The nurse would question a prescription for simvastatin in a patient with which condition
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Ed4Nurses.com, Sagamore Hills, Ohio Nursing Made Incredibly Easy!: July 2005 - Volume 3 - Issue 4 - p 51-52 Summary Simvastatin is an HMG-CoA reductase inhibitor used to lower lipid levels and reduce the risk of cardiovascular events including myocardial infarction and stroke. Brand NamesCholib, FloLipid, Simcor, Vytorin, Zocor Generic NameSimvastatinDrugBank Accession NumberDB00641BackgroundSimvastatin, also known as the brand name product Zocor, is a lipid-lowering drug derived synthetically from a fermentation product of Aspergillus terreus. It belongs to the statin class of medications, which are used to lower the risk of cardiovascular disease and manage abnormal lipid levels by inhibiting the endogenous production of cholesterol in the liver. More specifically, statin medications competitively inhibit the enzyme hydroxymethylglutaryl-coenzyme A (HMG-CoA) Reductase,2 which catalyzes the conversion of HMG-CoA to mevalonic acid and is the third step in a sequence of metabolic reactions involved in the production of several compounds involved in lipid metabolism and transport including cholesterol, low-density lipoprotein (LDL) (sometimes referred to as "bad cholesterol"), and very low-density lipoprotein (VLDL). Prescribing of statin medications is considered standard practice following any cardiovascular events and for people with a moderate to high risk of development of CVD, such as those with Type 2 Diabetes. The clear evidence of the benefit of statin use coupled with very minimal side effects or long term effects has resulted in this class becoming one of the most widely prescribed medications in North America.3,4 Simvastatin and other drugs from the statin class of medications including atorvastatin, pravastatin, rosuvastatin, fluvastatin, and lovastatin are considered first-line options for the treatment of dyslipidemia.3,4 Increasing use of the statin class of drugs is largely due to the fact that cardiovascular disease (CVD), which includes heart attack, atherosclerosis, angina, peripheral artery disease, and stroke, has become a leading cause of death in high-income countries and a major cause of morbidity around the world.5 Elevated cholesterol levels, and in particular, elevated low-density lipoprotein (LDL) levels, are an important risk factor for the development of CVD.3,16 Use of statins to target and reduce LDL levels has been shown in a number of landmark studies to significantly reduce the risk of development of CVD and all-cause mortality.6,7,8,9,10,14 Statins are considered a cost-effective treatment option for CVD due to their evidence of reducing all-cause mortality including fatal and non-fatal CVD as well as the need for surgical revascularization or angioplasty following a heart attack.3,4 Evidence has shown that even for low-risk individuals (with <10% risk of a major vascular event occurring within 5 years) statins cause a 20%-22% relative reduction in major cardiovascular events (heart attack, stroke, coronary revascularization, and coronary death) for every 1 mmol/L reduction in LDL without any significant side effects or risks.11,12 While all statin medications are considered equally effective from a clinical standpoint, rosuvastatin is considered the most potent; doses of 10 to 40mg rosuvastatin per day were found in clinical studies to result in a 45.8% to 54.6% decrease in LDL cholesterol levels, while simvastatin has been found to have an average decrease in LDL-C of ~35%.27,13,14,18 Potency is thought to correlate to tissue permeability as the more lipophilic statins such as simvastatin are thought to enter endothelial cells by passive diffusion, as opposed to hydrophilic statins such as pravastatin and rosuvastatin which are taken up into hepatocytes through OATP1B1 (organic anion transporter protein 1B1)-mediated transport.15,20 Despite these differences in potency, several trials have demonstrated only minimal differences in terms of clinical outcomes between statins.9 TypeSmall MoleculeGroupsApprovedStructureWeightAverage: 418.5662Monoisotopic: 418.271924326 Chemical FormulaC25H38O5Synonyms
