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| Simvastatin, sold under the brand name Zocor among others, is a statin, a type of lipid-lowering medication. It is used along with exercise, diet, and weight loss to decrease elevated lipid levels. It is also used to decrease the risk of heart problems in those at high risk. It is taken by mouth.
Common side effects include constipation, headaches, and nausea. Serious side effects may include muscle breakdown, liver problems, and increased blood sugar levels. A lower dose may be needed in people with kidney problems. There is evidence of harm to the developing baby when taken during pregnancy and it should not be used by those who are breastfeeding. It is in the statin class of medications and works by decreasing the manufacture of cholesterol by the liver.
Simvastatin is made from the fungus Aspergillus terreus. It was patented by Merck in 1980, and came into medical use in 1992. Simvastatin is available as a generic medication, and is on the World Health Organization's List of Essential Medicines. In 2022, it was the nineteenth most commonly prescribed medication in the United States, with more than 26 million prescriptions. |
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Read full article at Wikipedia
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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 |
| RYMZZMVNJRMUDD-HGQWONQESA-N |
| CCC(C)(C)C(=O)O[C@H]1C[C@@H](C)C=C2C=C[C@H](C)[C@H](CC[C@@H]3C[C@@H](O)CC(=O)O3)[C@@H]12 |
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EC 3.4.24.83 (anthrax lethal factor endopeptidase) inhibitor
An EC 3.4.24.* (metalloendopeptidase) inhibitor that interferes with the action of anthrax lethal factor endopeptidase (EC 3.4.24.83).
EC 1.1.1.34/EC 1.1.1.88 (hydroxymethylglutaryl-CoA reductase) inhibitor
Any EC 1.1.1.* (oxidoreductase acting on donor CH-OH group, NAD+ or NADP+ acceptor) inhibitor that inhibits HMG-CoA reductases. Hydroxymethylglutaryl-CoA reductase inhibitors have been shown to lower directly cholesterol synthesis. The Enzyme Commission designation is EC 1.1.1.34 for the NADPH-dependent enzyme and EC 1.1.1.88 for an NADH-dependent enzyme.
(via statin )
ferroptosis inducer
Any substance that induces or promotes ferroptosis (a type of programmed cell death dependent on iron and characterized by the accumulation of lipid peroxides) in organisms.
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prodrug
A compound that, on administration, must undergo chemical conversion by metabolic processes before becoming the pharmacologically active drug for which it is a prodrug.
geroprotector
Any compound that supports healthy aging, slows the biological aging process, or extends lifespan.
anticholesteremic drug
A substance used to lower plasma cholesterol levels.
(via statin )
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View more via ChEBI Ontology
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(1S,3R,7S,8S,8aR)-8-{2-[(2R,4R)-4-hydroxy-6-oxotetrahydro-2H-pyran-2-yl]ethyl}-3,7-dimethyl-1,2,3,7,8,8a-hexahydronaphthalen-1-yl 2,2-dimethylbutanoate
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2,2-dimethylbutyric acid, 8-ester with (4R,6R)-6-(2-((1S,2S,6R,8S,8aR)-1,2,6,7,8,8a-hexahydro-8-hydroxy-2,6-dimethyl-1-naphthyl)ethyl)tetrahydro-4-hydroxy-2H-pyran-2-one
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ChemIDplus
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MK-733
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KEGG DRUG
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Simvastatin
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KEGG DRUG
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Simvastatina
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ChemIDplus
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Simvastatine
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ChemIDplus
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Simvastatinum
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ChemIDplus
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Zocor
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ChemIDplus
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4768037
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Beilstein Registry Number
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Beilstein
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79902-63-9
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CAS Registry Number
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KEGG DRUG
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79902-63-9
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CAS Registry Number
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ChemIDplus
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Spindler SR, Li R, Dhahbi JM, Yamakawa A, Mote P, Bodmer R, Ocorr K, Williams RT, Wang Y, Ablao KP (2012)
Statin treatment increases lifespan and improves cardiac health in Drosophila by decreasing specific protein prenylation.
