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Fluvastatin

Fluvastatin is a synthetic, lipid-lowering medication used to treat high cholesterol and reduce the risk of cardiovascular disease.
As a member of the statin drug class, Fluvastatin works by inhibiting 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase, the enzyme responsible for cholesterol biosynthesis in the liver.
This leads to a decrease in intracellular cholesterol levels and upregulation of low-density lipoprotein (LDL) receptors, resulting in enhanced clearance of LDL cholesterol from the bloodstream.
Fluvastatin has been shown to effectively lower total cholesterol, LDL cholesterol, and triglyceride levels, while also slightly increaseing high-density lipoprotein (HDL) cholesterol.
Its use is indicated for the treatment of primary hypercholesterolemia and mixed dyslipidemia, as well as for the prevention of cardiovascular events in patients at high risk.
Fluvastatin is generally well-tolerated, with potential side effects including myalgia, gastrointestinal disturbances, and elvatated liver enzymes.
Careful monitoring is recommended, especially in patients with pre-existing liver or kidney disease.

Most cited protocols related to «Fluvastatin»

1
Extracting Lipid and Diabetes Traits from EMRs
Cited 8 times
EMRs contain structured [International Classification of Diseases or ICD-9 (billing) codes and Current Procedural Terminology or CPT (procedure) codes; clinical lab test results, semi-structured, and unstructured (clinical notes) data, all of which can be used for electronic phenotyping. The data types currently available in the SD that can be accessed for electronic phenotyping include narratives (such as clinical notes, discharge summaries, history and physicals, problem lists, surgical reports, progress notes, letters), ICD-9 codes, CPT codes, forms (intake, assessment), reports [pathology, electrocardiograms (ECGs), echocardiograms], clinical communications, lab values and vital signs, medication orders, TraceMaster (ECGs), and the tumor registry [41 (link)].
Electronic phenotyping has been previously described for BMI in EAGLE BioVU [42 ]. To extract lipid and type 2 diabetes traits from EAGLE BioVU EMRs, laboratory measurements were queried for glucose, HbA1c, HDL-C, insulin, LDL-C, total cholesterol, and triglycerides. Records were also queried for calculated LDL-C. Prescription medication is available in the SD through MedEx [43 (link)], an algorithm that extracts medications and their signature mentions from free-text entries available in the EMR.
For each adult patient (>18 years), median values were calculated for a) measurements taken when no medications are prescribed (“pre-medication” values) and b) measurements taken at first mention of medication and post mention of medication (“post-medication” values). We used the following medication class and list to identify lipid measurements determined at the time or after patients were prescribed lipid-lowering medications

Statins (also known as HMG CoA reductase inhibitors, atorvastatin (Lipitor®), fluvastatin (Lescol®), lovastatin (Mevacor®, Altoprev™), pravastatin (Pravachol®), rosuvastatin calcium (Crestor®), simvastatin (Zocor®), lovastatin + niacin (Advicor®), atorvastatin + amlodipine (Caduet®), and simvastatin + ezetimibe (Vytorin™)

Selective cholesterol absorption inhibitors (ezetimibe (Zetia®))

Resins (cholestyramine (Questran®, Questran® Light, Prevalite®, Locholest®, Locholest® Light), colestipol (Colestid®), colesevelam Hcl (WelChol®))

Fibrates (gemfibrozil (Lopid®), fenofibrate (Antara®, Lofibra®, Tricor®, and Triglide™), clofibrate (Atromid-S))

