Pitavastatin (NK-104) sodium 是有效的羟甲基戊二酰-CoA(HMG-CoA)还原酶抑制剂。Pitavastatin sodium 在 HepG2 细胞中抑制乙酸合成胆固醇的IC50为 5.8 nM。Pitavastatin sodium 是一种高效的肝细胞低密度脂蛋白胆固醇 (LDL-C) 受体诱导剂。Pitavastatin sodium 还具有抗动脉粥样硬化、抗哮喘、抗骨关节炎、抗肿瘤、神经保护、肝保护和肾保护作用。

Pitavastatin (NK-104) sodium is a potent hydroxymethylglutaryl-CoA (HMG-CoA) reductase inhibitor. Pitavastatin sodium inhibits cholesterol synthesis from acetic acid with an IC 50 of 5.8 nM in HepG2 cells. Pitavastatin sodium is an efficient hepatocyte low-density lipoprotein-cholesterol (LDL-C) receptor inducer. Pitavastatin sodium also possesses anti-atherosclerotic, anti-asthmatic, anti-osteoarthritis, antineoplastic, neuroprotective, hepatoprotective and reno-protective effects [1] [2] [3] [8].

Pitavastatin inhibits the growth of a panel of ovarian cancer cells, including those considered most likely to represent HGSOC, grown as a monolayers (IC 50 =0.4-5 μM) or as spheroids (IC 50 = 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.

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 O 2- 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 O 2-.

574705-92-3

C25H23FNNaO4

443.44

(< 1 mg/ml refers to the product slightly soluble or insoluble )
Powder: -20°C for 3 years
In solvent: -80°C for 2 years