Simvastatin is indicated for the treatment of hyperlipidemia to reduce elevated total cholesterol (total-C), low-density lipoprotein cholesterol (LDL‑C), apolipoprotein B (Apo B), and triglycerides (TG), and to increase high-density lipoprotein cholesterol (HDL-C).29,30 This includes the treatment of primary hyperlipidemia (Fredrickson type IIa, heterozygous familial and nonfamilial), mixed dyslipidemia (Fredrickson type IIb), hypertriglyceridemia (Fredrickson type IV hyperlipidemia), primary dysbetalipoproteinemia (Fredrickson type III hyperlipidemia), homozygous familial hypercholesterolemia (HoFH) as an adjunct to other lipid-lowering treatments, as well as adolescent patients with Heterozygous Familial Hypercholesterolemia (HeFH).29,30 Simvastatin is also indicated to reduce the risk of cardiovascular morbidity and mortality including myocardial infarction, stroke, and the need for revascularization procedures. It is primarily used in patients at high risk of coronary events because of existing coronary heart disease, diabetes, peripheral vessel disease, history of stroke or other cerebrovascular disease.29,30 Prescribing of statin medications is considered standard practice following any cardiovascular events and for people with a moderate to high risk of development of CVD. Statin-indicated conditions include diabetes mellitus, clinical atherosclerosis (including myocardial infarction, acute coronary syndromes, stable angina, documented coronary artery disease, stroke, trans ischemic attack (TIA), documented carotid disease, peripheral artery disease, and claudication), abdominal aortic aneurysm, chronic kidney disease, and severely elevated LDL-C levels.3,4 Reduce drug development failure rates Build, train, & validate machine-learning models Build, train, & validate predictive machine-learning models with structured datasets. Associated Conditions
Avoid life-threatening adverse drug events Improve clinical decision support with information on contraindications & blackbox warnings, population restrictions, harmful risks, & more. Avoid life-threatening adverse drug events & improve clinical decision support. PharmacodynamicsSimvastatin is an oral antilipemic agent which inhibits HMG-CoA reductase. It is used to lower total cholesterol, low density lipoprotein-cholesterol (LDL-C), apolipoprotein B (apoB), non-high density lipoprotein-cholesterol (non-HDL-C), and trigleride (TG) plasma concentrations while increasing HDL-C concentrations. High LDL-C, low HDL-C and high TG concentrations in the plasma are associated with increased risk of atherosclerosis and cardiovascular disease. The total cholesterol to HDL-C ratio is a strong predictor of coronary artery disease and high ratios are associated with higher risk of disease. Increased levels of HDL-C are associated with lower cardiovascular risk. By decreasing LDL-C and TG and increasing HDL-C, rosuvastatin reduces the risk of cardiovascular morbidity and mortality.3,4 Elevated cholesterol levels, and in particular, elevated low-density lipoprotein (LDL) levels, are an important risk factor for the development of CVD.3 Use of statins to target and reduce LDL levels has been shown in a number of landmark studies to significantly reduce the risk of development of CVD and all-cause mortality.6,7,8,9,10 Statins are considered a cost-effective treatment option for CVD due to their evidence of reducing all-cause mortality including fatal and non-fatal CVD as well as the need for surgical revascularization or angioplasty following a heart attack.3,4 Evidence has shown that even for low-risk individuals (with <10% risk of a major vascular event occurring within 5 years) statins cause a 20%-22% relative reduction in major cardiovascular events (heart attack, stroke, coronary revascularization, and coronary death) for every 1 mmol/L reduction in LDL without any significant side effects or risks.11,12 Skeletal Muscle Effects Simvastatin occasionally causes myopathy manifested as muscle pain, tenderness or weakness with creatine kinase (CK) above ten times the upper limit of normal (ULN). Myopathy sometimes takes the form of rhabdomyolysis with or without acute renal failure secondary to myoglobinuria, and rare fatalities have occurred. Predisposing factors for myopathy include advanced age (≥65 years), female gender, uncontrolled hypothyroidism, and renal impairment. Chinese patients may also be at increased risk for myopathy. In most cases, muscle symptoms and CK increases resolved when treatment was promptly discontinued.29,30 In a clinical trial database of 41,413 patients, the incidence of myopathy was approximately 0.03% and 0.08% at 20 and 40 mg/day, respectively, while the risk of myopathy with simvastatin 80 mg (0.61%) was disproportionately higher than that observed at the lower doses. It's therefore recommended that the 80mg dose of simvastatin should be used only in patients who have been taking simvastatin 80 mg