产品介绍 |
ARL67156 (FPL 67156) trisodium hydrate 是一种 ecto-ATPase 抑制剂。ARL67156 trisodium hydrate 是竞争性 NTPDase1 (CD39),NTPDase3 和 NPP1 抑制剂,Ki 分别为 11,18 和 12 μM。ARL67156 trisodium hydrate 可用于钙化性主动脉瓣疾病、哮喘等疾病的研究。
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生物活性 |
ARL67156 (FPL 67156) trisodium hydrate is a selective ecto-ATPase inhibitor. ARL67156 trisodium hydrate is a competitive inhibitor of NTPDase1 (CD39), NTPDase3 and NPP1, with Kis of 11, 18 and 12 μM, respectively. ARL67156 trisodium hydrate can be used in the research of disease like calcific aortic valve disease, asthma.
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体外研究 |
ARL67156 trisodium hydrate (1-100 μM) potentiates neurogenic contractions in a concentration-dependent manner[4].
ARL67156 trisodium hydrate (10 μg/mL, 24 h) increases the surface expression of CXCR3 on ATP-treated HMC-1 cells[5].
ARL67156 trisodium hydrate (30 μM, 5s) potentiates the norepinephrine release promoted by ATP in guinea pig heart synaptosomes[6].
ARL67156 trisodium hydrate (100 μM, 4h) significantly decreases HIV-1replication in macrophages[7].
西域 has not independently confirmed the accuracy of these methods. They are for reference only. |
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体内研究 |
ARL67156 trisodium hydrate (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.
ARL67156 trisodium hydrate (intraperitoneal injection, 2 mg/kg) prevents the increase of serum adenosine concentration induced by Fructose 1,6-bisphosphate (FBP).
西域 has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model: |
Warfarin-induced mineralization rat model |
Dosage: |
1.1 μg/kg/day |
Administration: |
Administered with osmotic pumps implanted subcutaneously, for 28 days |
Result: |
Prevented the development of aortic stenosis by lowering the level of apoptosis and mineralization of the aortic valve/aorta.
Normalized the level of pAkt (an important kinase involved in the survival pathway).
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Animal Model: |
C57BL/6 mice |
Dosage: |
2 mg/kg |
Administration: |
Intraperitoneal injection, 1 h before administration of FBP (100 mg/kg) |
Result: |
Completely abolished the anti-inflammatory effects of FBP (observed by the neutrophil infiltration, hyperalgesia and oedema of the joint).
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体内研究 |
ARL67156 trisodium hydrate (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.
ARL67156 trisodium hydrate (intraperitoneal injection, 2 mg/kg) prevents the increase of serum adenosine concentration induced by Fructose 1,6-bisphosphate (FBP).
西域 has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model: |
Warfarin-induced mineralization rat model |
Dosage: |
1.1 μg/kg/day |
Administration: |
Administered with osmotic pumps implanted subcutaneously, for 28 days |
Result: |
Prevented the development of aortic stenosis by lowering the level of apoptosis and mineralization of the aortic valve/aorta.
Normalized the level of pAkt (an important kinase involved in the survival pathway).
|
Animal Model: |
C57BL/6 mice |
Dosage: |
2 mg/kg |
Administration: |
Intraperitoneal injection, 1 h before administration of FBP (100 mg/kg) |
Result: |
Completely abolished the anti-inflammatory effects of FBP (observed by the neutrophil infiltration, hyperalgesia and oedema of the joint).
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性状 | Solid |
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溶解性数据 | |
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运输条件 |
Room temperature in continental US; may vary elsewhere.
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储存方式 |
-20°C, sealed storage, away from moisture
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参考文献 |
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. 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]
. 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]
. 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]
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