Niacin

Crawford D.C., Goodloe R., Farber-Eger E., Boston J., Pendergrass S.A., Haines J.L., Ritchie M.D, & Bush W.S. (2015). Leveraging epidemiologic and clinical collections for genomic studies of complex traits. Human heredity, 79(0), 137-146.
Publication 2015
Adult Advicor Amlodipine Anticholesteremic Agents Atorvastatin Atromid Caduet Cholesterol Clofibrate Colesevelam Hydrochloride Colestipol Crestor Diabetes Mellitus, Non-Insulin-Dependent Eagle Echocardiography Electrocardiogram Ezetimibe Fenofibrate Fibrates Fluvastatin Gemfibrozil Glucose Hydroxymethylglutaryl-CoA Reductase Inhibitors Insulin Lescol Light Lipids Lipitor Lofibra Lopid Lovastatin lovastatin-niacin combination Mevacor Neoplasms Niacin Operative Surgical Procedures Patient Discharge Patients Pharmaceutical Preparations Physical Examination Pravachol Pravastatin Questran Resin, Cholestyramine Resins, Plant Rosuvastatin Calcium Signs, Vital Simvastatin Tricor Triglycerides Vytorin Welchol Zetia Zocor
2
Angiotensin-II and PPE Induced AAA Models
Cited 7 times
Male ApoE−/−/C57BL/6J mice or wild type C57BL/6J mice at 10–12 wk of age were obtained from the Jackson Laboratory, Bar Harbor, Maine, and housed at the Stanford Animal Facility, Stanford, CA. Animal care and experimental procedures were conducted in compliance with Stanford Laboratory Animal Care Guidelines. The Administrative Panel on Laboratory Animal Care at Stanford University approved all procedures involving mice.
Two mechanistically distinct, but complementary mouse AAA models were used in this study: subcutaneous Ang II infusion in ApoE−/− mice (Ang II/ApoE−/− model) and intra-aortic PPE infusion in C57BL/6J mice (PPE model). In most experiments, ApoE−/− mice were fed chow supplemented with irbesartan (50 mg/kg), telmisartan (10 mg/kg) or bosentan (100 mg/kg), or were daily given drinking water supplemented with fluvastatin (40 mg/kg) or doxycycline (100 mg/kg). As controls, separate groups of ApoE−/− mice for individual experiments were given the standard chow and drinking water without drug supplementation. One week later, to induce AAAs, all mice were subcutaneously implanted with osmotic minipumps (Alzet model 2004, Durect Corporation, Cupertino, CA) for continuous infusion of Ang II at 1000 ng/kg/min, and treated continuously with their respective drugs for 28 days [9] (link). In additional experiments, C57BL/6J mice were fed telmisartan-supplemented chow (10 mg/kg) or the standard chow. One week thereafter, AAAs were created by transient intra-aortic infusion of PPE as described previously [93] (link), and these mice were continuously fed with the chow with or without telmisartan supplementation for additional 2 wk. In all experiments, doses for two ARBs and bosentan were selected based on published mouse studies in which each drug lowered blood pressure and/or suppressed cardiovascular pathology [94] (link)–[96] (link).
Iida Y., Xu B., Schultz G.M., Chow V., White J.J., Sulaimon S., Hezi-Yamit A., Peterson S.R, & Dalman R.L. (2012). Efficacy and Mechanism of Angiotensin II Receptor Blocker Treatment in Experimental Abdominal Aortic Aneurysms. PLoS ONE, 7(12), e49642.
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Publication 2012
Animals Animals, Laboratory Aorta ApoE protein, human Bosentan Cardiovascular System Doxycycline Fluvastatin Irbesartan Males Mice, House Mice, Inbred C57BL Osmosis Pharmaceutical Preparations Subcutaneous Infusions Telmisartan Transients Triple-A Syndrome
3
Statin Use in Taiwan from 2000-2013
Cited 5 times
Statins currently used in Taiwan from 2000 to 2013 were identified as follows: atorvastatin, lovastatin, fluvastatin, pravastatin, rosuvastatin, and simvastatin. Prescription history of statins and non-statin lipid-lowering drugs was collected. To reduce the biased results, subjects whose final prescriptions for statins were filled >12 months before the index date were excluded from the study. Therefore, only subjects whose final prescriptions for statins were filled within 12 months before the index date were included. Subjects who had at least one prescription of medications before the index date were defined as “ever use.” Subjects who never had one prescription of medications before the index date were defined as “never use.” The definition of medications use was adapted from previous studies (Lai et al., 2015 (link), 2016 (link)).
Liao K.F., Lin C.L, & Lai S.W. (2017). Population-Based Case-Control Study Assessing the Association between Statins Use and Pulmonary Tuberculosis in Taiwan. Frontiers in Pharmacology, 8, 597.
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Publication 2017
Atorvastatin Fluvastatin Hydroxymethylglutaryl-CoA Reductase Inhibitors Hypolipidemic Agents Lovastatin Pharmaceutical Preparations Pravastatin Prescription Drugs Prescriptions Rosuvastatin Simvastatin
4
Screening for Anti-Amoebic Compounds
Cited 4 times