PloS one 7, e39581 [PubMed:22737247]
[show Abstract]
Statins such as simvastatin are 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors and standard therapy for the prevention and treatment of cardiovascular diseases in mammals. Here we show that simvastatin significantly increased the mean and maximum lifespan of Drosophila melanogaster (Drosophila) and enhanced cardiac function in aging flies by significantly reducing heart arrhythmias and increasing the contraction proportion of the contraction/relaxation cycle. These results appeared independent of internal changes in ubiquinone or juvenile hormone levels. Rather, they appeared to involve decreased protein prenylation. Simvastatin decreased the membrane association (prenylation) of specific small Ras GTPases in mice. Both farnesyl (L744832) and type 1 geranylgeranyl transferase (GGTI-298) inhibitors increased Drosophila lifespan. These data are the most direct evidence to date that decreased protein prenylation can increase cardiac health and lifespan in any metazoan species, and may explain the pleiotropic (non-cholesterol related) health effects of statins. | deCathelineau AM, Bokoch GM (2009)
Inactivation of rho GTPases by statins attenuates anthrax lethal toxin activity.
Infection and immunity 77, 348-359 [PubMed:18936176]
[show Abstract]
Anthrax lethal factor (LF), secreted by Bacillus anthracis, interacts with protective antigen to form a bipartite toxin (lethal toxin [LT]) that exerts pleiotropic biological effects resulting in subversion of the innate immune response. Although the mitogen-activated protein kinase kinases (MKKs) are the major intracellular protein targets of LF, the pathology induced by LT is not well understood. The statin family of HMG-coenzyme A reductase inhibitors have potent anti-inflammatory effects independent of their cholesterol-lowering properties, which have been attributed to modulation of Rho family GTPase activity. The Rho GTPases regulate vesicular trafficking, cytoskeletal dynamics, and cell survival and proliferation. We hypothesized that disruption of Rho GTPase function by statins might alter LT action. We show here that statins delay LT-induced death and MKK cleavage in RAW macrophages and that statin-mediated effects on LT action are attributable to disruption of Rho GTPases. The Rho GTPase-inactivating toxin, toxin B, did not significantly affect LT binding or internalization, suggesting that the Rho GTPases regulate trafficking and/or localization of LT once internalized. The use of drugs capable of inhibiting Rho GTPase activity, such as statins, may provide a means to attenuate intoxication during B. anthracis infection. | Glynn SA, O'Sullivan D, Eustace AJ, Clynes M, O'Donovan N (2008)
The 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors, simvastatin, lovastatin and mevastatin inhibit proliferation and invasion of melanoma cells.
BMC cancer 8, 9 [PubMed:18199328]
[show Abstract]
BackgroundA number of recent studies have suggested that cancer incidence rates may be lower in patients receiving statin treatment for hypercholesterolemia. We examined the effects of statin drugs on in vitro proliferation, migration and invasion of melanoma cells.MethodsThe ability of lovastatin, mevastatin and simvastatin to inhibit the melanoma cell proliferation was examined using cytotoxicity and apoptosis assays. Effects on cell migration and invasion were assessed using transwell invasion and migration chambers. Hypothesis testing was performed using 1-way ANOVA, and Student's t-test.ResultsLovastatin, mevastatin and simvastatin inhibited the growth, cell migration and invasion of HT144, M14 and SK-MEL-28 melanoma cells. The concentrations required to inhibit proliferation of melanoma cells (0.8-2.1 microave previously been achieved in a phase I clinical trial of lovastatin in patients with solid tumours, (45 mg/kg/day resulted in peak plasma concentrations of approximately 3.9 microConclusionOur results suggest that statin treatment is unlikely to prevent melanoma development at standard doses. However, higher doses of statins may have a role to play in adjuvant therapy by inhibiting growth and invasion of melanoma cells. | Ahn KS, Sethi G, Chaturvedi MM, Aggarwal BB (2008)
Simvastatin, 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, suppresses osteoclastogenesis induced by receptor activator of nuclear factor-kappaB ligand through modulation of NF-kappaB pathway.
