ARL67156 (FPL 67156) triethylamine 是一种 ecto-ATPase 抑制剂。ARL67156 triethylamine 是竞争性 NTPDase1 (CD39)，NTPDase3 和 NPP1 抑制剂，Ki 分别为 11，18 和 12 μM。ARL67156 triethylamine 可用于钙化性主动脉瓣疾病、哮喘等疾病的研究。
货号:ajcx38910
CAS:N/A
分子式:C15H24Br2N5O12P3.(4.3C6H15N)
分子量：1154.23
溶解度:Methanol : 125 mg/mL (108.30 mM; Need ultrasonic)|DMSO : 100 mg/mL (86.64 mM; Need ultrasonic)
纯度：98%
存储：Store at -20°C
库存：现货

Background:

ARL67156 (FPL 67156) triethylamine is a selective ecto-ATPase inhibitor. ARL67156 triethylamine is a competitive inhibitor of NTPDase1 (CD39), NTPDase3 and NPP1, with Kis of 11, 18 and 12 μM, respectively. ARL67156 triethylamine can be used in the research of disease like calcific aortic valve disease, asthma[1][2].

ARL67156 triethylamine (1-100 μM) potentiates neurogenic contractions in a concentration-dependent manner[4].ARL67156 triethylamine (10 μg/mL, 24 h) increases the surface expression of CXCR3 on ATP-treated HMC-1 cells[5].ARL67156 triethylamine (30 μM, 5s) potentiates the norepinephrine release promoted by ATP in guinea pig heart synaptosomes[6].ARL67156 triethylamine (100 μM, 4h) significantly decreases HIV-1replication in macrophages[7].

ARL67156 triethylamine (1.1 μg/kg/day, administered with osmotic pumps implanted subcutaneously, for 28 days) prevents the development of calcific aortic valve disease in Warfarin -treated rats[2].ARL67156 triethylamine (intraperitoneal injection, 2 mg/kg) prevents the increase of serum adenosine concentration induced by Fructose 1,6-bisphosphate (FBP)[3].

[1]. Évesque SA, et al. Specificity of the ecto-ATPase inhibitor ARL 67156 on human and mouse ectonucleotidases. Br J Pharmacol. 2007 Sep;152(1):141-50. [2]. Nancy CÔtÉ, et al. Inhibition of Ectonucleotidase With ARL67156 Prevents the Development of Calcific Aortic Valve Disease in Warfarin-Treated Rats. Eur J Pharmacol. 2012 Aug 15;689(1-3):139-46. [3]. FlÁvio P Veras, et al. Fructose 1,6-bisphosphate, a high-energy intermediate of glycolysis, attenuates experimental arthritis by activating anti-inflammatory adenosinergic pathway. Sci Rep. 2015 Oct 19;5:15171. [4]. C Kennedy, et al. ATP as a co-transmitter with noradrenaline in sympathetic nerves--function and fate. Ciba Found Symp. 1996;198:223-35; discussion 235-8. [5]. Ya-Dong Gao, et al. Th2 cytokine-primed airway smooth muscle cells induce mast cell chemotaxis via secretion of ATP. J Asthma. 2014 Dec;51(10):997-1003. [6]. Casilde Sesti, et al. EctoNucleotidase in cardiac sympathetic nerve endings modulates ATP-mediated feedback of norepinephrine release. J Pharmacol Exp Ther. 2002 Feb;300(2):605-11. [7]. Julieta Schachter, et al. Inhibition of ecto-ATPase activities impairs HIV-1 infection of macrophages. Immunobiology. 2015 May;220(5):589-96.