Anandamide
(Synonyms: 花生四烯酸乙醇胺) 目录号 : GC35339
An endogenous cannabinoid
Cas No.:94421-68-8
Sample solution is provided at 25 µL, 10mM.
Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
|
Animal experiment: |
Mice[2]Eleven-week-old C57BL/6J male mice and global CB1R-/- mice are housed individually on a 12/12-h light/dark schedule at 22-23°C with ad libitum access to water and food. A group of mice is subject to a high-fat diet (30% lard). After 16 weeks of diet, animals with a weight gain less than +10 g compared with controls are excluded from the study. Diet-induced obesity (DIO) mice (39.1±1.1 vs. 27.3±0.9 g, DIO vs. control) are glucose intolerant and insulin resistant. On the day of each experiment, food is removed from the cages for 6 h (from 8:00 A.M. to 2:00 P.M.). Anandamide is administered intraperitoneally at 10 mg/kg. In control experiments, animals are injected with vehicle (4% DMSO/1% Tween 80)[2]. |
|
References: [1]. Malek N, et al. Anandamide, Acting via CB2 Receptors, Alleviates LPS-Induced Neuroinflammation in Rat Primary Microglial Cultures. Neural Plast. 2015;2015:130639. |
|
Arachidonoyl ethanolamide (AEA) is the ethanolamine amide of arachidonic acid, originally isolated from porcine brain.1 AEA is an endogenous cannabinoid neurotransmitter that binds to both cannabinoid 1 (CB1) and CB2 receptors.2 AEA has Ki values ranging from 61 to 543 nM for CB1 receptors and from 279 to 1,940 nM for CB2 receptors.3
1.Devane, W.A., Hanus, L., Breuer, A., et al.Isolation and structure of a brain constituent that binds to the cannabinoid receptorScience258(5090)1946-1949(1992) 2.Felder, C.C., Briley, E.M., Axelrod, J., et al.Anandamide, an endogenous cannabimimetic eicosanoid, binds to the cloned human cannabinoid receptor and stimulates receptor-mediated signal transductionProc. Natl. Acad. Sci. USA90(16)7656-7660(1993) 3.Pertwee, R.G.Pharmacology of cannabinoid receptor ligandsCurr. Med. Chem.6(8)635-664(1999)
| Cas No. | 94421-68-8 | SDF | |
| 别名 | 花生四烯酸乙醇胺 | ||
| 化学名 | N-(2-hydroxyethyl)-5Z,8Z,11Z,14Z-eicosatetraenamide | ||
| Canonical SMILES | CCCCC/C=C\C/C=C\C/C=C\C/C=C\CCCC(NCCO)=O | ||
| 分子式 | C22H37NO2 | 分子量 | 347.53 |
| 溶解度 | 30mg/mL in DMSO, or 10mg/mL in DMF | 储存条件 | Store at -20°C,stored under nitrogen |
| 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。 |
||
| 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 | 2.8774 mL | 14.3872 mL | 28.7745 mL |
| 5 mM | 0.5755 mL | 2.8774 mL | 5.7549 mL |
| 10 mM | 0.2877 mL | 1.4387 mL | 2.8774 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。
Cannabidiol enhances Anandamide signaling and alleviates psychotic symptoms of schizophrenia
Transl Psychiatry 2012 Mar 20;2(3):e94.PMID:22832859DOI:10.1038/tp.2012.15.
Cannabidiol is a component of marijuana that does not activate cannabinoid receptors, but moderately inhibits the degradation of the endocannabinoid Anandamide. We previously reported that an elevation of Anandamide levels in cerebrospinal fluid inversely correlated to psychotic symptoms. Furthermore, enhanced Anandamide signaling let to a lower transition rate from initial prodromal states into frank psychosis as well as postponed transition. In our translational approach, we performed a double-blind, randomized clinical trial of cannabidiol vs amisulpride, a potent antipsychotic, in acute schizophrenia to evaluate the clinical relevance of our initial findings. Either treatment was safe and led to significant clinical improvement, but cannabidiol displayed a markedly superior side-effect profile. Moreover, cannabidiol treatment was accompanied by a significant increase in serum Anandamide levels, which was significantly associated with clinical improvement. The results suggest that inhibition of Anandamide deactivation may contribute to the antipsychotic effects of cannabidiol potentially representing a completely new mechanism in the treatment of schizophrenia.
