ARL67156 trisodium  (Synonyms: FPL 67156 trisodium)

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

Ki: 11 μM (NTPDase1), 18 μM (NTPDase3), 12 μM (NPP1)^[1]

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

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

ARL67156 trisodium (1.1 μg/kg/day, administered with osmotic pumps implanted subcutaneously, for 28 days) prevents the development of calcific aortic valve disease in Warfarin (HY-B0687)-treated rats^[2].
ARL67156 trisodium (intraperitoneal injection, 2 mg/kg) prevents the increase of serum adenosine concentration induced by Fructose 1,6-bisphosphate (FBP)^[3].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

785.05

Solid

C₁₅H₂₁Br₂N₅Na₃O₁₂P₃

1021868-83-6

O[[email protected]]1[[email protected]@H](O[[email protected]](COP(OP(C(Br)(Br)P(O)(O[Na])=O)(O[Na])=O)(O[Na])=O)[[email protected]]1O)N2C3=NC=NC(N(CC)CC)=C3N=C2

Room temperature in continental US; may vary elsewhere.

-20°C, sealed storage, away from moisture

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

• [1]. Lévesque 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.  [Content Brief]

  [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.  [Content Brief]

  [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.  [Content Brief]

  [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.  [Content Brief]

  [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.  [Content Brief]

  [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.  [Content Brief]

  [7]. Julieta Schachter, et al. Inhibition of ecto-ATPase activities impairs HIV-1 infection of macrophages. Immunobiology. 2015 May;220(5):589-96.  [Content Brief]