Pitavastatin

Research use only, not for human use.

Pitavastatin (NK-104) is a potent inhibitor of hydroxymethylglutaryl-CoA (HMG-CoA) reductase, effectively inhibiting cholesterol synthesis from acetic acid in HepG2 cells with an IC50 of 5.8 nM.

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).?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.Pitavastatin (1?μM, 48?hours) causes PARP cleavage in Ovcar-8 cells.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..Western Blot Analysis Cell Line:Ovcar-8 cells Concentration:1?μM Incubation Time:48 hours Result:Induced PARP cleavage.

Pitavastatin (59?mg/kg; p.o.; twice daily for 28 days) causes significant tumour regression.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.Animal Model:4 week old female NCR Nu/Nu female mice?(bearing Ovcar-4 tumours)Dosage:59 mg/kg Administration:p.o.; twice daily for 28 days Result:Caused significant tumour regression.Animal Model:Female New Zealand white rabbits (diet induced severe hyperlipidemia)Dosage:0.1 mg/kg Administration:p.o; daily for 12 weeks Result:Retarded the progression of atherosclerosis formation and improved NO bioavailability by eNOS up-regulation and decrease of O2-.

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Autophagy

Autophagy

Autophagy | HMG-CoA Reductase | Apoptosis | Mitophagy

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147511-69-1

421.46

C25H24FNO4

>98% (HPLC)

In Vitro:?DMSO : 100 mg/mL (237.27 mM; Ultrasonic )

C(=C/[C@H](C[C@H](CC(O)=O)O)O)\C1=C(C2=C(N=C1C3CC3)C=CC=C2)C4=CC=C(F)C=C4

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(-20℃)

With Ice Pack

≥ 2 years