2. Membrane Transporter/Ion Channel Neuronal Signaling Metabolic Enzyme/Protease
  3. GlyT Endogenous Metabolite
  4. N-Arachidonylglycine

N-Arachidonylglycine (NA-Gly), a carboxylic analog of the endocannabinoid anandamide (AEA), is a GPR18 agonist (EC50 = 44.5 nM). Unlike AEA, N-Arachidonylglycine has no activity at either CB1 or CB2 receptors. N-Arachidonylglycine inhibits GLYT2 (IC50 = 5.1 μM). N-Arachidonylglycine also is an effective activator of endometrial cell migration.

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N-Arachidonylglycine

N-Arachidonylglycine Chemical Structure

CAS No. : 179113-91-8

Size Prix Stock Quantité
Solvent
5 mg (138.30 mM * 100 μL in Ethanol) En stock
Solvent
10 mg (138.30 mM * 200 μL in Ethanol) En stock
Solvent
25 mg (138.30 mM * 500 μL in Ethanol) En stock
Solvent
50 mg (138.30 mM * 1 mL in Ethanol) En stock
Solvent
100 mg (138.30 mM * 2 mL in Ethanol) En stock

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Based on 1 publication(s) in Google Scholar

Other Forms of N-Arachidonylglycine:

N-Arachidonylglycine Related Antibodies

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1 Publications Citing Use of MCE N-Arachidonylglycine

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Description

N-Arachidonylglycine (NA-Gly), a carboxylic analog of the endocannabinoid anandamide (AEA), is a GPR18 agonist (EC50 = 44.5 nM). Unlike AEA, N-Arachidonylglycine has no activity at either CB1 or CB2 receptors. N-Arachidonylglycine inhibits GLYT2 (IC50 = 5.1 μM). N-Arachidonylglycine also is an effective activator of endometrial cell migration[1][2].

IC50 & Target

GlyT2

5.1 μM (IC50)

Cellular Effect
Cell Line Type Value Description References
CHO IC50
> 10 3
Compound: 8, NAGly
Antagonist activity against human GPR18 expressed in CHO cells assessed as reduction in delta9-THC-induced beta-arrestin recruitment by beta-galactosidase enzyme fragment complementation method
Antagonist activity against human GPR18 expressed in CHO cells assessed as reduction in delta9-THC-induced beta-arrestin recruitment by beta-galactosidase enzyme fragment complementation method
10.1039/C3MD00394A
CHO IC50
> 10 3
Compound: 8, NAGly
Antagonist activity against human GPR55 expressed in CHO cells assessed as reduction in LPI-induced beta-arrestin recruitment by beta-galactosidase enzyme fragment complementation method
Antagonist activity against human GPR55 expressed in CHO cells assessed as reduction in LPI-induced beta-arrestin recruitment by beta-galactosidase enzyme fragment complementation method
10.1039/C3MD00394A
CHO IC50
>10 3
Compound: 8, NAGly
Antagonist activity against human GPR18 expressed in CHO cells assessed as reduction in delta9-THC-induced beta-arrestin recruitment by beta-galactosidase enzyme fragment complementation method
Antagonist activity against human GPR18 expressed in CHO cells assessed as reduction in delta9-THC-induced beta-arrestin recruitment by beta-galactosidase enzyme fragment complementation method
10.1039/C3MD00394A
CHO IC50
> 10 3
Compound: 8, NAGly
Antagonist activity against human GPR18 expressed in CHO cells assessed as reduction in delta9-THC-induced beta-arrestin recruitment by beta-galactosidase enzyme fragment complementation method
Antagonist activity against human GPR18 expressed in CHO cells assessed as reduction in delta9-THC-induced beta-arrestin recruitment by beta-galactosidase enzyme fragment complementation method
10.1039/C3MD00394A
CHO IC50
> 10 3
Compound: 8, NAGly
Antagonist activity against human GPR55 expressed in CHO cells assessed as reduction in LPI-induced beta-arrestin recruitment by beta-galactosidase enzyme fragment complementation method
Antagonist activity against human GPR55 expressed in CHO cells assessed as reduction in LPI-induced beta-arrestin recruitment by beta-galactosidase enzyme fragment complementation method
10.1039/C3MD00394A
In Vitro

N-Arachidonylglycine (0.1 nM-100 μM; 5 min) drives MAPK activation in GPR18-transfected HEK293 cells[1].
N-Arachidonylglycine shows no activity at GLYT1 or GAT1 at concentrations up to 100 μm[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

N-Arachidonylglycine Related Antibodies

Western Blot Analysis[1]

Cell Line: HEK293-GPR18 cells
Concentration: 0.1 nM-100 µM
Incubation Time: 5 min
Result: Drove MAPK activation.
In Vivo

N-Arachidonylglycine (10 mg/kg; oral) increases blood concentrations of anandamide 9-fold[3].
N-Arachidonylglycine (1.2 mg/kg; oral; once) results in a significant 70% reduction of peritoneal cells[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Rats[3]
Dosage: 10 mg/kg
Administration: Oral
Result: Inhibition of FAAH, causing a reduction in the hydrolytic cleavage of anandamid.
Animal Model: Mouse (peritonitis model)[3]
Dosage: 1.2 mg/kg
Administration: Oral; once
Result: Resulted in a significant 70% reduction of peritoneal cells.
Masse moléculaire

361.52

Formule

C22H35NO3
CAS No.
Appearance

Liquid

Color

Colorless to light yellow

SMILES

O=C(O)CNC(CCC/C=C\C/C=C\C/C=C\C/C=C\CCCCC)=O
Structure Classification
Initial Source
Livraison

Room temperature in continental US; may vary elsewhere.
Stockage

Solution, -20°C, 2 years
Pureté et documentation
Références
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N-Arachidonylglycine Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

N-Arachidonylglycine179113-91-8NA-GlyGlyTEndogenous MetaboliteGlycine transportersendocannabinoidanandamideAEAGLYT2endometrialInhibitorinhibitorinhibit

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