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| Â | MedlinePlus Drug Information: HMG-CoA Reductase Inhibitors (Systemic) |
 | | These medicines belong to the group of medicines called 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors. |  | | Children— Studies on this medicine have been done only in adult patients, and there is no specific information comparing use of HMG-CoA reductase inhibitors in children with use in other age groups. |  | | HMG-CoA reductase inhibitor --Atorvastatin; Cerivastatin #; Fluvastatin; Lovastatin; Pravastatin; Simvastatin |
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http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202284.html
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| Â | Texas Medicaid Vendor Drug Program, HMG-CoA Reductase Inhibitors |
 | | If atorvastatin, cerivastatin, lovastatin or simvastatin are used in concurrently with nefazodone, conservative HMG-CoA reductase inhibitor doses are recommended in addition to close monitoring for skeletal muscle damage (e.g., muscle pain, weakness, elevated muscle enzymes). |  | | Concurrent use of cyclosporine (or other immunosuppressive therapy) and lovastatin is not recommended and will be reviewed. |  | | Combined therapy with lovastatin or simvastatin and either itraconazole or ketoconazole is not recommended and will be reviewed. |
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http://www.hhsc.state.tx.us/HCF/vdp/Criteria/hmg-coa.html
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| Â | Texas Medicaid Vendor Drug Program, HMG-CoA Reductase Inhibitors |
 | | Patients requiring concurrent therapy with certain HMG CoA reductase inhibitors and some macrolide antibiotics should be monitored regularly for muscular symptoms such as pain, tenderness, or weakness. |  | | Fluvastatin and pravastatin appear to be less likely to interact with nefazodone and may be reasonable alternatives in patients requiring both nefazodone and HMG-CoA reductase inhibitor therapy. |  | | Due to an unknown mechanism, gemfibrozil treatment used concomitantly with an HMG-CoA reductase inhibitor substantially increases the risk of myopathy and life-threatening rhabdomyolysis to 3-5%. |
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http://www.hhsc.state.tx.us/HCF/vdp/Criteria/hmg-coa.html
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| Â | 5399a48_IND_molinate.doc |
 | | In times of demand the mouse is able to utilise the hydroxymethyl-glutaryl-CoA (HMG CoA) reductase/synthase pathway of endogenous cholesterol synthesis while upregulation of this pathway has been demonstrated to be poor in the rat. |  | | In studies comparing the responses of rat, hamster and rabbit adrenocortical cells to ACTH stimulation Spady and Dietschy (16) found that rat steroidogenic cells preferentially used HDL cholesterol from the culture medium while the ability to utilise the HMG CoA reductase pathway was extremely limited. |  | | In those species which use LDL cholesterol for steroidogenesis, or which can use de novo synthesis of cholesterol from the HMG CoA reductase/synthase pathway, molinate sulphoxide, even if produced, will not inhibit cholesterol availability and the steroidogenic cells are able to undergo steroidogenesis as normal. |
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http://ecb.jrc.it/classlab/5399a48_IND_molinate.doc
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| Â | 7-Dehydrocholesterol-dependent proteolysis of HMG-CoA reductase suppresses sterol biosynthesis in a mouse model of Smith-Lemli-Opitz/RSH syndrome -- Fitzky et al. 108 (6): 905 -- Journal of Clinical Investigation |
 | | HMG-CoA reductase, LDL receptor, and sterol response elementbinding |  | | reductase, HMG-CoA synthase, LDL receptor (LDLR), and squalene |  | | Northern blot analysis of (a) hepatic HMG-CoA reductase, HMG-CoA synthase, squalene synthase, LDLR, SREBP-1, and SREBP-2, and (b) RT-PCRamplified brain HMG-CoA reductase and LDLR mRNA extracted from Dhcr7/, Dhcr7+/, and Dhcr7+/+ newborn mice, demonstrating that expression of all of the genes is the same in the three genotypes. |
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http://www.jci.org/cgi/content/full/108/6/905
