PitavastatinPitavastatin
MedChemExpress (MCE)
HY-B0144A
147511-69-1
NK-104
99.83%
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month
Room temperature in continental US
may vary elsewhere.
Pitavastatin (NK-104) is a potent hydroxymethylglutaryl-CoA (HMG-CoA) reductase inhibitor. Pitavastatin inhibits cholesterol synthesis from acetic acid with an IC50 of 5.8 nM in HepG2 cells. Pitavastatin is an efficient hepatocyte low-density lipoprotein-cholesterol (LDL-C) receptor inducer. Pitavastatin also possesses anti-atherosclerotic, anti-asthmatic, anti-osteoarthritis, antineoplastic, neuroprotective, hepatoprotective and reno-protective effects.
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].
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].
HMG-CoA Reductase[1] 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]. MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. 0 --> Pitavastatin Related Antibodies Western Blot Analysis[4] Cell Line: Ovcar-8 cells
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[1]. Morikawa S, et al. Relative induction of mRNA for HMG CoA reductase and LDL receptor by five different HMG-CoA reductase inhibitors in cultured human cells. J Atheroscler Thromb. 2000
7(3):138-44. [Content Brief]
[2]. Katsuki S, et al. Nanoparticle-mediated delivery of pitavastatin inhibits atherosclerotic plaque destabilization/rupture in mice by regulating the recruitment of inflammatory monocytes. Circulation. 2014 Feb 25
129(8):896-906. [Content Brief]
[3]. Tajiri K, et al. Pitavastatin regulates helper T-cell differentiation and ameliorates autoimmune myocarditis in mice. Cardiovasc Drugs Ther. 2013 Oct
27(5):413-24. [Content Brief]
[4]. Hamano T, et al. Pitavastatin decreases tau levels via the inactivation of Rho/ROCK. Neurobiol Aging. 2012 Oct
33(10):2306-20. [Content Brief]
[5]. de Wolf E, et al.Dietary geranylgeraniol can limit the activity of pitavastatin as a potential treatment for drug-resistant ovarian cancer.Sci Rep. 2017 Jul 14
7(1):5410. [Content Brief]
[6]. Demir B, et al. The Effects of Pitavastatin on Nuclear Factor-Kappa B and ICAM-1 in Human Saphenous Vein Graft Endothelial Culture. Cardiovasc Ther. 2019 May 2
2019:2549432. [Content Brief]
[7]. Hayashi T, et al. A new HMG-CoA reductase inhibitor, pitavastatin remarkably retards the progression of high cholesterol induced atherosclerosis in rabbits. Atherosclerosis. 2004 Oct
176(2):255-63. [Content Brief]
[8]. Sahebkar A, et al. A comprehensive review on the lipid and pleiotropic effects of pitavastatin. Prog Lipid Res. 2021 Nov
84:101127. [Content Brief]
