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CAY10401 Sale

目录号 : GC43148

An exceptionally potent FAAH inhibitor

CAY10401 Chemical Structure

Cas No.:288862-89-5

规格 价格 库存 购买数量
100μg
¥479.00
现货
500μg
¥2,159.00
现货
1mg
¥3,838.00
现货
5mg
¥16,789.00
现货

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Sample solution is provided at 25 µL, 10mM.

产品文档

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产品描述

Fatty acid amide hydrolase (FAAH) is the enzyme responsible for hydrolysis and inactivation of fatty acid amides including anandamide and oleamide. CAY10401 is a selective, potent inhibitor of rat FAAH exhibiting a Ki value of 0.14 nM. CAY10401 is approximately 580 fold more potent than oleyl trifluoromethyl ketone when assayed under the same conditions.

Chemical Properties

Cas No. 288862-89-5 SDF
Canonical SMILES CCCCCCCCCCCCCCCCCC(=O)c1nc2ncccc2o1
分子式 C24H34N2O2 分子量 382.5
溶解度 DMF: 20 mg/ml,DMSO: 20 mg/ml,DMSO:PBS (pH 7.2)(1:1): .15 mg/ml,Ethanol: 20 mg/ml 储存条件 Store at -20°C
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储备液的保存方式和期限:-80°C 储存时,请在 6 个月内使用,-20°C 储存时,请在 1 个月内使用。
为了提高溶解度,请将管子加热至37℃,然后在超声波浴中震荡一段时间。
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溶解性数据

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1 mg 5 mg 10 mg
1 mM 2.6144 mL 13.0719 mL 26.1438 mL
5 mM 0.5229 mL 2.6144 mL 5.2288 mL
10 mM 0.2614 mL 1.3072 mL 2.6144 mL
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Research Update

Expression and function of fatty acid amide hydrolase in prostate cancer

Int J Cancer 2008 Sep 15;123(6):1318-26.PMID:18566995DOI:10.1002/ijc.23674.

The hydrolysis of endocannabinoids has profound effects on the function of the endocannabinoid signaling system in the regulation of prostate carcinoma cells. Prostate carcinoma cells exhibit a wide range of hydrolysis activity for 2-arachidonoylglycerol (2-AG), the major endocannabinoid. However, enzyme(s) responsible for 2-AG hydrolysis and their functions in prostate cancer have not been characterized. In this study, we demonstrated that fatty acid amide hydrolase (FAAH) was differentially expressed in normal and prostate carcinoma cells. In PC-3 cells, overexpression of FAAH resulted in increased FAAH protein, 2-AG hydrolysis, cell invasion and cell migration. Conversely, small-interfering RNA (siRNA) knockdown of FAAH in LNCaP cells decreased FAAH protein, 2-AG hydrolysis and cell invasion. Furthermore, CAY10401, a FAAH inhibitor, decreased cell invasion and it enhanced the reduction of invasion in FAAH siRNA-transfected LNCaP cells. Immunohistochemistry staining of commercial tissue microarrays (TMAs) demonstrated FAAH staining in 109 of 157 cores of prostate adenocarcinomas but weak staining in 1 of 8 cores of normal prostate tissues. These results suggest that FAAH regulates 2-AG hydrolysis and invasion of prostate carcinoma cells and is potentially involved in prostate tumorigenesis.

Inhibition of fatty acid amide hydrolase and monoacylglycerol lipase by the anandamide uptake inhibitor VDM11: evidence that VDM11 acts as an FAAH substrate

Br J Pharmacol 2005 Aug;145(7):885-93.PMID:15895107DOI:10.1038/sj.bjp.0706253.

There is some dispute concerning the extent to which the uptake inhibitor VDM11 (N-(4-hydroxy-2-methylphenyl) arachidonoyl amide) is capable of inhibiting the metabolism of the endocannabinoid anandamide (AEA) by fatty acid amide hydrolase (FAAH). In view of a recent study demonstrating that the closely related compound AM404 (N-(4-hydroxyphenyl)arachidonylamide) is a substrate for FAAH, we re-examined the interaction of VDM11 with FAAH. In the presence of fatty acid-free bovine serum albumin (BSA, 0.125% w v(-1)), both AM404 and VDM11 inhibited the metabolism of AEA by rat brain FAAH with similar potencies (IC(50) values of 2.1 and 2.6 microM, respectively). The compounds were about 10-fold less potent as inhibitors of the metabolism of 2-oleoylglycerol (2-OG) by cytosolic monoacylglycerol lipase (MAGL). The potency of VDM11 towards FAAH was dependent upon the assay concentration of fatty acid-free bovine serum albumin (BSA). Thus, in the absence of fatty acid-free BSA, the IC(50) value for inhibition of FAAH was reduced by a factor of about two (from 2.9 to 1.6 microM). A similar reduction in the IC(50) value for the inhibition of membrane bound MAGL by both this compound (from 14 to 6 microM) and by arachidonoyl serinol (from 24 to 13 microM) was seen. An HPLC assay was set up to measure 4-amino-m-cresol, the hypothesised product of FAAH-catalysed VDM11 hydrolysis. 4-Amino-m-cresol was eluted with a retention time of approximately 2.4 min, but showed a time-dependent degradation to compounds eluting at peaks of approximately 5.6 and approximately 8 min. Peaks with the same retention times were also found following incubation of the membranes with VDM11, but were not seen when the membranes were preincubated with the FAAH inhibitors URB597 (3'-carbamoyl-biphenyl-3-yl-cyclohexylcarbamate) and CAY10401 (1-oxazolo[4,5-b]pyridin-2-yl-9-octadecyn-1-one) prior to addition of VDM11. The rate of metabolism of VDM11 was estimated to be roughly 15-20% of that for anandamide. It is concluded that VDM11 is an inhibitor of FAAH under the assay conditions used here, and that the inhibition may at least in part be a consequence of the compound acting as an alternative substrate.