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| Â | HMG-CoA reductase inhibitor mevastatin enhances the growth inhibitory effect of butyrate in the colorectal carcinoma cell line Caco-2 -- Wächtershäuser et al. 22 (7): 1061 -- Carcinogenesis |
 | | HMG-CoA reductase inhibitor mevastatin enhances the growth inhibitory effect of butyrate in the colorectal carcinoma cell line Caco-2 -- Wächtershäuser et al. |  | | Narisawa,T., Morotomi,M., Fukaura,Y., Hasebe,M., Ito,M. and Aizawa,R. (1996) Chemoprevention by pravastatin, a 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor, of N-methyl-N-nitrosourea-induced colon carcinogenesis in F344 rats. |  | | Lee,S.J., Ha,M.J., Lee,J., Nguyen,P., Choi,Y.H., Pirnia,F., Kang,W.K., Wang,X.F., Kim,S.J. and Trepel,J.B. (1998) Inhibition of the 3-hydroxy-3-methylglutaryl-coenzyme A reductase pathway induces p53-independent transcriptional regulation of p21(WAF1/CIP1) in human prostate carcinoma cells. |
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http://carcin.oxfordjournals.org/cgi/content/full/22/7/1061
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| Â | What is an HMG-CoA reductase inhibitor? |
 | | Wang, P.S. “HMG-CoA Reductase Inhibitors and the Risk of Hip Fractures in Elderly Patients,” Journal of the American Medical Association 283 (2000). |  | | HMG-CoA reductase inhibitors are a group of prescription drugs used to lower cholesterol, a white waxy substance that can stick to the inside of blood vessels, resulting in clogged arteries, heart disease, and strokes. |  | | These medicines work by slowing down the body’s ability to make cholesterol. |
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http://www.drugstore.com/qxa1026_332828_sespider-what_is_an_hmg_coa_reductase_inhibitor.htm
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| Â | Terpenoid |
 | | Many organisms manifacture terpenoids/isoprenoids through the HMG-CoA reductase pathway, |  | | DMAPP is a common metabolite in both pathways and and exchange of |  | | independent pathway is located in the plastids of plants. |
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http://www.infothis.com/find/Terpenoid
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| Â | Dyslipidemia: HMG-CoA Reductase |
 | | The statins are metabolized by the CYP3A4 pathway. |  | | Since protease inhibitors inhibit this pathway, the resulting increased levels of statins may place patients at a greater risk for skeletal muscle toxicity. |
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http://www.hivandhepatitis.com/recent/metabolic/dyslipidemias/1h.html
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| Â | Modulatory effects of HMG-CoA reductase inhibitors in diabetic microangiopathy -- DANESH and KANWAR 18 (7): 805 -- The FASEB Journal |
 | | Evans, M., Rees, A. (2002) Effects of HMG-CoA reductase inhibitors on skeletal muscle: are all statins the same?. |  | | Vincent, L., Soria, C., Mirshahi, F., et al (2002) Cerivastatin, an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme a reductase, inhibits endothelial cell proliferation induced by angiogenic factors in vitro and angiogenesis in in vivo models. |  | | Blanco-Colio, L. M., Villa, A., Ortego, M., et al (2002) 3-Hydroxy-3-methyl-glutaryl coenzyme A reductase inhibitors, atorvastatin and simvastatin, induce apoptosis of vascular smooth muscle cells by downregulation of Bcl-2 expression and Rho A prenylation. |
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http://www.fasebj.org/cgi/content/full/18/7/805
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| Â | Dolichol |
 | | It is a product of the HMG-CoA reductase pathway. |
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http://www.worldhistory.com/wiki/D/Dolichol.htm
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| Â | British Journal of Pharmacology - HMG-CoA reductase inhibitors and P-glycoprotein modulation |
 | | The 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) represent an established class of drugs for the treatment of hypercholesterolaemia, with potentially fatal adverse events (such as rhabdomyolysis). |  | | Identification of a liver-specific human organic anion transporting polypeptide and identification of rat and human hydroxymethylglutaryl- CoA reductase inhibitor transporters.. |  | | It is of interest to note that the cytochrome P450 system, especially the isoform P450 3A, has an overlapping substrate specificity to that of P-gp (Kim et al., 1999; Wacher et al., 1995). |