The phenotypic drug susceptibility assays were performed as previously described using CellTiter-Glo v2.0 (CTG) (Promega, Madison, WI)44,49,63. The ReFrame collection of 12,000 compounds assembled at Calibr–Scripps were prepared in 384-well (Corning, White Flat bottom 3570) plate format at screening concentrations of 5μM (30nL of 10mM stock concentration/well in dimethylsulfoxide (DMSO)) using the Labcyte Echo 555 for acoustic compound dispensing. The first round was to screen in a single-point assay with 3,000 Naegleria/well, 600 Acanthamoeba/well or 4,000 Balamuthia/well in a total volume of 60μl. Prior to initiating drug screening, a maximum of 2% total hits from the library were predetermined for follow up from Calibr-Scripps for all screening projects. Drug spotted plates from Calibr-Scripps were left, at room temperature, to thaw overnight and parasites were plated using the Biomek NXp automated liquid handler (Beckman Coulter). Hits were defined as compounds that produced > -40% (for Naegleria) or > -50% (for Acanthamoeba and Balamuthia) of normalized growth inhibition compared to the negative growth control (0.5% DMSO) and positive controls that produced ~100% inhibition of amoebae cell populations. Posaconazole, azithromycin and DB2385A all at 1μM were used for controls for Naegleria and Acanthamoeba; artovastatin, fluvastatin and simvastatin all at 1μM were used as controls for Balamuthia. The second round was to verify the initial active hits from round I, hits were identified and serially diluted in duplicate from 5μM to 2nM in a 1:3, 8 point dilution series in 384-well plates with the same number of amoebae for Naegleria, Acanthamoeba and Balamuthia with the exact same controls and concentrations for each respective amoebae to generate the concentration for half-maximal activity derived from the hill equation model (qAC50). Dose-response curve fitting was analysed with Genedata Analyser software using the Smart Fit function. All assayed plates were incubated at the genus optimum growth temperature described above and tested for a period of 72 hours.
Rice C.A., Colon B.L., Chen E., Hull M.V, & Kyle D.E. (2020). Discovery of repurposing drug candidates for the treatment of diseases caused by pathogenic free-living amoebae. PLoS Neglected Tropical Diseases, 14(9), e0008353.
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Publication 2020
Acanthamoeba Acoustics Amoeba Azithromycin cDNA Library Cells ECHO protocol Fluvastatin Naegleria Parasites Pharmaceutical Preparations Phenotype Population Group posaconazole Promega Psychological Inhibition Simvastatin Sulfoxide, Dimethyl Susceptibility, Disease Technique, Dilution
5
Measuring Statin Medication Use
Cited 4 times
All patients who were prescribed statin medications in any VA pharmacy during the study observation period were identified. Statin prescriptions included simvastatin, lovastatin, fluvastatin, pravastatin, atorvastatin and cerivastatin. We collected the dates of prescriptions ordered, the number of days prescribed, number of pills per prescription and number of refills ordered. With this information the statin “defined daily dose” (DDD) was calculated for each subject. The DDD is a validated unit for measuring a prescribed drug amount, and is defined as the average maintenance dose per day of a drug consumed in an adult [33 ]. It is calculated as:
DDD=(total amount of drug prescribed on a daily basis to a patient)/(amount of drug in a DDD)[33]. The DDD was re-calculated annually for each year of the study observation period.
The “cumulative defined daily dose” (cDDD) was calculated from the DDD. The cDDD is defined as the total sum of dispensed DDDs of a given medication. Both the DDD and cDDD are recommended by the World Health Organization (WHO) and are widely used for comparison of medications, including statins, along a similar standard [33 ]. Statin use was defined as >28 cDDDs of statin medications prescribed during the study period. Similar information was collected for non-statin lipid lowering agents (cholestyramine, colesevelam, colestipol, ezetimibe, niacin, niacinimide), triglyceride-lowering agents (clofibrate, fenofibrate, gemfibrozil), as well as the antidiabetic agents Metformin, sulfonylureas and thiazolidinedione.
Simon T.G., Bonilla H., Yan P., Chung R.T, & Butt A.A. (2016). Atorvastatin and fluvastatin are associated with dose-dependent reductions in cirrhosis and HCC, among patients with HCV Results from ERCHIVES. Hepatology (Baltimore, Md.), 64(1), 47-57.
Publication 2016
2,4-thiazolidinedione Adult Antidiabetics Atorvastatin cerivastatin Clofibrate Colesevelam Colestipol Contraceptives, Oral Ezetimibe Fenofibrate Fluvastatin Gemfibrozil Hydroxymethylglutaryl-CoA Reductase Inhibitors Hypolipidemic Agents Lovastatin Metformin Niacin Patients Pharmaceutical Preparations Pravastatin Resin, Cholestyramine Simvastatin Sulfonylurea Compounds Triglycerides

