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Literature summary for 3.5.1.99 extracted from

  • Naidu, P.S.; Kinsey, S.G.; Guo, T.L.; Cravatt, B.F.; Lichtman, A.H.
    Regulation of inflammatory pain by inhibition of fatty acid amide hydrolase (2010), J. Pharmacol. Exp. Ther., 334, 182-190.
    View publication on PubMedView publication on EuropePMC
Search for more literature for 3.5.1.99

Application

Application Comment Organism
drug development FAAH is an attractive target for treating pain Mus musculus

Inhibitors

Inhibitors Comment Organism Structure
cyclohexylcarbamic acid 3'-carbamoylbiphenyl-3-yl ester i.e. URB597, attenuates the development of lipopolysaccharide-induced paw edema and reverses lipopolysaccharide-induced hyperalgesia through the respective CB2 and CB1 mechanisms of action. The inhibition is not affected by capsazepine, a transient receptor potential vanilloid type 1 antagonist Mus musculus

Natural Substrates/ Products (Substrates)

Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
anandamide + H2O Mus musculus i.e. N-arachidonoylethanolamine arachidonic acid + ethanolamine
-
 ?

Organism

Organism UniProt Comment Textmining
Mus musculus
-
 male C57BL/6J mice
-

Source Tissue

Source Tissue Comment Organism Textmining
neuron
-
 Mus musculus
-

Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
anandamide + H2O i.e. N-arachidonoylethanolamine Mus musculus arachidonic acid + ethanolamine
-
 ?

Synonyms

Synonyms Comment Organism
FAAH
-
 Mus musculus

General Information

General Information Comment Organism
physiological function FAAH is the chief catabolic enzyme regulating the endogenous cannabinoid N-arachidonoylethanolamine, i.e. anandamide Mus musculus