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http://www.nature.com/bjp/journal/v132/n6/full/0703920a.html
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| Â | Pravastatin, pravastatin sodium, apo pravastatin |
 | | Pravastatin is a member of the HMG-CoA reductase inhibitor family of drugs, also called "statins," such as lovastatin and simvastatin. |  | | Pravastatin is a member of the HMG-CoA reductase inhibitor family of drugs, also called “statins,” such as lovastatin and simvastatin. |  | | Pravastatin sodium is one of a new class of lipid-lowering compounds, the HMG-CoA reductase inhibitors, which reduce cholesterol biosynthesis. |
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http://www.healthinquire.com/pravastatin.html
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| Â | Pfam 16.0 : HMG-CoA_red |
 | | Complex of the catalytic portion of human hmg-coa reductase with hmg and coa |  | | Crystal structure of Pseudomonas mevalonii HMG-CoA reductase at 3.0 angstrom resolution. |  | | Although little sequence similarity is found between the transmembrane domains of HMG-CoA reductases from different species, the C-terminal catalytic domain is well conserved. |
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http://pfam.wustl.edu/cgi-bin/getdesc?name=HMG-CoA_red
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| Â | HMG-CoA_reductase_pathway |
 | | A number of drugs targets the HMG-CoA reductase pathway: |  | | The HMG-CoA reductase pathway, also known as MVA pathway or mevalonate-dependent (MAD) route, is an important cellular metabolic pathway present in virtually all organisms. |  | | Regulation of this pathway is also achieved by controlling the rate of translation of the mRNA, degradation of reductase and phosphorylation. |
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http://www.freecaviar.com/search.php?title=HMG-CoA_reductase_pathway
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| Â | Heart and Stroke Encyclopedia |
 | | HMG CoA Reductase Inhibitor Drugs — see Cholesterol-Lowering Drugs |  | | HMO (Health Maintenance Organizations) — see Managed Health Care Plans |  | | HERS (Heart and Estrogen-progestin Replacement Study) — see Estrogen and Cardiovascular Diseases in Women |
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http://www.americanheart.org/presenter.jhtml?identifier=10000056
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| Â | HMG-CoA Reductase Inhibitors Prevent Migration of Human Coronary Smooth Muscle Cells Through Suppression of Increase in Oxidative Stress -- Yasunari et al. 21 (6): 937 -- Arteriosclerosis, Thrombosis, and Vascular Biology |
 | | Soma MR, Donetti E, Parolini C, Mazzini G, Ferrari C, Fumagalli R, Paoletti R. HMG CoA reductase inhibitors: in vivo effects on carotid intimal thickening in normocholesterolemic rabbits. |  | | Hamelin BA, Turgeon J. Hydrophilicity/lipophilicity: relevance for the pharmacology and clinical effects of HMG-CoA reductase inhibitors. |  | | reductase inhibitory action than does simvastatin, have antioxidation |
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http://atvb.ahajournals.org/cgi/content/full/21/6/937
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| Â | AstraZeneca letter to The Lancet in response to publication of a letter by Public Citizen about Crestor |
 | | In response to the letter from Public Citizen (June 26, p 2189),1 rosuvastatin (Crestor) is a highly efficacious 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor (statin) with a safety profile comparable to those of other marketed statins. |  | | AstraZeneca’s ongoing review of post-marketed safety data as well as a recent review of data by health authorities worldwide, including the US Food and Drug Administration, supports this conclusion. |  | | AstraZeneca letter to The Lancet in response to publication of a letter by Public Citizen about Crestor |
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http://www.medicalnewstoday.com/medicalnews.php?newsid=10018
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