Palmidrol

Research use only, not for human use.

Palmitoylethanolamide(PEA) , an endogenous fatty acid amide, activates PPAR-α selectively in vitro (EC50=3.1±0.4 μM).

Palmitoylethanolamide(PEA) , an endogenous fatty acid amide, activates PPAR-α selectively in vitro (EC50=3.1±0.4 μM).

Palmitoylethanolamide (Palmidrol) itself does not stimulate interferon production in mice treated per os or intravenously. But repeated application of this drug per os induces a macrophage activation, reflected by enhanced interferon production in vitro. When the interferon stimulation is delayed until 4 to 10 days after the first dose of Palmitoylethanolamide, interferon response to ds-RNA is slightly increased. After this phase of enhanced activity a decreased production of interferon is observed. Palmitoylethanolamide is not significantly effective in protecting mice from lethal dose of EMC virus. Application of this drug has an inhibitory effect on the toxicity of ds-RNA. A possible explanation of the mechanism by which Palmitoylethanolamide decreased the toxicity of virus in the organism is discussed.

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AM 3112 | Loramine P 256 | Mackpeart DR 14V

GPCR/G Protein

Histamine Receptor

PPARα

Others-Field

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544-31-0

299.49

C18H37NO2

>98% (HPLC)

In Vitro:?DMSO : 2.6 mg/mL (8.68 mM)

CCCCCCCCCCCCCCCC(=O)NCCO

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(-20℃)

With Ice Pack

≥ 2 years