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| 5mg |
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| 10mg |
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| 25mg |
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| 100mg |
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| 250mg |
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Purity: ≥98%
| Targets |
CB1; CB2; PPAR; TRPV1; Microbial Metabolite; Human Endogenous Metabolite
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| 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].
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| 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 |
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| 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. |
| Molecular Formula |
C22H37NO2
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|---|---|
| Molecular Weight |
347.53468
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| Exact Mass |
347.282
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| Elemental Analysis |
C, 73.09; H, 9.76; N, 3.87; O, 13.28
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| CAS # |
94421-68-8
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| PubChem CID |
5281969
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| Appearance |
Colorless to light yellow liquid
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| Density |
0.9±0.1 g/cm3
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| Boiling Point |
522.3±50.0 °C at 760 mmHg
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| Flash Point |
269.7±30.1 °C
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| Vapour Pressure |
0.0±3.1 mmHg at 25°C
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| Index of Refraction |
1.504
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| LogP |
5.66
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| Hydrogen Bond Donor Count |
2
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| Hydrogen Bond Acceptor Count |
2
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| Rotatable Bond Count |
16
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| Heavy Atom Count |
25
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| Complexity |
408
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| Defined Atom Stereocenter Count |
0
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| SMILES |
C(CC(=O)NCCO)C/C=C\C/C=C\C/C=C\C/C=C\CCCCC
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| InChi Key |
LGEQQWMQCRIYKG-DOFZRALJSA-N
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| 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-
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| Chemical Name |
(5Z,8Z,11Z,14Z)-N-(2-hydroxyethyl)icosa-5,8,11,14-tetraenamide
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| Synonyms |
Arachidonylethanolamide; Anandamide; AEA; Arachidonylethanolamide; 94421-68-8; Arachidonoyl ethanolamide; N-Arachidonoylethanolamine; N-arachidonoyl ethanolamine; arachidonoylethanolamide; AEA; Arachidonoyl ethanolamide
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| HS Tariff Code |
2934.99.9001
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| 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)
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| Solubility (In Vitro) |
DMSO: ≥ 100 mg/mL (~287.7 mM)
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| 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. View More
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. |
| 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 |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
| NCT Number | Recruitment | interventions | Conditions | Sponsor/Collaborators | Start Date | Phases |
| NCT02727023 | Completed | Other: Osteopathic Manipulative Medicine |
Anandamide Endocannabinoids |
New York Institute of Technology | December 2015 | Not Applicable |
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