147511-69-1

HMGA reductase inhibitor

ChEBI: A hydroxy monocarboxylic acid anion that is the conjugate base of pitavastatin, obtained by deprotonation of the carboxy group.

[Name previously used: Itavastatin].

pitavastatin (nk-104) is a potent hmg-coa reductase inhibitor, pitavastatin inhibited cholesterol synthesis from acetic acid with an ic50 of 5.8 nm in a human liver cancer cell line (hepg2).

This HMG-CoA reductase inhibitor (FW = 421.46 g/mol; CAS 147511-69- 1; IUPAC Name: (3R,5S,6E)-7-[2-cyclopropyl-4-(4-fluorophenyl)quinolin- 3-yl]-3,5-dihydroxyhept-6-enoic acid), also known as itavastatin, itabavastin, nisvastatin, NK-104, NKS-104, and the trade name Livalo?, is indicated for ameliorating hypercholesterolemia and preventing cardiovascular disease. NK-104 potency is dose-dependent and is roughly equivalent to that of atorvastatin. It is well-tolerated in the treatment of patients with hypercholesterolemia. Pitavastatin uptake is carrier-mediated. Target(s): Reduces inflammatory cytokine production from human bronchial epithelial cells; Decreases microtubule tau protein levels via the inactivation of Rho/ROCK; Inhibits hepatic steatosis and fibrosis in non-alcoholic steatohepatitis model; Suppresses therosclerosis induced by chronic inhibition of the synthesis of nitric oxide in moderately hypercholesterolemic rabbits; Decreases the expression of endothelial lipase both in vitro and in vivo; Inhibits NFkB pathway in brain; Inactivates NFkB and decreases IL-6 production through Rho kinase pathway in MCF-7 human breast cancer cells; Reduces C-reactive-protein-induced interleukin-8 production in human aortic endothelial cells; Inhibits lysophosphatidic acid-induced proliferation and monocyte chemoattractant protein-1 expression in aortic smooth muscle cells by suppressing Rac-1-mediated reactive oxygen species generation; Inhibits upregulation of intermediate conductance calcium-activated potassium channels and coronary arteriolar remodeling induced by long-term blockade of nitric oxide synthesis; Inhibits migration and proliferation of rat vascular smooth muscle cells.