JNJ-1661010

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Chemical Structure| 681136-29-8 同义名 : Takeda-25
CAS号 : 681136-29-8
货号 : A167983
分子式 : C19H19N5OS
纯度 : 99%
分子量 : 365.452
MDL号 : MFCD00209157
存储条件：

Pure form Keep in dark place,Inert atmosphere,Room temperature

In solvent -20°C:3-6个月-80°C:12个月
溶解度 :

DMSO: 105 mg/mL(287.32 mM)，配合低频超声助溶，注意：DMSO长时间开封后，会吸水并导致溶解能力下降，请避免使用长期开封的DMSO
动物实验配方：

5% DMSO+95% Corn oil 5 mg/mL

生物活性
靶点

  • FAAH

    FAAH (rat), IC50:10 nM

    FAAH (human), IC50:12 nM
描述 Fatty acid amides (FAA) are a diverse group of lipid mediators including arachidonoyl ethanolamide (AEA), oleoyl ethanolamide (OEA), palmitoyl ethanolamide (PEA) and N-arachidonoyl glycine. FAAs are hydrolyzed by several different enzymes with different substrate preferences. The metabolizing enzymes that hydrolyze FAA include fatty acid amide hydrolase (FAAH), and N-acylethanolamine-hydrolyzing acid amidase[3]. JNJ-1661010 is a selective inhibitor of FAAH with IC50 of 10 nM (rat) and 12 nM (human)[3]. The level of FAAH activity in the rat brain was decreased by at least 85% for up to 4 h after intraperitoneal dosing of 20 mg/kg JNJ-1661010, and only 25% of FAAH activity had returned by 24 h postdose, compared to control levels[3]. Treatment of wild-type mice with 10 mg/kg JNJ-1661010, intraperitoneally four times a day, resulted in prominent exacerbation of bleomycin-induced fibrosis and dermal thickening, myofibroblast counts and hydroxyproline content are significantly increased compared with sham-treated, bleomycin-challenged mice[4].
作用机制 The acyl piperazinyl fragment of JNJ-1661010 forms a covalent bond with the FAAH.
实验方案
1mg 5mg 10mg

1 mM

5 mM

10 mM

2.74mL

0.55mL

0.27mL

13.68mL

2.74mL

1.37mL

27.36mL

5.47mL

2.74mL
参考文献

[1]Karbarz MJ, Luo L, et al. Biochemical and biological properties of 4-(3-phenyl-[1,2,4] thiadiazol-5-yl)-piperazine-1-carboxylic acid phenylamide, a mechanism-based inhibitor of fatty acid amide hydrolase. Anesth Analg. 2009 Jan;108(1):316-29.

[2]Keith JM, Apodaca R, et al. Thiadiazolopiperazinyl ureas as inhibitors of fatty acid amide hydrolase. Bioorg Med Chem Lett. 2008 Sep 1;18(17):4838-43.

[3]Karbarz MJ, Luo L, Chang L, Tham CS, Palmer JA, Wilson SJ, Wennerholm ML, Brown SM, Scott BP, Apodaca RL, Keith JM, Wu J, Breitenbucher JG, Chaplan SR, Webb M. Biochemical and biological properties of 4-(3-phenyl-[1,2,4] thiadiazol-5-yl)-piperazine-1-carboxylic acid phenylamide, a mechanism-based inhibitor of fatty acid amide hydrolase. Anesth Analg. 2009 Jan;108(1):316-29. doi: 10.1213/ane.0b013e31818c7cbd. PMID: 19095868.

[4]Palumbo-Zerr K, Horn A, Distler A, Zerr P, Dees C, Beyer C, Selvi E, Cravatt BF, Distler O, Schett G, Distler JH. Inactivation of fatty acid amide hydrolase exacerbates experimental fibrosis by enhanced endocannabinoid-mediated activation of CB1. Ann Rheum Dis. 2012 Dec;71(12):2051-4. doi: 10.1136/annrheumdis-2012-201823. Epub 2012 Aug 22. PMID: 22915616.