Fluvastatin Sodium - CAS 93957-55-2
Catalog number: 93957-55-2
Category: Inhibitor
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
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HMG-CoA Reductase (HMGCR)
Fluvastatin Sodium inhibits HMG-CoA reductase activity with IC50 of 8 nM.
Publictions citing BOC Sciences Products
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1.Simvastatin Sodium Salt and Fluvastatin Interact with Human Gap Junction Gamma-3 Protein.
Marsh A1, Casey-Green K1, Probert F1, Withall D1, Mitchell DA2, Dilly SJ3, James S4, Dimitri W4, Ladwa SR3, Taylor PC1, Singer DR4,5,2. PLoS One. 2016 Feb 10;11(2):e0148266. doi: 10.1371/journal.pone.0148266. eCollection 2016.
Finding pleiomorphic targets for drugs allows new indications or warnings for treatment to be identified. As test of concept, we applied a new chemical genomics approach to uncover additional targets for the widely prescribed lipid-lowering pro-drug simvastatin. We used mRNA extracted from internal mammary artery from patients undergoing coronary artery surgery to prepare a viral cardiovascular protein library, using T7 bacteriophage. We then studied interactions of clones of the bacteriophage, each expressing a different cardiovascular polypeptide, with surface-bound simvastatin in 96-well plates. To maximise likelihood of identifying meaningful interactions between simvastatin and vascular peptides, we used a validated photo-immobilisation method to apply a series of different chemical linkers to bind simvastatin so as to present multiple orientations of its constituent components to potential targets. Three rounds of biopanning identified consistent interaction with the clone expressing part of the gene GJC3, which maps to Homo sapiens chromosome 7, and codes for gap junction gamma-3 protein, also known as connexin 30.
2.Involvement of Monocarboxylate Transporter 4 Expression in Statin-Induced Cytotoxicity.
Kikutani Y1, Kobayashi M1, Konishi T1, Sasaki S1, Narumi K1, Furugen A1, Takahashi N2, Iseki K3. J Pharm Sci. 2016 Apr;105(4):1544-9. doi: 10.1016/j.xphs.2016.01.014. Epub 2016 Feb 28.
Statins, 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, are the most widely used cholesterol-lowering agents for prevention of obstructive cardiovascular events. However, statins can cause a variety of skeletal muscle problems, and exercise leads to an increase in statin-induced muscle injury. Exercise induces the protein content of monocarboxylate transporter 4 (MCT4), which is expressed strongly in skeletal muscle and is thought to play a major role in the transport of metabolically important monocarboxylates such as l-lactate. We previously reported that α-cyano-4-hydroxycinnamate, an MCT4 inhibitor, increased the inhibition of growth of RD cells, a prototypic embryonal rhabdomyosarcoma cell line (an RD cell line), as a model of in vitro skeletal muscle, induced by a statin. However, it is unclear whether statin-induced RD cell cytotoxicity is associated with MCT4 expression. We, therefore, examined the relationship between statin-induced cytotoxicity and MCT4 expression in RD cells.
3.A Clinical Study Evaluating The Effects of Fluvastatin on Serum Osteoprotegerin Levels in Rheumatoid Arthritis Patients.
Hegazy SK1, El-Ghany SE2, El-Hefnawy ME2. J Clin Pharmacol. 2016 Feb 22. doi: 10.1002/jcph.725. [Epub ahead of print]
Osteoprotegerin (OPG), a member of the tumor necrosis factor receptor family, has been identified as a critical regulator of bone resorption. Considering the possible role of OPG in the rheumatoid arthritis disease (RA), and osteoclastogenesis suppression effects of statins, the present study aims to investigate the effects of fluvastatin on serum levels of OPG and disease activity score (DAS) in patients with RA. Forty patients with rheumatoid arthritis were randomized in a placebo-controlled trial to receive 40 mg fluvastatin or placebo as an adjunct to existing disease-modifying antirheumatic drugs (DMARDS) therapy (methotrexate, leflunomide, hydroxychloroquine). Patients were followed up over 12 weeks. OPG and disease activity variables were measured at baseline and after 12 weeks of treatment. After 12 weeks, the OPG level was significantly increased in the fluvastatin group compared to the placebo group. DAS-28 was significantly decreased in the fluvastatin group compared to the placebo group.
4.Drosophila Lung Cancer Models Identify Trametinib plus Statin as Candidate Therapeutic.
Levine BD1, Cagan RL2. Cell Rep. 2016 Feb 16;14(6):1477-87. doi: 10.1016/j.celrep.2015.12.105. Epub 2016 Jan 28.
We have developed a Drosophila lung cancer model by targeting Ras1(G12V)-alone or in combination with PTEN knockdown-to the Drosophila tracheal system. This led to overproliferation of tracheal tissue, formation of tumor-like growths, and animal lethality. Screening a library of FDA-approved drugs identified several that improved overall animal survival. We explored two hits: the MEK inhibitor trametinib and the HMG-CoA reductase inhibitor fluvastatin. Oral administration of these drugs inhibited Ras and PI3K pathway activity, respectively; in addition, fluvastatin inhibited protein prenylation downstream of HMG-CoA reductase to promote survival. Combining drugs led to synergistic suppression of tumor formation and rescue lethality; similar synergy was observed in human A549 lung adenocarcinoma cells. Notably, fluvastatin acted both within transformed cells and also to reduce whole-body trametinib toxicity in flies. Our work supports and provides further context for exploring the potential of combining statins with MAPK inhibitors such as trametinib to improve overall therapeutic index.
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