chronically (e.g., for 12 months or more) without evidence of muscle toxicity. As well, patients already stabilized on simvastatin 80mg should be monitored closely for evidence of muscle toxicity; if they need to be initiated on an interacting drug that is contraindicated or is associated with a dose cap for simvastatin, that patient should be switched to an alternative statin with less potential for the drug-drug interaction.29,30 The risk of myopathy during treatment with simvastatin may be increased with concurrent administration of interacting drugs such as fenofibrate, niacin, gemfibrozil, cyclosporine, and strong inhibitors of the CYP3A4 enzyme. Cases of myopathy, including rhabdomyolysis, have been reported with HMG-CoA reductase inhibitors coadministered with colchicine, and caution should therefore be exercised when prescribing these two medications together.29,30 Liver Enzyme Abnormalities Persistent increases (to more than 3X the ULN) in serum transaminases have occurred in approximately 1% of patients who received simvastatin in clinical studies. When drug treatment was interrupted or discontinued in these patients, the transaminase levels usually fell slowly to pretreatment levels. The increases were not associated with jaundice or other clinical signs or symptoms. 29,30 In the Scandinavian Simvastatin Survival Study (4S),14 the number of patients with more than one transaminase elevation to >3 times the ULN, over the course of the study, was not significantly different between the simvastatin and placebo groups (14 [0.7%] vs. 12 [0.6%]). The frequency of single elevations of ALT to 3 times the ULN was significantly higher in the simvastatin group in the first year of the study (20 vs. 8, p=0.023), but not thereafter. In the HPS (Heart Protection Study),10 in which 20,536 patients were randomized to receive simvastatin 40 mg/day or placebo, the incidences of elevated transaminases (>3X ULN confirmed by repeat test) were 0.21% (n=21) for patients treated with simvastatin and 0.09% (n=9) for patients treated with placebo.29,30 Endocrine Effects Increases in HbA1c and fasting serum glucose levels have been reported with HMG-CoA reductase inhibitors, including simvastatin.29 Although cholesterol is the precursor of all steroid hormones, studies with simvastatin have suggested that this agent has no clinical effect on steroidogenesis. Simvastatin caused no increase in biliary lithogenicity and, therefore, would not be expected to increase the incidence of gallstones.30 Mechanism of actionSimvastatin is a prodrug in which the 6-membered lactone ring of simvastatin is hydrolyzed in vivo to generate the beta,delta-dihydroxy acid, an active metabolite structurally similar to HMG-CoA (hydroxymethylglutaryl CoA). Once hydrolyzed, simvastatin competes with HMG-CoA for HMG-CoA reductase, a hepatic microsomal enzyme, which catalyzes the conversion of HMG-CoA to mevalonate, an early rate-limiting step in cholesterol biosynthesis.2 Simvastatin acts primarily in the liver, where decreased hepatic cholesterol concentrations stimulate the upregulation of hepatic low density lipoprotein (LDL) receptors which increases hepatic uptake of LDL. Simvastatin also inhibits hepatic synthesis of very low density lipoprotein (VLDL).29,30 The overall effect is a decrease in plasma LDL and VLDL. At therapeutic doses, the HMG-CoA enzyme is not completely blocked by simvastatin activity, thereby allowing biologically necessary amounts of mevalonate to remain available. As mevalonate is an early step in the biosynthetic pathway for cholesterol, therapy with simvastatin would also not be expected to cause any accumulation of potentially toxic sterols. In addition, HMG-CoA is metabolized readily back to acetyl-CoA, which participates in many biosynthetic processes in the body.30 In vitro and in vivo animal studies also demonstrate that simvastatin exerts vasculoprotective effects independent of its lipid-lowering properties, also known as the pleiotropic effects of statins.15 This includes improvement in endothelial function, enhanced stability of atherosclerotic plaques, reduced oxidative stress and inflammation, and inhibition of the thrombogenic response. Statins have also been found to bind allosterically to β2 integrin function-associated antigen-1 (LFA-1), which plays an important role in leukocyte trafficking and in T cell activation.17
