Pitavastatin sodium

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Pitavastatin sodium

本产品不向个人销售，仅用作科学研究，不用于任何人体实验及非科研性质的动物实验。

CAS NO:	574705-92-3
规格:	≥98%

包装与价格：

包装	价格(元)
25mg	电议
50mg	电议
100mg	电议
250mg	电议
500mg	电议

产品介绍

理化性质和储存条件

Molecular Formula: C25H23FNNaO4;

Molecular Weight: 443.44

In Vitro	Pitavastatin inhibits the growth of a panel of ovarian cancer cells, including those considered most likely to represent HGSOC, grown as a monolayers (IC50=0.4-5 μM) or as spheroids (IC50 = 0.6-4 μM)[4]. Pitavastatin (1 μM; 48 hours) induces apoptosis, evidenced by the increased activity of executioner caspases-3,7 as well as caspase-8 and caspase-9 in Ovcar-8 cells and Ovcar-3 cells[4]. Pitavastatin (1 μM, 48 hours) causes PARP cleavage in Ovcar-8 cells[4]. Pitavastatin (0.1 and 1 μM; 1 h, then cells incubate with TNF-α for 6 h) increases the expression of ICAM-1 mRNA through suppressing NF-κB pathway in TNF-α-stimulated human saphenous vein endothelial cells[6]. Western Blot Analysis[4] Cell Line: Ovcar-8 cells Concentration: 1 μM Incubation Time: 48 hours Result: Induced PARP cleavage.
In Vivo	Pitavastatin (59 mg/kg; p.o.; twice daily for 28 days) causes significant tumour regression[4]. Pitavastatin (0.1 mg/kg; p.o; daily for 12 weeks) retards the progression of atherosclerosis formation and improves NO bioavailability by eNOS up-regulation and decrease of O2- in diet induced severe hyperlipidemia rabbit model[7]. Animal Model: 4 week old female NCR Nu/Nu female mice (bearing Ovcar-4 tumours)[4] Dosage: 59 mg/kg Administration: p.o.; twice daily for 28 days Result: Caused significant tumour regression. Animal Model: Female New Zealand white rabbits (diet induced severe hyperlipidemia)[7] Dosage: 0.1 mg/kg Administration: p.o; daily for 12 weeks Result: Retarded the progression of atherosclerosis formation and improved NO bioavailability by eNOS up-regulation and decrease of O2-.

In Vitro

Pitavastatin inhibits the growth of a panel of ovarian cancer cells, including those considered most likely to represent HGSOC, grown as a monolayers (IC50=0.4-5 μM) or as spheroids (IC50 = 0.6-4 μM)[4]. Pitavastatin (1 μM; 48 hours) induces apoptosis, evidenced by the increased activity of executioner caspases-3,7 as well as caspase-8 and caspase-9 in Ovcar-8 cells and Ovcar-3 cells[4]. Pitavastatin (1 μM, 48 hours) causes PARP cleavage in Ovcar-8 cells[4]. Pitavastatin (0.1 and 1 μM; 1 h, then cells incubate with TNF-α for 6 h) increases the expression of ICAM-1 mRNA through suppressing NF-κB pathway in TNF-α-stimulated human saphenous vein endothelial cells[6]. Western Blot Analysis[4] Cell Line: Ovcar-8 cells Concentration: 1 μM Incubation Time: 48 hours Result: Induced PARP cleavage.

In Vivo

Pitavastatin (59 mg/kg; p.o.; twice daily for 28 days) causes significant tumour regression[4]. Pitavastatin (0.1 mg/kg; p.o; daily for 12 weeks) retards the progression of atherosclerosis formation and improves NO bioavailability by eNOS up-regulation and decrease of O2- in diet induced severe hyperlipidemia rabbit model[7]. Animal Model: 4 week old female NCR Nu/Nu female mice (bearing Ovcar-4 tumours)[4] Dosage: 59 mg/kg Administration: p.o.; twice daily for 28 days Result: Caused significant tumour regression. Animal Model: Female New Zealand white rabbits (diet induced severe hyperlipidemia)[7] Dosage: 0.1 mg/kg Administration: p.o; daily for 12 weeks Result: Retarded the progression of atherosclerosis formation and improved NO bioavailability by eNOS up-regulation and decrease of O2-.