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SML0257
JZL195
≥98% (HPLC)
Synonim(y):
4-[(3-Phenoxyphenyl)methyl]-1-piperazinecarboxylic acid 4-nitrophenyl ester
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About This Item
Wzór empiryczny (zapis Hilla):
C24H23N3O5
Numer CAS:
Masa cząsteczkowa:
433.46
Numer MDL:
Kod UNSPSC:
12352200
Identyfikator substancji w PubChem:
NACRES:
NA.77
Polecane produkty
Próba
≥98% (HPLC)
Formularz
powder
kolor
white to beige
rozpuszczalność
DMSO: ≥5 mg/mL at warmed
temp. przechowywania
−20°C
ciąg SMILES
[O-][N+](=O)c1ccc(OC(=O)N2CCN(CC2)Cc3cccc(Oc4ccccc4)c3)cc1
InChI
1S/C24H23N3O5/c28-24(32-22-11-9-20(10-12-22)27(29)30)26-15-13-25(14-16-26)18-19-5-4-8-23(17-19)31-21-6-2-1-3-7-21/h1-12,17H,13-16,18H2
Klucz InChI
QNYRAEKLMNDRFY-UHFFFAOYSA-N
Zastosowanie
JZL195 has been used:
- as a selective inhibitor of endocannabinoid (eCB) clearance enzymes to induce in vivo long-term depression at CA3-CA1 synapses and at prelimbic (PrL)-nucleus accumbens (NAc)synapses, to study the neuroprotective action of eCB
- to inhibit the action of hydrolytic enzymes that limit eCB activity, to study the effect of 2-linoleoylglycerol (2-LG) on the human CB1 receptor activity
- as a dual fatty acid amide hydrolase (FAAH)/monoacylglycerol lipase (MAGL) inhibitor to study its dose-related antipruritic effect on the serotonin (5-HT)-induced scratching model
Działania biochem./fizjol.
JZL195 is a dual inhibitor of FAAH and MAGL.
JZL195 is a potent dual inhibitor of Monoacylglycerol lipase (MAGL) and fatty acid amide hydrolase (FAAH), enzymes that degrade the endocannabinoids 2-arachidonoylglycerol (2-AG) and anandamide (AEA), the endogenous ligands for the cannabinoid G-protein coupled receptors CB1 and CB2. IC50 values are 2 nM for MAGL and 4 nM for FAAH. JZL195 has been shown to inhibit endocannabinoid hydrolysis and elevate 2-AG and AEA levels in vivo.
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Kod klasy składowania
11 - Combustible Solids
Klasa zagrożenia wodnego (WGK)
WGK 3
Temperatura zapłonu (°F)
Not applicable
Temperatura zapłonu (°C)
Not applicable
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Feng Wang et al.
Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 39(6), 1122-1137 (2018-02-13)
Ischemia not only activates cell death pathways but also triggers endogenous protective mechanisms. However, it is largely unknown what is the essence of the endogenous neuroprotective mechanisms induced by preconditioning. In this study we demonstrated that systemic injection of JZL195
Ozgur Yesilyurt et al.
Archives of dermatological research, 308(5), 335-345 (2016-04-30)
The increase of endocannabinoid tonus by inhibiting fatty acid amide hydrolase (FAAH) or monoacylglycerol lipase (MAGL) represents a promising therapeutic approach in a variety of disease to overcome serious central side effects of exocannabinoids. Recent studies reported that systemic administration
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Evidence has accumulated that obesity-related metabolic dysregulation is associated with overactivation of the endocannabinoid system (ECS), which involves cannabinoid receptor 1 (CB1R), in peripheral tissues, including adipose tissue (AT). The functional consequences of CB1R activation on AT metabolism remain unclear.
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Fatty acid amide hydrolase (FAAH) represents a potential therapeutic target for number of peripheral and nervous system related disorders including neuropathic pain and neuroinflammation. A library of N-(2,4-dichlorobenzoyl) isatin Schiff bases 7a-7l and 8a-8c were designed using the contemporary scaffold-hopping
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