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MedChemExpress - Model Arachidonoyl ethanolamide phosphate - 183323-26-4

Arachidonoyl ethanolamide phosphate, an endocannabinoid, is an endogenous ligand for cannabinoid receptors in the central nervous system (CB1 subtype) and peripheral immune cells (CB2 subtype)[1][2].

Arachidonoyl ethanolamide phosphate

MCE China：Arachidonoyl ethanolamide phosphate

Brand：MedChemExpress (MCE)

Cat. No.HY-134173

CAS：183323-26-4

Storage：Please store the product under the recommended conditions in the Certificate of Analysis.

Shipping：Room temperature in continental US; may vary elsewhere.

Description：Arachidonoyl ethanolamide phosphate, an endocannabinoid, is an endogenous ligand for cannabinoid receptors in the central nervous system (CB1 subtype) and peripheral immune cells (CB2 subtype).

In Vitro：Arachidonoyl ethanolamide phosphate (AEA; 1 μM) is shown to induce apoptotic bodies formation and DNA fragmentation, hallmarks of programmed cell death, in human neuroblastoma CHP100 and lymphoma U937 cells[1]. An anti-proliferative action of Arachidonoyl ethanolamide phosphate in human breast carcinoma cells, due to a CB1-like receptor-mediated inhibition of the action of endogenous prolactin at its receptor. Arachidonoyl ethanolamide phosphate has an activation of cell proliferation in hematopoietic cell lines. Arachidonoyl ethanolamide phosphate is a neuromodulator that mediate a retrograde signaling pathway to modulate neurotransmitter release at the presynaptic terminal[1]. Arachidonoyl ethanolamide phosphate (0.1-10 μM; for 5 days) time- and concentration-dependently inhibits rat C6 glioma cell proliferation[2].

References：

[1]. M Maccarrone, et al. Anandamide induces apoptosis in human cells via vanilloid receptors. Evidence for a protective role of cannabinoid receptors. J Biol Chem. 2000 Oct 13;275(41):31938-45. [Content Brief]

[2]. S O Jacobsson, et al. Inhibition of rat C6 glioma cell proliferation by endogenous and synthetic cannabinoids. Relative involvement of cannabinoid and vanilloid receptors. J Pharmacol Exp Ther. 2001 Dec;299(3):951-9. [Content Brief]

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