추천 제품
Quality Level
분석
≥98% (HPLC)
양식
powder
색상
white
solubility
DMSO: soluble ~14 mg/mL
저장 온도
2-8°C
SMILES string
NC(=O)c1cccc(c1)-c2cccc(OC(=O)NC3CCCCC3)c2
InChI
1S/C20H22N2O3/c21-19(23)16-8-4-6-14(12-16)15-7-5-11-18(13-15)25-20(24)22-17-9-2-1-3-10-17/h4-8,11-13,17H,1-3,9-10H2,(H2,21,23)(H,22,24)
InChI key
ROFVXGGUISEHAM-UHFFFAOYSA-N
일반 설명
URB597 binds to active sites of fatty acid amide hydrolases and inhibits their activity. URB597 alters expression of tyrosine hydroxylase and interacts with abnormal-cannabidiol (Abn-CBD) and peroxisome proliferator-activated receptors (PPARs). URB597 elicits antinociception property via cannabinoid receptor by maintaining endocannabinoid anandamide (AEA) levels. URB597 reduces abnormal hyperactivity in neurons and could be for treatment of seizures and improving synaptic plasticity.
생화학적/생리학적 작용
Potent, selective fatty acid amide hydrolase (FAAH) inhibitor.
제조 메모
URB597 is soluble in DMSO at a concentration that is approximately 14 mg/ml.
Storage Class Code
11 - Combustible Solids
WGK
WGK 3
개인 보호 장비
Eyeshields, Gloves
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시험 성적서(COA)
Lot/Batch Number
The FAAH inhibitor URB597 efficiently reduces tyrosine hydroxylase expression through CB1-and FAAH-independent mechanisms
Bosier B, et al.
British Journal of Pharmacology, 169(4), 794-807 (2013)
Mechanism of carbamate inactivation of FAAH: implications for the design of covalent inhibitors and in vivo functional probes for enzymes
Alexander JP and Cravatt BF
Chemistry & Biology, 12(11), 1179-1187 (2005)
The FAAH inhibitor URB597 suppresses hippocampal maximal dentate afterdischarges and restores seizure-induced impairment of short and long-term synaptic plasticity
Colangeli R, et al.
Scientific Reports, 7(1), 11152-11152 (2017)
Interaction between the cholecystokinin and endogenous cannabinoid systems in cued fear expression and extinction retention
Bowers ME and Ressler KJ
Neuropsychopharmacology, 30, 688-688 (2015)
Lucas Albrechet-Souza et al.
Neurobiology of stress, 15, 100387-100387 (2021-09-16)
Understanding sex differences in behavioral and molecular effects of stress has important implications for understanding the vulnerability to chronic psychiatric disorders associated with stress response circuitry. The amygdala is critical for emotional learning and generating behavioral responses to stressful stimuli
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