ARL 67156 trisodium salt is a selective inhibitor of ecto-ATPases[1]. The Ki values of ARL 67156 trisodium salt against human NTPDase1(CD39), NTPDase3, and NPP1 were 11±3, 18±4, and 12±3μM, respectively[1].
In vitro, treatment with 10μg/ml ARL 67156 trisodium salt for 24 hours increased the surface expression of CXCR3 on ATP-treated HMC-1 cells[2]. Treatment with 100μM ARL 67156 trisodium salt for 4 hours reduced HIV-1 replication in macrophages[3]. Treatment with 30μM ARL 67156 trisodium salt for 5 seconds enhanced ATP-promoted norepinephrine release in the synaptosome of guinea pig hearts[4].
In vivo, administration of ARL 67156 trisodium salt(2mg/kg; i.p.) for 24 hours completely prevented the FBP-induced increase in serum adenosine concentration in mice[5].
References:
[1] Lévesque SA, Lavoie EG, Lecka J, Bigonnesse F, Sévigny J. Specificity of the ecto-ATPase inhibitor ARL 67156 on human and mouse ectonucleotidases. Br J Pharmacol. 2007;152(1):141-150.
[2] Gao YD, Cao J, Li P, Huang G, Yang J. Th2 cytokine-primed airway smooth muscle cells induce mast cell chemotaxis via secretion of ATP. J Asthma. 2014;51(10):997-1003.
[3] Schachter J, Delgado KV, Barreto-de-Souza V, Bou-Habib DC, Persechini PM, Meyer-Fernandes JR. Inhibition of ecto-ATPase activities impairs HIV-1 infection of macrophages. Immunobiology. 2015;220(5):589-596.
[4] Sesti C, Broekman MJ, Drosopoulos JH, Islam N, Marcus AJ, Levi R. EctoNucleotidase in cardiac sympathetic nerve endings modulates ATP-mediated feedback of norepinephrine release. J Pharmacol Exp Ther. 2002;300(2):605-611.
[5]Veras FP, Peres RS, Saraiva AL, et al. Fructose 1,6-bisphosphate, a high-energy intermediate of glycolysis, attenuates experimental arthritis by activating anti-inflammatory adenosinergic pathway. Sci Rep. 2015;5:15171.
ARL 67156 trisodium salt是一种选择性的细胞外ATP酶抑制剂[1]。ARL 67156 trisodium salt对人NTPDase1（CD39）、NTPDase3和NPP1的Ki值分别为11±3μM、18±4μM和12±3μM[1]。
体外实验中，10μg/ml ARL 67156 trisodium salt处理24小时可增加ATP处理的HMC-1细胞表面CXCR3的表达水平[2]。100μM ARL 67156 trisodium salt处理4小时可降低巨噬细胞中的HIV-1复制[3]。30μM ARL 67156 trisodium salt处理5秒后，增强了豚鼠心脏突触体中ATP促进的去甲肾上腺素的释放[4]。
体内实验中，给予ARL 67156 trisodium salt（2mg/kg；腹腔注射）处理24小时可完全阻止小鼠中FBP诱导的血清腺苷浓度升高[5]。