Pitavastatin sodium  (Synonyms: NK-104 sodium)

Pitavastatin (NK-104) sodium is a potent hydroxymethylglutaryl-CoA (HMG-CoA) reductase inhibitor. Pitavastatin sodium inhibits cholesterol synthesis from acetic acid with an IC₅₀ 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].

HMG-CoA Reductase^[1]

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.

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].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

443.44

C₂₅H₂₃FNNaO₄

574705-92-3

O=C(O[Na])C[C@H](O)C[C@H](O)/C=C/C1=C(C2=CC=C(C=C2)F)C3=C(C=CC=C3)N=C1C4CC4

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [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]