Most recents protocols related to «Fluvastatin»

1
Statins Alleviate LS Membrane Remodeling
Not available on PMC !

Example 2

This example demonstrates that statins alleviate LS membrane remodeling phenotypes.

Statins decrease cholesterol (Cho) biosynthesis by inhibiting 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase (FIG. 2A and McFarland et al., Int J Mol Sci 15: 20607-20637 (2014)); consequently, they also down-modulate the downstream synthesis of two intermediates (farnesyl-pyrophosphate and geranyl-geranyl-pyrophosphate) required for RhoA prenylation, which in turn is essential for GTPase membrane anchoring and activation (del Real et al., J Exp Med 200: 541-547 (2004); Demierre et al., Nat Rev Cancer 5: 930-942 (2005); and FIG. 2A). They also have been shown to be active against the RhoA hyperactivation observed in certain cancers (Zhong et al., Cancer Treat Rev 41: 554-567 (2015)).

Several generation statins (Maji et al., Indian J Endocrinol Metab 17: 636-646 (2013)), including fluvastatin, atorvastatin, pitavastatin and rosuvastatin, were tested for their ability to ameliorate LS spreading defects. All statins mitigated to a certain extent the LS spreading phenotype; however, rosuvastatin produced the best results (rosuvastatin>pitavastatin>>>simvastatin and others) in terms of maximizing rescue effect over needed dose and toxicity (FIG. 2B and data not shown).

Phenotype alleviation was observed following the use of an acute rosuvastatin dose (100 μM for 1 h), but similar effect was also evident using lower concentrations (1-10 μM) sustained over longer periods of time (≥72 h; FIG. 2B). Importantly, the latter usage scheme better emulated currently approved treatment conditions with statins that render an effective concentration of free drug in plasma of up to 10 μM (Bjorkhem-Bergman et al., Br J Clin Pharmacol 72: 164-165 (2011)). Following exposure to statins, viability and stress-induced changes in morphology were determined for LS cells (FIG. 2C). Our results showed that rosuvastatin had minimal toxicity, while other statins including pitavastatin and cerivastatin were substantially toxic (FIG. 2C, D). It should be noted that the latter was recalled from the market due to severe rhabdomyolysis effects (Maji et al. (2013), supra). In addition, and to monitor the magnitude of the statins' effects on HMG-CoA reductase in LS cells, we incubated patient fibroblasts in Cho-free media supplemented with vehicle or statins and determined the uptake of fluorescently labeled Cho. While vehicle-treated cells had normal production of endogenous Cho, the ones exposed to statins (due to their HMG-CoA reductase inhibitory activity) were Cho-depleted at a different extent as evidenced by a substantial increase in the uptake of exogenous, fluorescently labeled Cho (FIG. 2E). Our results suggested that rosuvastatin in addition to being less toxic at the chronic dose, led to a less acute inhibition of cholesterol biosynthesis (and consequently to a lower demand of exogenous, fluorescent-analog uptake). However, in contrast with the relatively innocuous chronic exposure (10 μM for ≥72 h), we observed that acute doses of rosuvastatin (100 μM) induced toxicity when exposure time≥15 h (data not shown).

