Physicochemical Properties
| Molecular Formula | C22H37NO2 |
| Molecular Weight | 347.53468 |
| Exact Mass | 347.282 |
| Elemental Analysis | C, 73.09; H, 9.76; N, 3.87; O, 13.28 |
| CAS # | 94421-68-8 |
| PubChem CID | 5281969 |
| Appearance | Colorless to light yellow liquid |
| Density | 0.9±0.1 g/cm3 |
| Boiling Point | 522.3±50.0 °C at 760 mmHg |
| Flash Point | 269.7±30.1 °C |
| Vapour Pressure | 0.0±3.1 mmHg at 25°C |
| Index of Refraction | 1.504 |
| LogP | 5.66 |
| Hydrogen Bond Donor Count | 2 |
| Hydrogen Bond Acceptor Count | 2 |
| Rotatable Bond Count | 16 |
| Heavy Atom Count | 25 |
| Complexity | 408 |
| Defined Atom Stereocenter Count | 0 |
| SMILES | C(CC(=O)NCCO)C/C=C\C/C=C\C/C=C\C/C=C\CCCCC |
| InChi Key | LGEQQWMQCRIYKG-DOFZRALJSA-N |
| InChi Code | InChI=1S/C22H37NO2/c1-2-3-4-5-6-7-8-9-10-11-12-13-14-15-16-17-18-19-22(25)23-20-21-24/h6-7,9-10,12-13,15-16,24H,2-5,8,11,14,17-21H2,1H3,(H,23,25)/b7-6-,10-9-,13-12-,16-15- |
| Chemical Name | (5Z,8Z,11Z,14Z)-N-(2-hydroxyethyl)icosa-5,8,11,14-tetraenamide |
| Synonyms | Arachidonylethanolamide; Anandamide; AEA; Arachidonylethanolamide; 94421-68-8; Arachidonoyl ethanolamide; N-Arachidonoylethanolamine; N-arachidonoyl ethanolamine; arachidonoylethanolamide; AEA; Arachidonoyl ethanolamide |
| HS Tariff Code | 2934.99.9001 |
| Storage |
Powder-20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture. |
| Shipping Condition | Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs) |
Biological Activity
| Targets | CB1; CB2; PPAR; TRPV1; Microbial Metabolite; Human Endogenous Metabolite |
| ln Vitro |
Anandamide (0-250 μg/ml, 1 h) inhibits the growth of Candida albicans hyphae and stops them from adhering to epithelial cells[4]. Anandamide (0-250 μg/ml, 2 h) modifies the expression of genes related to hyphal morphogenesis and adhesion[4]. Anandamide inhibits the activity of protein kinases, which lowers tau phosphorylation[3]. |
| ln Vivo |
Anandamide (10 mg/kg, IP, once) improves glucose tolerance by significantly reducing the rise in glycemia in response to glucose ingestion when compared to control[2]. Anandamide (100 ng, ICV bilateral injection, single) partially mitigates the cognitive deficits, alterations in synaptic markers, and ventricle enlargement caused by streptozotocin (STZ)[3]. Anandamide reduces the development of inflammation by acting as an anti-inflammatory in a mouse model of ulcerative colitis[4]. Anandamide reduces lipopolysaccharide (LPS)-induced neuroinflammation in rat primary microglial cultures[1]. |
| Enzyme Assay | Microglial activation is a polarized process divided into potentially neuroprotective phenotype M2 and neurotoxic phenotype M1, predominant during chronic neuroinflammation. Endocannabinoid system provides an attractive target to control the balance between microglial phenotypes. Anandamide as an immune modulator in the central nervous system acts via not only cannabinoid receptors (CB1 and CB2) but also other targets (e.g., GPR18/GPR55). We studied the effect of anandamide on lipopolysaccharide-induced changes in rat primary microglial cultures. Microglial activation was assessed based on nitric oxide (NO) production. Analysis of mRNA was conducted for M1 and M2 phenotype markers possibly affected by the treatment. Our results showed that lipopolysaccharide-induced NO release in microglia was significantly attenuated, with concomitant downregulation of M1 phenotypic markers, after pretreatment with anandamide. This effect was not sensitive to CB1 or GPR18/GPR55 antagonism. Administration of CB2 antagonist partially abolished the effects of anandamide on microglia. Interestingly, administration of a GPR18/GPR55 antagonist by itself suppressed NO release. In summary, we showed that the endocannabinoid system plays a crucial role in the management of neuroinflammation by dampening the activation of an M1 phenotype. This effect was primarily controlled by the CB2 receptor, although functional cross talk with GPR18/GPR55 may occur[1]. |
