Pitavastatin: Efficacy and Safety Profiles of A Novel Synthetic HMG‐CoA Reductase Inhibitor
Abstract
The use of 3‐hydroxy‐3‐methylglutaryl coenzyme A (HMG‐CoA) reductase inhibitors, statins, has been shown to reduce major cardiovascular events in both primary and secondary prevention, and statins became one of the most widely prescribed classes of drugs throughout the world. Previously, statins have been well tolerated and have shown favorable safety profiles. However, the voluntary withdrawal of cerivastatin from the market because of a disproportionate number of reports of rhabdomyolysis‐associated deaths drew attention to the pharmacokinetic profile of statins, which may possibly have been related to serious drug‐drug interactions. Pitavastatin (NK‐104, previously called itavastatin or nisvastatin, Kowa Company Ltd., Tokyo) is a novel, fully synthetic statin, which has a potent cholesterol‐lowering action. The short‐term and long‐term lipid‐modifying effects of pitavastatin have already been investigated in subjects with primary hypercholesterolemia, heterozygous familial hypercholesterolemia, hypertriglyceridemia, and type‐2 diabetes mellitus accompanied by hyperlipidemia. Within the range of daily doses from 1 to 4 mg, the efficacy of pitavastatin as a lipid‐lowering drug seems to be similar, or potentially superior, to that of atorvastatin. According to the results of pharmacokinetic studies, pitavastatin showed favorable and promising safety profile; it was only slightly metabolized by the cytochrome P450 (CYP) system, its lactone form had no inhibitory effects on the CYP3A4‐mediated metabolism of concomitantly administered drugs; P‐glycoprotein‐mediated transport did not play a major role in its disposition, and pitavastatin did not inhibit P‐glycoprotein activity. It could be concluded that pitavastatin could provide a new and potentially better thera‐peutic choice for lipid‐modifying therapy than do the currently available statins. The ef‐ficacy and safety of higher dose treatment, as well as its long‐term effects in the pre‐vention of coronary artery disease, should be further investigated.
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Statins are not applicable as single antifungal agents for treatment of IFI because their MICs are about one order of magnitude higher than their maximum achievable concentrations in human serum.
“Statins are not applicable as single antifungal agents for the treatment of IFI because their MICs are much higher (about 1 order of magnitude) than their maximum achievable concentrations in human serum [11,[40][41][42][43][44][45] .”
From Statins as antifungal agents (2011) · cites this paper as [40]
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- Authors
- Kajinami, K., Takekoshi, N., & Saito, Y.
- Affiliations
- Kanazawa Medical University (JP)
- Chiba University (JP)
- Corresponding author
- Kajinami, Kouji
- ORCID
- Saito, Yasushi
- Venue
- Cardiovascular Drug Reviews
- Publisher
- Wiley
- Published
- 2003-09
- Volume
- 21
- Issue
- 3
- Pages
- 199-215
- ISSN
- 0897-5957 (ISSN-L)
- 1527-3466
- OpenAlex
- W2074541010
- Cited by
- 136
- References
- 77
- Citations by year
- 2026: 5 · 2025: 4 · 2024: 2 · 2023: 3 · 2022: 8 · 2021: 8 · 2020: 4 · 2019: 3 · 2018: 1 · 2017: 5 · 2016: 6 · 2015: 3 · 2014: 6 · 2013: 4 · 2012: 2
- FWCI
- 8.31
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Cardiovascular Drug Reviews (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Lipids, and Metabolism
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Keywords
- pitavastatin, statins, lipid-lowering therapy, hypercholesterolemia, familial hypercholesterolemia, hypertriglyceridemia, type 2 diabetes, pharmacokinetics, drug-drug interactions, cytochrome P450, P-glycoprotein, rhabdomyolysis, atorvastatin comparison, coronary heart disease prevention
- MeSH terms
- Animals, Arteriosclerosis, Clinical Trials as Topic, Cytochrome P-450 Enzyme System, Drug Interactions, Humans, Hypercholesterolemia, Lipoproteins, Quinolines, Hydroxymethylglutaryl-CoA Reductase Inhibitors, ATP Binding Cassette Transporter, Subfamily B, Member 1
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