US11857549B2. Compositions and methods for the treatment of Lowe syndrome (2024-01-02). Purdue Research Foundation [US]. Inventors: Ruben Claudio Aguilar [US].
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Patent 2024
Anabolism Atorvastatin Cells cerivastatin Cholesterol cholesterol reductase Coenzyme A farnesyl pyrophosphate Fibroblasts Fluvastatin geranylgeranyl pyrophosphate Guanosine Triphosphate Phosphohydrolases Lanugo Malignant Neoplasms Oculocerebrorenal Syndrome Oxidoreductase Patients Pharmaceutical Preparations Phenotype pitavastatin Plasma Prenylation Psychological Inhibition Rhabdomyolysis RHOA protein, human Rosuvastatin Simvastatin Tissue, Membrane Training Programs
2
Ethnic Differences in Statin Response

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Publication 2023
African American Animals Arabs Asian Persons Atorvastatin Caribbean People Caucasoid Races Chinese Chromosomes, Human, Pair 12 Coenzymes Ethnic Groups Ethnicity Females Fluvastatin Genes Genetic Polymorphism Genome Haplotypes Hepatocyte Hispanics Hydrolysis Hydroxymethylglutaryl-CoA Reductase Inhibitors Japanese Lipids Lovastatin Males Metabolic Clearance Rate Metabolism Muscle Tissue Organic Anion Transport Polypeptides Patients Pharmaceutical Preparations Physicians Plasma Pravastatin Rosuvastatin Secondary Prevention Simvastatin Single Nucleotide Polymorphism Therapeutic Effect Therapeutics Tissue, Membrane vastatin Woman
3
Cardiovascular Disease Risk Factors
We extracted information on each subject on demographics, survey data, cholesterol, LDL-C, and triglyceride levels, as well as use of statins and PCSK9 inhibitor use. ASCVD was defined based on all listed manifestations of coronary artery disease, cerebrovascular disease (excluding hemorrhagic stroke), and peripheral arterial disease. Statin use was defined as a documented prescription (generic or branded) of atorvastatin, cerivastatin, fluvastatin, lovastatin, pitavastatin, pravastatin, rosuvastatin, and/or simvastatin. Statin intensity was categorized into those at high and low/moderate intensities according to US guidelines [12 (link)]. Ezetimibe and icosapent ethyl use was also captured, and PCSK9 inhibitors included evolocumab and alirocumab. We additionally obtained survey data on health insurance status, types of health insurance, BMI, education level, cigarette smoking status, and income.
Akbarpour M., Devineni D., Gong Y, & Wong N.D. (2023). Dyslipidemia Treatment and Lipid Control in US Adults with Diabetes by Sociodemographic and Cardiovascular Risk Groups in the NIH Precision Medicine Initiative All of Us Research Program. Journal of Clinical Medicine, 12(4), 1668.
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Publication 2023
alirocumab Atorvastatin Cerebrovascular Disorders cerivastatin Cholesterol Coronary Arteriosclerosis evolocumab Ezetimibe Fluvastatin Generic Drugs Health Insurance Hemorrhagic Stroke Hydroxymethylglutaryl-CoA Reductase Inhibitors icosapent ethyl Lovastatin PCSK9 Inhibitors PCSK9 protein, human Peripheral Arterial Diseases pitavastatin Pravastatin Rosuvastatin Simvastatin Triglycerides
4
Routine Therapies for Acute Coronary Syndrome
We included therapies widely embraced by the clinical community as routine therapies. Specifically, therapies were considered routine if they were strongly (i.e., Recommendation Class I) and consistently recommended by clinical practice guidelines (CPGs) based on sufficient evidence (i.e., Level of Evidence A) in both mainland China and the US.
In April 2021, we screened the CPGs developed by the Chinese Society of Cardiology and the American College of Cardiology/American Heart Association. We identified four routine therapies:

Reperfusion, including primary percutaneous coronary intervention (PCI) and fibrinolytic therapy. Fibrinolytic therapy could be performed by tenecteplase, reteplase, alteplase, streptokinase, urokinase, or prourokinase. RCTs evaluating delayed PCI or fibrinolytic therapy were excluded.

P2Y12 receptor inhibitors, including clopidogrel, ticagrelor, and prasugrel. RCTs evaluating loading P2Y12 receptor inhibitors administered before PCI or fibrinolytic therapy were excluded.

Statins, including atorvastatin, fluvastatin, lovastatin, pravastatin, rosuvastatin, simvastatin, and pitavastatin. We excluded RCTs evaluating loading statin therapy administered before PCI or fibrinolytic therapy.