International journal of cancer 123, 1733-1740 [PubMed:18688862]
[show Abstract]
Simvastatin, an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, is a cholesterol-lowering drug that may play a role in bone metabolism through a mechanism that is not fully understood. Recently, receptor activator of NF-kappaB ligand (RANKL), a member of the TNF superfamily, has emerged as a major mediator of bone loss via activation of osteoclastogenesis. The latter is also associated with certain cancers such as multiple myeloma and breast cancer. Whether simvastatin can modulate RANKL-induced or cancer induced osteoclastogenesis was investigated. The effect of simvastatin on RANKL signaling and consequent osteoclastogenesis was investigated. RANKL induced NF-kappaB activation, whereas pretreatment with simvastatin completely suppressed such activation and correlated with suppression of RANKL-induced activation of IkappaBalpha kinase, IkappaBalpha phosphorylation and IkappaBalpha degradation. Similarly, RANKL induced the differentiation of monocytic cells to osteoclasts, whereas simvastatin suppressed it. The inhibition was maximal when cells were exposed to both simvastatin and RANKL simultaneously and minimal when simvastatin was added 1 day after RANKL treatment. Simvastatin also inhibited the osteoclastogenesis induced by human breast cancer and by multiple myeloma cells. Together, our results indicate that simvastatin inhibits the RANKL-induced NF-kappaB activation pathway that leads to suppression of osteoclastogenesis induced by RANKL and by tumor cells, thereby suggesting its therapeutic potential in osteoporosis and in cancer-related bone loss. | Wolozin B, Wang SW, Li NC, Lee A, Lee TA, Kazis LE (2007)
Simvastatin is associated with a reduced incidence of dementia and Parkinson's disease.
BMC medicine 5, 20 [PubMed:17640385]
[show Abstract]
BackgroundStatins are a class of medications that reduce cholesterol by inhibiting 3-hydroxy-3-methylglutaryl-coenzyme A reductase. Whether statins can benefit patients with dementia remains unclear because of conflicting results. We hypothesized that some of the confusion in the literature might arise from differences in efficacy of different statins. We used a large database to compare the action of several different statins to investigate whether some statins might be differentially associated with a reduction in the incidence of dementia and Parkinson's disease.MethodsWe analyzed data from the decision support system of the US Veterans Affairs database, which contains diagnostic, medication and demographic information on 4.5 million subjects. The association of lovastatin, simvastatin and atorvastatin with dementia was examined with Cox proportional hazard models for subjects taking statins compared with subjects taking cardiovascular medications other than statins, after adjusting for covariates associated with dementia or Parkinson's disease.ResultsWe observed that simvastatin is associated with a significant reduction in the incidence of dementia in subjects > or =65 years, using any of three models. The first model incorporated adjustment for age, the second model included adjusted for three known risk factors for dementia, hypertension, cardiovascular disease or diabetes, and the third model incorporated adjustment for the Charlson index, which is an index that provides a broad assessment of chronic disease. Data were obtained for over 700,000 subjects taking simvastatin and over 50,000 subjects taking atorvastatin who were aged >64 years. Using model 3, the hazard ratio for incident dementia for simvastatin and atorvastatin are 0.46 (CI 0.44-0.48, p < 0.0001) and 0.91 (CI 0.80-1.02, p = 0.11), respectively. Lovastatin was not associated with a reduction in the incidence of dementia. Simvastatin also exhibited a reduced hazard ratio for newly acquired Parkinson's disease (HR 0.51, CI 0.4-0.55, p < 0.0001).ConclusionSimvastatin is associated with a strong reduction in the incidence of dementia and Parkinson's disease, whereas atorvastatin is associated with a modest reduction in incident dementia and Parkinson's disease, which shows only a trend towards significance. | Finsterer J, Zuntner G (2005)
Rhabdomyolysis from Simvastatin triggered by infection and muscle exertion.