Peak plasma concentrations of both active and total inhibitors were attained within 1.3 to 2.4 hours post-dose. While the recommended therapeutic dose range is 10 to 40 mg/day, there was no substantial deviation from linearity of AUC with an increase in dose to as high as 120 mg. Relative to the fasting state, the plasma profile of inhibitors was not affected when simvastatin was administered immediately before a test meal.29,30 In a pharmacokinetic study of 17 healthy Chinese volunteers, the major PK parameters were as follows: Tmax 1.44 hours, Cmax 9.83 ug/L, t1/2 4.85 hours, and AUC 40.32ug·h/L.19 Simvastatin undergoes extensive first-pass extraction in the liver, the target organ for the inhibition of HMG-CoA reductase and the primary site of action. This tissue selectivity (and consequent low systemic exposure) of orally administered simvastatin has been shown to be far greater than that observed when the drug is administered as the enzymatically active form, i.e. as the open hydroxyacid.30 In animal studies, after oral dosing, simvastatin achieved substantially higher concentrations in the liver than in non-target tissues. However, because simvastatin undergoes extensive first-pass metabolism, the bioavailability of the drug in the systemic system is low. In a single-dose study in nine healthy subjects, it was estimated that less than 5% of an oral dose of simvastatin reached the general circulation in the form of active inhibitors.30 Genetic differences in the OATP1B1 (Organic-Anion-Transporting Polypeptide 1B1) hepatic transporter encoded by the SCLCO1B1 gene (Solute Carrier Organic Anion Transporter family member 1B1) have been shown to impact simvastatin pharmacokinetics. Evidence from pharmacogenetic studies of the c.521T>C single nucleotide polymorphism (SNP) showed that simvastatin plasma concentrations were increased on average 3.2-fold for individuals homozygous for 521CC compared to homozygous 521TT individuals.22,21 The 521CC genotype is also associated with a marked increase in the risk of developing myopathy, likely secondary to increased systemic exposure.23 Other statin drugs impacted by this polymorphism include rosuvastatin, pitavastatin, atorvastatin, lovastatin, and pravastatin.20 For patients known to have the above-mentioned c.521CC OATP1B1 genotype, a maximum daily dose of 20mg of simvastatin is recommended to avoid adverse effects from the increased exposure to the drug, such as muscle pain and risk of rhabdomyolysis.30 Evidence has also been obtained with other statins such as rosuvastatin that concurrent use of statins and inhibitors of Breast Cancer Resistance Protein (BCRP) such as elbasvir and grazoprevir increased the plasma concentration of these statins. Further evidence is needed, however a dose adjustment of simvastatin may be necessary. Other statin drugs impacted by this polymorphism include fluvastatin and atorvastatin.21 Volume of distributionRat studies indicate that when radiolabeled simvastatin was administered, simvastatin-derived radioactivity crossed the blood-brain barrier.29 Protein bindingBoth simvastatin and its β-hydroxyacid metabolite are highly bound (approximately 95%) to human plasma proteins.29,30 MetabolismSimvastatin is administered as the inactive lactone derivative that is then metabolically activated to its β-hydroxyacid form by a combination of spontaneous chemical conversion and enzyme-mediated hydrolysis by nonspecific carboxyesterases in the intestinal wall, liver, and plasma. Oxidative metabolism in the liver is primarily mediated by CYP3A4 and CYP3A5, with the remaining metabolism occurring through CYP2C8 and CYP2C9.25 The major active metabolites of simvastatin are β-hydroxyacid metabolite and its 6'-hydroxy, 6'-hydroxymethyl, and 6'-exomethylene derivatives.29,30 Polymorphisms in the CYP3A5 gene have been shown to affect the disposition of simvastatin and may provide a plausible explanation for interindividual variability of simvastatin disposition and pharmacokinetics.24 Hover over products below to view reaction partners Route of eliminationFollowing an oral dose of 14C-labeled simvastatin in man, 13% of the dose was excreted in urine and 60% in feces.29,30 Half-life4.85 hours19 ClearanceNot Available Adverse EffectsImprove decision support & research outcomes With structured adverse effects data, including: blackbox warnings, adverse reactions, warning & precautions, & incidence rates. Improve decision support & research outcomes with our structured adverse effects data. ToxicityNot Available Pathways
This information should not be interpreted without the help of a healthcare provider. If you believe you are experiencing an interaction, contact a healthcare provider immediately. The absence of an interaction does not necessarily mean no interactions exist.
