ARL67156 trisodium salt hydrate

ARL67156trisodiumsalthydrate是一种ecto-ATPase抑制剂。ARL67156trisodiumsalthydrate是弱的竞争性NTPDase1(CD39)，NTPDase3和NPP1抑制剂，Ki分别为11，18和12μM。ARL67156trisodiumsalthydrate可预防体内主动脉瓣钙化。

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1mg

￥1962.00

1570.00

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Background

ARL67156 trisodium salt hydrate is an inhibitor of ecto-ATPase. ARL67156 trisodium salt hydrate is a weak competitive inhibitor of NTPDase1 (CD39), NTPDase3 and NPP1, with Kis of 11, 18 and 12 μM, respectively[1]. ARL67156 trisodium salt hydrate prevents in vivo the development of calcific aortic valve disease[2].

ARL67156 trisodium salt is also an effective inhibitor of UTP breakdown by superior cervical ganglion cells and to potentiate contractions elicited by this nucleotide in isolated tail artery of rat. ARL67156 is not an effective inhibitor of NTPDase2, NTPDase8, NPP3 and ecto-5′-nucleotidase (CD73), although it also reduces the activity of these enzymes[1].

Pre-treatment of mice with ARL67156 (2 mg/kg, i.p.), a selective inhibitor of CD39 (CD39i), completely prevents the increase of serum adenosine concentration induced by Fructose 1,6-bisphosphate (FBP; 100 mg/kg)[3]. Animal Model: C57BL/6 mice[3]

[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. [2]. Nancy C?té, 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.