Pitavastatin (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]. IC50 & Target: 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]. 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 O^2- in diet induced severe hyperlipidemia rabbit model^[7].