Drug product information from 10+ global regions Our datasets provide approved product information including: Access drug product information from over 10 global regions. Product ImagesInternational/Other BrandsCholestat (Kalbe) / Colemin (Biohorm) / Labistatin (Sandoz) / Lipex (Merck Sharp & Dohme) / Medipo (Mediolanum Farmaceutici) / Nivelipol (Temis-Lostalo) / Simovil (Merck Sharp & Dohme) / Sinvacor (Merck Sharp & Dohme) / Sivastin (Sigma-Tau) / Sivatin (Rowex) / Sivinar (Anfarm) / Sorfox (Galex) / Sotovastin (Bros) / Starezin (Leovan Pharmaceuticals) / Starstat (Lupin) / Starzoko (Daewoong) / Stasiva (Pharmanel) / Statex (Pliva) / Staticor (Darnitsa) / Statinal (Alet Pharmaceuticals) / Stativer (Iapharm) / SynvinolinBrand Name Prescription Products
InChI=1S/C25H38O5/c1-6-25(4,5)24(28)30-21-12-15(2)11-17-8-7-16(3)20(23(17)21)10-9-19-13-18(26)14-22(27)29-19/h7-8,11,15-16,18-21,23,26H,6,9-10,12-14H2,1-5H3/t15-,16-,18+,19+,20-,21-,23-/m0/s1 IUPAC Name(1S,3R,7S,8S,8aR)-8-{2-[(2R,4R)-4-hydroxy-6-oxooxan-2-yl]ethyl}-3,7-dimethyl-1,2,3,7,8,8a-hexahydronaphthalen-1-yl 2,2-dimethylbutanoate SMILES[H][C@]12[C@H](C[C@@H](C)C=C1C=C[C@H](C)[C@@H]2CC[C@@H]1C[C@@H](O)CC(=O)O1)OC(=O)C(C)(C)CC Synthesis ReferenceShieh-Shung J. Chen, Byron H. Arison, "Process for the preparation of 3-keto, 5-hydroxy simvastatin analogs." U.S. Patent US4965200, issued April, 1981. US4965200General References
DrugBank does not sell nor buy drugs. Pricing information is supplied for informational purposes only. Patents
ADMET data is predicted using admetSAR, a free tool for evaluating chemical ADMET properties. (23092397) Mass Spec (NIST)Not AvailableSpectra
TargetsBuild, predict & validate machine-learning models Use our structured and evidence-based datasets to unlock new Use our structured and evidence-based datasets to unlock new insights and accelerate drug research. KindProteinOrganismHumansPharmacological action Yes ActionsInhibitor General FunctionNadph bindingSpecific FunctionTransmembrane glycoprotein that is the rate-limiting enzyme in cholesterol biosynthesis as well as in the biosynthesis of nonsterol isoprenoids that are essential for normal cell function including...Gene NameHMGCRUniprot IDP04035Uniprot Name3-hydroxy-3-methylglutaryl-coenzyme A reductaseMolecular Weight97475.155 Da References
KindProtein OrganismHumansPharmacological action Unknown ActionsInhibitory allosteric modulator General FunctionMetal ion bindingSpecific FunctionIntegrin alpha-L/beta-2 is a receptor for ICAM1, ICAM2, ICAM3 and ICAM4. It is involved in a variety of immune phenomena including leukocyte-endothelial cell interaction, cytotoxic T-cell mediated ...Gene NameITGALUniprot IDP20701Uniprot NameIntegrin alpha-LMolecular Weight128768.495 Da References
KindProteinOrganismHumansPharmacological action Unknown ActionsInhibitor General FunctionTranscription factor bindingSpecific FunctionResponsible for the deacetylation of lysine residues on the N-terminal part of the core histones (H2A, H2B, H3 and H4). Histone deacetylation gives a tag for epigenetic repression and plays an impo...Gene NameHDAC2Uniprot IDQ92769Uniprot NameHistone deacetylase 2Molecular Weight55363.855 Da References
EnzymesKindProteinOrganismHumansPharmacological action Unknown ActionsSubstrate General FunctionVitamin d3 25-hydroxylase activitySpecific FunctionCytochromes P450 are a group of heme-thiolate monooxygenases. In liver microsomes, this enzyme is involved in an NADPH-dependent electron transport pathway. It performs a variety of oxidation react...Gene NameCYP3A4Uniprot IDP08684Uniprot NameCytochrome P450 3A4Molecular Weight57342.67 Da References
Kind ProteinOrganismHumansPharmacological action Unknown ActionsSubstrate General FunctionOxygen bindingSpecific FunctionCytochromes P450 are a group of heme-thiolate monooxygenases. In liver microsomes, this enzyme is involved in an NADPH-dependent electron transport pathway. It oxidizes a variety of structurally un...Gene NameCYP3A5Uniprot IDP20815Uniprot NameCytochrome P450 3A5Molecular Weight57108.065 Da References
