of Caspase-3 was also reported. This is the first-ever report for the isolation of PEA from C. gloeosporioides with anticancer activity against human breast cancer cells and therefore holds great potential for future therapeutics.
A review on garcinia kola heckel: traditional uses, phytochemistry, pharmacological activities, and toxicology
Biomarkers 2022 Mar;27(2):101-117.PMID:34904497DOI:10.1080/1354750X.2021.2016974.
Purpose: Garcinia kola is a medicinal plant commonly known as bitter kola. It is utilised in ethnomedicine for the treatment of diarrhoea, bronchitis, bacterial infection, cough, hepatitis, gonorrhoea, laryngitis, food poison, liver and gastric diseases. Objective: This study reviewed the phytochemistry, pharmacological activities, and ethnomedicinal potentials of G. kola. Materials and methods: An extensive review was performed using electronic literature collated from ScienceDirect, Springer, Wiley, and PubMed databases. Results: Phytochemical analysis revealed the isolation of several chemical compounds including 9-octadecenoic acid, linoleic acid, 14-methylpentadecanoic acid, 1-butanol, Hexadecanamide, I-4',II-4',I-5,II-5,I-7,II-7-hexahydroxy-I-3,II-8-biflavanone, lanost-7-en-3-one, kolaflavanone (8E)-4-geranyl-3,5-dihydroxybenzophenone, glutinol, Garcinia biflavonoid (GB-2a-II-4'-OMe), 9,19-cyclolanost-24-en-3-ol, 24-methylene, tirucallol, lupeol, β-amyrin, obtusifoliol and Kolaviron. Diverse pharmacological in-vivo and in vitro investigations revealed that G. kola has anti-inflammatory, antimalarial, hepatoprotective, cardioprotective, anti-asthmatic, neuroprotective, antioxidant, and antidiabetic activities. Conclusion: The present study revealed that G. kola has preventive and therapeutic potentials against various diseases in both in vivo and in vitro studies and therefore can be utilised as a raw material in the pharmaceutical industries for the development of therapeutic products. However, there is a need for clinical trial experiments to validate and provide accurate and substantial information on the required safe dosage and efficacy for the treatment of several diseases.
Identification and characterization of PPARα ligands in the hippocampus
Nat Chem Biol 2016 Dec;12(12):1075-1083.PMID:27748752DOI:10.1038/nchembio.2204.
Peroxisome proliferator-activated receptor-α (PPARα) regulates hepatic fatty acid catabolism and mediates the metabolic response to starvation. Recently we found that PPARα is constitutively activated in nuclei of hippocampal neurons and controls plasticity via direct transcriptional activation of CREB. Here we report the discovery of three endogenous PPARα ligands-3-hydroxy-(2,2)-dimethyl butyrate, Hexadecanamide, and 9-octadecenamide-in mouse brain hippocampus. Mass spectrometric detection of these compounds in mouse hippocampal nuclear extracts, in silico interaction studies, time-resolved FRET analyses, and thermal shift assay results clearly indicated that these three compounds served as ligands of PPARα. Site-directed mutagenesis studies further revealed that PPARα Y464 and Y314 are involved in binding these hippocampal ligands. Moreover, these ligands activated PPARα and upregulated the synaptic function of hippocampal neurons. These results highlight the discovery of hippocampal ligands of PPARα capable of modulating synaptic functions.