| Cell Assay |
Cell Line: HeLa cervical epithelial cells Concentration: 0, 10, 50, 125, 250 μg/ml Incubation Time: 2 h Result: Repressed the expression of the HWP1 and ALS3 adhesins involved in Candida adhesion to epithelial cells and the HGC1, RAS1, EFG1 and ZAP1 regulators of hyphal morphogenesis and cell adherence. Increased the expression of NRG1, a transcriptional repressor of filamentous growth. |
| Animal Protocol |
Male Wistar rats (3-4 months, 350-400 g, STZ-induced AD-like sporadic dementia model) 100 ng ICV bilateral injection, single Anandamide was prepared in 4% DMSO/1% Tween 80 and administered intraperitoneally at 10 mg/kg. In control experiments, animals were injected with vehicle (4% DMSO/1% Tween 80).[2] Glucose, Xylose, and Insulin Tolerance Tests For glucose tolerance test (GTT) and insulin tolerance test, mice respectively received a glucose load (2 g/kg) or insulin intraperitoneal injection (0.5 UI/kg). For GTT, a d-glucose solution (20% weight for volume) was either injected intraperitoneally (intraperitoneal GTT) or given orally (oral GTT [OGTT]). Oral d-xylose loading test (OXT) consisted in the administration of a d-xylose solution (10% weight for volume; 1 g/kg body weight). Drugs were administered intraperitoneally to 6-h fasting mice 10 min before glucose, xylose, or insulin. Each treatment was tested with a 1-week interval on the same series of mice in the same conditions. Glycemia was measured directly in blood sampled from the tail with a My Life Pura glucose meter. In some OGTT experiments, blood (25 µL) from tail vein was collected in chilled tubes containing EGTA and DPPIV inhibitor for determination of insulin, glucose-dependent insulinotropic peptide (GIP), and GLP-1 concentration with a Bio-Plex Mouse Diabetes Assay. In OXT, some control experiments included oral administration of phlorizin as a sodium-dependent glucose transporter 1 (SGLT-1) inhibitor, 15 min before the first injection. Plasma xylose concentrations were measured with a spectrophotometric kit [2]. |
| References |
[1]. Anandamide, Acting via CB2 Receptors, Alleviates LPS-Induced Neuroinflammation in Rat Primary Microglial Cultures. Neural Plast. 2015;2015:130639. [2]. Acute activation of cannabinoid receptors by Anandamide reduces gastrointestinal motility and improves postprandial glycemia in mice. Diabetes. 2015 Mar;64(3):808-18. [3]. Anandamide Effects in a Streptozotocin-Induced Alzheimer's Disease-Like Sporadic Dementia in Rats. Front Neurosci. 2018 Sep 21;12:653. [4]. Anandamide prevents the adhesion of filamentous Candida albicans to cervical epithelial cells. Sci Rep. 2020 Aug 13;10(1):13728. [5]. The endocannabinoid anandamide has an anti-inflammatory effect on CCL2 expression in vascular smooth muscle cells. Basic Res Cardiol. 2020 Apr 22;115(3):34. |
| Additional Infomation |
Anandamide is an N-acylethanolamine 20:4 resulting from the formal condensation of carboxy group of arachidonic acid with the amino group of ethanolamine. It has a role as a neurotransmitter, a vasodilator agent and a human blood serum metabolite. It is an endocannabinoid and a N-acylethanolamine 20:4. It is functionally related to an arachidonic acid. Anandamide has been reported in Homo sapiens and Caenorhabditis elegans with data available. |
Solubility Data
| Solubility (In Vitro) | DMSO: ≥ 100 mg/mL (~287.7 mM) |
| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.08 mg/mL (5.99 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 2.08 mg/mL (5.99 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. Solubility in Formulation 3: ≥ 2.08 mg/mL (5.99 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly. (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 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 |