Anandamide transport
Pharmacol Ther 2004 Nov;104(2):117-35.PMID:15518883DOI:10.1016/j.pharmthera.2004.07.008.
N-Arachidonylethanolamine (Anandamide) is an endogenous agonist of the cannabinoid CB1 and CB2 receptors and displays many of the same receptor-mediated physiological effects as delta9-tetrahydrocannabinol (delta9-THC), the active component of marijuana. As with any neurotransmitter, there must be tight control of Anandamide receptor-mediated signaling and a means of rapid removal of the molecule from the system. Thus, the process by which Anandamide is transported into the cell for metabolism has been a topic of much interest and has been implicated as a potential drug target in the treatment of several disease states that are reported to have an association with the endocannabinoid system. In this review, we will discuss the current models proposed for the mechanism of Anandamide transport, the progress that has been made in the development of compounds that specifically inhibit Anandamide transport, the observed effects of Anandamide transport inhibition in vivo, and finally, potential therapeutic applications of compounds that inhibit Anandamide transport.
Anandamide uptake explained?
Trends Pharmacol Sci 2012 Apr;33(4):181-5.PMID:22297258DOI:10.1016/j.tips.2012.01.001.
The endocannabinoids Anandamide (AEA) and 2-arachidonoylglycerol are removed from the extracellular space by a process of cellular uptake followed by metabolism. Although the enzymes responsible for endocannabinoid metabolism have been well characterised, the processes involved in uptake have been the subject of much controversy. Recent studies, however, have identified intracellular transport proteins (fatty acid binding proteins 5 and 7, heat shock protein 70, albumin, and fatty acid amide hydrolase-like AEA transporter protein) that shuttle AEA from the plasma membrane to its metabolic enzymes. Proteins such as the fatty acid amide hydrolase-like Anandamide transporter protein may be useful targets for novel therapeutic strategies aimed at potentiating AEA signalling. In this article I review the current state of the art of endocannabinoid uptake.
Brain activity of Anandamide: a rewarding bliss?
Acta Pharmacol Sin 2019 Mar;40(3):309-323.PMID:30050084DOI:10.1038/s41401-018-0075-x.
Anandamide is a lipid mediator that acts as an endogenous ligand of CB1 receptors. These receptors are also the primary molecular target responsible for the pharmacological effects of Δ9-tetrahydrocannabinol, the psychoactive ingredient in Cannabis sativa. Several studies demonstrate that Anandamide exerts an overall modulatory effect on the brain reward circuitry. Several reports suggest its involvement in the addiction-producing actions of other abused drugs, and it can also act as a behavioral reinforcer in animal models of drug abuse. Importantly, all these effects of Anandamide appear to be potentiated by pharmacological inhibition of its metabolic degradation. Enhanced brain levels of Anandamide after treatment with inhibitors of fatty acid amide hydrolase, the main enzyme responsible for its degradation, seem to affect the rewarding and reinforcing actions of many drugs of abuse. In this review, we will provide an overview from a preclinical perspective of the current state of knowledge regarding the behavioral pharmacology of Anandamide, with a particular emphasis on its motivational/reinforcing properties. We will also discuss how modulation of Anandamide levels through inhibition of enzymatic metabolic pathways could provide a basis for developing new pharmaco-therapeutic tools for the treatment of substance use disorders.
Anandamide receptor signal transduction
Vitam Horm 2009;81:79-110.PMID:19647109DOI:10.1016/S0083-6729(09)81004-2.
In the 15 years since its discovery Anandamide has been implicated in many physiological processes. The signaling pathways mediating many of these processes are now coming to light, particularly in the CNS. The complexity of the cannabinoid system and the identification of many potential other receptors for Anandamide have made conclusive evidence of molecular pathways stimulated by this molecule significantly more difficult to achieve. It is becoming obvious that Anandamide receptor signal transduction is not a simple process and that many different cascades can be activated depending on a range of both experimental and physiological variables. This chapter explores the signaling pathways activated by Anandamide both through the cannabinoid receptors and through other cellular targets.