KindProteinOrganismHumansPharmacological action Unknown ActionsSubstrate Inhibitor General FunctionSteroid hydroxylase activitySpecific FunctionCytochromes P450 are a group of heme-thiolate monooxygenases. In liver microsomes, this enzyme is involved in an NADPH-dependent electron transport pathway. It oxidizes a variety of structurally un...Gene Name CYP2C8Uniprot IDP10632Uniprot NameCytochrome P450 2C8Molecular Weight55824.275 Da References
KindProteinOrganismHumansPharmacological action Unknown ActionsInhibitor Supporting data are limited to findings of in vitro studies.General FunctionSteroid hydroxylase activitySpecific FunctionCytochromes P450 are a group of heme-thiolate monooxygenases. In liver microsomes, this enzyme is involved in an NADPH-dependent electron transport pathway. It oxidizes a variety of structurally un...Gene NameCYP2C9Uniprot IDP11712Uniprot NameCytochrome P450 2C9Molecular Weight55627.365 Da References
KindProteinOrganismHumansPharmacological action Unknown ActionsSubstrate General FunctionSteroid hydroxylase activitySpecific FunctionResponsible for the metabolism of many drugs and environmental chemicals that it oxidizes. It is involved in the metabolism of drugs such as antiarrhythmics, adrenoceptor antagonists, and tricyclic...Gene NameCYP2D6Uniprot IDP10635Uniprot NameCytochrome P450 2D6Molecular Weight55768.94 Da References
KindProteinOrganismHumansPharmacological action Unknown ActionsInhibitor Inducer General FunctionSteroid hydroxylase activitySpecific FunctionCytochromes P450 are a group of heme-thiolate monooxygenases. In liver microsomes, this enzyme is involved in an NADPH-dependent electron transport pathway. It oxidizes a variety of structurally un...Gene NameCYP2B6Uniprot IDP20813Uniprot NameCytochrome P450 2B6Molecular Weight56277.81 Da References
KindProtein OrganismHumansPharmacological action Unknown ActionsSubstrate General FunctionSteroid bindingSpecific FunctionUDPGT is of major importance in the conjugation and subsequent elimination of potentially toxic xenobiotics and endogenous compounds. This isoform glucuronidates bilirubin IX-alpha to form both the...Gene NameUGT1A1Uniprot IDP22309Uniprot NameUDP-glucuronosyltransferase 1-1Molecular Weight59590.91 Da References
KindProteinOrganismHumansPharmacological action Unknown ActionsSubstrate General FunctionRetinoic acid bindingSpecific FunctionUDPGT is of major importance in the conjugation and subsequent elimination of potentially toxic xenobiotics and endogenous compounds. Isoform 2 lacks transferase activity but acts as a negative reg...Gene NameUGT1A3Uniprot IDP35503Uniprot NameUDP-glucuronosyltransferase 1-3Molecular Weight60337.835 Da References
KindProteinOrganismHumansPharmacological action Unknown ActionsSubstrate General FunctionGlucuronosyltransferase activity Specific FunctionUDPGT is of major importance in the conjugation and subsequent elimination of potentially toxic xenobiotics and endogenous compounds.Its unique specificity for 3,4-catechol estrogens and estriol su...Gene NameUGT2B7Uniprot IDP16662Uniprot NameUDP-glucuronosyltransferase 2B7Molecular Weight60694.12 Da References
KindProteinOrganismHumansPharmacological action Unknown ActionsSubstrate General FunctionSteroid hydroxylase activitySpecific FunctionResponsible for the metabolism of a number of therapeutic agents such as the anticonvulsant drug S-mephenytoin, omeprazole, proguanil, certain barbiturates, diazepam, propranolol, citalopram and im...Gene NameCYP2C19Uniprot IDP33261Uniprot NameCytochrome P450 2C19Molecular Weight55930.545 Da References
KindProteinOrganismHumansPharmacological action Unknown ActionsInhibitor General FunctionMethylumbelliferyl-acetate deacetylase activitySpecific FunctionInvolved in the detoxification of xenobiotics and in the activation of ester and amide prodrugs. Shows high catalytic efficiency for hydrolysis of cocaine, 4-methylumbelliferyl acetate, heroin and ...Gene NameCES2 Uniprot IDO00748Uniprot NameCocaine esteraseMolecular Weight61806.41 Da References
KindProteinOrganismHumansPharmacological action Unknown ActionsInhibitor General FunctionTriglyceride lipase activitySpecific FunctionInvolved in the detoxification of xenobiotics and in the activation of ester and amide prodrugs. Hydrolyzes aromatic and aliphatic esters, but has no catalytic activity toward amides or a fatty acy...Gene NameCES1Uniprot IDP23141Uniprot NameLiver carboxylesterase 1Molecular Weight62520.62 Da References