Southern medical journal 98, 827-829 [PubMed:16144183]
[show Abstract]
A 42-year-old woman received a 6-month course of simvastatin (20 mg/d) for hypercholesterolemia. Despite an infection with fever, fatigue, myalgias, and lumbar pain, she continued to perform her regular sports activities. Neurologic examination revealed bilateral ptosis and slight upper limb weakness. Serum creatine kinase was 41,000 U/L. Needle electromyography was nonspecifically abnormal. Discontinuation of simvastatin and reduction of the sports activities was followed by a prompt continual lowering of the elevated muscle enzymes to normal values over a 2-week period. The patient's infection, regular sports activity despite the infection, and a suspected mitochondrial defect were regarded as triggers of rhabdomyolysis. | Ucar M, Neuvonen M, Luurila H, Dahlqvist R, Neuvonen PJ, Mjörndal T (2004)
Carbamazepine markedly reduces serum concentrations of simvastatin and simvastatin acid.
European journal of clinical pharmacology 59, 879-882 [PubMed:14691614]
[show Abstract]
ObjectiveThe aim of this study was to examine the effect of carbamazepine on the pharmacokinetics of orally administered simvastatin in healthy volunteers.MethodsIn a randomised, two-phase crossover study and a wash out of 2 weeks, 12 healthy volunteers took carbamazepine for 14 days (600 mg daily except 200 mg daily for the first 2 days) or no drug. On day 15, each subject ingested 80 mg simvastatin. Serum concentrations of simvastatin and its active metabolite simvastatin acid were measured up to 24 h.ResultsCarbamazepine decreased the mean total area under the serum concentration-time curve of simvastatin and simvastatin acid by 75% ( P<0.001) and 82% ( P<0.001), respectively. The mean peak concentrations of both simvastatin and simvastatin acid were reduced by 68% ( P<0.01), and half-life of simvastatin acid was shortened from 5.9+/-0.3 h to 3.7+/-0.5 h ( P<0.01) by carbamazepine.ConclusionCarbamazepine greatly reduces the serum concentrations of simvastatin and simvastatin acid, probably by inducing their metabolism. Concomitant administration of carbamazepine and simvastatin should be avoided or the dose of simvastatin should be considerably increased. | Hwang R, Lee EJ, Kim MH, Li SZ, Jin YJ, Rhee Y, Kim YM, Lim SK (2004)
Calcyclin, a Ca2+ ion-binding protein, contributes to the anabolic effects of simvastatin on bone.
The Journal of biological chemistry 279, 21239-21247 [PubMed:14973129]
[show Abstract]
In vitro treatment with a pharmacological dose of simvastatin, a potent pro-drug of a 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor, stimulates bone formation. In our study, simvastatin stimulated differentiation of osteoblasts remarkably in a dose-dependent manner, with minimal effect on proliferation. To identify the mediators of the anabolic effects of simvastatin on osteoblasts, we tried to identify and characterize simvastatin-induced proteins by using proteomic analysis. Calcyclin was significantly up-regulated by more than 10 times, and annexin I was also up-regulated by simvastatin. However, annexin III, vimentin, and tropomyosin were down-regulated. Up-regulated calcyclin mRNA by simvastatin was validated by reverse transcription in mouse calvarial cells. In confocal microscope analysis, green fluorescence protein-calcyclin fusion protein was ubiquitously observed in the of MC3T3-E1 cells transfected with green fluorescence protein-calcyclin cDNA containing plasmid and was quickly concentrated in the nucleus 20 min after simvastatin treatment. Overexpression of calcyclin cDNA stimulated both the proliferation and expression of alkaline phosphatase mRNA significantly, without exposure to simvastatin in MC3T3-E1 cells. However, both the rate of proliferation of the osteoblasts and the expression of alkaline phosphatase mRNA were suppressed significantly 1 day after treatment with the calcyclin-specific small interference RNA, and furthermore, simvastatin did not overcome this suppression in the small interference RNA-pretreated MC3T3-E1 cells. In conclusion, calcyclin is one of the candidate proteins that plays a role in osteoblastogenesis in response to simvastatin, although the precise functions of calcyclin in osteoblast remain to be verified. | Qin XZ (2003)
Collision-induced dissociation of the negative ions of simvastatin hydroxy acid and related species.