Anticoagulants, including unfractionated heparin, enoxaparin, fondaparinux, and bivalirudin. We only included RCTs evaluating anticoagulants administered with fibrinolytic therapy.

Jia Y., Liang J., Wang W., Wei X., Xiao S, & Robinson K.A. (2023). Assessment of redundant randomized clinical trials among patients with ST segment elevation myocardial infarction. BMC Medicine, 21, 69.
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Publication 2023
Alteplase Anticoagulants Atorvastatin bivalirudin Cardiovascular System Chinese Clopidogrel Enoxaparin Fluvastatin Fondaparinux Heparin Hydroxymethylglutaryl-CoA Reductase Inhibitors inhibitors Lovastatin Percutaneous Coronary Intervention pitavastatin Prasugrel Pravastatin Reperfusion reteplase Rosuvastatin saruplase Simvastatin Streptokinase Tenecteplase Therapeutics Thrombolytic Therapy Ticagrelor Urokinase
5
Assessing Statin Dispensing Policy Impact
We used proxies to assess the dispensing policy and the number of SRM. The first outcome was “the difference in dose change”. This was measured by comparing the dose category of the first dispensing to dose category of the last dispensing. The dose categories of simvastatin (ATC code C10AA01) were 10, 20 and 40 mg and atorvastatin (ATC code C10AA05) were 5, 10, 20, 40, and 80 mg based on the defined daily dose equivalent (DDD-E).
The second outcome was any change in drug use. This was categorized by discontinuation and switching. Discontinuation was defined as no new statins dispensed within 90 days after the theoretical end date of the last dispensing and no other cholesterol-lowering drug within 90 days after the end of the last dispensing or no further dispensing issued for any cholesterol-lowering drug and more than 90 days available to the right censoring date. Switching was defined as no new statins dispensed within 90 days after the theoretical end date of the last dispensing and another cholesterol-lowering drug within 90 days after the theoretical end date of the last dispensing [44 (link),45 (link)]. Switching was specified by changing from simvastatin or atorvastatin to another statin (simvastatin, atorvastatin, rosuvastatin, pravastatin, or fluvastatin) or cholesterol-lowering drug (acipimox, ezetimibe, bezafibrate, ciprofibrate, fenofibrate, gemfibrozil, colesevelam, cholestyramine, nicotinic acid, docosapentaenoic acid, or eicosapentaenoic acid) [46 ].
The third outcome was the difference in time to establish stable dosing, defined as the time until three times successively the same dose was dispensed based on DDD-E. After this moment, the dosing regimen was assumed to be stable. The time to establish stable dosing was used as a measure for health impact, i.e., when a patient has a stable dosing regimen sooner, they are assumed to have less SRM and need less health care visits.
Jansen M.E., Rigter T., Fleur T.M., Souverein P.C., Verschuren W.M., Vijverberg S.J., Swen J.J., Rodenburg W, & Cornel M.C. (2023). Predictive Value of SLCO1B1 c.521T>C Polymorphism on Observed Changes in the Treatment of 1136 Statin-Users. Genes, 14(2), 456.
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Publication 2023
acipimox Anticholesteremic Agents Atorvastatin Bezafibrate ciprofibrate Colesevelam docosapentaenoic acid Eicosapentaenoic Acid Ezetimibe Fenofibrate Fluvastatin Gemfibrozil Hydroxymethylglutaryl-CoA Reductase Inhibitors Niacin Patients Pharmaceutical Preparations Pravastatin Resin, Cholestyramine Rosuvastatin Simvastatin Treatment Protocols

Top products related to «Fluvastatin»

