The fatty acid amide hydrolase (FAAH) inhibitor PF-3845 acts in the nervous system to reverse LPS-induced tactile allodynia in mice.
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Rational Design of Fatty Acid Amide Hydrolase Inhibitors That Act by Covalently Bonding to Two Active Site ResiduesThe CB2 receptor and its role as a regulator of inflammationElevating endocannabinoid levels: pharmacological strategies and potential therapeutic applicationsA chemical genetic screen uncovers a small molecule enhancer of the N-acylethanolamine degrading enzyme, fatty acid amide hydrolase, in ArabidopsisFatty-acid-binding protein inhibition produces analgesic effects through peripheral and central mechanisms.α-Ketoheterocycle inhibitors of fatty acid amide hydrolase: exploration of conformational constraints in the acyl side chain.The discovery and development of inhibitors of fatty acid amide hydrolase (FAAH).Selective inhibition of FAAH produces antidiarrheal and antinociceptive effect mediated by endocannabinoids and cannabinoid-like fatty acid amides.Regulation of inflammation by cannabinoids, the endocannabinoids 2-arachidonoyl-glycerol and arachidonoyl-ethanolamide, and their metabolites.Role of FAAH-like anandamide transporter in anandamide inactivation.Inhibition of fatty acid binding proteins elevates brain anandamide levels and produces analgesia.Fatty acid amide hydrolase blockade attenuates the development of collagen-induced arthritis and related thermal hyperalgesia in mice.Simultaneous inhibition of fatty acid amide hydrolase and monoacylglycerol lipase shares discriminative stimulus effects with Δ9-tetrahydrocannabinol in mice.The fatty acid amide hydrolase inhibitor PF-3845 promotes neuronal survival, attenuates inflammation and improves functional recovery in mice with traumatic brain injury.Attenuation of persistent pain-related behavior by fatty acid amide hydrolase (FAAH) inhibitors in a rat model of HIV sensory neuropathy.Efficacy, Tolerability, and Safety of Cannabinoid Treatments in the Rheumatic Diseases: A Systematic Review of Randomized Controlled Trials.α-Ketoheterocycle-based Inhibitors of Fatty Acid Amide Hydrolase (FAAH).Effects of alterations in cannabinoid signaling, alone and in combination with morphine, on pain-elicited and pain-suppressed behavior in mice.Diacylglycerol lipase β inhibition reverses nociceptive behaviour in mouse models of inflammatory and neuropathic pain.Repeated low-dose administration of the monoacylglycerol lipase inhibitor JZL184 retains cannabinoid receptor type 1-mediated antinociceptive and gastroprotective effects.The monoacylglycerol lipase inhibitor JZL184 suppresses inflammatory pain in the mouse carrageenan model.Protective Action of Anandamide and Its COX-2 Metabolite against l-Homocysteine-Induced NLRP3 Inflammasome Activation and Injury in Podocytes.Design, synthesis, and characterization of α-ketoheterocycles that additionally target the cytosolic port Cys269 of fatty acid amide hydrolaseIn vivo characterization of the highly selective monoacylglycerol lipase inhibitor KML29: antinociceptive activity without cannabimimetic side effects.No more pain upon Gq-protein-coupled receptor activation: role of endocannabinoids.Cannabinoids in pain management: CB1, CB2 and non-classic receptor ligands.The Endogenous Cannabinoid System: A Budding Source of Targets for Treating Inflammatory and Neuropathic Pain.The cannabinoid system and pain.Immunofluorescent spectral analysis reveals the intrathecal cannabinoid agonist, AM1241, produces spinal anti-inflammatory cytokine responses in neuropathic rats exhibiting relief from allodynia.Endocannabinoids exert CB1 receptor-mediated neuroprotective effects in models of neuronal damage induced by HIV-1 Tat protein.O-hydroxyacetamide carbamates as a highly potent and selective class of endocannabinoid hydrolase inhibitors.The α7 nicotinic receptor dual allosteric agonist and positive allosteric modulator GAT107 reverses nociception in mouse models of inflammatory and neuropathic pain.The effect of FAAH, MAGL, and Dual FAAH/MAGL inhibition on inflammatory and colorectal distension-induced visceral pain models in Rodents.Liposomal Delivery of Diacylglycerol Lipase-Beta Inhibitors to Macrophages Dramatically Enhances Selectivity and Efficacy in Vivo.The monoacylglycerol lipase inhibitor KML29 with gabapentin synergistically produces analgesia in mice.Investigation of Diacylglycerol Lipase Alpha Inhibition in the Mouse Lipopolysaccharide Inflammatory Pain Model.The Difference a Single Atom Can Make: Synthesis and Design at the Chemistry-Biology Interface.Inhibition of Endocannabinoid-Metabolizing Enzymes in Peripheral Tissues Following Developmental Chlorpyrifos Exposure in Rats.Endocannabinoid System and Migraine Pain: An Update.Evaluation of different drug classes on transient sciatic nerve injury-depressed marble burying in mice.
P2860
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P2860
The fatty acid amide hydrolase (FAAH) inhibitor PF-3845 acts in the nervous system to reverse LPS-induced tactile allodynia in mice.
description
2012 nî lūn-bûn
@nan
2012年の論文
@ja
2012年論文
@yue
2012年論文
@zh-hant
2012年論文
@zh-hk
2012年論文
@zh-mo
2012年論文
@zh-tw
2012年论文
@wuu
2012年论文
@zh
2012年论文
@zh-cn
name
The fatty acid amide hydrolase ...... ced tactile allodynia in mice.
@ast
The fatty acid amide hydrolase ...... ced tactile allodynia in mice.
@en
type
label
The fatty acid amide hydrolase ...... ced tactile allodynia in mice.
@ast
The fatty acid amide hydrolase ...... ced tactile allodynia in mice.
@en
prefLabel
The fatty acid amide hydrolase ...... ced tactile allodynia in mice.
@ast
The fatty acid amide hydrolase ...... ced tactile allodynia in mice.
@en
P2093
P2860
P1476
The fatty acid amide hydrolase ...... ced tactile allodynia in mice.
@en
P2093
Aron H Lichtman
Cyrine Ezzili
Dale L Boger
Jacqueline L Blankman
Jonathan Z Long
Lamont Booker
Rehab A Abdullah
Steven G Kinsey
P2860
P304
P356
10.1111/J.1476-5381.2011.01445.X
P407
P577
2012-04-01T00:00:00Z