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.