1
Fluvastatin by Merck Group
Sourced in United States, Germany
Fluvastatin is a synthetic statin medication used for the treatment of hypercholesterolemia. It is a potent inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, the rate-limiting enzyme in cholesterol biosynthesis.
2
Simvastatin by Merck Group
Sourced in United States, Germany, China, United Kingdom, France, Sao Tome and Principe, Japan, Slovenia, Sweden, Italy
Simvastatin is a laboratory instrument used for the analysis and measurement of chemical compounds. It is designed to accurately quantify the presence and concentration of specific substances in a given sample. The core function of Simvastatin is to provide precise and reliable data for research and scientific applications.
3
Lovastatin by Merck Group
Sourced in United States, Germany, United Kingdom
Lovastatin is a pharmaceutical compound used as an active ingredient in certain laboratory equipment. It is a naturally occurring statin medication that helps lower cholesterol levels.
4
Atorvastatin by Merck Group
Sourced in United States, Germany, United Kingdom, China
Atorvastatin is a laboratory equipment product manufactured by Merck Group. It is a type of statin, a class of medications used to lower cholesterol levels. The core function of Atorvastatin is to inhibit the enzyme HMG-CoA reductase, which plays a crucial role in the production of cholesterol in the body.
5
Fluvastatin by Selleck Chemicals
Sourced in United States
Fluvastatin is a laboratory equipment product used for research and analysis. It is a statin drug that inhibits the enzyme HMG-CoA reductase, which is involved in the production of cholesterol in the body. Fluvastatin is widely used in the pharmaceutical and scientific research fields.
6
Pravastatin by Merck Group
Sourced in United States, France, Spain, United Kingdom
Pravastatin is a pharmaceutical product developed by Merck Group for use in laboratory settings. It is a statin drug that helps lower cholesterol levels by inhibiting the enzyme HMG-CoA reductase, which plays a crucial role in the production of cholesterol in the body. Pravastatin can be used in research and testing applications that require the regulation of cholesterol levels.
7
Fluvastatin by Cayman Chemical
Sourced in United States
Fluvastatin is a synthetic statin compound used as a laboratory reagent. It is a member of the HMG-CoA reductase inhibitor class of drugs. Fluvastatin functions by inhibiting the enzyme HMG-CoA reductase, which is a key enzyme involved in the biosynthesis of cholesterol.
8
Mevalonate by Merck Group
Sourced in United States
Mevalonate is a chemical compound used in laboratory settings for research and analysis purposes. It serves as a key intermediate in the biosynthesis of various molecules, including sterols, terpenes, and isoprenoids. Mevalonate plays a critical role in cellular metabolism and is essential for the proper functioning of various biological processes.
9
Mevalonolactone by Merck Group
Sourced in United States, Switzerland, Germany
Mevalonolactone is a chemical compound used as a laboratory reagent. It is a precursor in the biosynthesis of various isoprenoids, such as cholesterol, steroids, and terpenes. Mevalonolactone is commonly used in biochemical and cell biology research applications.
10
Fluvastatin sodium hydrate by Merck Group
Sourced in United States
Fluvastatin sodium hydrate is a white to off-white crystalline powder that is used as a reference standard in analytical applications. It is the sodium salt of the active ingredient in the statin medication fluvastatin.

More about "Fluvastatin"

Fluvastatin is a member of the statin drug class, which are synthetic lipid-lowering medications used to treat high cholesterol (hypercholesterolemia) and reduce the risk of cardiovascular disease.
Statins, such as Simvastatin, Lovastatin, Atorvastatin, and Pravastatin, work by inhibiting the enzyme 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase, which is responsible for cholesterol biosynthesis in the liver.
This leads to a decrease in intracellular cholesterol levels and an upregulation of low-density lipoprotein (LDL) receptors, resulting in enhanced clearance of LDL cholesterol from the bloodstream.
Fluvastatin has been shown to effectively lower total cholesterol, LDL cholesterol, and triglyceride levels, while also slightly increasing high-density lipoprotein (HDL) cholesterol.
Its use is indicated for the treatment of primary hypercholesterolemia and mixed dyslipidemia, as well as for the prevention of cardiovascular events in patients at high risk.
Fluvastatin is generally well-tolerated, with potential side effects including myalgia, gastrointestinal disturbances, and elevated liver enzymes.
Careful monitoring is recommended, especially in patients with pre-existing liver or kidney disease.
Fluvastatin sodium hydrate is the active ingredient in the Fluvastatin medication, and Mevalonolactone is a key intermediate in the cholesterol biosynthesis pathway that is inhibited by statins.
By understanding the mechanisms of action and pharmacological properties of Fluvastatin and related statins, researchers can optimize their studies and enhance the reproducibility and accuracy of their findings using tools like PubCompare.ai.