Pitavastatin sodium
Modify Date: 2024-01-23 12:22:31
Pitavastatin sodium structure
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Common Name | Pitavastatin sodium | ||
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| CAS Number | 574705-92-3 | Molecular Weight | 443.44300 | |
| Density | N/A | Boiling Point | N/A | |
| Molecular Formula | C25H23FNNaO4 | Melting Point | N/A | |
| MSDS | N/A | Flash Point | N/A | |
Use of Pitavastatin sodiumPitavastatin (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]. |
| Name | sodium (3R,5S,6E)-7-[2-cyclopropyl-4-(4-fluorophenyl)quinolin-3-yl]-3,5-dihydroxyhept-6-enoate |
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| Synonym | More Synonyms |
| Description | 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]. |
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| Related Catalog | |
| 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]. Western Blot Analysis[4] Cell Line: Ovcar-8 cells Concentration: 1 μM Incubation Time: 48 hours Result: Induced PARP cleavage. |
| 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 O2- in diet induced severe hyperlipidemia rabbit model[7]. Animal Model: 4 week old female NCR Nu/Nu female mice (bearing Ovcar-4 tumours)[4] 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)[7] 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-. |
| References |
| Molecular Formula | C25H23FNNaO4 |
|---|---|
| Molecular Weight | 443.44300 |
| Exact Mass | 443.15100 |
| PSA | 93.48000 |
| LogP | 3.18340 |
| pitavastatin sodium |