Journal of mass spectrometry : JMS 38, 677-686 [PubMed:12827636]
[show Abstract]
Simvastatin hydroxy acid (1) is a well-known, potent HMG-CoA reductase inhibitor for the treatment of hypercholesterolemia. Its lactone, simvastatin (commercial name Zocor) (a prodrug of 1), has been widely prescribed in the USA and throughout the world. In this work, collision-induced dissociation (CID) of the negative ion of 1 (m/z 435), a carboxylic anion, was analyzed in detail. The major fragmentation pathway of this ion is a novel de-esterification to form the negative product ions at m/z 319 and 115. The ion at m/z 319 undergoes further collision-induced rearrangements to form the negative ions at m/z 215, 159 and 85. Possible mechanisms of the de-esterification are discussed in terms of both charge-initiated and charge-remote fragmentations. The de-esterification of the negative ion of 1 and the rearrangements of the ion at m/z 319 are rationalized by charge transfer and negative-charge initiated fragmentation. This study deepens our understanding of collision-induced fragmentations of carboxylic anions with multi-functional groups. A comparison of the CID data for the negative ions of 1 and 5 (a major oxidation degradate of 1) indicates that the analysis of the CID data for 1 can serve as a basis for identification of oxidation degradation products or metabolites of 1. The analysis of the CID data for the negative ion of 1 also reveals the fundamental characteristics of the CID data for the negative ions of other statin hydroxy acids such as lovastatin (3) and pravastatin (4). | Zapata R, Piulachs MD, Bellés X (2003)
Inhibitors of 3-hydroxy-3-methylglutaryl-CoA reductase lower fecundity in the German cockroach: correlation between the effects on fecundity in vivo with the inhibition of enzymatic activity in embryo cells.
Pest management science 59, 1111-1117 [PubMed:14561068]
[show Abstract]
The enzyme 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase is crucial to insect development and reproduction, as revealed by the sterilising properties of some specific inhibitors of it. In the present paper, we study the sterilising effects of a number of HMG-CoA reductase inhibitors on the German cockroach, Blattella germanica (L). The inhibitors tested were naringenin, lovastatin, mevastatin, simvastatin, atorvastatin and fluvastatin. The first two compounds were ineffective or scarcely effective as HMG-CoA reductase inhibitors. The most active compounds in vivo were fluvastatin and atorvastatin, followed by simvastatin and mevastatin. They were equally ranked when tested as HMG-CoA reductase inhibitors in the B germanica embryonic derived cell line UM-BGE-1. This suggests that this cell line may be an appropriate tool for testing HMG-CoA reductase inhibitors and so to predict their properties as insect sterilising agents with insecticide potential. | Hess DC, Fagan SC (2001)
Pharmacology and clinical experience with simvastatin.
Expert opinion on pharmacotherapy 2, 153-163 [PubMed:11336576]
[show Abstract]
Simvastatin (Zocortrade mark, Merck) is a safe and effective 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor. Simvastatin potently lowers total and low density lipoprotein (LDL) cholesterol. Simvastatin was the first cholesterol-lowering agent that reduced total mortality in a randomised clinical trial. Simvastatin is effective at reducing total mortality, myocardial infarction, coronary mortality and the incidence of stroke or transient ischemic attack in patients with coronary heart disease and hypercholesterolemia. Simvastatin, like other statins, also has non-lipid mechanisms of action. These include anti-inflammatory effects, antiproliferative effects on smooth muscle cells and an upregulation of endothelial nitric oxide synthase. Overall, simvastatin has an excellent safety profile. Simvastatin, along with other statins, has made a significant impact on the morbidity and mortality from coronary heart disease. |
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