TransportersKindProteinOrganismHumansPharmacological action Unknown ActionsInhibitor General FunctionXenobiotic-transporting atpase activitySpecific FunctionEnergy-dependent efflux pump responsible for decreased drug accumulation in multidrug-resistant cells.Gene NameABCB1Uniprot IDP08183Uniprot Name Multidrug resistance protein 1Molecular Weight141477.255 Da References
KindProteinOrganismHumansPharmacological action Unknown ActionsInhibitor General FunctionSodium-independent organic anion transmembrane transporter activitySpecific FunctionMediates the Na(+)-independent transport of organic anions such as sulfobromophthalein (BSP) and conjugated (taurocholate) and unconjugated (cholate) bile acids (By similarity). Selectively inhibit...Gene NameSLCO1A2Uniprot IDP46721Uniprot NameSolute carrier organic anion transporter family member 1A2Molecular Weight74144.105 Da References
KindProteinOrganismHumansPharmacological action Unknown ActionsSubstrate Inhibitor General FunctionSodium-independent organic anion transmembrane transporter activitySpecific FunctionMediates the Na(+)-independent uptake of organic anions such as pravastatin, taurocholate, methotrexate, dehydroepiandrosterone sulfate, 17-beta-glucuronosyl estradiol, estrone sulfate, prostagland...Gene NameSLCO1B1Uniprot IDQ9Y6L6Uniprot NameSolute carrier organic anion transporter family member 1B1Molecular Weight76447.99 Da References
KindProteinOrganismHumansPharmacological action Unknown ActionsSubstrate General FunctionOrganic anion transmembrane transporter activitySpecific FunctionMediates hepatobiliary excretion of numerous organic anions. May function as a cellular cisplatin transporter.Gene NameABCC2Uniprot IDQ92887Uniprot NameCanalicular multispecific organic anion transporter 1Molecular Weight174205.64 Da References
KindProteinOrganismHumansPharmacological action No ActionsSubstrate General FunctionTransporter activitySpecific Function Involved in the ATP-dependent secretion of bile salts into the canaliculus of hepatocytes.Gene NameABCB11Uniprot IDO95342Uniprot NameBile salt export pumpMolecular Weight146405.83 Da References
KindProteinOrganismHumansPharmacological action Unknown General FunctionSodium-independent organic anion transmembrane transporter activitySpecific FunctionMediates the Na(+)-independent transport of organic anions such as taurocholate, the prostaglandins PGD2, PGE1, PGE2, leukotriene C4, thromboxane B2 and iloprost.Gene NameSLCO2B1Uniprot IDO94956Uniprot NameSolute carrier organic anion transporter family member 2B1Molecular Weight76709.98 Da References
KindProteinOrganismHumansPharmacological action Unknown General FunctionSodium-independent organic anion transmembrane transporter activitySpecific FunctionMediates the Na(+)-independent uptake of organic anions such as 17-beta-glucuronosyl estradiol, taurocholate, triiodothyronine (T3), leukotriene C4, dehydroepiandrosterone sulfate (DHEAS), methotre...Gene NameSLCO1B3Uniprot IDQ9NPD5Uniprot NameSolute carrier organic anion transporter family member 1B3Molecular Weight77402.175 Da References
Drug created at June 13, 2005 13:24 / Updated at October 25, 2022 10:47 What is simvastatin prescribed for?Simvastatin: a medicine to treat high cholesterol - NHS.
When should you not take simvastatin?Your doctor will probably tell you not to take simvastatin if you have liver disease or if the tests show that you may be developing liver disease. tell your doctor if you drink more than two alcoholic beverages per day, if you are 65 years of age or older, or if you are Asian, especially if you are Chinese.
Who needs to take simvastatin?Who needs to take statins?. Have high cholesterol (LDL above 190 mg/dL) that exercise and diet changes couldn't reduce.. Had a stroke, heart attack or peripheral artery disease.. Have diabetes and an LDL of at least 70 mg/dL and are 40 to 75 years old.. What is simvastatin used for and side effects?Simvastatin is used together with a proper diet to treat high cholesterol and triglyceride (fat) levels in the blood. This medicine may help prevent medical problems (eg, heart or blood vessel problems, heart attacks, or strokes) caused by clogged blood vessels.
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