Fluvastatin - CAS 93957-54-1
Catalog number: 93957-54-1
Category: Inhibitor
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Molecular Formula:
Molecular Weight:
HMG-CoA Reductase (HMGCR)
Fluvastatin is a competitive inhibitor of hydroxymethylglutaryl-coenzyme A reductase (HMGCR) with IC50 of 8 nM. It belongs to a class of the statin drug and is structurally distinct from the fungal derivatives of this therapeutic class. It binds of the substrate HMG-CoA with Ki value of 0.3 nM but not with respect to binding of NADPH. It is marketed under the trade name Lescol® and is used to treat hypercholesterolemia and to prevent cardiovascular disease. It induces G2/M phase arrest and has antilipemic effect.
Solid powder
XU-62320; XU 62320; XU62320; Cranoc;Lescol;(+)-(3R,5S)-fluvastati;(E,3R,5S)-7-[3-(4-fluorophenyl)-1-propan-2-ylindol-2-yl]-3,5-dihydroxyhept-6-enoic acid;6-Heptenoic acid,7-[3-(4-fluorophenyl)-1-(1-methylethyl)-1H-indol-2-yl]-3,5-dihydroxy-,[R*,S*-(E)]-
10 mM in DMSO
-20°C Freezer
Fluvastatin is used to treat hypercholesterolemia and to prevent cardiovascular disease. It has antilipemic effect.
Quality Standard:
In-house standard
Shelf Life:
2 month in rt, long time
Kilogram to ton
Boiling Point:
681.8±55.0 °C | Condition: Press: 760 Torr
Melting Point:
193.9-196.9 °C
1.23±0.1 g/cm3 | Condition: Temp: 20 °C Press: 760 Torr
Canonical SMILES:
1.Statin-related aminotransferase elevation according to baseline aminotransferases level in real practice in Korea.
Kim HS1,2, Lee SH3, Kim H4, Lee SH2, Cho JH2, Lee H5, Yim HW6, Kim SH7, Choi IY1, Yoon KH1,2, Kim JH3. J Clin Pharm Ther. 2016 Mar 25. doi: 10.1111/jcpt.12377. [Epub ahead of print]
WHAT IS KNOWN AND OBJECTIVE: Higher rate of statin-related hepatotoxicity has been reported for Koreans than for Westerners. Moreover, statin-related aminotransferase elevation for those who show borderline levels of aspartate transaminase (AST) and alanine transaminase (ALT) (≤×3 of UNL) at baseline has not been fully investigated.
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.Repositioning "old" drugs for new causes: identifying new inhibitors of prostate cancer cell migration and invasion.
Shah ET1,2, Upadhyaya A1,2, Philp LK1,2, Tang T1, Skalamera D3,2, Gunter J1,2, Nelson CC1,2, Williams ED1,2, Hollier BG4,5. Clin Exp Metastasis. 2016 Apr;33(4):385-99. doi: 10.1007/s10585-016-9785-y. Epub 2016 Mar 1.
The majority of prostate cancer (PCa) deaths occur due to the metastatic spread of tumor cells to distant organs. Currently, there is a lack of effective therapies once tumor cells have spread outside the prostate. It is therefore imperative to rapidly develop therapeutics to inhibit the metastatic spread of tumor cells. Gain of cell motility and invasive properties is the first step of metastasis and by inhibiting motility one can potentially inhibit metastasis. Using the drug repositioning strategy, we developed a cell-based multi-parameter primary screening assay to identify drugs that inhibit the migratory and invasive properties of metastatic PC-3 PCa cells. Following the completion of the primary screening assay, 33 drugs were identified from an FDA approved drug library that either inhibited migration or were cytotoxic to the PC-3 cells. Based on the data obtained from the subsequent validation studies, mitoxantrone hydrochloride, simvastatin, fluvastatin and vandetanib were identified as strong candidates that can inhibit both the migration and invasion of PC-3 cells without significantly affecting cell viability.
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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