Pitavastatin acid

• CAT Number: I001803
• CAS Number: 147511-69-1
• Molecular Formula: C25H24FNO4
• Molecular Weight: 421.46
• Purity: ≥95%
• Synonyms: Pitavastatin; Itavastatin; Livalo; NK 104; 147511-69-1; Pitavastatin [INN]
• Target: HMG-CoA Reductase
• Solubility: 10 mM in DMSO
• Storage: Refrigerator
• Related CAS: 147526-32-7 (calcium)
• IC50: 5.8 nM(cholesterol synthesis from aceticacid in HepG2)
• InChI: 1S/C25H24FNO4/c26-17-9-7-15(8-10-17)24-20-3-1-2-4-22(20)27-25(16-5-6-16)21(24)12-11-18(28)13-19(29)14-23(30)31/h1-4,7-12,16,18-19,28-29H,5-6,13-14H2,(H,30,31)/b12-11+/t18-,19-/m1/s1
• InChIKey: VGYFMXBACGZSIL-MCBHFWOFSA-N
• SMILES: C1CC1C2=NC3=CC=CC=C3C(=C2C=CC(CC(CC(=O)O)O)O)C4=CC=C(C=C4)F

Pitavastatin acid(cas 147511-69-1) is the free acid of Pitavastatin, which 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).

 

Reference

1. Curr Opin Investig Drugs. 2002 Sep;3(9):1334-41.
Pitavastatin Nissan/Kowa Yakuhin/Novartis/Sankyo.
Flores NA(1).
Author information:
(1)University College London, Institute of Urology and Nephrology, Division of Applied Physiology, 48 Riding House Street, London, W1W 7EY, UK.
Pitavastatin (nisvastatin) is an HMG CoA reductase inhibitor being developed jointly by Nissan, Kowa Kogyo, Novartis and Sankyo for the potential treatment of atherosclerosis and hyperlipidemia.
2. J Clin Pharmacol. 2002 Aug;42(8):835-45.
Pharmacology of 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors (statins), including rosuvastatin and pitavastatin.
Igel M(1), Sudhop T, von Bergmann K.
Author information:
(1)Department of Clinical Pharmacology, University of Bonn, Germany.
Coronary heart disease (CHD) is the leading cause of morbidity and mortality in the Western world, with hypercholesterolemia as the major risk factor. The 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors represent the most efficient drugsfor the treatment of hypercholesterolemia. They lower plasma cholesterol due to the inhibition of endogenous cholesterol synthesis in the liverand subsequent increased expression of low-density lipoprotein (LDL) receptors, resulting in an up-regulated catabolic rate for plasma LDL. The beneficial effect of statins on the incidence of CHD was clearly demonstrated in several large-scale clinical trials. Currently, five statins (atorvastatin, fluvastatin, lovastatin, pravastatin, and simvastatin) are available, and two novel compounds (pitavastatin, rosuvastatin) are undergoing clinical investigation. To point out potential mechanisms leading to increased toxicity and to compare the novel statins with the established ones, this article summarizes their pharmacological data since the prevalence of adverse events can be explained at least in part by their pharmacokinetic differences.